Clinical Applications of Electrocardiography

*Practical Applications of Electrocardiogram*

[17] Zheng J, Zhang W, Luo J, Zhou W, Shen R. Variant map system to simulate complex properties of DNA interactions using binary sequences. Advances in

[18] Zheng J, Luo J, Zhou W. Pseudo DNA sequence generation of noncoding distributions using variant maps on cellular automata. Applied

[19] Zheng J, Zhang W, Luo J, Zhou W, Liesaputra V. Variant map construction to detect symmetric properties of genomes on 2D distributions. Journal of Data Mining in Genomics &

[20] Heim D, Heim O, Zeng PA, Zheng J. Successful creation of regular patterns in variant maps from bat echolocation calls. Biological Systems: Open Access.

[21] Ji Y, Zheng J, Xie Y, Shou T. Variant maps on normal and abnormal ECG data sequences. Biology and Medicine

[22] Hou Z, Zheng J. Mapping ECG signals on variant maps. In: Proceedings of the 2017 IEEE/ACM International Conference on Advances in Social Networks Analysis and Mining

(ASONAM'17); 31 July–03 August 2017;

Sydney, Australia: ACM; 2017

BMEI'10); 14-16; IEEE; 2017

Springer-Nature. 2019. DOI: 10.1007/978-981-13-2282-2

[24] Zheng J. Variant construction from theoretical foundation to applications.

[23] Hou Z, Zheng J. Visualization of P wave characteristics in ECG. In: Proceedings of the 2017 IEEE International Conference on Image and Signal Processing, Biomedical Engineering and Informatics (CISP-

Pure Mathematics. 2013;**3**:5

Mathematics. 2014;**5**:153

Proteomics. 2014;**5**:1

(Aligarh). 2016;**8**:336

2016;**5**:166

**58**

Chapter 4

Abstract

variant maps

1. Introduction

the test results more conveniently.

61

Characteristics of Atrial Premature

Beat ECG Signals on Variant Maps

Premature heartbeat is also known as extrasystole. It means the foundation of sinus or ectopic heart rhythm, a certain pacemaker in the heart excitable earlier than the basic rhythm, cause the heart to be local or all happening prematurely remove pole. Premature atrial beats may lead to cardiomyopathy. The experimental data in this chapter are provided by Xishan People's Hospital of Wuxi city, including normal ECG signals and abnormal ECG signals (atrial premature beat). The two types of ECG data sequences are processed experimentally through the variant measurement model, and the differences in the variant maps are compared.

Keywords: atrial premature beat, ECG signal, data sequence, arrhythmia,

beat ECG signals obtained through variant measurement schemes.

of feature clustering to study the variant measurement of ECG signal data sequences. ECG signal utilizes multivalued logic function and variant principle to form variant logic symbol on n-element ECG signal sequence and output variant maps and observe the difference between different ECG signal data. The obtained variant maps can analyze the ECG data from the macroscopic level and express the information that cannot be reflected by the traditional ECG in an intuitive way. The application of variant maps in ECG signal is an extension of the original ECG signal methods. In practical applications, it is expected that the variant maps can assist the application of traditional ECG in the medical field and help clinicians to diagnose

Cardiovascular diseases are common diseases that seriously threaten human health [1], and the mortality rate caused by cardiovascular diseases continues to increase globally. ECG signal is the direct response of heart activity and the most effective way to analyze cardiovascular diseases. The object of this chapter is the atrial premature beat ECG signal in atrial arrhythmia. The experimental method is variant measurement model [2]. The provider of ECG data is Xishan People's Hospital of Wuxi city, Jiangsu Province China, and the later calibrator of ECG data is the First People's Hospital of Yunnan Province China. This chapter includes relevant background to introduce atrial premature beat [3], variant measurement model, experimental data, and variant maps of atrial premature beat signals. There is a significant difference between the variant maps of normal and atrial premature

This chapter uses the variant measurement model and the visualization method

Lihua Leng, Jeffery Zheng and Jing Zhang

#### Chapter 4

## Characteristics of Atrial Premature Beat ECG Signals on Variant Maps

Lihua Leng, Jeffery Zheng and Jing Zhang

#### Abstract

Premature heartbeat is also known as extrasystole. It means the foundation of sinus or ectopic heart rhythm, a certain pacemaker in the heart excitable earlier than the basic rhythm, cause the heart to be local or all happening prematurely remove pole. Premature atrial beats may lead to cardiomyopathy. The experimental data in this chapter are provided by Xishan People's Hospital of Wuxi city, including normal ECG signals and abnormal ECG signals (atrial premature beat). The two types of ECG data sequences are processed experimentally through the variant measurement model, and the differences in the variant maps are compared.

Keywords: atrial premature beat, ECG signal, data sequence, arrhythmia, variant maps

#### 1. Introduction

Cardiovascular diseases are common diseases that seriously threaten human health [1], and the mortality rate caused by cardiovascular diseases continues to increase globally. ECG signal is the direct response of heart activity and the most effective way to analyze cardiovascular diseases. The object of this chapter is the atrial premature beat ECG signal in atrial arrhythmia. The experimental method is variant measurement model [2]. The provider of ECG data is Xishan People's Hospital of Wuxi city, Jiangsu Province China, and the later calibrator of ECG data is the First People's Hospital of Yunnan Province China. This chapter includes relevant background to introduce atrial premature beat [3], variant measurement model, experimental data, and variant maps of atrial premature beat signals. There is a significant difference between the variant maps of normal and atrial premature beat ECG signals obtained through variant measurement schemes.

This chapter uses the variant measurement model and the visualization method of feature clustering to study the variant measurement of ECG signal data sequences. ECG signal utilizes multivalued logic function and variant principle to form variant logic symbol on n-element ECG signal sequence and output variant maps and observe the difference between different ECG signal data. The obtained variant maps can analyze the ECG data from the macroscopic level and express the information that cannot be reflected by the traditional ECG in an intuitive way. The application of variant maps in ECG signal is an extension of the original ECG signal methods. In practical applications, it is expected that the variant maps can assist the application of traditional ECG in the medical field and help clinicians to diagnose the test results more conveniently.

#### 2. Relevant background

#### 2.1 Atrial premature beats

Atrial arrhythmia is the most common arrhythmia clinically, which refers to a kind of arrhythmia caused by conduction obstruction when ectopic excitations are located in the atrium or conduction system passing through the atrium. It is mainly active arrhythmia, and atrial premature beat is the most common type of atrial arrhythmia. Atrial premature beats can be seen in normal healthy people, but in healthy people, there are few frequent atrial premature beats [4]. Atrial premature beats is more common in organic heart disease patients, Hyperthyroidism, Coronary heart disease, Cardiomyopathy patients if frequent atrial premature beat, is the precursor of Atrial fibrillation, Acute myocardial infarction can also occur frequent atrial premature beat. Figure 1 shows the comparison between normal ECG and atrial premature beat ECG.

. The transformation rules of the four variant symbols are shown in Table 1. Therefore, in this chapter, long ECG signal is converted into long

The variant measurement model describes the measurement as the four meta symbols: . The 16 subsets of meta symbol set are as follows: , , , , , , , , , , , , , , , and .

If any measure is selected as the value of in the variant maps and any measure

quantity of is defined as 0 and the corresponding definitions of 16 variant

combinations of such two-dimensional maps, which are specifically shown in Table 3. In this chapter, the three-dimensional variant maps are also adopted, and the Z-axis is added on the basis of the two-dimensional maps. The selection princi-

Variant measurement structure is composed of three components: input, processing, and output. The input ECG signal is provided by Wuxi Xishan People's Hospital. The data processing module is the core module of variant measurement and consists of variant module, statistical measurement module, and visualization

Conversion type Variant sign Statistical sign Statistical total

Sign subset Variant measure Sign subset Variant measure

is selected as the value of in the variant maps, there are a total of

Here, the statistical

variant logical operator through variant logical function.

DOI: http://dx.doi.org/10.5772/intechopen.83551

Characteristics of Atrial Premature Beat ECG Signals on Variant Maps

The 16 subsets correspond to the 16 measures:

ple is the same as the selection method of and .

2.5 ECG signal variant measurement structure

2.4 Variant visualization

measures are shown in Table 2.

Table 1.

Table 2.

63

Definition of 16 variant measures.

Variant sign conversion rule.

The picture is the atrial premature beat ECG. Patient information: male, 46 years old, arrhythmia, mean heart rate 62 bpm, early occurrence of P0 -QRS-T in limb leads, 160 ms in P'R interval, incomplete compensatory interval, such expression is a atrial premature beat.

#### 2.2 Variant measurement model

In 2010, variant model [5] was proposed with the stability of cellular automata as an example; the effect of variant and non-variant functions on binary logic functional space was explained. In 2011, the conditional probability statistical distribution of the variant measurement structure [6] is discussed. By simulating the two-state quantum interaction system, the variant two-path simulation model was established. With the continuous development of variant construction, this model has been applied in many fields: coding and non-coding DNA [7] sequence detection, random sequence testing [8], classification of cellular automata [7], classification of echolocation in bats [9], ECG signals [10, 11], and variant construction [12].

#### 2.3 Variant logic

The core theory of variant measurement model is variant logic, which is extended and evolved on the basis of classical logic. In the variant logic function, assuming that the input sequence is long , the output data sequence is N-1 according to the variant rule. On the basis of the variant logical function, the variant measurement model defines four basic variant logical symbols:

Figure 1. Atrial premature beats ECG.

. The transformation rules of the four variant symbols are shown in Table 1. Therefore, in this chapter, long ECG signal is converted into long variant logical operator through variant logical function.

#### 2.4 Variant visualization

2. Relevant background

Practical Applications of Electrocardiogram

2.1 Atrial premature beats

atrial premature beat ECG.

a atrial premature beat.

2.3 Variant logic

Figure 1.

62

Atrial premature beats ECG.

2.2 Variant measurement model

Atrial arrhythmia is the most common arrhythmia clinically, which refers to a kind of arrhythmia caused by conduction obstruction when ectopic excitations are located in the atrium or conduction system passing through the atrium. It is mainly active arrhythmia, and atrial premature beat is the most common type of atrial arrhythmia. Atrial premature beats can be seen in normal healthy people, but in healthy people, there are few frequent atrial premature beats [4]. Atrial premature beats is more common in organic heart disease patients, Hyperthyroidism, Coronary heart disease, Cardiomyopathy patients if frequent atrial premature beat, is the precursor of Atrial fibrillation, Acute myocardial infarction can also occur frequent atrial premature beat. Figure 1 shows the comparison between normal ECG and

The picture is the atrial premature beat ECG. Patient information: male, 46 years

leads, 160 ms in P'R interval, incomplete compensatory interval, such expression is

In 2010, variant model [5] was proposed with the stability of cellular automata

as an example; the effect of variant and non-variant functions on binary logic functional space was explained. In 2011, the conditional probability statistical distribution of the variant measurement structure [6] is discussed. By simulating the two-state quantum interaction system, the variant two-path simulation model was established. With the continuous development of variant construction, this model has been applied in many fields: coding and non-coding DNA [7] sequence detection, random sequence testing [8], classification of cellular automata [7], classification of echolocation in bats [9], ECG signals [10, 11], and variant construction [12].

The core theory of variant measurement model is variant logic, which is extended and evolved on the basis of classical logic. In the variant logic function, assuming that the input sequence is long , the output data sequence

function, the variant measurement model defines four basic variant logical symbols:

is N-1 according to the variant rule. On the basis of the variant logical

old, arrhythmia, mean heart rate 62 bpm, early occurrence of P0

The variant measurement model describes the measurement as the four meta symbols: . The 16 subsets of meta symbol set are as follows: , , , , , , , , , , , , , , , and . The 16 subsets correspond to the 16 measures:

Here, the statistical quantity of is defined as 0 and the corresponding definitions of 16 variant measures are shown in Table 2.

If any measure is selected as the value of in the variant maps and any measure is selected as the value of in the variant maps, there are a total of combinations of such two-dimensional maps, which are specifically shown in Table 3. In this chapter, the three-dimensional variant maps are also adopted, and the Z-axis is added on the basis of the two-dimensional maps. The selection principle is the same as the selection method of and .

#### 2.5 ECG signal variant measurement structure

Variant measurement structure is composed of three components: input, processing, and output. The input ECG signal is provided by Wuxi Xishan People's Hospital. The data processing module is the core module of variant measurement and consists of variant module, statistical measurement module, and visualization

#### Table 1.

Variant sign conversion rule.

Table 2. Definition of 16 variant measures.

#### Table 3.

Combinations of visualization of 256 variant measures.

#### Figure 2.

Structure diagram of ECG sequence variant measurement.

module. The final output is variant maps. The structure of ECG signal variant measurement is shown in Figure 2.

#### 2.6 Data processing module

The data processing module is divided into three parts: variant module, measurement statistics module, and visualization module. The variant module is the most important part of the variant measurement model. It is mainly responsible for transforming the original ECG signal sequence into the sequence of four basic variant logic symbols through mapping rules. The specific definitions of the parameters involved in the transformation process will be given in the core module. The measurement statistics module is mainly responsible for grouping the variant logical symbol sequence by setting a reasonable segment length M according to total length of the sequence. After grouping, the sequence in each group is counted and denoted as . The visualization module is to generate the final variant maps, in which the variant maps can be two-dimensional map and three-dimensional map. The specific visualization process will be given in the chapter of the core module. The structure diagram of the data processing module is shown in Figure 3.

#### 2.7 Core module

#### 2.7.1 Variant module

The variant module is the most core module in the variant measurement model. It is mainly responsible for converting the obtained ECG signal sequence into four variant logical symbol sequences through variant logic. The transformation process involves parameters , and the definition is shown in Eqs. (1)–(4).

$$X = A\_{i+1} \cdot A\_i \tag{1}$$

(3)

(4)

(5)

Considering that the difference value can reflect the increase or decrease of adjacent ECG data, the difference value of the overall ECG data can reflect the fluctuation of the sequence; the mean value can reflect the level of adjacent ECG data, so the mean value of the overall ECG data can reflect the overall level of the sequence. In the process of data transformation, the variant module selects the difference, global difference, mean, and global mean as the measurement parame-

parameter values can be calculated for the input n-long ECG signal sequence as the parameter support of the variant module. According to the mapping principle of Eq. (5), the original ECG sequence was mapped to sequence by setting

As shown in Figure 3, for n-1 long variant logic symbol sequence, set the segment length parameter , the number of groups is , and then . According to the grouping situation, the number of " " ," " ," " and " " in each group is recorded

ters. Using the parameters defined in Eqs. (1)–(4), the corresponding

Characteristics of Atrial Premature Beat ECG Signals on Variant Maps

DOI: http://dx.doi.org/10.5772/intechopen.83551

parameters.

65

Figure 3.

Structure diagram of ECG data processing.

2.7.2 Measurement statistics module

$$\mathbf{T} = \frac{\sum\_{l=1}^{N-1} |A\_{l+1} \cdot A\_l|}{N} \tag{2}$$

Characteristics of Atrial Premature Beat ECG Signals on Variant Maps DOI: http://dx.doi.org/10.5772/intechopen.83551

Figure 3. Structure diagram of ECG data processing.

module. The final output is variant maps. The structure of ECG signal variant

... ... ... ... ... ...

length M according to total length of the sequence. After grouping, the

The data processing module is divided into three parts: variant module, measurement statistics module, and visualization module. The variant module is the most important part of the variant measurement model. It is mainly responsible for transforming the original ECG signal sequence into the sequence of four basic variant logic symbols through mapping rules. The specific definitions of the parameters involved in the transformation process will be given in the core module. The measurement statistics module is mainly responsible for grouping the variant logical symbol sequence by setting a reasonable segment

...

... ...

... ...

sequence in each group is counted and denoted as . The visualization module is to generate the final variant maps, in which the variant maps can be two-dimensional map and three-dimensional map. The specific visualization process will be given in the chapter of the core module. The structure diagram of the

The variant module is the most core module in the variant measurement model. It is mainly responsible for converting the obtained ECG signal sequence into four variant logical symbol sequences through variant logic. The transformation process involves parameters , and the definition is shown in Eqs. (1)–(4).

(1)

(2)

measurement is shown in Figure 2.

Combinations of visualization of 256 variant measures.

Practical Applications of Electrocardiogram

Structure diagram of ECG sequence variant measurement.

data processing module is shown in Figure 3.

2.7 Core module

64

2.7.1 Variant module

2.6 Data processing module

Table 3.

Figure 2.

$$\mathcal{L} = \frac{A\_l + A\_{l+1}}{2} \tag{3}$$

$$N = \frac{\sum\_{l=1}^{N-1} \frac{\{A\_l + A\_{l+1}\}}{Z}}{N} \tag{4}$$

Considering that the difference value can reflect the increase or decrease of adjacent ECG data, the difference value of the overall ECG data can reflect the fluctuation of the sequence; the mean value can reflect the level of adjacent ECG data, so the mean value of the overall ECG data can reflect the overall level of the sequence. In the process of data transformation, the variant module selects the difference, global difference, mean, and global mean as the measurement parameters. Using the parameters defined in Eqs. (1)–(4), the corresponding parameter values can be calculated for the input n-long ECG signal sequence as the parameter support of the variant module. According to the mapping principle of Eq. (5), the original ECG sequence was mapped to sequence by setting parameters.

$$\begin{cases} if \quad X > T \quad and \quad X > 0 \colon B\_{l} = + \\ if \quad X > T \quad and \quad X \le 0 \colon B\_{l} = - \\ if \quad X \le T \quad and \quad L > V \colon B\_{l} = \top \\ if \quad X \le T \quad and \quad L \le V \colon B\_{l} = \bot \end{cases} \tag{5}$$

#### 2.7.2 Measurement statistics module

As shown in Figure 3, for n-1 long variant logic symbol sequence, set the segment length parameter , the number of groups is , and then . According to the grouping situation, the number of " " ," " ," " and " " in each group is recorded as " ", " ", " " and " ", " " represents the number of statistics of the variant logic symbol " " in this group. After statistical process, the whole output group is generated . For each set of statistical results, including meet long variant logical symbol sequence is converted into S group statistical array .

4. Experimental results

Figure 5.

Figure 6.

67

4.1 Two-dimensional overall maps

DOI: http://dx.doi.org/10.5772/intechopen.83551

As shown in Figure 5, the red diagram on the left is a variant map of normal ECG signals; the blue on the right is a variant map of atrial premature ECG signals,

Characteristics of Atrial Premature Beat ECG Signals on Variant Maps

Overall two-dimensional maps of normal ECG data and atrial premature beat.

Two-dimensional combination maps of normal ECG data and atrial premature beat.

#### 2.7.3 Visualization module

The visualization module determines the selection of coordinates and generates a variant graph. According to the results obtained from the measurement statistics module and the definition of variant visualization, this chapter selects overall two-dimensional maps, two-dimensional combination maps, and threedimensional combination maps to display the visualization results. The overall twodimensional maps define normal and abnormal ECG signals as of 256 combinations, respectively. The two-dimensional combination maps is to form the scatter diagram of normal and abnormal ECG signals by the same mapping method, and it is easier to observe the differences between them on the same maps. Threedimensional combination maps are a combination method added on the basis of two-dimensional combination maps. In three-dimensional space, the characteristics between normal ECG signal and abnormal ECG signal are more abundant.

#### 3. Data sets

The ECG data is provided by the people's hospital of Wuxi Xishan. The CB series ECG review analyzer is used to measure blood pressure of ECG data. Through the system of the patient's ECG information is stored in 18 data files, one of .dat files is stored in the patient's ECG data, by reviewing the ECG blood pressure of CB series data of ECG analysis system is read as shown in Figure 4.

As shown in Figure 4, the patient's ECG was collected with three-lead, and the heart rate data of CH1 lead was recorded at a sampling point of 1.5 s on average. The ECG signal was imported into the database for variant measurement experiment. This set of ECG data includes 105 patients. By analyzing the diagnosis results of each patient, this data set can be divided into two categories: normal and abnormal.  In this chapter, atrial premature beat and normal ECG data were selected for variant measurement.

Figure 4. ECG data diagram of Xishan People's Hospital.

Characteristics of Atrial Premature Beat ECG Signals on Variant Maps DOI: http://dx.doi.org/10.5772/intechopen.83551

### 4. Experimental results

as " ", " ", " " and " ", " " represents the number of statistics of the variant logic symbol " " in this group. After statistical process, the whole output group is

meet long variant logical sym-

The visualization module determines the selection of coordinates and generates a variant graph. According to the results obtained from the measurement statistics module and the definition of variant visualization, this chapter selects overall two-dimensional maps, two-dimensional combination maps, and threedimensional combination maps to display the visualization results. The overall twodimensional maps define normal and abnormal ECG signals as of 256 combinations, respectively. The two-dimensional combination maps is to form the scatter diagram of normal and abnormal ECG signals by the same mapping method, and it is easier to observe the differences between them on the same maps. Threedimensional combination maps are a combination method added on the basis of two-dimensional combination maps. In three-dimensional space, the characteristics

generated . For each set of statistical results, including

bol sequence is converted into S group statistical array .

between normal ECG signal and abnormal ECG signal are more abundant.

data of ECG analysis system is read as shown in Figure 4.

The ECG data is provided by the people's hospital of Wuxi Xishan. The CB series ECG review analyzer is used to measure blood pressure of ECG data. Through the system of the patient's ECG information is stored in 18 data files, one of .dat files is stored in the patient's ECG data, by reviewing the ECG blood pressure of CB series

As shown in Figure 4, the patient's ECG was collected with three-lead, and the heart rate data of CH1 lead was recorded at a sampling point of 1.5 s on average. The ECG signal was imported into the database for variant measurement experiment. This set of ECG data includes 105 patients. By analyzing the diagnosis results of each patient, this data set can be divided into two categories: normal and abnormal.  In this chapter, atrial premature beat and normal ECG data were selected for variant measurement.

2.7.3 Visualization module

Practical Applications of Electrocardiogram

3. Data sets

Figure 4.

66

ECG data diagram of Xishan People's Hospital.

#### 4.1 Two-dimensional overall maps

As shown in Figure 5, the red diagram on the left is a variant map of normal ECG signals; the blue on the right is a variant map of atrial premature ECG signals,

Figure 5. Overall two-dimensional maps of normal ECG data and atrial premature beat.

Figure 6. Two-dimensional combination maps of normal ECG data and atrial premature beat.

with the same mapping of , formed when the insets. At the top of each small map is the mapping mode corresponding to that diagram.

4.3 Three-dimensional combination maps

DOI: http://dx.doi.org/10.5772/intechopen.83551

Characteristics of Atrial Premature Beat ECG Signals on Variant Maps

sum of the three subsets.

Figure 8.

69

Three-dimensional combination maps of normal ECG data and atrial premature beat.

As shown in Figures 8–10, the three-dimensional combination maps are a combination of the normal ECG signal and the atrial premature beat ECG signal in the three-dimensional space. The mode of the (X, Y, Z) combination in Figure 8 is the combination of (X, Y, Z) in Figure 9 is and the

combination of (X, Y, Z) in Figure 10 is ; the values of X and Y are both defined as the sum of the two subsets, and the values of Z are all limited to the

#### 4.2 Two-dimensional combination maps

As shown in Figure 6, the two-dimensional combination maps put the results of the variant of the normal ECG signal and the atrial premature beat ECG signal in one picture, and the four combinations in Figure 6 are and ; the values of are all limited to the sum of the two subsets.

As shown in Figure 7, the two-dimensional combination maps also put the results of the variant of the normal ECG signal and the atrial premature beat ECG signal in a single graph. The 12 combinations in Figure 7 are

and

the value of is limited to the sum of two subsets, and the value of is limited to the sum of the three subsets.

Figure 7. Two-dimensional combination maps of normal ECG data and atrial premature beat.

Characteristics of Atrial Premature Beat ECG Signals on Variant Maps DOI: http://dx.doi.org/10.5772/intechopen.83551

#### 4.3 Three-dimensional combination maps

with the same mapping of , formed when the

As shown in Figure 6, the two-dimensional combination maps put the results of the variant of the normal ECG signal and the atrial premature beat ECG signal in

is limited to the sum of two subsets, and the value of is limited to the sum of the

and

the value of

and ; the values of are all limited to the sum of the two subsets. As shown in Figure 7, the two-dimensional combination maps also put the results of the variant of the normal ECG signal and the atrial premature beat ECG

to that diagram.

three subsets.

Figure 7.

68

4.2 Two-dimensional combination maps

Practical Applications of Electrocardiogram

one picture, and the four combinations in Figure 6 are

signal in a single graph. The 12 combinations in Figure 7 are

Two-dimensional combination maps of normal ECG data and atrial premature beat.

insets. At the top of each small map is the mapping mode corresponding

As shown in Figures 8–10, the three-dimensional combination maps are a combination of the normal ECG signal and the atrial premature beat ECG signal in the three-dimensional space. The mode of the (X, Y, Z) combination in Figure 8 is the combination of (X, Y, Z) in Figure 9 is and the combination of (X, Y, Z) in Figure 10 is ; the values of X and Y are both defined as the sum of the two subsets, and the values of Z are all limited to the sum of the three subsets.

Figure 9. Three-dimensional combination maps of normal ECG data and atrial premature beat.

#### 5. Results analysis

Through the display of two-dimensional integral maps, two-dimensional combination maps, and three-dimensional combination maps, we can observe that:

beat ECG signal appears as an irregular cone. As the mapping mode changes, the shape of the variant maps also change, but the normal and abnormal ECG signals

Three-dimensional combination maps of normal ECG data and atrial premature beat.

Characteristics of Atrial Premature Beat ECG Signals on Variant Maps

DOI: http://dx.doi.org/10.5772/intechopen.83551

The two-dimensional combination map puts the variant maps of the two types of ECG signals on one canvas, and the difference between the normal and abnormal variant obtained by the same mapping method is more clear on one canvas. The mapping method selected in this chapter is more comprehensive, so the obtained

The three-dimensional combination map is based on the two-dimensional combination maps subjoining the Z-axis to form a spatial distribution display of the

always exhibit different variant characteristics.

variant map results are also universal.

Figure 10.

71

The two-dimensional integral maps are to show the macro difference between the normal ECG signal and the atrial premature beat ECG signal through the variant experiment. From the two-dimensional whole figure, there are significant differences in the distribution shape and range between normal and abnormal ECG signals. The variant maps of the normal ECG signal show that the scattered points are disperse, even spreading the entire canvas, and the shape of the atrial premature

Characteristics of Atrial Premature Beat ECG Signals on Variant Maps DOI: http://dx.doi.org/10.5772/intechopen.83551

Figure 10. Three-dimensional combination maps of normal ECG data and atrial premature beat.

beat ECG signal appears as an irregular cone. As the mapping mode changes, the shape of the variant maps also change, but the normal and abnormal ECG signals always exhibit different variant characteristics.

The two-dimensional combination map puts the variant maps of the two types of ECG signals on one canvas, and the difference between the normal and abnormal variant obtained by the same mapping method is more clear on one canvas. The mapping method selected in this chapter is more comprehensive, so the obtained variant map results are also universal.

The three-dimensional combination map is based on the two-dimensional combination maps subjoining the Z-axis to form a spatial distribution display of the

5. Results analysis

Practical Applications of Electrocardiogram

Figure 9.

70

Through the display of two-dimensional integral maps, two-dimensional combination maps, and three-dimensional combination maps, we can observe that: The two-dimensional integral maps are to show the macro difference between the normal ECG signal and the atrial premature beat ECG signal through the variant experiment. From the two-dimensional whole figure, there are significant differences in the distribution shape and range between normal and abnormal ECG signals. The variant maps of the normal ECG signal show that the scattered points are disperse, even spreading the entire canvas, and the shape of the atrial premature

Three-dimensional combination maps of normal ECG data and atrial premature beat.

variant maps. The (X, Y, Z) combination of the three-dimensional combination map selects , and and combines the two subsets and three subsets. The combination of the two is well integrated and is a more comprehensive illustration of the variant of normal and abnormal ECG signals. In the graphic display, five kinds of views are selected for each mapping method, which are (X, Y, Z), (Y, X, Z), (X, Z), (Y, Z), and (X, Y) as the screenshot of the main view. Through the results, we can see that there are also large differences in the three-dimensional spatial distribution of normal ECG signals and atrial premature beat ECG signals.

#### 6. Summary and outlook

In this chapter, the variant measurement model is used to perform the variant experiment on the acquired batch ECG data. Finally, the experimental results of the variant measurement are displayed through three visualization methods. It is found through experiments that the variant measurement model can be well applied to the classification of normal ECG signals and atrial premature beat ECG signals.

In the future, we hope to get more abundant ECG data and can cooperate with the hospital to implement the application of the variant measurement model in the classification of ECG signals, so that it can assist the traditional ECG application in the clinical field.

#### Acknowledgements

Thanks to the Xishan People's Hospital of Wuxi City of Jiangsu Province for ECG datasets, to First People's Hospital of Yunnan Province for calibrator of ECG data, and to the Key Project of Electric Information and Next Generation IT Technology of Yunnan (2018ZI002), National Science Foundation of China NSFC (61362014), and the Overseas Higher Level Scholar Project of Yunnan for financial supports of the project.

Author details

, Jeffery Zheng2

provided the original work is properly cited.

Yunnan Branch, Kunming, China

\* and Jing Zhang3

2 School of Software, Yunnan University, Kunming, China

Characteristics of Atrial Premature Beat ECG Signals on Variant Maps

DOI: http://dx.doi.org/10.5772/intechopen.83551

\*Address all correspondence to<EMAIL_ADDRESS>
1 Technology and Product Management Department, Agricultural Bank of China,

3 Department of Cadre Health, Yunnan First People's Hospital, Kunming, China

© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

Lihua Leng1

73

Characteristics of Atrial Premature Beat ECG Signals on Variant Maps DOI: http://dx.doi.org/10.5772/intechopen.83551

#### Author details

variant maps. The (X, Y, Z) combination of the three-dimensional combination map selects , and and combines the two subsets and three subsets. The combination of the two is well integrated and is a more comprehensive illustration of the variant of normal and abnormal ECG signals. In the graphic display, five kinds of views are selected for each mapping method, which are (X, Y, Z), (Y, X, Z), (X, Z), (Y, Z), and (X, Y) as the screenshot of the main view. Through the results, we can see that there are also large differences in the three-dimensional spatial distribution of normal ECG signals and atrial

In this chapter, the variant measurement model is used to perform the variant experiment on the acquired batch ECG data. Finally, the experimental results of the variant measurement are displayed through three visualization methods. It is found through experiments that the variant measurement model can be well applied to the

In the future, we hope to get more abundant ECG data and can cooperate with the hospital to implement the application of the variant measurement model in the classification of ECG signals, so that it can assist the traditional ECG application in

Thanks to the Xishan People's Hospital of Wuxi City of Jiangsu Province for ECG datasets, to First People's Hospital of Yunnan Province for calibrator of ECG data, and to the Key Project of Electric Information and Next Generation IT Technology of Yunnan (2018ZI002), National Science Foundation of China NSFC (61362014), and the Overseas Higher Level Scholar Project of Yunnan for financial supports of

classification of normal ECG signals and atrial premature beat ECG signals.

premature beat ECG signals.

Practical Applications of Electrocardiogram

6. Summary and outlook

the clinical field.

the project.

72

Acknowledgements

Lihua Leng1 , Jeffery Zheng2 \* and Jing Zhang3

1 Technology and Product Management Department, Agricultural Bank of China, Yunnan Branch, Kunming, China

2 School of Software, Yunnan University, Kunming, China

3 Department of Cadre Health, Yunnan First People's Hospital, Kunming, China

\*Address all correspondence to<EMAIL_ADDRESS>
© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

### References

[1] Thompson SC, Ting SA. Avoidance denial versus optimistic denial in reaction to the threat of future cardiovascular disease. Health Education & Behavior the Official Publication of the Society for Public Health Education. 2012;39(5):620

[2] Zheng J, Zheng C. Variant measures and visualized statistical distributions. Acta Photonica Sinica. 2011;40(9): 1397-1404

[3] Mitchell LB. Atrial Premature Beats. The ECG. Springer. 2004:239-335

[4] Wallmann D, Tüller D, Wustmann K, et al. Frequent atrial premature beats predict paroxysmal atrial fibrillation in stroke patients: An opportunity for a new diagnostic strategy. Stroke. 2007; 38(8):2292-2294

[5] Zheng J, Zheng C. A framework to express variant and invariant functional spaces for binary logic. Frontiers of Electrical and Electronic Engineering in China. 2010;5(2):163-172

[6] Zheng J, Zheng C, Kunii TL. A Framework of Variant Logic Construction for Cellular Automata, Cellular Automata—Innovative Modelling for Science and Engineering. Rijeka, Croatia: InTech Press; 2011

[7] Zheng J, Luo J, Zhou W. Pseudo DNA sequence generation of non-coding distributions using variant maps on cellular automata. Applied Mathematics. 2014;5(1):153-174

[8] Zheng J. Novel Pseudo Random Number Generation Using Varian Logic Framework. Australian Security Congress. 2011:100-104

[9] Heim DM, Heim O, Zeng PA, Zheng J. Successful creation of regular patterns in variant maps from bat echolocation

calls. Biological Systems: Open Access. 2016;5:166. DOI: 10.4172/2329-6577. 1000166

[10] Leng L, Zheng J. Mapping ECG signal sequences on variant maps. In: 2017 IEEE Trustcom/BigDataSE/ICESS; 2017. pp. 881-884. DOI: 10.1109/ Trustcom/BigDataSE/ICESS.2017.326

[11] Leng L, Zheng J. Visualization research of ECG sequence in sinus arrhythmia. Computer Science. 2016;43 (s2):183-185 (in Chinese)

[12] Zheng J. Variant Construction from Theoretical Foundation to Applications. Springer-Nature. 2019. DOI: 10.1007/ 978-981-13-2282-2

**75**

**Chapter 5**

Failure

*Hakan Altay*

**1. Introduction**

fibrillation [1].

condition related with VT and HF.

reduced ejection fraction (HFREF).

**Abstract**

Ventricular Tachycardia and Heart

Ventricular tachycardia (VT) is a common arrhythmia seen in patients with heart failure (HF) and is now seen more frequently as these patients survive longer with modern therapies. In patients with HF, half of the deaths are sudden due to life-threatening ventricular arrhythmias, including VT. Although disease modifying drugs, such as beta blockers, mineralocorticoid drugs, and angiotensin receptor neprilysin inhibitors, prevent the occurrence of VT to some extent, the mainstay of therapy is the antiarrhythmic drug therapy, implantable cardioverter-defibrillator (ICD) implantation, and traditional radiofrequency catheter ablation. Autonomic nerve system modulation and stereotactic body radiation therapy have emerged as novel techniques for the management of refractory VT cases. Patients with refractory VT and repetitive ICD shocks should be further evaluated regarding the

candidacy for left ventricular assist device and transplantation.

implantable-cardioverter defibrillator, ablation

**Keywords:** ventricular tachycardia, heart failure, antiarrhythmic therapy,

Ventricular tachycardia (VT) is common in patients with heart failure (HF). The presence and severity of VT increase as the severity of HF increases. Larger infarcts with greater left ventricle (LV) systolic dysfunction are more likely to be associated with VT. VT forms one of the most common electrical mechanisms responsible for sudden cardiac death (SCD) in HF. Patients with LV systolic dysfunction who develop VT are at increased risk of SCD from subsequent VT or ventricular

Patients with VT and HF may present either with cardiac arrest to the emergency department or with palpitations, syncope, chest pain, or ICD shocks to cardiology outpatient clinics, varying according to the hemodynamic stability of VT. Both non-sustained VT (VT duration < 30 sec) and sustained VT (VT duration > 30 sec) in patients with HF are associated with significant morbidity and mortality. VT storm (three or more separate episodes of sustained VT requiring intervention (such as ICD shock or ATP) within 24 hours) is the most troublesome

Although half of the patients with HF have preserved ejection fraction and SCD is also a common issue in these patients, there is no proved treatment either by ICD or drugs [2]. Because of this, VT and HF will be discussed in the context of HF with

#### **Chapter 5**

References

1397-1404

38(8):2292-2294

China. 2010;5(2):163-172

2014;5(1):153-174

74

[1] Thompson SC, Ting SA. Avoidance denial versus optimistic denial in reaction to the threat of future cardiovascular disease. Health Education & Behavior the Official Publication of the Society for Public Health Education. 2012;39(5):620

Practical Applications of Electrocardiogram

calls. Biological Systems: Open Access. 2016;5:166. DOI: 10.4172/2329-6577.

[10] Leng L, Zheng J. Mapping ECG signal sequences on variant maps. In: 2017 IEEE Trustcom/BigDataSE/ICESS; 2017. pp. 881-884. DOI: 10.1109/ Trustcom/BigDataSE/ICESS.2017.326

[11] Leng L, Zheng J. Visualization research of ECG sequence in sinus arrhythmia. Computer Science. 2016;43

[12] Zheng J. Variant Construction from Theoretical Foundation to Applications. Springer-Nature. 2019. DOI: 10.1007/

(s2):183-185 (in Chinese)

978-981-13-2282-2

1000166

[2] Zheng J, Zheng C. Variant measures and visualized statistical distributions. Acta Photonica Sinica. 2011;40(9):

[3] Mitchell LB. Atrial Premature Beats. The ECG. Springer. 2004:239-335

[4] Wallmann D, Tüller D, Wustmann K, et al. Frequent atrial premature beats predict paroxysmal atrial fibrillation in stroke patients: An opportunity for a new diagnostic strategy. Stroke. 2007;

[5] Zheng J, Zheng C. A framework to express variant and invariant functional spaces for binary logic. Frontiers of Electrical and Electronic Engineering in

[6] Zheng J, Zheng C, Kunii TL. A Framework of Variant Logic

Construction for Cellular Automata, Cellular Automata—Innovative

Modelling for Science and Engineering. Rijeka, Croatia: InTech Press; 2011

[7] Zheng J, Luo J, Zhou W. Pseudo DNA sequence generation of non-coding distributions using variant maps on cellular automata. Applied Mathematics.

[8] Zheng J. Novel Pseudo Random Number Generation Using Varian Logic

[9] Heim DM, Heim O, Zeng PA, Zheng J. Successful creation of regular patterns in variant maps from bat echolocation

Framework. Australian Security

Congress. 2011:100-104

## Ventricular Tachycardia and Heart Failure

*Hakan Altay*

#### **Abstract**

Ventricular tachycardia (VT) is a common arrhythmia seen in patients with heart failure (HF) and is now seen more frequently as these patients survive longer with modern therapies. In patients with HF, half of the deaths are sudden due to life-threatening ventricular arrhythmias, including VT. Although disease modifying drugs, such as beta blockers, mineralocorticoid drugs, and angiotensin receptor neprilysin inhibitors, prevent the occurrence of VT to some extent, the mainstay of therapy is the antiarrhythmic drug therapy, implantable cardioverter-defibrillator (ICD) implantation, and traditional radiofrequency catheter ablation. Autonomic nerve system modulation and stereotactic body radiation therapy have emerged as novel techniques for the management of refractory VT cases. Patients with refractory VT and repetitive ICD shocks should be further evaluated regarding the candidacy for left ventricular assist device and transplantation.

**Keywords:** ventricular tachycardia, heart failure, antiarrhythmic therapy, implantable-cardioverter defibrillator, ablation

#### **1. Introduction**

Ventricular tachycardia (VT) is common in patients with heart failure (HF). The presence and severity of VT increase as the severity of HF increases. Larger infarcts with greater left ventricle (LV) systolic dysfunction are more likely to be associated with VT. VT forms one of the most common electrical mechanisms responsible for sudden cardiac death (SCD) in HF. Patients with LV systolic dysfunction who develop VT are at increased risk of SCD from subsequent VT or ventricular fibrillation [1].

Patients with VT and HF may present either with cardiac arrest to the emergency department or with palpitations, syncope, chest pain, or ICD shocks to cardiology outpatient clinics, varying according to the hemodynamic stability of VT. Both non-sustained VT (VT duration < 30 sec) and sustained VT (VT duration > 30 sec) in patients with HF are associated with significant morbidity and mortality. VT storm (three or more separate episodes of sustained VT requiring intervention (such as ICD shock or ATP) within 24 hours) is the most troublesome condition related with VT and HF.

Although half of the patients with HF have preserved ejection fraction and SCD is also a common issue in these patients, there is no proved treatment either by ICD or drugs [2]. Because of this, VT and HF will be discussed in the context of HF with reduced ejection fraction (HFREF).

### **2. Epidemiology**

Ventricular tachycardia is common in patients with HF, with up to 20% of patients developing VT in 5 years after an ICD was placed [3]. In patients with HF, SCD occurs 6–9 times more often than the general population [4]. The most studied and proven predictor of ventricular tachyarrhythmia and SCD is left ventricle ejection fraction (LVEF) [5]. It has been shown that once the LVEF recovered, the incidence of ventricular tachyarrhythmia decreases [6].

The threshold of LVEF <35% represents an accepted threshold at which SCD risk is increased and primary prevention is indicated. Several other risk predictors of VT, such as non-sustained VT, programmed ventricular stimulation on electrophysiological study (EPS), microvolt T-wave alternans, late potentials on signalaveraged electrocardiogram, absence of heart rate variability, QT wave dispersion, baroreflex sensitivity, and heart rate turbulence have been proposed for patients with HF. However, none of these predictors has influenced the clinical practice.

#### **3. Pathophysiology**

There are multiple mechanisms that play a role in the occurrence of VT in patients with HF (**Table 1**). Adverse remodeling and progressive fibrosis occur in the ventricle following myocardial infarction (MI) or in association with nonischemic cardiomyopathy. These structural alterations as well as the ion channel changes form the essential substrate for the induction of VT [7].

The most common mechanism for VT is electrical reentry within and around patches of heterogenous myocardial fibrosis, most commonly occurring in areas of scar post-myocardial infarction or non-ischemic cardiomyopathy [8]. The scarrelated VT is typically monomorphic with single QRS morphology. Induction of monomorphic VT during EPS predicts patients who have the risk of spontaneous VT. Polymorphic VT is defined as a continually changing QRS morphology, often associated with acute ischemia, drugs which lead to QT prolongation or electrolyte imbalance.

Increased sympathetic nervous system (SNS) activation is another trigger for induction of VT. SNS activation, via beta-adrenoreceptors activates ryanodine receptor on the sarcoplasmic reticulum inside the cardiomyocytes leading to efflux of calcium and increase of intracellular concentration which is a trigger for VT. This is the rationale under the effect of beta blockers in suppressing VT, as well as SCD in HF patients.

**77**

*Ventricular Tachycardia and Heart Failure DOI: http://dx.doi.org/10.5772/intechopen.85256*

clinical outcomes.

**4. Management**

antiarrhythmic treatment in this case [12].

VT occurring within 24–48 hours of acute MI is called primary VT, and acute ischemia is considered to be the transient or correctable cause of VT in this case. Revascularization is the primary management form of primary VT. VT occurring after 48 hours of acute MI is called secondary VT, which is associated with worse

Increased diastolic calcium levels, early and delayed after depolarizations, and some of the drugs also cause VT. Antiarrhythmic drugs are the foremost drugs causing VT. Digoxin that is commonly used in the management of HF is an arrhythmogenic drug. Dobutamine treatment for acute decompensated HF has also been associated with VT [9]. Because of this, patients should be continuously monitorized during treatment with dobutamine. VT can also present as a complication of left ventricular assist device in an advanced HF patient. Most of these types of VT occur perioperatively [10]. It is important to find out the definite mechanism of VT in order to implement the best effective treatment. In patients with sarcoidosis, for example, VT can occur as a result of inflammation, scar or both. If VT is thought to be due to inflammation, best treatment is antiarrhythmic drug and immunosuppressive, whereas if VT is of scar related, best treatment is antiarrhythmic drug and catheter ablation [11].

Management of VT in heart failure poses a great challenge to cardiologists since antiarrhythmic drugs are limited by incomplete efficacy and unfavorable adverse effect profile, ICD is complex and expensive and may affect the quality of life adversely because of inappropriate shocks, and invasive catheter ablation owns the risk of complication and recurrence. Therefore, multidisciplinary team approach including electrophysiologists, heart failure specialists, general cardiologists, intensivists, and cardiovascular surgeon should be used to tackle such a difficult disease. VT is a life-threatening condition and needs urgent management. Acute management of VT in HF patients depends on the hemodynamic stability of the patient. In hemodynamically unstable VT, the priority is electrical direct current cardioversion [12]. If the patient is hemodynamically stable, a trial of antiarrhythmic treatment should be applied. Intravenous amiodarone is the most effective and safe

Slow VT (<150 beats/minute) may be tolerated in the short term (**Figure 1**). However, slow VT in the presence of poor ventricular function may cause hemodynamic compromise in the long term. It is important to closely monitor the patient while administering antiarrhythmic therapy. If the antiarrhythmic therapy does not cardiovert the patient, shock should be applied as early as possible since sustained VT can compromise hemodynamic status of the patient with left ventricular dysfunction in due course. The initial approach to the management of VT should include evaluation for correctable causes of VT (e.g., electrolyte abnormalities and ischemia). Electrolyte abnormalities, particularly hypokalemia and hypomagnesemia which are known to facilitate VT in HF patients should be corrected. Potassium and magnesium levels should be kept >4 meq/l and > 2 meq/l, respectively. Agents,

for example, digoxin, that may induce arrhythmia should be withheld.

For chronic management of VT, optimization of guideline-directed medical treatment is very important especially in patients with HFREF. Until recently, these treatments consisted of angiotensin converting enzyme inhibitors (ACEis) or angiotensin receptor blockers (ARBs), beta blockers (BBs), and mineralocorticoid receptor antagonists (MRAs). Of these guideline-directed medical treatments, BB and MRA have been proved to prevent sudden cardiac death [13, 14]. These drugs have the ability to improve reverse modeling which reduces VT. BBs are the

#### **Table 1.**

*Mechanisms of VT occurrence in patients with heart failure.*

#### *Ventricular Tachycardia and Heart Failure DOI: http://dx.doi.org/10.5772/intechopen.85256*

*Practical Applications of Electrocardiogram*

incidence of ventricular tachyarrhythmia decreases [6].

Ventricular tachycardia is common in patients with HF, with up to 20% of patients developing VT in 5 years after an ICD was placed [3]. In patients with HF, SCD occurs 6–9 times more often than the general population [4]. The most studied and proven predictor of ventricular tachyarrhythmia and SCD is left ventricle ejection fraction (LVEF) [5]. It has been shown that once the LVEF recovered, the

The threshold of LVEF <35% represents an accepted threshold at which SCD risk is increased and primary prevention is indicated. Several other risk predictors of VT, such as non-sustained VT, programmed ventricular stimulation on electrophysiological study (EPS), microvolt T-wave alternans, late potentials on signalaveraged electrocardiogram, absence of heart rate variability, QT wave dispersion, baroreflex sensitivity, and heart rate turbulence have been proposed for patients with HF. However, none of these predictors has influenced the clinical practice.

There are multiple mechanisms that play a role in the occurrence of VT in patients with HF (**Table 1**). Adverse remodeling and progressive fibrosis occur in the ventricle following myocardial infarction (MI) or in association with nonischemic cardiomyopathy. These structural alterations as well as the ion channel

The most common mechanism for VT is electrical reentry within and around patches of heterogenous myocardial fibrosis, most commonly occurring in areas of scar post-myocardial infarction or non-ischemic cardiomyopathy [8]. The scarrelated VT is typically monomorphic with single QRS morphology. Induction of monomorphic VT during EPS predicts patients who have the risk of spontaneous VT. Polymorphic VT is defined as a continually changing QRS morphology, often associated with acute ischemia, drugs which lead to QT prolongation or electrolyte

Increased sympathetic nervous system (SNS) activation is another trigger for induction of VT. SNS activation, via beta-adrenoreceptors activates ryanodine receptor on the sarcoplasmic reticulum inside the cardiomyocytes leading to efflux of calcium and increase of intracellular concentration which is a trigger for VT. This is the rationale under the effect of beta blockers in suppressing VT, as well as SCD in

changes form the essential substrate for the induction of VT [7].

**2. Epidemiology**

**3. Pathophysiology**

imbalance.

HF patients.

**Mechanisms**

Myocardial scar

Ischemia

Drugs

**Table 1.**

Positive remodeling and fibrosis

Electrolyte abnormalities Increased sympathetic tone

Abnormal calcium handling Delayed after depolarization

*Mechanisms of VT occurrence in patients with heart failure.*

**76**

VT occurring within 24–48 hours of acute MI is called primary VT, and acute ischemia is considered to be the transient or correctable cause of VT in this case. Revascularization is the primary management form of primary VT. VT occurring after 48 hours of acute MI is called secondary VT, which is associated with worse clinical outcomes.

Increased diastolic calcium levels, early and delayed after depolarizations, and some of the drugs also cause VT. Antiarrhythmic drugs are the foremost drugs causing VT. Digoxin that is commonly used in the management of HF is an arrhythmogenic drug. Dobutamine treatment for acute decompensated HF has also been associated with VT [9]. Because of this, patients should be continuously monitorized during treatment with dobutamine. VT can also present as a complication of left ventricular assist device in an advanced HF patient. Most of these types of VT occur perioperatively [10]. It is important to find out the definite mechanism of VT in order to implement the best effective treatment. In patients with sarcoidosis, for example, VT can occur as a result of inflammation, scar or both. If VT is thought to be due to inflammation, best treatment is antiarrhythmic drug and immunosuppressive, whereas if VT is of scar related, best treatment is antiarrhythmic drug and catheter ablation [11].

#### **4. Management**

Management of VT in heart failure poses a great challenge to cardiologists since antiarrhythmic drugs are limited by incomplete efficacy and unfavorable adverse effect profile, ICD is complex and expensive and may affect the quality of life adversely because of inappropriate shocks, and invasive catheter ablation owns the risk of complication and recurrence. Therefore, multidisciplinary team approach including electrophysiologists, heart failure specialists, general cardiologists, intensivists, and cardiovascular surgeon should be used to tackle such a difficult disease.

VT is a life-threatening condition and needs urgent management. Acute management of VT in HF patients depends on the hemodynamic stability of the patient. In hemodynamically unstable VT, the priority is electrical direct current cardioversion [12]. If the patient is hemodynamically stable, a trial of antiarrhythmic treatment should be applied. Intravenous amiodarone is the most effective and safe antiarrhythmic treatment in this case [12].

Slow VT (<150 beats/minute) may be tolerated in the short term (**Figure 1**). However, slow VT in the presence of poor ventricular function may cause hemodynamic compromise in the long term. It is important to closely monitor the patient while administering antiarrhythmic therapy. If the antiarrhythmic therapy does not cardiovert the patient, shock should be applied as early as possible since sustained VT can compromise hemodynamic status of the patient with left ventricular dysfunction in due course. The initial approach to the management of VT should include evaluation for correctable causes of VT (e.g., electrolyte abnormalities and ischemia). Electrolyte abnormalities, particularly hypokalemia and hypomagnesemia which are known to facilitate VT in HF patients should be corrected. Potassium and magnesium levels should be kept >4 meq/l and > 2 meq/l, respectively. Agents, for example, digoxin, that may induce arrhythmia should be withheld.

For chronic management of VT, optimization of guideline-directed medical treatment is very important especially in patients with HFREF. Until recently, these treatments consisted of angiotensin converting enzyme inhibitors (ACEis) or angiotensin receptor blockers (ARBs), beta blockers (BBs), and mineralocorticoid receptor antagonists (MRAs). Of these guideline-directed medical treatments, BB and MRA have been proved to prevent sudden cardiac death [13, 14]. These drugs have the ability to improve reverse modeling which reduces VT. BBs are the

**Figure 1.** *Slow VT at a rate of approximately 125/bpm in a patient on high dose of beta blocker and amiodarone.*

first-line therapy for the management of VT in HF patients. In MADIT-II trial (the Multicenter Automatic Defibrillator Implantation Trial II), patients with ICD treated with the highest dose of BB experienced less ICD treatment compared to patients not taking BB [15].

A meta-analysis compared medical treatment with ICD preventing SCD in patients with HF and left ventricular systolic dysfunction. MRAs were found to be the most effective drug when added to ACEi and BB, in preventing SCD [16]. Zannad et al. also showed that MRAs were equally effective in preventing SCD in patients with ICD as without ICD [17].

A newly emerged drug in HFREF, angiotensin receptor neprilysin inhibitor (ARNi), was compared with enalapril in PARADIGM-HF trial (prospective comparison of angiotensin neprilysin inhibitor (ARNI) with ACE-i to determine impact on global morbidity and mortality in heart failure) [18]. ARNi was shown to be superior in reducing cardiovascular death and hospitalization compared to enalapril. ARNi also reduced SCD by 20% compared to enalapril. European Society of Cardiology 2016 HF guideline has made a class 1 recommendation regarding the use of BB, MRA, and ARNi in patients with HFREF and VT [19].

Optimum use of guideline-directed medical treatment prevents development of VT to some extent. If the patient continues to be at risk of VT because of low ejection fraction, non-sustained or sustained VT, antiarrhythmic drugs, ICD implantation, and VT ablation are the subsequent treatment options for chronic management of VT. General use of antiarrhythmic drugs in HF is not recommended for VT since these drugs, except amiodarone, have been shown to increase mortality in patients with HF due to proarrhythmic or negative inotropic effects.

Notorious CAST trial (Cardiac Arrhythmia Suppression Trial) showed that class 1C agents, encainide, and flecainide increases mortality and non-fatal cardiac arrest when used to suppress VT post-myocardial infarction [20]. CAST trial was planned to answer the question of whether suppressing ventricular premature beats (VPB) also aid in reducing mortality. Patients who had myocardial infarction within the preceding 2 years and >6 VPBs on holter recording were enrolled. Those who had MI within 90 days were required to have EF < 55%, and those who had MI after this period were required to have EF < 40%. Patients were randomly assigned to class1C agents (encainide, flecainide, or moricizine). Patients whose PVBs were suppressed were allocated to the treatment with one of the class 1C agent or placebo. The trial was prematurely stopped based on the in-term analysis that showed that encainide and flecainide used to suppress VPBs increased the mortality by 2.5 times. It is likely that mortality excess can be attributed to the proarrhythmic effects of encainide and flecainide.

**79**

**Figure 2.**

*Ventricular Tachycardia and Heart Failure DOI: http://dx.doi.org/10.5772/intechopen.85256*

amiodarone have been noted to be high [22].

assessed whether VT could be induced again [26].

amiodarone.

primary prevention.

Amiodarone is the sole agent that can be used safely for suppression of VT in HF patients. Amiodarone has been studied extensively in patients with left ventricular dysfunction. Its efficacy for decreasing mortality in patients with VT and LV dysfunction has not been shown in SCD-HeFT trial (the Sudden Cardiac Death in Heart Failure Trial) [21]. However, a meta-analysis including 8522 patients post-myocardial infarction or with systolic HF showed that amiodarone reduced SCD and cardiovascular mortality [22]. Its safety, unlike class 1 antiarrhythmic agents, has been confirmed in this patient population. In patients with more severe HF, amiodarone use is associated with adverse prognosis [21]. Amiodarone cannot be used for a long period of time because it is associated with multiple side effects, primarily affecting thyroid, lung, liver, skin, and eye [23]. Therefore, regular monitoring of lung, liver, and thyroid function is required. Due to these side effects, discontinuation rates of

Sotalol, a group III antiarrhythmic drug, with BB properties, is highly effective in suppressing VT but it is contraindicated in HF patients since increased mortality was demonstrated when D-sotalol was used in patients with left ventricular dysfunction after myocardial infarction in SWORD trial [24]. Dofetilide, another class III antiarrhythmic drug, failed to reduce arrhythmic death in patients with HF [25]. If VT occurs despite amiodarone therapy, mexiletine can be used as an adjunct to

Electrophysiologic study was once used for identification of successful antiarrhythmic therapy and also the patients who require other advanced therapies. Patients were given certain antiarrhythmic drugs after VT was induced at programmed stimulation. Patients on chronic oral antiarrhythmic drug were then

Of the therapies currently available to manage VT, ICD is by far the most effective one and has the best supported safety and efficacy data from the trials and registries. An ICD has two important components: an ICD generator and a lead for sensing, pacing, and shock delivery (**Figure 2**). ICD improves the survival of patients who had VT and syncope, patients who had VT and LVEF<40%, and hemodynamic compromise [27]. ICD has been shown to prevent sudden cardiac death prophylactically in patents with LVEF <35% resulting both from ischemic or non-ischemic cardiomyopathy [21, 28, 29]. The important issue in these primary prevention groups is that they should have already received guideline-directed medical treatment for at least 3 months before ICD implantation is planned. Electrophysiologic study is no longer a required procedure before planning ICD for

*A schematic representation of an intracardiac defibrillator implanted to right ventricle of heart failure patient.*

#### *Ventricular Tachycardia and Heart Failure DOI: http://dx.doi.org/10.5772/intechopen.85256*

*Practical Applications of Electrocardiogram*

patients not taking BB [15].

**Figure 1.**

patients with ICD as without ICD [17].

first-line therapy for the management of VT in HF patients. In MADIT-II trial (the Multicenter Automatic Defibrillator Implantation Trial II), patients with ICD treated with the highest dose of BB experienced less ICD treatment compared to

*Slow VT at a rate of approximately 125/bpm in a patient on high dose of beta blocker and amiodarone.*

A meta-analysis compared medical treatment with ICD preventing SCD in patients with HF and left ventricular systolic dysfunction. MRAs were found to be the most effective drug when added to ACEi and BB, in preventing SCD [16]. Zannad et al. also showed that MRAs were equally effective in preventing SCD in

A newly emerged drug in HFREF, angiotensin receptor neprilysin inhibitor (ARNi), was compared with enalapril in PARADIGM-HF trial (prospective comparison of angiotensin neprilysin inhibitor (ARNI) with ACE-i to determine impact on global morbidity and mortality in heart failure) [18]. ARNi was shown to be superior in reducing cardiovascular death and hospitalization compared to enalapril. ARNi also reduced SCD by 20% compared to enalapril. European Society of Cardiology 2016 HF guideline has made a class 1 recommendation regarding the

Optimum use of guideline-directed medical treatment prevents development of VT to some extent. If the patient continues to be at risk of VT because of low ejection fraction, non-sustained or sustained VT, antiarrhythmic drugs, ICD implantation, and VT ablation are the subsequent treatment options for chronic management of VT. General use of antiarrhythmic drugs in HF is not recommended for VT since these drugs, except amiodarone, have been shown to increase mortality

Notorious CAST trial (Cardiac Arrhythmia Suppression Trial) showed that class 1C agents, encainide, and flecainide increases mortality and non-fatal cardiac arrest when used to suppress VT post-myocardial infarction [20]. CAST trial was planned to answer the question of whether suppressing ventricular premature beats (VPB) also aid in reducing mortality. Patients who had myocardial infarction within the preceding 2 years and >6 VPBs on holter recording were enrolled. Those who had MI within 90 days were required to have EF < 55%, and those who had MI after this period were required to have EF < 40%. Patients were randomly assigned to class1C agents (encainide, flecainide, or moricizine). Patients whose PVBs were suppressed were allocated to the treatment with one of the class 1C agent or placebo. The trial was prematurely stopped based on the in-term analysis that showed that encainide and flecainide used to suppress VPBs increased the mortality by 2.5 times. It is likely that mortality excess can be attributed to the proarrhythmic effects of encainide and flecainide.

use of BB, MRA, and ARNi in patients with HFREF and VT [19].

in patients with HF due to proarrhythmic or negative inotropic effects.

**78**

Amiodarone is the sole agent that can be used safely for suppression of VT in HF patients. Amiodarone has been studied extensively in patients with left ventricular dysfunction. Its efficacy for decreasing mortality in patients with VT and LV dysfunction has not been shown in SCD-HeFT trial (the Sudden Cardiac Death in Heart Failure Trial) [21]. However, a meta-analysis including 8522 patients post-myocardial infarction or with systolic HF showed that amiodarone reduced SCD and cardiovascular mortality [22]. Its safety, unlike class 1 antiarrhythmic agents, has been confirmed in this patient population. In patients with more severe HF, amiodarone use is associated with adverse prognosis [21]. Amiodarone cannot be used for a long period of time because it is associated with multiple side effects, primarily affecting thyroid, lung, liver, skin, and eye [23]. Therefore, regular monitoring of lung, liver, and thyroid function is required. Due to these side effects, discontinuation rates of amiodarone have been noted to be high [22].

Sotalol, a group III antiarrhythmic drug, with BB properties, is highly effective in suppressing VT but it is contraindicated in HF patients since increased mortality was demonstrated when D-sotalol was used in patients with left ventricular dysfunction after myocardial infarction in SWORD trial [24]. Dofetilide, another class III antiarrhythmic drug, failed to reduce arrhythmic death in patients with HF [25]. If VT occurs despite amiodarone therapy, mexiletine can be used as an adjunct to amiodarone.

Electrophysiologic study was once used for identification of successful antiarrhythmic therapy and also the patients who require other advanced therapies. Patients were given certain antiarrhythmic drugs after VT was induced at programmed stimulation. Patients on chronic oral antiarrhythmic drug were then assessed whether VT could be induced again [26].

Of the therapies currently available to manage VT, ICD is by far the most effective one and has the best supported safety and efficacy data from the trials and registries. An ICD has two important components: an ICD generator and a lead for sensing, pacing, and shock delivery (**Figure 2**). ICD improves the survival of patients who had VT and syncope, patients who had VT and LVEF<40%, and hemodynamic compromise [27]. ICD has been shown to prevent sudden cardiac death prophylactically in patents with LVEF <35% resulting both from ischemic or non-ischemic cardiomyopathy [21, 28, 29]. The important issue in these primary prevention groups is that they should have already received guideline-directed medical treatment for at least 3 months before ICD implantation is planned. Electrophysiologic study is no longer a required procedure before planning ICD for primary prevention.

#### **Figure 2.**

*A schematic representation of an intracardiac defibrillator implanted to right ventricle of heart failure patient.*

ICD has antitachycardia pacing (ATP) treatment in addition to defibrillator shock and also programs which can discriminate supraventricular tachycardia from VT which aids to minimize inappropriate shocks. ATP consists of one or more sequence of pacing stimuli, generally expressed as a percentage of tachycardia cycle length for a given RR interval. In case of burst ATP, pacing stimuli is delivered at constant coupling intervals, whereas ramp ATP consists of pacing stimuli with decrement coupling interval (**Figure 3**). Once VT is confirmed, first therapy in the form of ATP was given, and if ATP does not work, then shock is delivered. Generally ICD's VT detection zone is programmed to >167 beats/min and ventricular fibrillation detection zone to >185–200 beats/min. Antiarrhythmic drugs commonly prolong VT cycle length and hence cause slow VT, a condition which may require to lower the detection zone for VT (**Figure 1**). In secondary prevention patients with HF, the programming of detection zone depends on the cycle length of the VT occurred. Generally, the detection zone is programmed 20 bpm slower than the rate of the VT occurred before. ATP for faster VT (188–250 bpm) may also be programmed with the aim for reducing shocks. ICD shocks are related with poor prognosis and quality of life. For this reason, every effort should be made to reduce shocks. It was shown that reducing defibrillator shocks was associated with increased survival [30].

Cardiac resynchronization therapy (CRT) is also an important milestone in the management of moderate to severe HF patients with prolonged QRS duration (>150 msn and LBBB morphology). CRT without defibrillator (CRT-P) can prevent SCD by improving reverse remodeling. CARE-HF Trial (Cardiac Resynchronization—Heart Failure) showed that CRT-P prevents SCD by 46% in the long term follow-up [31]. Although CRT was shown to reduce new onset VT, it had no effect on recurrent VTs [32].

In patients with HF who are refractory to antiarrhythmic therapy, radiofrequency catheter ablation has emerged as an important therapeutic option. The success rate of this technique varies according to the type of cardiomyopathy. The American Heart Association(AHA)/the Heart Rhythm Society (HRS) recommends the use of VT ablation in patients with prior myocardial infarction and recurrent VT, unresponsive or intolerant to antiarrhythmic treatment [8]. Electrophysiologic study (EPS) with programmed electrical stimulation is recommended before ablation in case of sustained monomorphic VT in patients with prior MI [33]. Catheter ablation can be effective, but acute complications and long-term VT recurrence risk necessitating repeat ablation should be recognized. And worth notifying, procedure

#### **Figure 3.**

*Antitachycardia pacing (ATP) therapy of intracardiac defibrillator. (A) Burst ATP; pacing stimuli at lower than VT and constant coupling interval. (B) Ramp ATP; pacing stimuli starting with lower than VT cycle length and coupling intervals decreasing at each stimuli.*

**81**

for repetitive VTs [40].

*Ventricular Tachycardia and Heart Failure DOI: http://dx.doi.org/10.5772/intechopen.85256*

operation [34].

of ablation lasts for long hours with extended recovery times. If VT remains refractory to catheter ablation, repeat ablation may be tried. If the first ablation was done by endocardial mapping, repeat ablations may be carried by epicardial mapping. Surgical ablation is indicated in patients with VT refractory to antiarrhythmic drugs whose catheter ablation has failed [12]. It was shown that surgical cryoablation guided by endocardial and epicardial mapping along with aneurysmectomy when indicated was a successful way of terminating VT in patients who underwent bypass

Due to multiple mechanisms of VT in idiopathic dilated cardiomyopathy, the success rate of catheter ablation is less than in ischemic cardiomyopathy. It has been shown that ablation in this type of cardiomyopathy results in higher recurrence rate of VT than ischemic cardiomyopathy [35]. Catheter ablation of VT in dilated cardiomyopathy should only be done in patients with clear mechanism of VT (e.g., bundle branch reentry) only in experienced centers. Despite these shortcomings, successful VT ablation in non-ischemic dilated cardiomyopathy has increased. Predictors of recurrence after VT ablation in non-ischemic dilated cardiomyopathy were found to be inducibility of sustained VT in the programmed stimulation study,

Worth mentioning, there are some types of VTs occurring in the structurally normal heart, termed idiopathic VT. Idiopathic VT is further categorized according to the anatomic location in the heart. Most of them originate from the right ventricular outflow tract (RVOT) and have left bundle branch block (LBBB) pattern on the electrocardiogram. The second most common idiopathic VT originating from the conduction system is termed as fascicular VT. The other idiopathic VT originates from the mitral or tricuspid annulus and termed as annular VT. The clinical course of idiopathic VT is usually benign; however, if they occur in the form of incessant VT, they may cause LV systolic dysfunction, termed as arrhythmia-induced cardiomyopathy (AIC). It is important to differentiate AIC from non-ischemic dilated cardiomyopathy because RF ablation is the first line treatment and curative in the former [8]. VT originating from left ventricular outflow tract (LVOT) is rare compared to VT originating from RVOT. Some form of VTs originating from LVOT cannot be ablated by using conventional approach. This unique type of VT with LBBB inferior axis and early precordial transition can successfully be ablated from the aortic root, using either the left or non-coronary aortic sinus of valsalva [37]. VTs can also originate from papillary muscle of left or right ventricle. Ablation of papillary muscle VT is difficult compared to other idiopathic VTs. However, there is a case report showing successful ablation of incessant VT originating from posterior papillary muscle of right ventricle [38]. EPS is highly recommended before ablation of VT in structurally normal hearts which are suspected to be originated from RVOT, LVOT, aortic cusps, and epicardial VT [33]. EPS has also a role in case of sustained monomorphic VT in patients with arrhythmogenic right ventricular dysplasia (ARVD). It was shown that inducibility of sustained monomorphic VT during EPS highly predicts SCD, heart transplantation, VT with hemodynamic

Another form of VT occurring in the structurally normal heart is catecholaminergic polymorphic VT. This type of VT should be suspected when syncope triggered by emotion or physical effort occurs in young patients with normal heart and QT interval. First line treatment is BBs. Hypertrophic cardiomyopathy (HCM), a common cause of SCD in young athletes, is a heterogenous group of cardiomyopathy with increased wall thickness. HCM with mid-ventricular obstruction and apical aneurysm is a rare form of HCM which is associated with frequent occurrence of VT. Prophylactic ICD is the main treatment, but RF ablation is required

poor systolic function (EF < 35%), and delayed intervention time [36].

compromise, or syncope in patients with ARVD [39].

#### *Ventricular Tachycardia and Heart Failure DOI: http://dx.doi.org/10.5772/intechopen.85256*

*Practical Applications of Electrocardiogram*

increased survival [30].

no effect on recurrent VTs [32].

ICD has antitachycardia pacing (ATP) treatment in addition to defibrillator shock and also programs which can discriminate supraventricular tachycardia from VT which aids to minimize inappropriate shocks. ATP consists of one or more sequence of pacing stimuli, generally expressed as a percentage of tachycardia cycle length for a given RR interval. In case of burst ATP, pacing stimuli is delivered at constant coupling intervals, whereas ramp ATP consists of pacing stimuli with decrement coupling interval (**Figure 3**). Once VT is confirmed, first therapy in the form of ATP was given, and if ATP does not work, then shock is delivered. Generally ICD's VT detection zone is programmed to >167 beats/min and ventricular fibrillation detection zone to >185–200 beats/min. Antiarrhythmic drugs commonly prolong VT cycle length and hence cause slow VT, a condition which may require to lower the detection zone for VT (**Figure 1**). In secondary prevention patients with HF, the programming of detection zone depends on the cycle length of the VT occurred. Generally, the detection zone is programmed 20 bpm slower than the rate of the VT occurred before. ATP for faster VT (188–250 bpm) may also be programmed with the aim for reducing shocks. ICD shocks are related with poor prognosis and quality of life. For this reason, every effort should be made to reduce shocks. It was shown that reducing defibrillator shocks was associated with

Cardiac resynchronization therapy (CRT) is also an important milestone in the management of moderate to severe HF patients with prolonged QRS duration (>150 msn and LBBB morphology). CRT without defibrillator (CRT-P) can prevent SCD by improving reverse remodeling. CARE-HF Trial (Cardiac Resynchronization—Heart Failure) showed that CRT-P prevents SCD by 46% in the long term follow-up [31]. Although CRT was shown to reduce new onset VT, it had

In patients with HF who are refractory to antiarrhythmic therapy, radiofrequency catheter ablation has emerged as an important therapeutic option. The success rate of this technique varies according to the type of cardiomyopathy. The American Heart Association(AHA)/the Heart Rhythm Society (HRS) recommends the use of VT ablation in patients with prior myocardial infarction and recurrent VT, unresponsive or intolerant to antiarrhythmic treatment [8]. Electrophysiologic study (EPS) with programmed electrical stimulation is recommended before ablation in case of sustained monomorphic VT in patients with prior MI [33]. Catheter ablation can be effective, but acute complications and long-term VT recurrence risk necessitating repeat ablation should be recognized. And worth notifying, procedure

*Antitachycardia pacing (ATP) therapy of intracardiac defibrillator. (A) Burst ATP; pacing stimuli at lower than VT and constant coupling interval. (B) Ramp ATP; pacing stimuli starting with lower than VT cycle*

**80**

**Figure 3.**

*length and coupling intervals decreasing at each stimuli.*

of ablation lasts for long hours with extended recovery times. If VT remains refractory to catheter ablation, repeat ablation may be tried. If the first ablation was done by endocardial mapping, repeat ablations may be carried by epicardial mapping. Surgical ablation is indicated in patients with VT refractory to antiarrhythmic drugs whose catheter ablation has failed [12]. It was shown that surgical cryoablation guided by endocardial and epicardial mapping along with aneurysmectomy when indicated was a successful way of terminating VT in patients who underwent bypass operation [34].

Due to multiple mechanisms of VT in idiopathic dilated cardiomyopathy, the success rate of catheter ablation is less than in ischemic cardiomyopathy. It has been shown that ablation in this type of cardiomyopathy results in higher recurrence rate of VT than ischemic cardiomyopathy [35]. Catheter ablation of VT in dilated cardiomyopathy should only be done in patients with clear mechanism of VT (e.g., bundle branch reentry) only in experienced centers. Despite these shortcomings, successful VT ablation in non-ischemic dilated cardiomyopathy has increased. Predictors of recurrence after VT ablation in non-ischemic dilated cardiomyopathy were found to be inducibility of sustained VT in the programmed stimulation study, poor systolic function (EF < 35%), and delayed intervention time [36].

Worth mentioning, there are some types of VTs occurring in the structurally normal heart, termed idiopathic VT. Idiopathic VT is further categorized according to the anatomic location in the heart. Most of them originate from the right ventricular outflow tract (RVOT) and have left bundle branch block (LBBB) pattern on the electrocardiogram. The second most common idiopathic VT originating from the conduction system is termed as fascicular VT. The other idiopathic VT originates from the mitral or tricuspid annulus and termed as annular VT. The clinical course of idiopathic VT is usually benign; however, if they occur in the form of incessant VT, they may cause LV systolic dysfunction, termed as arrhythmia-induced cardiomyopathy (AIC). It is important to differentiate AIC from non-ischemic dilated cardiomyopathy because RF ablation is the first line treatment and curative in the former [8]. VT originating from left ventricular outflow tract (LVOT) is rare compared to VT originating from RVOT. Some form of VTs originating from LVOT cannot be ablated by using conventional approach. This unique type of VT with LBBB inferior axis and early precordial transition can successfully be ablated from the aortic root, using either the left or non-coronary aortic sinus of valsalva [37]. VTs can also originate from papillary muscle of left or right ventricle. Ablation of papillary muscle VT is difficult compared to other idiopathic VTs. However, there is a case report showing successful ablation of incessant VT originating from posterior papillary muscle of right ventricle [38]. EPS is highly recommended before ablation of VT in structurally normal hearts which are suspected to be originated from RVOT, LVOT, aortic cusps, and epicardial VT [33]. EPS has also a role in case of sustained monomorphic VT in patients with arrhythmogenic right ventricular dysplasia (ARVD). It was shown that inducibility of sustained monomorphic VT during EPS highly predicts SCD, heart transplantation, VT with hemodynamic compromise, or syncope in patients with ARVD [39].

Another form of VT occurring in the structurally normal heart is catecholaminergic polymorphic VT. This type of VT should be suspected when syncope triggered by emotion or physical effort occurs in young patients with normal heart and QT interval. First line treatment is BBs. Hypertrophic cardiomyopathy (HCM), a common cause of SCD in young athletes, is a heterogenous group of cardiomyopathy with increased wall thickness. HCM with mid-ventricular obstruction and apical aneurysm is a rare form of HCM which is associated with frequent occurrence of VT. Prophylactic ICD is the main treatment, but RF ablation is required for repetitive VTs [40].

#### **5. Management of ICD repetitive shocks**

Despite ICD can effectively terminate ventricular tachycardia either by antitachycardia pacing or defibrillation shock, it cannot prevent VT recurrences. In patients with ICD, prevention of VT recurrence is required to minimize ICD shocks which can not only be quite uncomfortable for the patient leading to poor quality of life but also cause early battery depletion. Apart from these, recurrent shocks lead to HF progression, frequent hospitalization, and mortality. Use of antiarrhythmic drugs, particularly amiodarone can reduce ICD appropriate shocks by 34% [41]. In the OPTIC study (the Optimal Pharmacological Therapy in Cardioverter Defibrillator Patients), beta blocker and amiodarone combination were shown to be superior in suppression of VT recurrence compared to BB alone or sotalol [42]. Drug discontinuation rate at 1 year was found to be 18.2% for amiodarone, 23.5% for sotalol, and 5.3% for BB. Mexiletine, a class 1b antiarrhythmic drug, was shown to reduce VT recurrence as an adjunct to amiodarone in amiodarone-refractory VT in patients with ICD [43]. Ranolazine, a late Na channel inhibitor, was also shown to reduce VT burden and ICD shocks in patients with drug refractory VT and ICD [44].

Radiofrequency catheter ablation can be lifesaving in patients with ICD and repetitive shocks. In ischemic cardiomyopathy, some trials such as SMASH-VT (Substrate Mapping and Ablation in Sinus Rhythm to Halt Ventricular Tachycardia), VTACH (Ventricular Tachycardia Ablation in Coronary Heart Disease), and VANISH trials have shown the superiority of ablation for reducing ICD shocks [45–47]. The SMASH-VT trial compared ICD implantation plus prophylactic ablation to ICD implantation alone in patients with recent VT. Ablation reduced ICD shocks significantly from 31 to 9% and reduced VT from 33 to 12%. The VTACH trial assessed the effect of catheter ablation in patients with ischemic cardiomyopathy and mappable VT. Ablation significantly prolonged time to recurrent VT. The VANISH trial compared catheter ablation to escalation of antiarrhythmic therapy on top of first-line antiarrhythmic therapy in patients with VT. Ablation significantly reduced composite outcome of death, appropriate ICD shocks, and VT storm. Repetitive ICD shocks should also warrant referral to an advanced heart failure unit, capable for left ventricular assist device (LVAD) implantation and transplantation [48]. Catheter ablation of VT has risk of complication like all other invasive procedures. Complications related to these procedures are cardiac perforation, systemic embolism including myocardial infarction/stroke, vascular complications, and mortality.

Autonomic modulation procedures may also be applied for VT refractory to ablation. It was shown that videoscopic surgical cardiac sympathetic denervation may reduce the number of ICD shocks in refractory cases [49]. The surgery involves removal of the lower half of the stellate ganglion and T2-T4 stellate ganglia. This technique is especially effective when sympathetic denervation was made bilaterally. Renal denervation was also shown to reduce VT recurrences [50].

Stereotactic body radiation therapy (SBRT) for VT in HF patients has recently emerged as a new way of suppression of VT. SBRT is a technique that delivers high dose of radiation (25 gray) to target tissues with reduced exposure to normal adjacent tissues. SBRT has been used for decades to target various cancers. First, Cuculich et al. showed a 99.9% reduction in VT burden with cardiac SBRT in a case series of five patients with a high burden of drug-refractory VT, who had been suffering through repeated ICD shocks [51]. And recently, ENCORE VT trial showed that SBRT reduced VT and premature ventricular contraction episodes 94% at 6 months among 18 patients with treatmentrefractory VT, over half of whom presented with VT storm [52].

**83**

**Figure 4.**

*taking blood from left ventricle and pumping it to aorta.*

*Ventricular Tachycardia and Heart Failure DOI: http://dx.doi.org/10.5772/intechopen.85256*

may be applied in these patients.

In selected cases with recurrent VT which cannot be managed with the treatment recommendation given above, implantation of LVAD could temporarily stabilize patient hemodynamically, as well as improve reverse remodeling. LVAD is a battery-operated mechanical pump, which takes the blood from failed LV and pumps it to the aorta to be transmitted to the rest of the body (**Figure 4**). There are not many heart failure patients with LVAD. However, the management of VT in this patient population requires mention since it is somewhat different than HF patients without LVAD. LVAD may be able to continue maintaining cardiac output in spite of sustained VT, and most of the LVAD patients have ICD in place. When such patients present to the emergency department, first patient hemodynamic status should be assessed. If the blood pressure checked by Doppler ultrasonography is okay, it is reasonable to transfer the patient to a tertiary center where there is LVAD specialist and electrophysiologist. If there is hemodynamic compromise, then the patient should be immediately converted to normal sinus rhythm with electrical shock [53]. If the patient is a candidate neither for transplantation nor LVAD, end-of-life care should be applied for palliation. Shared decision making with the patient and relatives should be done, and discussion regarding measures such as ICD deactivation

*A schematic representation of a left ventricle assist device (LVAD) showing battery-operated mechanical pump*

*Ventricular Tachycardia and Heart Failure DOI: http://dx.doi.org/10.5772/intechopen.85256*

*Practical Applications of Electrocardiogram*

drug refractory VT and ICD [44].

vascular complications, and mortality.

presented with VT storm [52].

**5. Management of ICD repetitive shocks**

Despite ICD can effectively terminate ventricular tachycardia either by antitachycardia pacing or defibrillation shock, it cannot prevent VT recurrences. In patients with ICD, prevention of VT recurrence is required to minimize ICD shocks which can not only be quite uncomfortable for the patient leading to poor quality of life but also cause early battery depletion. Apart from these, recurrent shocks lead to HF progression, frequent hospitalization, and mortality. Use of antiarrhythmic drugs, particularly amiodarone can reduce ICD appropriate shocks by 34% [41]. In the OPTIC study (the Optimal Pharmacological Therapy in Cardioverter Defibrillator Patients), beta blocker and amiodarone combination were shown to be superior in suppression of VT recurrence compared to BB alone or sotalol [42]. Drug discontinuation rate at 1 year was found to be 18.2% for amiodarone, 23.5% for sotalol, and 5.3% for BB. Mexiletine, a class 1b antiarrhythmic drug, was shown to reduce VT recurrence as an adjunct to amiodarone in amiodarone-refractory VT in patients with ICD [43]. Ranolazine, a late Na channel inhibitor, was also shown to reduce VT burden and ICD shocks in patients with

Radiofrequency catheter ablation can be lifesaving in patients with ICD and repetitive shocks. In ischemic cardiomyopathy, some trials such as SMASH-VT

Autonomic modulation procedures may also be applied for VT refractory to ablation. It was shown that videoscopic surgical cardiac sympathetic denervation may reduce the number of ICD shocks in refractory cases [49]. The surgery involves removal of the lower half of the stellate ganglion and T2-T4 stellate ganglia. This technique is especially effective when sympathetic denervation was made bilater-

Stereotactic body radiation therapy (SBRT) for VT in HF patients has recently

emerged as a new way of suppression of VT. SBRT is a technique that delivers high dose of radiation (25 gray) to target tissues with reduced exposure to normal adjacent tissues. SBRT has been used for decades to target various cancers. First, Cuculich et al. showed a 99.9% reduction in VT burden with cardiac SBRT in a case series of five patients with a high burden of drug-refractory VT, who had been suffering through repeated ICD shocks [51]. And recently, ENCORE VT trial showed that SBRT reduced VT and premature ventricular contraction episodes 94% at 6 months among 18 patients with treatmentrefractory VT, over half of whom

ally. Renal denervation was also shown to reduce VT recurrences [50].

(Substrate Mapping and Ablation in Sinus Rhythm to Halt Ventricular Tachycardia), VTACH (Ventricular Tachycardia Ablation in Coronary Heart Disease), and VANISH trials have shown the superiority of ablation for reducing ICD shocks [45–47]. The SMASH-VT trial compared ICD implantation plus prophylactic ablation to ICD implantation alone in patients with recent VT. Ablation reduced ICD shocks significantly from 31 to 9% and reduced VT from 33 to 12%. The VTACH trial assessed the effect of catheter ablation in patients with ischemic cardiomyopathy and mappable VT. Ablation significantly prolonged time to recurrent VT. The VANISH trial compared catheter ablation to escalation of antiarrhythmic therapy on top of first-line antiarrhythmic therapy in patients with VT. Ablation significantly reduced composite outcome of death, appropriate ICD shocks, and VT storm. Repetitive ICD shocks should also warrant referral to an advanced heart failure unit, capable for left ventricular assist device (LVAD) implantation and transplantation [48]. Catheter ablation of VT has risk of complication like all other invasive procedures. Complications related to these procedures are cardiac perforation, systemic embolism including myocardial infarction/stroke,

**82**

In selected cases with recurrent VT which cannot be managed with the treatment recommendation given above, implantation of LVAD could temporarily stabilize patient hemodynamically, as well as improve reverse remodeling. LVAD is a battery-operated mechanical pump, which takes the blood from failed LV and pumps it to the aorta to be transmitted to the rest of the body (**Figure 4**). There are not many heart failure patients with LVAD. However, the management of VT in this patient population requires mention since it is somewhat different than HF patients without LVAD. LVAD may be able to continue maintaining cardiac output in spite of sustained VT, and most of the LVAD patients have ICD in place. When such patients present to the emergency department, first patient hemodynamic status should be assessed. If the blood pressure checked by Doppler ultrasonography is okay, it is reasonable to transfer the patient to a tertiary center where there is LVAD specialist and electrophysiologist. If there is hemodynamic compromise, then the patient should be immediately converted to normal sinus rhythm with electrical shock [53]. If the patient is a candidate neither for transplantation nor LVAD, end-of-life care should be applied for palliation. Shared decision making with the patient and relatives should be done, and discussion regarding measures such as ICD deactivation may be applied in these patients.

#### **Figure 4.**

*A schematic representation of a left ventricle assist device (LVAD) showing battery-operated mechanical pump taking blood from left ventricle and pumping it to aorta.*

VT storm is a medical emergency requiring prompt intervention. Reversible causes of VT, such as hypokalemia, hypomagnesemia, ischemia, and hypoxia should be sought and corrected where applicable. Beta blocker dose should be uptitrated to decrease the sympathetic tone. Another intervention to reduce sympathetic drive is sedation. Radiofrequency catheter ablation has been shown to be effective in controlling VT storm [54].

#### **6. Conclusion**

Ventricular tachycardia is a frequent event in HF population and is one of the poor prognostic factors related with HF. Management of VT is important because it is associated with SCD which is the responsible cause of death in 50% of patients with HF. Optimization of guideline-directed treatment is the most important step to prevent occurrence of VT in these patients. ICD has resulted marked improvement in survival of patients with HF and VT. However, repetitive ICD shocks due to recurrent VT poses a great problem and decreases survival. Antiarrhythmic therapy and VT ablation generally offer a complementary treatment in patients with ICD. Patients with VT who have failed standard therapy (antiarrhythmic therapy and catheter ablation) have limited options, with one-year survival below 20%. Autonomic modulation procedures and stereotactic body radiation therapy could be applied in patients with refractory VT. Patients with recurrent VT despite all other measures should be referred to tertiary centers where they are evaluated in respect of indications for LVAD implantation and transplantation.

#### **Author details**

Hakan Altay Baskent University, Faculty of Medicine, Istanbul Hospital, Turkey

\*Address all correspondence to<EMAIL_ADDRESS>
© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

**85**

*Ventricular Tachycardia and Heart Failure DOI: http://dx.doi.org/10.5772/intechopen.85256*

[1] Antiarrhythmics versus Implantable Defibrillators (AVID) Investigators. A comparison of antiarrhythmic-drug therapy with implantable defibrillators in patients resuscitated from nearfatal ventricular arrhythmias. NEJM.

prevention of sudden cardiac death: Executive summary: A Report of the American College of Cardiology/ American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Heart Rhythm. 2018;**15**(10):e190-e252. DOI: 10.1016/j. hrthm.2017.10.035. Epub 2017 Oct 30

[9] Tisdale JE, Patel R, Webb CR, Borzak S, Zarowitz BJ. Electrophysiologic and prodysrhythmic effects of intravenous inotropic agents. Progress in Cardiovascular Diseases.

[10] Nakahara S, Chien C, Gelow J, et al. Ventricular dysrhythmias after left ventricular assist device. Circulation: Arrhythmia and Electrophysiology.

[11] Yalagudri S, Zin Thu N, Devidutta S, Saggu D, Thachil A, Chennapragada S, et al. Tailored approach for management of ventricular tachycardia in cardiac sarcoidosis. Journal of Cardiovascular Electrophysiology. 2017;**28**(8):893-902.

[12] Priori SG, Blomström-Lundqvist C, Mazzanti A, Blom N, Borggrefe M, Camm J, et al. Task Force for the Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death of the European Society of Cardiology (ESC) 2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: The Task Force for the Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death of the European Society of Cardiology (ESC)Endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC). Europace. 2015;**17**(11):1601-1687. DOI: 10.1093/europace/euv319. Epub

1995;**38**:167-180

2013;**6**:648-654

DOI: 10.1111/jce.13228

2015 Aug 29

[2] Chan MM, Lam CS. How do patients with heart failure with preserved ejection fraction die? European Journal of Heart Failure. 2013;**15**:604-613

[4] Kunz R, Burnand B, Schünemann HJ, et al. Das GRADE-system. Der Internist.

[5] Klein L, Hsia H. Sudden cardiac death in heart failure. Cardiology

[6] Smer A, Saurav A, Azzouz MS, Salih M, Ayan M, Abuzaid A, et al. Meta-analysis of risk of ventricular arrhythmias after improvement in left ventricular ejection fraction during follow-up in patients with primary prevention implantable cardioverter defibrillators. The American Journal of Cardiology. 2017;**120**(2):279-286. DOI: 10.1016/j.amjcard.2017.04.020. Epub

[7] Baldinger SH, Stevenson WG, John RM. Ablation of ischemic ventricular tachycardia: Evidence, techniques, results, and future directions. Current Opinion in Cardiology. 2016;**31**:29-36

[8] Al-Khatib SM, Stevenson WG, Ackerman MJ, Bryant WJ, Callans DJ, Curtis AB, et al. 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the

[3] Moss AJ, Greenberg H, Case RB, et al. Long-term clinical course of patients after termination of ven-tricular tachyarrhythmia by an implanted defibrillator. Circulation.

2004;**110**(25):3760-3765

Clinics. 2014;**32**:135-144

2008;**49**:673-680

2017 Apr 27

1997;**337**:1576-1583

**References**

*Ventricular Tachycardia and Heart Failure DOI: http://dx.doi.org/10.5772/intechopen.85256*

#### **References**

*Practical Applications of Electrocardiogram*

effective in controlling VT storm [54].

**6. Conclusion**

VT storm is a medical emergency requiring prompt intervention. Reversible causes of VT, such as hypokalemia, hypomagnesemia, ischemia, and hypoxia should be sought and corrected where applicable. Beta blocker dose should be uptitrated to decrease the sympathetic tone. Another intervention to reduce sympathetic drive is sedation. Radiofrequency catheter ablation has been shown to be

Ventricular tachycardia is a frequent event in HF population and is one of the poor prognostic factors related with HF. Management of VT is important because it is associated with SCD which is the responsible cause of death in 50% of patients with HF. Optimization of guideline-directed treatment is the most important step to prevent occurrence of VT in these patients. ICD has resulted marked improvement in survival of patients with HF and VT. However, repetitive ICD shocks due to recurrent VT poses a great problem and decreases survival. Antiarrhythmic therapy and VT ablation generally offer a complementary treatment in patients with ICD. Patients with VT who have failed standard therapy (antiarrhythmic therapy and catheter ablation) have limited options, with one-year survival below 20%. Autonomic modulation procedures and stereotactic body radiation therapy could be applied in patients with refractory VT. Patients with recurrent VT despite all other measures should be referred to tertiary centers where they are evaluated in respect

**84**

**Author details**

Hakan Altay

provided the original work is properly cited.

© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

Baskent University, Faculty of Medicine, Istanbul Hospital, Turkey

\*Address all correspondence to<EMAIL_ADDRESS>
of indications for LVAD implantation and transplantation.

[1] Antiarrhythmics versus Implantable Defibrillators (AVID) Investigators. A comparison of antiarrhythmic-drug therapy with implantable defibrillators in patients resuscitated from nearfatal ventricular arrhythmias. NEJM. 1997;**337**:1576-1583

[2] Chan MM, Lam CS. How do patients with heart failure with preserved ejection fraction die? European Journal of Heart Failure. 2013;**15**:604-613

[3] Moss AJ, Greenberg H, Case RB, et al. Long-term clinical course of patients after termination of ven-tricular tachyarrhythmia by an implanted defibrillator. Circulation. 2004;**110**(25):3760-3765

[4] Kunz R, Burnand B, Schünemann HJ, et al. Das GRADE-system. Der Internist. 2008;**49**:673-680

[5] Klein L, Hsia H. Sudden cardiac death in heart failure. Cardiology Clinics. 2014;**32**:135-144

[6] Smer A, Saurav A, Azzouz MS, Salih M, Ayan M, Abuzaid A, et al. Meta-analysis of risk of ventricular arrhythmias after improvement in left ventricular ejection fraction during follow-up in patients with primary prevention implantable cardioverter defibrillators. The American Journal of Cardiology. 2017;**120**(2):279-286. DOI: 10.1016/j.amjcard.2017.04.020. Epub 2017 Apr 27

[7] Baldinger SH, Stevenson WG, John RM. Ablation of ischemic ventricular tachycardia: Evidence, techniques, results, and future directions. Current Opinion in Cardiology. 2016;**31**:29-36

[8] Al-Khatib SM, Stevenson WG, Ackerman MJ, Bryant WJ, Callans DJ, Curtis AB, et al. 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the

prevention of sudden cardiac death: Executive summary: A Report of the American College of Cardiology/ American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Heart Rhythm. 2018;**15**(10):e190-e252. DOI: 10.1016/j. hrthm.2017.10.035. Epub 2017 Oct 30

[9] Tisdale JE, Patel R, Webb CR, Borzak S, Zarowitz BJ. Electrophysiologic and prodysrhythmic effects of intravenous inotropic agents. Progress in Cardiovascular Diseases. 1995;**38**:167-180

[10] Nakahara S, Chien C, Gelow J, et al. Ventricular dysrhythmias after left ventricular assist device. Circulation: Arrhythmia and Electrophysiology. 2013;**6**:648-654

[11] Yalagudri S, Zin Thu N, Devidutta S, Saggu D, Thachil A, Chennapragada S, et al. Tailored approach for management of ventricular tachycardia in cardiac sarcoidosis. Journal of Cardiovascular Electrophysiology. 2017;**28**(8):893-902. DOI: 10.1111/jce.13228

[12] Priori SG, Blomström-Lundqvist C, Mazzanti A, Blom N, Borggrefe M, Camm J, et al. Task Force for the Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death of the European Society of Cardiology (ESC) 2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: The Task Force for the Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death of the European Society of Cardiology (ESC)Endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC). Europace. 2015;**17**(11):1601-1687. DOI: 10.1093/europace/euv319. Epub 2015 Aug 29

[13] Al-Gobari M, El Khatib C, Pillon F, Gueyffier F. β-Blockers for the prevention of sudden cardiac death in heart failure patients: a meta-analysis of randomized controlled trials. BMC Cardiovascular Disorders. 2013;**13**(52):1-9. DOI: 10.1186/1471-2261-13-52

[14] Pitt B, Remme W, Zannad F, Neaton J, Martinez F, Roniker B, et al. Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study Investigators. Epub 2003 Mar 31. Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. The New England Journal of Medicine. 2003;**348**(14):1309-1321

[15] Moss AJ, Zareba W, Hall WJ, Klein H, Wilber DJ, Cannom DS, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. The New England Journal of Medicine. 2002;**346**:877-883

[16] Peck KY, Lim YZ, Hopper I, Krum H. Medical therapy versus implantable cardioverter-defibrillator in preventing sudden cardiac death in patients with left ventricular systolic dysfunction and heart failure: A meta-analysis of >35,000 patients. International Journal of Cardiology. 2014;**173**(2):197-203. DOI: 10.1016/j.ijcard.2014.02.014. Epub 2014 Feb 22

[17] Zannad F, McMurray JJ, Krum H, van Veldhuisen DJ, Swedberg K, Shi H, et al. Eplerenone in patients with systolic heart failure and mild symptoms. The New England Journal of Medicine. 2011;**364**:11-21

[18] McMurray JJ, Packer M, Desai AS, et al. Angiotensin-neprilysin inhibition versus enalapril in heart failure. The New England Journal of Medicine. 2014;**371**:993-1004

[19] Ponikowski P, Voors AA, Anker SD, Bueno H, Cleland JG, Coats AJ, et al.

Authors/task force members; document reviewers.2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The task force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. European Journal of Heart Failure. 2016;**18**(8):891-975. DOI: 10.1002/ejhf.592. Epub 2016 May 20

[20] Cardiac Arrhythmia Suppression Trial (CAST) Investigators. Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction. The New England Journal of Medicine. 1989;**321**:406-412

[21] Bardy GH, Lee KL, Mark DB, Poole JE, Packer DL, Boineau R, et al. Sudden cardiac death in heart failure trial (SCD-HeFT) Investigators. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. The New England Journal of Medicine. 2005;**352**:225-237. DOI: 10.1056/ NEJMoa043399

[22] Piccini JP, Berger JS, O'Connor CM. Amiodarone for the prevention of sudden cardiac death: a meta-analysis of randomized controlled trials. European Heart Journal. 2009;**30**:1245-1253

[23] Bokhari F, Newman D, Greene M, Ko-rley V, Mangat I, Dorian P. Longterm comparison of the implantable cardioverter defibrillator versus amiodarone: Eleven-year follow-up of a subset of patients in the Canadian Implantable Defibrillator Study (CIDS). Circulation. 2004;**110**:112-116

[24] Waldo AL, Camm AJ, deRuyter H, Friedman PL, MacNeil DJ, Pauls JF, et al. Effect of d-sotalol on mortality in patients with left ventricular dysfunction after recent and remote myocardial infarction. The SWORD

**87**

*Ventricular Tachycardia and Heart Failure DOI: http://dx.doi.org/10.5772/intechopen.85256*

Investigators. Survival With Oral d-Sotalol. Lancet. 1996;**348**:7-12

[26] Horowitz LN, Josephson ME, Farshidi A, Spielman SR, Michelson EL, Greenspan AM. Recurrent sustained ventricular tachycardia 3. Role of the electrophysiologic study in selection of antiarrhythmic regimens. Circulation.

[27] Connolly SJ, Hallstrom AP, Cappato R, Schron EB, Kuck KH, Zipes DP, et al. Meta-analysis of the implantable cardioverter defibrillator secondary prevention trials. AVID, CASH and CIDS studies. Antiar-rhythmics vs Implantable Defibrillator study. Cardiac Arrest Study Hamburg. Canadian Implantable Defibrillator Study. European Heart Journal. 2000;**21**: 2071-2078. DOI: 10.1053/euhj.2000.2476

[28] Moss AJ, Zareba W, Hall WJ, Klein H, Wilber DJ, Cannom DS, et al. Multicenter automatic defibrillator implantation trial II investigators. Prophylactic implantation of a

NEJMoa013474

defibrillator in patients with myocardial infarction and reduced ejection fraction. The New England Journal of Medicine. 2002;**346**:877-883. DOI: 10.1056/

[29] Kadish A, Dyer A, Daubert JP, Quigg R, Estes NA, Anderson KP, et al. Defibrillators in non-ischemic cardiomy-opathy treatment evaluation (DEFINITE) Investigators. Prophylactic defibrillator implantation in patients with nonischemic dilated. NEJM.

2004;**350**(21):2151-2158

[30] Sweeney MO, Sherfesee L, DeGroot PJ, Wathen MS, Wilkoff

2000;**356**:2052-2058

1978;**58**(6):986-997

[25] Kober L, Bloch Thomsen PE, Moller M, Torp-Pedersen C, Carlsen J, Sandoe E, et al. Effect of dofetilide in patients with recent myocardial infarction and left-ventricular dysfunction: A randomised trial. Lancet.

BL. Differences in effects of

arrhythmias on mortality in

electrical therapy type for ventricular

implantable cardioverter-defibrillator patients. Heart Rhythm. 2010;**7**:353- 360. DOI: 10.1016/j. hrthm.2009.11.027

[31] Cleland JG, Daubert JC, Erdmann E, Freemantle N, Gras D, Kappenberger

L, et al. Longer-term effects of cardiac resynchronization therapy on mortality in heart failure [the CArdiac REsynchronization-Heart Failure (CARE-HF) trial ex- tension phase]. European Heart Journal.

[32] Sapp JL, Parkash R, Wells GA, Yetisir E, Gardner MJ, Healey JS, et al. Cardiac resynchronization therapy reduces ven-tricular arrhythmias in primary but not secondary prophylactic implantable cardioverter defibrillator patients: Insight from the resynchronization in ambulatory heart failure trial. Circulation. Arrhythmia and Electrophysiology. 2017;**10**. pii:

[33] Muresan L, Cismaru G, Martins RP, Bataglia A, Rosu R, Puiu M, et al. Recommendations for the use of electrophysiological study: Update 2018. Hellenic Journal of Cardiology. 2018S;**1109- 9666**(18)30352-X:1-19. DOI: 10.1016/j.

[34] Pagé PL, Cardinal R, Shenasa M, Kaltenbrunner W, Cossette R, Nadeau R. Surgical treatment of ventricular tachycardia. Regional cryoablation guided by computerized epicardial and endocardial mapping. Circulation.

[35] Dinov B, Fiedler L, Schönbauer R, et al. Outcomes in catheter ablation of ventricular tachycardia in dilated nonischemic cardiomyopathy in comparison to ischemic cardiomyopathy: Results from the Prospective HEart Centre of LeiPzig VT (HELP-VT) Study. Circulation. 2014;**129**:728-736

2006;**27**:1928-1932

004875

hjc.2018.09.002

1989;**80**(3 Pt 1):I124-I134

*Ventricular Tachycardia and Heart Failure DOI: http://dx.doi.org/10.5772/intechopen.85256*

Investigators. Survival With Oral d-Sotalol. Lancet. 1996;**348**:7-12

*Practical Applications of Electrocardiogram*

Authors/task force members; document reviewers.2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The task force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. European Journal of Heart Failure. 2016;**18**(8):891-975. DOI: 10.1002/ejhf.592. Epub 2016 May 20

[20] Cardiac Arrhythmia Suppression Trial (CAST) Investigators. Preliminary

flecainide on mortality in a randomized

[21] Bardy GH, Lee KL, Mark DB, Poole JE, Packer DL, Boineau R, et al. Sudden cardiac death in heart failure trial (SCD-HeFT) Investigators. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. The New England Journal of Medicine. 2005;**352**:225-237. DOI: 10.1056/

[22] Piccini JP, Berger JS, O'Connor CM. Amiodarone for the prevention of sudden cardiac death: a meta-analysis of randomized controlled trials. European Heart Journal. 2009;**30**:1245-1253

[23] Bokhari F, Newman D, Greene M, Ko-rley V, Mangat I, Dorian P. Longterm comparison of the implantable cardioverter defibrillator versus amiodarone: Eleven-year follow-up of a subset of patients in the Canadian Implantable Defibrillator Study (CIDS).

Circulation. 2004;**110**:112-116

[24] Waldo AL, Camm AJ, deRuyter H, Friedman PL, MacNeil DJ, Pauls JF, et al. Effect of d-sotalol on mortality in patients with left ventricular dysfunction after recent and remote myocardial infarction. The SWORD

report: effect of encainide and

trial of arrhythmia suppression after myocardial infarction. The New England Journal of Medicine.

1989;**321**:406-412

NEJMoa043399

[13] Al-Gobari M, El Khatib C, Pillon F, Gueyffier F. β-Blockers for the prevention of sudden cardiac death in heart failure patients: a meta-analysis of randomized controlled trials. BMC Cardiovascular Disorders. 2013;**13**(52):1-9. DOI:

10.1186/1471-2261-13-52

[14] Pitt B, Remme W, Zannad F, Neaton J, Martinez F, Roniker B, et al. Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study Investigators. Epub 2003 Mar 31. Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. The New England Journal of Medicine. 2003;**348**(14):1309-1321

[15] Moss AJ, Zareba W, Hall WJ, Klein H, Wilber DJ, Cannom DS, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. The New England Journal of Medicine.

[16] Peck KY, Lim YZ, Hopper I, Krum H. Medical therapy versus implantable cardioverter-defibrillator in preventing sudden cardiac death in patients with left ventricular systolic dysfunction and heart failure: A meta-analysis of >35,000 patients. International Journal of Cardiology. 2014;**173**(2):197-203. DOI: 10.1016/j.ijcard.2014.02.014. Epub

[17] Zannad F, McMurray JJ, Krum H, van Veldhuisen DJ, Swedberg K, Shi H, et al. Eplerenone in patients with systolic heart failure and mild symptoms. The New England Journal of

[18] McMurray JJ, Packer M, Desai AS, et al. Angiotensin-neprilysin inhibition versus enalapril in heart failure. The New England Journal of Medicine.

[19] Ponikowski P, Voors AA, Anker SD, Bueno H, Cleland JG, Coats AJ, et al.

Medicine. 2011;**364**:11-21

2014;**371**:993-1004

2002;**346**:877-883

2014 Feb 22

**86**

[25] Kober L, Bloch Thomsen PE, Moller M, Torp-Pedersen C, Carlsen J, Sandoe E, et al. Effect of dofetilide in patients with recent myocardial infarction and left-ventricular dysfunction: A randomised trial. Lancet. 2000;**356**:2052-2058

[26] Horowitz LN, Josephson ME, Farshidi A, Spielman SR, Michelson EL, Greenspan AM. Recurrent sustained ventricular tachycardia 3. Role of the electrophysiologic study in selection of antiarrhythmic regimens. Circulation. 1978;**58**(6):986-997

[27] Connolly SJ, Hallstrom AP, Cappato R, Schron EB, Kuck KH, Zipes DP, et al. Meta-analysis of the implantable cardioverter defibrillator secondary prevention trials. AVID, CASH and CIDS studies. Antiar-rhythmics vs Implantable Defibrillator study. Cardiac Arrest Study Hamburg. Canadian Implantable Defibrillator Study. European Heart Journal. 2000;**21**: 2071-2078. DOI: 10.1053/euhj.2000.2476

[28] Moss AJ, Zareba W, Hall WJ, Klein H, Wilber DJ, Cannom DS, et al. Multicenter automatic defibrillator implantation trial II investigators. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. The New England Journal of Medicine. 2002;**346**:877-883. DOI: 10.1056/ NEJMoa013474

[29] Kadish A, Dyer A, Daubert JP, Quigg R, Estes NA, Anderson KP, et al. Defibrillators in non-ischemic cardiomy-opathy treatment evaluation (DEFINITE) Investigators. Prophylactic defibrillator implantation in patients with nonischemic dilated. NEJM. 2004;**350**(21):2151-2158

[30] Sweeney MO, Sherfesee L, DeGroot PJ, Wathen MS, Wilkoff BL. Differences in effects of electrical therapy type for ventricular arrhythmias on mortality in implantable cardioverter-defibrillator patients. Heart Rhythm. 2010;**7**:353- 360. DOI: 10.1016/j. hrthm.2009.11.027

[31] Cleland JG, Daubert JC, Erdmann E, Freemantle N, Gras D, Kappenberger L, et al. Longer-term effects of cardiac resynchronization therapy on mortality in heart failure [the CArdiac REsynchronization-Heart Failure (CARE-HF) trial ex- tension phase]. European Heart Journal. 2006;**27**:1928-1932

[32] Sapp JL, Parkash R, Wells GA, Yetisir E, Gardner MJ, Healey JS, et al. Cardiac resynchronization therapy reduces ven-tricular arrhythmias in primary but not secondary prophylactic implantable cardioverter defibrillator patients: Insight from the resynchronization in ambulatory heart failure trial. Circulation. Arrhythmia and Electrophysiology. 2017;**10**. pii: 004875

[33] Muresan L, Cismaru G, Martins RP, Bataglia A, Rosu R, Puiu M, et al. Recommendations for the use of electrophysiological study: Update 2018. Hellenic Journal of Cardiology. 2018S;**1109- 9666**(18)30352-X:1-19. DOI: 10.1016/j. hjc.2018.09.002

[34] Pagé PL, Cardinal R, Shenasa M, Kaltenbrunner W, Cossette R, Nadeau R. Surgical treatment of ventricular tachycardia. Regional cryoablation guided by computerized epicardial and endocardial mapping. Circulation. 1989;**80**(3 Pt 1):I124-I134

[35] Dinov B, Fiedler L, Schönbauer R, et al. Outcomes in catheter ablation of ventricular tachycardia in dilated nonischemic cardiomyopathy in comparison to ischemic cardiomyopathy: Results from the Prospective HEart Centre of LeiPzig VT (HELP-VT) Study. Circulation. 2014;**129**:728-736

[36] Della Bella P, Trevisi N. Catheter ablation of ventricular tachycardia in nonischemic dilated cardiomyopathy: A difficult field where we should focus our efforts. Circulation. Arrhythmia and Electrophysiology 2016;**9**(10). pii: e004649

[37] Kanagaratnam L, Tomassoni G, Schweikert R, Pavia S, Bash D, Beheiry S, et al. Ventricular tachycardias arising from the aortic sinus of valsalva: An under-recognized variant of left outflow tract ventricular tachycardia. Journal of the American College of Cardiology. 2001;**37**(5):1408-1414

[38] Fragakis N, Karamitsos TD, Vassilikos V. Successful catheter ablation of an incessant ventricular tachycardia originating from the posterior papillary muscle in a structurally normal right ventricle. Hellenic Journal of Cardiology. 2016;**57**:286-288

[39] Saguner AM, Medeiros-Domingo A, Schwyzer MA, On CJ, Haegeli LM, Wolber T, et al. Usefulness of inducible ventricular tachycardia to predict long-term adverse outcomes in arrhythmogenic right ventricular cardiomyopathy. The American Journal of Cardiology. 2013;**111**(2):250-257. DOI: 10.1016/j. amjcard.2012.09.025

[40] Lim KK, Maron BJ, Knight BP. Successful catheter ablation of hemodynamically unstable monomorphic ventricular tachycardia in a patient with hypertrophic cardiomyopathy and apical aneurysm. Journal of Cardiovascular Electrophysiology. 2009;**20**(4):445-447. DOI: 10.1111/j.1540-8167.2008.01366.x

[41] Antangeli P, Muser D, Maeda S, et al. Comparitive effectiveness of antiarrhythmic drugs and catheter ablation for the prevention of recurrent ventricular tachycardia in patients with implantable cardioverter-defibrillators: A systematic review and meta-analysis

of randomized contolled trials. Heart Rhythm. 2016;**13**:1552-1559. DOI: 10.1016/j. hrthm.2016.03.004. PMID: 26961297

[42] Connolly SJ, Dorian P, Roberts RS, et al. Comparison of beta-blockers, amiodarone plus beta-blockers, or sotalol for prevention of shocks from implantable cardioverter defibrillators: The optic study: A randomized trial. JAMA. 2006;**295**:165-171

[43] Gao D, Van Herendael H, Alshengeiti L, et al. Mexiletine as an adjunctive therapy to amiodarone reduces the frequency of ventricular tachyarrhythmia events in patients with an implantable defibrillator. Journal of Cardiovascular Pharmacology. 2013;**62**:199-204. DOI: 10.1097/ FJC.0b013e31829651fe. PMID: 23609328

[44] Bunch TJ, Mahapatra S, Murdock D, Molden J, Weiss JP, May HT, et al. Ranolazine reduces ventricular tachycardia burden and ICD shocks in patients with drug-refractory ICD shocks. Pacing and Clinical Electrophysiology. 2011;**34**:1600-1606

[45] Reddy VY, Reynolds MR, Neuzil P, et al. Prophylactic catheter ablation for the prevention of defibrillator therapy. The New England Journal of Medicine. 2007;**357**:2657-2665. DOI: 10.1056/ NEJMoa065457. PMID: 18160685

[46] Kuck KH, Schaumann A, Eckhardt L, et al. Catheter ablation of stable ventricular tachycardia before defibrillator implantation in patients with coronary heart disease (VTACH): A multicentre randomised controlled trial. Lancet. 2010;**375**:31-40. DOI: 10.1111/jce.12073. PMID: 23350967

[47] Sapp JL, Wells GA, Parkash R, Stevenson WG, Blier L, Sarrazin JF, et al. Ventricular tachycardia ablation versus escalation of antiarrhythmic drugs. The New England Journal of Medicine. 2016;**375**(2):111-121

**89**

*Ventricular Tachycardia and Heart Failure DOI: http://dx.doi.org/10.5772/intechopen.85256*

[48] Yancy CW, Januzzi JL Jr, Allen LA, Butler J, Davis LL, Fonarow GC, et al. 2017 ACC expert consensus decision pathway for optimization of heart failure treatment: Answers to 10 pivotal issues about heart failure with reduced ejection fraction: A report of the American College of Cardiology Task Force on Expert Consensus Decision Pathways. Journal of the American College of Cardiology. 2018;**71**(2): 201-230. DOI: 10.1016/j.jacc.2017.11.025. [54] Carbucicchio C, Santamaria M, Trevisi N, Maccabelli G, Giraldi F, Fassini G, et al. Catheter ablation for the treatment of electrical storm in patients with implantable cardioverterdefibrillators: Short and long-term outcomes in a prospective single-center study. Circulation. 2008;**117**:462-469