**3. Different parameters affecting the explosive welded products**

There are various parameters which influence the final product of the explosive welding process. Therefore, careful control of welding parameters is very critical. The criteria for selection of the welding parameters depends upon the mechanical properties of the matting surfaces [32, 33]. Many researchers change the magnitude of these parameters by playing with the different parameters such as detonation velocity, stand-off distance, explosive type etc. The various process parameters are discussed below.

**Explosive:** In explosive welding, controlled energy of explosive is used to accelerate the flyer plate and help to impact on to the base plate, to produce a strong metallurgical bond. Explosive is generally characterized by their velocity of detonation (VoD) and density. In most of the engineering materials, the velocity of sound is between 4.5–6 km/s and most of the common explosives have VoD ranging between 6 and 7 km/s. Therefore, high VoD in explosive welding is not preferable as in case of joining the weld will get dismantle or in some cases it will destroy the material. In explosive welding, VoD is mostly applied in the range of 2–3 km/s to obtain a uniform detonation across the joining metal plates [32–34]. Many researchers have worked with different explosives to obtain a sound weld. A. Loureiro et al. have studied the effect of explosive mixture i.e. emulsion explosive with two different sensitizers i.e. hollow glass microspheres (HGMS) and expanded polystyrene spheres (EPS) on the weld interface of copper-aluminum. They observed improved surface using HGMS and higher wave amplitude was witnessed by employing EPS [35]. Similarly, many works related to explosive optimization have been done in the past in explosive welding [36, 37]. Recently Sherpa et al. have developed a low velocity of detonation (VoD) explosive welding process (LVEW)

**29**

**Table 1.**

*Explosive Welding Process to Clad Materials with Dissimilar Metallurgical Properties*

explosives used for explosive welding process are shown in **Table 1**.

interface which lead to the increase in corrosion rate [49].

defined limit it will cause entrapment of jet [33, 52].

melt pockets across the weld interface [20].

*Different explosives used in the explosive welding process.*

**3.1 Weldability window**

ANFO (ammonium nitrate

with fuel oil)

flyer plate [50, 51].

in which VoD was less than 2 km/s and obtained a sound joint [38]. Some of the

**Stand-off distance:** Stand-off distance is normally selected based on the thickness of the flyer plate and the explosive parameters. It is one of the critical parameters which influence the bond quality. Stand-off distance is selected basically to provide necessary dynamic bend angle and the impact velocity for proper bond to form. Durgutlu et al. studied the effect of stand-off distance on copper and stainless steel bond. They observed an increase in wavelength and amplitude of the wave with an increase in stand-off distance. As well as hardness value across the weld interface also increased with increasing stand-off distance [48]. M.R. Jandaghi et al. studied the effect of stand-off distance on the copper and aluminum interface. They observed that with an increase in stand-off distance, plastic deformation, kinetic energy at the collision point and as well as the melting increases at the weld

**Flyer plate velocity:** It is the velocity at which the flyer plate strike into the base plate after the detonation has started. To obtain good bonding, the flyer plate velocity should be in the described limits i.e. between the minimum and maximum flyer velocity. Experimenting with flyer plate velocity above defined range can lead to certain defects such as melting zone, cracks, brittle phases, bend and damage of

**Collision angle (β):** It is the angle formed between the flyer plate and the base plate during the collision process. Collision angle should be selected very carefully to meet the requirement of the bonding parameters. If the angle is selected below the critical collision angle, a jet-less phenomenon will occur and if β is chosen above

**Collision velocity (Vc):** It is the velocity with which collision point moves along the area being welded. For proper welding to occur there should be some plastic flow ahead of the collision point. Hence, the collision point velocity should be less than the sonic velocity in the metals. The smooth interface is observed at lower collision velocity while the wavy interface is observed at higher collision velocity at the weld interface. Increasing the collision velocity may also increase the chances of

The condition that should satisfy for proper bonding to take place is defined by weldability window. Detailed view with the description of weldability window is shown in **Figure 3**. It is plotted between collision angle (β) and collision velocity (Vp), where it is well defined by four different lines [50, 51]. The first limit is placed at the rightmost side in which formation of the jet at the collision point

SEP 7000 1300 [41, 42] Emulsion explosive 2200 1150 [43] Elbar-5 3000–3800 700–800 [44–46] PAVEX 2000–3000 530 [37, 47]

**) Ref.**

2300–2800 650–700 [39, 40]

**Explosive Velocity of detonation (m/s) Density (kg/m3**

*DOI: http://dx.doi.org/10.5772/intechopen.94448*

#### *Explosive Welding Process to Clad Materials with Dissimilar Metallurgical Properties DOI: http://dx.doi.org/10.5772/intechopen.94448*

in which VoD was less than 2 km/s and obtained a sound joint [38]. Some of the explosives used for explosive welding process are shown in **Table 1**.

**Stand-off distance:** Stand-off distance is normally selected based on the thickness of the flyer plate and the explosive parameters. It is one of the critical parameters which influence the bond quality. Stand-off distance is selected basically to provide necessary dynamic bend angle and the impact velocity for proper bond to form. Durgutlu et al. studied the effect of stand-off distance on copper and stainless steel bond. They observed an increase in wavelength and amplitude of the wave with an increase in stand-off distance. As well as hardness value across the weld interface also increased with increasing stand-off distance [48]. M.R. Jandaghi et al. studied the effect of stand-off distance on the copper and aluminum interface. They observed that with an increase in stand-off distance, plastic deformation, kinetic energy at the collision point and as well as the melting increases at the weld interface which lead to the increase in corrosion rate [49].

**Flyer plate velocity:** It is the velocity at which the flyer plate strike into the base plate after the detonation has started. To obtain good bonding, the flyer plate velocity should be in the described limits i.e. between the minimum and maximum flyer velocity. Experimenting with flyer plate velocity above defined range can lead to certain defects such as melting zone, cracks, brittle phases, bend and damage of flyer plate [50, 51].

**Collision angle (β):** It is the angle formed between the flyer plate and the base plate during the collision process. Collision angle should be selected very carefully to meet the requirement of the bonding parameters. If the angle is selected below the critical collision angle, a jet-less phenomenon will occur and if β is chosen above defined limit it will cause entrapment of jet [33, 52].

**Collision velocity (Vc):** It is the velocity with which collision point moves along the area being welded. For proper welding to occur there should be some plastic flow ahead of the collision point. Hence, the collision point velocity should be less than the sonic velocity in the metals. The smooth interface is observed at lower collision velocity while the wavy interface is observed at higher collision velocity at the weld interface. Increasing the collision velocity may also increase the chances of melt pockets across the weld interface [20].

## **3.1 Weldability window**

*Material Flow Analysis*

ness of flyer plate.

uniformly.

discussed below.

**2.3 Terminology used in explosive welding**

occur during collision due to explosion effects.

**Base plate:** It is the one which is placed at the open ground or at the anvil. This is kept stationary and is the one on which the cladding is performed. Both the base plate and the flyer plate are cleaned thoroughly and polished gently before welding. **Flyer plate:** It is the one which is placed above the base plate and during collision this plate hits onto the base plate. The selection of flyer plate and base plate is done on the basis of mass per unit area, whoever is less is placed as flyer plate. As com-

**Stand-off distance:** It is the one which maintains the distance between the flyer plate and the base plate. Stand-off distance helps the flyer plate to accelerate and acquire the required impact velocity to generate jetting. Apart from this, it also provides the exit path to the jet and the air formed between the flyer and base plate during the collision. In general stand-off distance is kept half or equal to the thick-

**Buffer sheet:** This sheet is placed over the flyer plate. It is made up of rubber or PVC. The main role of this sheet is to protect the flyer plate from damage which can

**Explosive box:** It is placed over the metal plates to be welded. This acts as a source of energy which provides the required forces to weld the materials. Explosive can be used as powder, slurry or sheet form which is spread over the buffer sheet

**Detonator:** This is placed at the top of the explosive box. The main function of the detonator is to help in initiating the main explosive. The detonator is detonated

There are various parameters which influence the final product of the explosive welding process. Therefore, careful control of welding parameters is very critical. The criteria for selection of the welding parameters depends upon the mechanical properties of the matting surfaces [32, 33]. Many researchers change the magnitude of these parameters by playing with the different parameters such as detonation velocity, stand-off distance, explosive type etc. The various process parameters are

**Explosive:** In explosive welding, controlled energy of explosive is used to accelerate the flyer plate and help to impact on to the base plate, to produce a strong metallurgical bond. Explosive is generally characterized by their velocity of detonation (VoD) and density. In most of the engineering materials, the velocity of sound is between 4.5–6 km/s and most of the common explosives have VoD ranging between 6 and 7 km/s. Therefore, high VoD in explosive welding is not preferable as in case of joining the weld will get dismantle or in some cases it will destroy the material. In explosive welding, VoD is mostly applied in the range of 2–3 km/s to obtain a uniform detonation across the joining metal plates [32–34]. Many researchers have worked with different explosives to obtain a sound weld. A. Loureiro et al. have studied the effect of explosive mixture i.e. emulsion explosive with two different sensitizers i.e. hollow glass microspheres (HGMS) and expanded polystyrene spheres (EPS) on the weld interface of copper-aluminum. They observed improved surface using HGMS and higher wave amplitude was witnessed by employing EPS [35]. Similarly, many works related to explosive optimization have been done in the past in explosive welding [36, 37]. Recently Sherpa et al. have developed a low velocity of detonation (VoD) explosive welding process (LVEW)

pared to base plate it has the lowest density as well as tensile strength.

with the help of dynamo placed at some distance from the trial site.

**3. Different parameters affecting the explosive welded products**

**28**

The condition that should satisfy for proper bonding to take place is defined by weldability window. Detailed view with the description of weldability window is shown in **Figure 3**. It is plotted between collision angle (β) and collision velocity (Vp), where it is well defined by four different lines [50, 51]. The first limit is placed at the rightmost side in which formation of the jet at the collision point

**Table 1.**

*Different explosives used in the explosive welding process.*

**Figure 3.** *Weldability window concepts for explosive welding process.*

is considered. As jetting is one of the important criteria in explosive welding. Abrahamson [53] linked welding velocity with the collision angle β as shown in Eq. 1 for the first limit. The second limit is placed at the left side of the weldability window which is related to the formation of wavy morphology at the weld interface. Cowan et al. introduced Reynolds number for describing the laminar and turbulent flow [20] as shown in Eq. 2. The third limit is related to the minimum flyer plate velocity (Vpmin) which ensure that the impact pressure developed at the collision point exceeds the yield strength of the materials. Lower boundary equation was developed for third limit as shown in Eq. 3. While the fourth limit corresponds to the maximum flyer plate velocity (Vpmax) which maintains the required impact pressure below the value so that the melting does not occur at the weld interface. To avoid melting Eq. 4 was developed by Wittman [50]. Therefore, in order to obtain good bond, selection of welding parameters should be with in the described limits of weldability window [20, 34, 50, 54].

$$V\_{\epsilon} = \frac{\beta}{10} + 5.5\tag{1}$$

$$R\_t = \frac{\left(\rho\_a + \rho\_b\right)V\_\epsilon^2}{2\left(\mathbf{H}\_a + \mathbf{H}\_b\right)}\tag{2}$$

**31**

**Table 2.**

*Explosive Welding Process to Clad Materials with Dissimilar Metallurgical Properties*

H sin =

1.2: Imperfectly cleaned plate surface

22 V

( )

Explosive welding process is capable of joining similar and dissimilar material combinations irrespective of the difference in physical and chemical properties.

**Material combination Welding configuration Explosive used Ref.** Al alloy -Al alloy Tube PETN [55] Steel-steel plates Parallel set-up Elbar-5 [56–58]

Copper-copper \_\_ \_\_ [59]

**Material combination Welding configuration Interlayer used Ref.**

Inclined set-up (Under

Aluminum to stainless steel Parallel set-up Cu, Ti & Ta [16]

Titanium and aluminum Parallel set-up Not used [61, 62] Aluminum and copper Parallel set-up Al5052, Cu & SS304 [63]

Al and Mg alloy Parallel set-up Not used [64, 65]

Aluminum and copper Parallel set-up Not used [67–69] Aluminum and steel Parallel set-up Not used [70–73]

Steel-steel Cylindrical Emulsion explosive/

Copper-copper alloy Parallel set-up Powder emulsion

water)

water)

Sn and Cu Inclined set-up (Under

*Material combinations joined using explosive welding process.*

=

2 c

*T Cm o KC Cp b N h*

β

*k*

V 2

*V*

ρ

*C*

1/2 1/4

ρ

ANFO

explosive

Parallel set-up Not used [17]

Parallel set-up Aluminum AA1050 [66]

Thin AZ31 [60]

Not used [41]

(3)

(4)

[36]

[43]

*DOI: http://dx.doi.org/10.5772/intechopen.94448*

Where HV : Vickers hardness no.

K: Constant value

Where Tm: Melting temperature,

**Similar materials combinations**

**Dissimilar materials combinations**

Titanium and magnesium alloy

C103 niobium alloy and C263

Aluminum and carbon steel and Aluminum-stainless steel

AZ31

nimonic alloy

Cp: Specific heat capacity, K: Thermal conductivity, h: Thickness of flyer plate, Cb: Bulk sound speed

Ρ: Density of the material

Take value 0.6: Plate surface is very clean

1 sin

**3.2 Different materials combination joined by explosive welding**

β

Where ρ ρ *a b* & : ρ Density of flyer plate and base plate

H &H *a b* : Hardness value of flyer plate and base plate

: *Rt* Reynolds number

*Explosive Welding Process to Clad Materials with Dissimilar Metallurgical Properties DOI: http://dx.doi.org/10.5772/intechopen.94448*

$$k\sin\beta = k\sqrt{\frac{\mathcal{H}\_\mathcal{V}}{\rho V\_\mathcal{C}^2}}\tag{3}$$

Where HV : Vickers hardness no.

*Material Flow Analysis*

is considered. As jetting is one of the important criteria in explosive welding. Abrahamson [53] linked welding velocity with the collision angle β as shown in Eq. 1 for the first limit. The second limit is placed at the left side of the weldability window which is related to the formation of wavy morphology at the weld interface. Cowan et al. introduced Reynolds number for describing the laminar and turbulent flow [20] as shown in Eq. 2. The third limit is related to the minimum flyer plate velocity (Vpmin) which ensure that the impact pressure developed at the collision point exceeds the yield strength of the materials. Lower boundary equation was developed for third limit as shown in Eq. 3. While the fourth limit corresponds to the maximum flyer plate velocity (Vpmax) which maintains the required impact pressure below the value so that the melting does not occur at the weld interface. To avoid melting Eq. 4 was developed by Wittman [50]. Therefore, in order to obtain good bond, selection of welding parameters should be with in the described limits

5.5

2

*V*

(1)

(2)

10 *Vc* = + β

*R* ρ +ρ = +

H &H *a b* : Hardness value of flyer plate and base plate

*t*

Where ρ ρ *a b* & : ρ Density of flyer plate and base plate

: *Rt* Reynolds number

( ) ( )

2H H *a bc*

*a b*

**30**

**Figure 3.**

of weldability window [20, 34, 50, 54].

*Weldability window concepts for explosive welding process.*

Ρ: Density of the material K: Constant value Take value 0.6: Plate surface is very clean 1.2: Imperfectly cleaned plate surface

$$\sin\left(\frac{\beta}{2}\right) = \frac{1}{2N} \frac{\left(T\_m \mathbf{C}\_o\right)^{1/2}}{\mathbf{V}\_c^2} \left(\frac{\mathbf{K} \mathbf{C}\_p \mathbf{C}\_b}{\rho h}\right)^{1/4} \tag{4}$$

Where Tm: Melting temperature,

Cp: Specific heat capacity, K: Thermal conductivity, h: Thickness of flyer plate, Cb: Bulk sound speed


**4. HIV infection may affect the natural history of atherogenesis**

Individuals infected with human immunodeficiency virus (HIV) have a different condition of life of the population free of infection with regard to morbidity and mortality from pre‐ mature atherosclerosis and cardiovascular, and its related complications[44]-[47].

Atherosclerosis is a systemic disorder characterized by the formation of cholesterol plaques, especially at the level of the intima of the arterial wall. All arteries can be affected, but the clinical consequences are more important at the level of coronary and carotid arteries of the lower limbs (LL).

Arterial disease is chronic, along with coronary artery disease and ischemic stroke, one of three clinical manifestations of the same pathophysiological process: atherothrombosis. The classic risk factors of atherosclerosis are: smoking, hypertension (HTN), diabetes mellitus (DM), hypercholesterolemia, and obesidade[48]. Atherosclerosisisamajor cause ofmortality worldwidemobility, andlow life expectancyis mainly due to heart attack and stroke(CVA)[49]-[51].

The morbidity and mortality among HIV-infected individuals with advanced disease was very high until the advent of potent antiretroviral therapy (HAART), which produced an improvement in quality and increased expectation [52]-[55].

This therapy, however has been associated with a variety of adverse effects, which in‐ clude metabolic changes such as changes lypodistrophy, insulin resistance, lactic acidosis and dislipidemia[46],[56]. All these changes are pro-atherogenic and its consequences are often fatal. The development of cardiovascular disease in HIV-infected individuals is re‐ lated to endothelial dysfunction. This dysfunction and accelerated atherosclerosis is a consequence of HIV itself that activates the endothelial directly or indirectly through production of citocinas[57].

comparisons. Questions that might be raised concerning loss of sensitivity with this type of equipment have already been addressed in a comparison with conventional machines[42].

The carotid artery ensures easy access to the examiner; for its anatomy, as it is a superfi‐ cial artery and follows a more or less straight path along the cervical segment, in addi‐ tion to being a vessel with abundant elastic fibers that respond promptly to

A study with populations at difference ages showed that IMT increases at a rate of [IMTmm

The means for IMT values of common and internal carotids are higher among patients with some risk factor (hypertension, age and smoking). This pattern occurs in normal subjects and patients with hepatosplenic schistosomiasis mansoni clinical and surgical treated, but this phenomenon is not observed in these patients without any treatment[43]. These find‐ ings lend support to the hypothesis that hepatosplenic schistosomiasis mansoni may be a

Individuals infected with human immunodeficiency virus (HIV) have a different condition of life of the population free of infection with regard to morbidity and mortality from pre‐

Atherosclerosis is a systemic disorder characterized by the formation of cholesterol plaques, especially at the level of the intima of the arterial wall. All arteries can be affected, but the clinical consequences are more important at the level of coronary and carotid arteries of the

Arterial disease is chronic, along with coronary artery disease and ischemic stroke, one of three clinical manifestations of the same pathophysiological process: atherothrombosis. The classic risk factors of atherosclerosis are: smoking, hypertension (HTN), diabetes mellitus (DM), hypercholesterolemia, and obesidade[48]. Atherosclerosisisamajor cause ofmortality worldwidemobility, andlow life expectancyis mainly due to heart attack and

The morbidity and mortality among HIV-infected individuals with advanced disease was very high until the advent of potent antiretroviral therapy (HAART), which produced an

This therapy, however has been associated with a variety of adverse effects, which in‐ clude metabolic changes such as changes lypodistrophy, insulin resistance, lactic acidosis and dislipidemia[46],[56]. All these changes are pro-atherogenic and its consequences are often fatal. The development of cardiovascular disease in HIV-infected individuals is re‐ lated to endothelial dysfunction. This dysfunction and accelerated atherosclerosis is a

improvement in quality and increased expectation [52]-[55].

= 0.009 x age+0.35], i.e., it is a biological phenomenon that can be quantified[30].

**4. HIV infection may affect the natural history of atherogenesis**

mature atherosclerosis and cardiovascular, and its related complications[44]-[47].

hemodynamic "stress"[23].

86 Current Trends in Atherogenesis

lower limbs (LL).

stroke(CVA)[49]-[51].

protective factor against atherogenesis[30].

There is evidence that both pathophysiological HIV to antiretroviral therapy may affect the profile lipídico[58],[59], insulina resistance[60],[61] and the response of vasodilatação[62]. The increased mortality in individuals with HIV due to cardiovascular events in young pa‐ tients, often without classic risk factors for atherosclerosis, is cause for concern and the sub‐ ject of new studies[44],[46].

Antiretroviral therapy is associated with pro-atherogenic metabolic abnormalities such as metabolic syndrome, type II diabetes, abnormal distribution of body fat, these conditions al‐ so associated with arterial disease coronariana[63],[64]. Some studies suggest that class of drugs known as protease inhibitors (PI) can be associated with premature atherosclerosis and cardiovascular events, vasculares[47]. It is not clear, but what is the real contribution of ART in HIV and increased risk of cardiovascular disease.

The measurement of intima-media complex (IMT) by ultrasonography (USG) is a nonin‐ vasive marker of early atherosclerosis and may reflect the increased overall cardiovascu‐ lar risk and is associated with increased risk of acute myocardial infarction (AMI) and / or AVC[65]-[67].

The IMT can be used as a predictor of atherosclerotic disease in coronary arteries independ‐ ently of classical risk factors: age, sex, smoking, hypertension, dyslipidemia, diabetes and family history of coronary artery disease (CAD). IMTcan be consideredas a markerfor the evaluation ofatherosclerosissubclínica[68]-[70].

The study using IMT has been performed in patients with acquired immunodeficiency syn‐ drome (AIDS) in the investigation of risk factors for atherosclerosis as an early marker, but there are few studies prospectivos[71],[72].

In AIDS patients the automatic measurement of MIC performed in right and left common carotid, with software determining produces the following measures: average, maximum and minimum (Figure 1). In this same place three manual measurements can be performed. Thus, it is possible to calculate the arithmetic mean of the measure in manual right and left common carotid and the maximum and minimum extent (Figure 2). In the right and left in‐ ternal carotid it can be performed as manual. The gold standard can be represented by the mean of automatic measurements from the right common carotid (RCA) and left common carotid (LCA)[73],[74]. We have measured population of 50 years AIDS patients, the MIC was considered thickened if > 0.8 mm[75] was considered the presence of a thickening dem‐ onstrated plate when WCC > 1.5mm[73],[76].

The ankle-brachial index (ABI) is a simple, noninvasive, high predictive value for peripheral artery disease and has significant association with risk of cardiovascular mortality. It is a good method to be safe, reproducible, low cost, outpatient use and validated in the general population. Early diagnosis of atherosclerosis identifies people at high risk for cardiovascu‐ lar events and thus provides effective treatment and control of factors risco[55].

The reduction of the ABI values below 0.9 is associated with a significantly increased cardio‐ vascular risk, particularly by acute myocardial infarction and ischemic stroke, independent of other factors[77],[78]. The increase in ABI (> 1.3) is due more to changes in arterial compli‐ ance than the stenosis, which would be responsible for a decrease in ABI. The high preva‐ lence of high ABI in patients with HIV may be mediated by the involvement of vascular elasticity as well as the formation of atheromatous plaques. A meta-analysis of six retrospec‐ tive studies the ABI has been studied in patients with HIV. The populations were selected with varying criteria and there was no consensus about the risk factors responsible for ab‐ normal ABI. The increased prevalence of ABI was higher than in the general population. In the population with HIV/AIDS remains whether the high prevalence of altered ABI is asso‐

Atherogenesis: Diseases that May Affect the Natural History "Schistosomiasis and HIV Infection"

http://dx.doi.org/10.5772/54018

89

We selected 70 cases with HIV in use antirratrovirais (ARV) for at least five years of service reference in the State of Pernambuco and 70 controls without HIV, matched by sex and age, which were assessed by automatic measurement of carotid IMT in and ABI. It was taken in‐ to account the classical risk factors of atherosclerosis, anthropometric measurements and treatment with protease inhibitors (PI). We performed the analysis of homogeneity of

The ABI was raised in a single patient in the case group (0.7%) and no change in the control group ABI. The WCC was not thickened in any individual. There was no statistically signifi‐ cant difference between case and control groups with respect to the ABI and the WCC, even when considering the type of treatment. There was no significant difference between the

Maggi et al. evaluating patients with HIV and advocate the hypothesis that CMI is thick‐ ened more in the HIV group, which use the IP protocol is the cause of the thickening and that the lesions found in these patients are similar to arteritis and substantially different from atherosclerotic plaques[66],[69],[71],[72]. The present study does not confirm this hy‐ pothesis of thickening CMI in patients with HIV. In 70 patients there was no thickening in the common carotid, while also presenting the same classic risk factors for atherosclerosis, including having more hypercholesterolemia and hypertriglyceridemia than the control group. One possible explanation for the lack of thickening of the WCC in this population is the fact that the patients are young (mean 40.5 years), having long-term treatment (mean 8.16 years), have fewer risk factors than other atherosclerosis studies and found to be clini‐ cally stable (84% had an undetectable current CV with current median CD4 670.57) with less

It can be concluded that HIV-infected individuals do not run a higher risk of atherosclerosis than the control population, taking into consideration the classical risk factors of atheroscle‐

The result of this study is essential because as the population was very young, phase detec‐ tion of atherosclerotic disease earlier period can be after cutting realized. The follow-up of a cohort for a new sectional assessment later is very important for early detection of athero‐

ciated with increased incidence of cardiovascular events.

groups. The groups were homogeneous at the 95% confidence.

rosis and the specific characteristics of HIV-infected patients.

sclerosis in HIV patients on antiretroviral therapy.

aggression endothelium.

groups regarding presence of atheromatous plaques in the common carotid.

**Figure 1.** Medida automática do CMI em CCD

**Figure 2.** Medida manual do CMI em CCD

The reduction of the ABI values below 0.9 is associated with a significantly increased cardio‐ vascular risk, particularly by acute myocardial infarction and ischemic stroke, independent of other factors[77],[78]. The increase in ABI (> 1.3) is due more to changes in arterial compli‐ ance than the stenosis, which would be responsible for a decrease in ABI. The high preva‐ lence of high ABI in patients with HIV may be mediated by the involvement of vascular elasticity as well as the formation of atheromatous plaques. A meta-analysis of six retrospec‐ tive studies the ABI has been studied in patients with HIV. The populations were selected with varying criteria and there was no consensus about the risk factors responsible for ab‐ normal ABI. The increased prevalence of ABI was higher than in the general population. In the population with HIV/AIDS remains whether the high prevalence of altered ABI is asso‐ ciated with increased incidence of cardiovascular events.

We selected 70 cases with HIV in use antirratrovirais (ARV) for at least five years of service reference in the State of Pernambuco and 70 controls without HIV, matched by sex and age, which were assessed by automatic measurement of carotid IMT in and ABI. It was taken in‐ to account the classical risk factors of atherosclerosis, anthropometric measurements and treatment with protease inhibitors (PI). We performed the analysis of homogeneity of groups. The groups were homogeneous at the 95% confidence.

The ABI was raised in a single patient in the case group (0.7%) and no change in the control group ABI. The WCC was not thickened in any individual. There was no statistically signifi‐ cant difference between case and control groups with respect to the ABI and the WCC, even when considering the type of treatment. There was no significant difference between the groups regarding presence of atheromatous plaques in the common carotid.

**Figure 1.** Medida automática do CMI em CCD

88 Current Trends in Atherogenesis

**Figure 2.** Medida manual do CMI em CCD

Maggi et al. evaluating patients with HIV and advocate the hypothesis that CMI is thick‐ ened more in the HIV group, which use the IP protocol is the cause of the thickening and that the lesions found in these patients are similar to arteritis and substantially different from atherosclerotic plaques[66],[69],[71],[72]. The present study does not confirm this hy‐ pothesis of thickening CMI in patients with HIV. In 70 patients there was no thickening in the common carotid, while also presenting the same classic risk factors for atherosclerosis, including having more hypercholesterolemia and hypertriglyceridemia than the control group. One possible explanation for the lack of thickening of the WCC in this population is the fact that the patients are young (mean 40.5 years), having long-term treatment (mean 8.16 years), have fewer risk factors than other atherosclerosis studies and found to be clini‐ cally stable (84% had an undetectable current CV with current median CD4 670.57) with less aggression endothelium.

It can be concluded that HIV-infected individuals do not run a higher risk of atherosclerosis than the control population, taking into consideration the classical risk factors of atheroscle‐ rosis and the specific characteristics of HIV-infected patients.

The result of this study is essential because as the population was very young, phase detec‐ tion of atherosclerotic disease earlier period can be after cutting realized. The follow-up of a cohort for a new sectional assessment later is very important for early detection of athero‐ sclerosis in HIV patients on antiretroviral therapy.

## **Author details**

Carlos Teixeira Brandt, Emanuelle Tenório A. M. Godoi, André Valença, Guilherme Veras Mascena and Jocelene Tenório A. M. Godoi

Federal University of Pernambuco, Pernambuco, Recife, Brazil

### **References**

[14] Gensini GF, Dilaghi B. The unstable plaque. Eur Heart J Supplements. 2002; (4);

Atherogenesis: Diseases that May Affect the Natural History "Schistosomiasis and HIV Infection"

http://dx.doi.org/10.5772/54018

91

[15] Weber C, Noels H. Atherosclerosis: current pathogenesis and therapeutic op‐

[16] Stanley RG, Jackson CL, Griffiths K, Doenhoff MJ. Effects of Schistosomamansoni worms and eggs on circulating cholesterol and liver lipids in mice. Atherosclerosis.

[17] La Flamme AC, Harvie M, Kenwright D, Cameron K, Rawlence N, Low YS, McKen‐ zie S. Chronic exposure to schistosome eggs reduces serum cholesterol but has no ef‐ fect on atherosclerotic lesion development. Parasite Immunol. 2007;29(5):259-66.

[18] Lane HA, Smith JC, Davies JS. Noninvasive assessment of preclinical atherosclerosis.

[19] Raitakari OT, Juonala M, Kahonen M, Taittonen L, Laitinen T, Makittorko N, et al. Cardiovascular risk factors in childhood and carotid intima-media thickness in adult‐ hood: The cardiovascular risk in young Finns study. JAMA. 2003; 290(17): 2277-83.

[20] Bonithon-Kopp C, Touboul PJ, Berr C, Leroux C, Mainard F, Courbon D, et al. Rela‐ tion of intima-media thickness to atherosclerotic plaques in carotid arteries. The Vas‐

[21] Ishizu T, Ishimitsu T, Yanagi H, Seo Y, Obara K, Moriyama N, et al Effect of age on carotid arterial intima-media thickness in chilhood. Heart and Vessel. 2004;

[22] Pignoli P, Tremoli E, Poli A, Oreste P, Paoletti R. Intimal plus medial thickness of the arterial wall. A direct measurement with ultrasound imaging. Circulation. 1986;

[23] Ebrahim S, Papacosta O, Whincup P, Wannamethee G, Walker M, Nicolaides AN, et al. Carotid plaque, intima-media thickness, cardiovascular risk factors, and prevalent cardiovascular disease in men and women: the British Regional Heart Study. Stroke.

[24] Baldassarre D, Amato Mauro, Bondioli A, Sirtori CR, Tremoli E. Carotid artery inti‐ ma-media thickness measured by ultrasonography in normal clinical practice corre‐

[25] Espínola-Klein C, Hans-Jürgen R, Blankenberg S, Bickel C, Kopp H, Rippin G, et al. Are morphological or functional changes in the carotid artery wall associated with Chlamydia pneumoniae, Helicobacter pylori, Cytomegalovirus, or Herpes simplex

[26] WHO. World Health Organization. The Control of Schistosomiasis, Technical Report

lates well with aterosclerotic risk factors. Stroke. 2000; 31(10):2426-38.

virus infection? Stroke. 2002; 31(9):2127-38.

cular Aging Study (EVA). ArteriosclerThrombVasc Biol. 1996; 16(10):310-6.

(Suppl B):22-27.

2009;207(1):131-8.

19(4)189-95.

74(6):1399-1406.

1999; 30(4):841-50.

Series; 1993. p.86.

tions.Nat Med. 2011;17;11:1410-22.

Vasc Health Risk Manag. 2006; 2(1): 19-30.

[14] Gensini GF, Dilaghi B. The unstable plaque. Eur Heart J Supplements. 2002; (4); (Suppl B):22-27.

**Author details**

90 Current Trends in Atherogenesis

**References**

2004;109:III-27–III-32.

2001;15:2623–30.

2002;105:1135-1143.

2002;105:1135-1143.

2011; 22(5): 327–334

Carlos Teixeira Brandt, Emanuelle Tenório A. M. Godoi, André Valença,

[1] Ross R. Atherosclerois - an inflammatory disease. N Engl J Med. 1999; 340:115–126. [2] Davignon J, Ganz P. Role of endothelial dysfunction in atherosclerosis. Circulation.

[3] Fuster V, Moreno PR, Fayad ZA, Corti R, Badimon JJ. Atherothrombosis and high-

[4] Moghadasian MH, McManus BM, Nguyen LB, Shefer S, Nadji M, Godin DV, Green TJ, Hill J, Yang Y, Scudamore CH, Frohlich JJ. Pathophys- iology of apolipoprotein E deficiency in mice: relevance to apo E-related disorders in humans. FASEB J.

[5] Stoll G, Bendszus M. Inflammation and atherosclerosis: Novel insights Intoplaque formation and destabilization. Downloaded from http://stroke.ahajournals.org∕ 2012.

[6] Ross R. Atherosclerois - an inflammatory disease. N Engl J Med. 1999; 340:115–126. [7] Libby P, Ridker PM, Maseri A. Inflammation and atherosclerosis. Circulation.

[8] Libby P, Ridker PM, Hansson GK. Progress and challenges in translating the biology

[9] Lonn E, Bosch J, Yusuf S, et al.; HOPE and HOPE‑TOO Trial Investigators. Effects of long‑term vitamin E supplementation on cardiovascular events and cancer: a

[10] Lee SW, Antiga L, Spence JD, Steinman DA. Geometry of the carotid bifurcation pre‐

[11] Lee SW, Antiga L, Spence JD, Steinman DA. Geometry of the carotid bifurcation pre‐

[12] Libby P, Ridker PM, Maseri A. Inflammation and atherosclerosis. Circulation.

[13] GrundtmanC, Wick G. The autoimmune concept of atherosclerosis.CurrOpinLipidol.

Guilherme Veras Mascena and Jocelene Tenório A. M. Godoi

Federal University of Pernambuco, Pernambuco, Recife, Brazil

risk plaque. J Am CollCardiol. 2005;46:937–54.

DOI: 10.1161/01.STR.0000226901.34927.10.

of atherosclerosis. Nature. 2011; 473: 317-325.

randomized controlled trial. JAMA. 2005; 293: 1338-1347.

dicts its exposure to disturbed flow. Stroke. 2008;39:2341–2347.

dicts its exposure to disturbed flow. Stroke. 2008;39:2341–2347.

[27] Brandt CT, Maciel DT, Caneca AOF. Esplenose associada ao tratamento cirúrgico da hipertensão porta esquistossomótica na criança: avaliação de 10 anos. AnFac Med Univ Fed Pernamb. 1999; 44(1):15-20.

[40] Liuba P, Persson J, Luoma J, Ylä-Hertuala S, Pesonen E. Acute infections in children are accompanied by oxidative modification of LDL and decrease of HDL cholesterol, and are followed by thickening of carotid intima-media. European Heart Journal.

Atherogenesis: Diseases that May Affect the Natural History "Schistosomiasis and HIV Infection"

http://dx.doi.org/10.5772/54018

93

[41] Helft G, Worthley SG, Fuster V, Fayad ZA, Zaman AG, Corti R, et al. Progression and regression of atherosclerotic lesions: Monitoring with serial noninvasive magnet‐

[42] Magnussen CG, Fryer J, Laakkonen M, Raitakari OT. Evaluating the use of a portable ultrasound machine to quantify intima-media thickness and flow-mediated dilation: Agreement between measurements from two ultrasound machines. Ultrasound Med

[43] Hodis HN, Mack WJ, LaBree L, Selzer RH, Liu C, Liu C, et al. Reduction in carotid arterial wall thickness using lovastatin and dietary therapy: a randomized controlled

[44] Friis-Moler N, Weber R, Reiss P, Thiébaut R, Kirk O, d'ArminioMonforte A, Pradier C, Morfeldt L, Mateu S, Law M, El-Sadr W, De Wit S, Sabin CA, Phillips AN, Lundg‐ ren JD. Cardiovascular risk factors in HIV patients-association with antirretroviral

[45] Bozkurt B. Cardiovascular toxicity with highly active antirretroviral therapy: review

[46] Grover SA, Coupal L, Gilmore N, Mukherjee J. Impact of dyslipidemia associated with Highly Active Antirretroviral Therapy (HAART) on cardiovascular risk and life

[47] Friis-Moller N, Reiss P, Sabin CA, Weber R, Monforte A, El-Sadr W, Thiébaut R, De Wit S, Kirk O, Fontas E, Law MG, Phillips A, Lundgren JD. Class of antirretroviral drugs and the risk of myocardial infarction. N Engl J Med. 2007;356(17):1723-35. [48] Dedola M, Godoi E, Coppé G, Cambou JP, Cantet C, Mas JL, Guérillot M, Vahanian A, Herrman MA, Jullien G, Leizorovicz A, Boccalon H. Risk factors management in 5708 ambulatory patients suffering from peripheral vascular disease followed in ur‐

[49] Bots ML, Hoes AW, Koudstaal PJ, Hofman A, Grobbee DE. Common carotid intimamedia thickness and risk of stroke and myocardial infarction: the Rotterdam Study.

[50] Kung HC, Hoyert DL, Xu J, Murphy SL. Deaths: final data for 2005. Natl Vital Stat

[51] Ministério da Saúde. Estatísticas Vitais. 2006. Brasília. [citado 2009 mai 02]. Disponí‐

[52] Palella FJ Jr, Delaney KM, Moorman AC, Loveless MO, Fuhrer J, Satten GA, Asch‐ man DJ, Holmberg SD. Declining morbidity and mortality among patients with ad‐

ic resonance imaging. Circulation. 2002; 105(8):993-8.

clinical trial. Ann Intern Med. 1996; 124(6):548-56.

therapy. Results from DAD study. AIDS. 2003;17(8):1179-93.

of clinical studies. CardiovascToxicol. 2004;4(3):243-60.

ban practic. Arch Mal Coeur Vaiss. 2005;98(12):1177-88.

expectancy. Am J Cardiol. 2005;95(5):586-91.

Circulation. 1997;96(5):1432-7.

vel em:http://www.w3.datasus.gov.br/.

Rep. 2008;56(10):1-120.

2002; 24(6):515-21.

Biol. 2006; 33(9): 1323-9.

[40] Liuba P, Persson J, Luoma J, Ylä-Hertuala S, Pesonen E. Acute infections in children are accompanied by oxidative modification of LDL and decrease of HDL cholesterol, and are followed by thickening of carotid intima-media. European Heart Journal. 2002; 24(6):515-21.

[27] Brandt CT, Maciel DT, Caneca AOF. Esplenose associada ao tratamento cirúrgico da hipertensão porta esquistossomótica na criança: avaliação de 10 anos. AnFac Med

[28] Gillet MPT, Coêlho LCBB. The effect of splenectomy on plasma phosphatidylcholinecolesterolacyltranferase activity and blood lipids in human schistosomiasismansoni.

[29] Facundo HTF, Brandt CT, Owen JS, Lima VLM. Elevated levels of erythrocyte-conju‐ gated dienes indicate increased lipid peroxidation in schistosomiasismansoni pa‐ tients. Braz J Med Biol Res. 2004; 37(7): 957-962. Available from: http://www.scielo.br/

[30] Guimarães AV, Brandt CT, Ferraz A. Complexo miointimal das carótidas comum e interna em portadores de esquistossomose mansônica hepatoesplênica.*Rev. Col. Bras. Cir.*[online]. 2009;36 (4) 292-299. Available from: http://www.scielo.br/scielo. ISSN

[31] Silva SN, Oliveira KF, Brandt CT, Lima VLM. A lipid study of schistosomotic young

[32] Verschuren WM, Jacobs DR, Bloemberg BP, Kromhout D, Menotti A, Aravanis C, et al. Serum total cholesterol and long-term coronary heart disease mortality in differ‐ ent cultures. Twenty-five-years follow-up of the seven countries study. JAMA.1995;

[33] Khovindhunkit W, Memon RA, Feingold KR, Grunfekd C. Infection and inflamma‐ tion-induced proatherogenic changes of lipoproteins. J Infect Dis. 2000; 81(Suppl.3):

[34] Feingold KR, Soued M, Serio MK, Adi S, Moser AH, Grunfeld C. The effect of diet on tumor necrosis factor stimulation of hepatic lipogenesis. Metabolism. 1990;39(6):

[35] Mendall MA, Goggin PM, Molineaux N, Levy J, Toosy T, Strachan D et al. Relation of Helicobacter pylori infection and coronary heart disease. Br Heart J. 1994; 71(5):437-9.

[36] DeStefano F, Anda RF, Kahn HS, Williamson DF, Russell CM. Dental disease and

[37] Yudkin JS, Kumari M, Humphries SE. Inflammation, obesity, stress and coronary heart disease: is interleukin-6 the link? Atherosclerosis. 2000; 148(2): 209-14.

[38] Sunnemark D, Harris RA, Frostegard J, Orn A. Induction of early atherosclerosis in CBA/J mice by combination of Tripanossomacruzi infection and a high cholesterol

[39] Doenhoff M.J, Stanley RG, Griffiths, Jackson CL. An anti-atherogenic effect of Schis‐ tosomiasismansoni infection in mice associated with a parasite-induced lowering of

risk of coronary heart disease and mortality. BMJ. 1993; 306(6879):688-91.

diet. Atherosclerosis. 2000; 153(2):273-82.

blood total cholesterol.Parasitology. 2003;(9)337-50.

Univ Fed Pernamb. 1999; 44(1):15-20.

Bioch Soc Trans. 1979; 7(5):988-990.

27(4): 131-6.

462-72.

92 Current Trends in Atherogenesis

623-632.

scielo.doi.org/10.1590/S0100-879X2004000700003.

0100-6991. http://dx.doi.org/10.1590/S0100-69912009000400004.

people underwent surgical treatment. Acta Cir. Bras. 2002; 17(4):251-7.

vanced human immunodeficiency virus infection. HIV Outpatient Study Investiga. N Engl J Med. 1998, 338(13): 853-60.

[64] Depairon M, Chessex S, Sudre P, Rodondi N, Doser N, Chave JP, Riesen W, Nicod P, Darioli R, Telenti A, Mooser V. Premature atherosclerosis in HIV-infected individu‐

Atherogenesis: Diseases that May Affect the Natural History "Schistosomiasis and HIV Infection"

http://dx.doi.org/10.5772/54018

95

[65] Simon A, Gariepy J, Chironi G, Megnien JL, Levenson J. Intima-media thickness: a new tool for diagnosis and treatment of cardiovascular risk. J Hypertens. 2002;20(2):

[66] Bots ML, Evans GW, Riley WA, Grobbee DE. Carotid intima-media thickness meas‐ urements in intervention studies design options, progression rates, and sample Size

[67] Barros FS, Pontes SM. Doença carotídea aterosclerótica. In: Engeelhorn CA, Morais Filho D, Barros FS, editores. Guia prático de ultra-sonografia vascular. 1ª ed. Rio de

[68] Lekakis JP, Papamichael CM, Cimponeriu AT, Stamatelopoulos KS, Papaioannou TG, Kanakakis J, Alevizaki MK, Papapanagiotou A, Kalofoutis AT, Stamatelopoulos SF. Atherosclerotic changes of extracoronary arteries are associated with the extent of

[69] Maggi P, Lillo A, Perilli F, Maserati R, Chirianni A. Colour-Doppler ultrasonography of carotid vessels in patients treated with antirretroviral therapy: a comparative

[70] Allison MA, Tiefenbrun J, Langer RD, Wright CM. Atherosclerotic calcification and intimal medial thickness of the carotid arteries.Int J Cardiol. 2005;103(1):98-104. [71] Maggi P, Perilli F, Lillo A, Carito V, Epifani G, Bellacosa C, Pastore G, Regina G. An ultrasound-based comparative study on carotid plaques in HIV-positive patients vs. atherosclerotic and arteritis patients: atherosclerotic or inflammatory lesions? Coron

[72] Maggi P, Perilli F, Lillo A, Gargiulo M, Ferraro S, Grisorio B, Ferrara S, Carito V, Bel‐ lacosa C, Pastore G, Chirianni A, Regina G. Rapid progression of carotid lesions in

[73] Touboul PJ, Hennerici MG, Meairs S, *et al*. Mannheim carotid intima-media thickness

[74] Touboul PJ, Vicaut E, Labreuche J, *et al*. Correlation between the Framingham risk score and intima media thickness: the Paroi Artérielle et Risque Cardio-vasculaire

[75] Engelhorn CA, Engelhorn AL, Cassou MF, *et al*. Espessamento médio-intimal na ori‐ gem da artéria subclávia direita como marcador precoce de risco cardiovascular. *Arq*

[76] Labropoulos N, Ashraf Mansour M, Kang SS, *et al*. Viscoelastic properties of normal and atherosclerotic carotid arteries. *Eur J Vasc Endovasc Surg* 2000;19:221-5.

HAART-treated HIV-1 patients. Atherosclerosis. 2007;192(2):407-12.

consensus (2004-2006). *Cerebrovasc Dis* 2007;23:75-80.

(PARC) study. *Atherosclerosis* 2007;192:363-9.

*Bras de Cardiol*. 2006; 87:609-14.

als-focus on protease inhibitor therapy. AIDS, 2001;15(3):329-34.

considerations: a point of view. Stroke. 2003;34:2985-94.

coronary atherosclerosis. Am J Cardiol. 2000; 85(8):949-52.

Janeiro: Dilivros; 2007. p.17-37.

study. AIDS. 2004;18(7):1023-8.

Artery Dis. 2007;18(1):23-9.

159-69.

[64] Depairon M, Chessex S, Sudre P, Rodondi N, Doser N, Chave JP, Riesen W, Nicod P, Darioli R, Telenti A, Mooser V. Premature atherosclerosis in HIV-infected individu‐ als-focus on protease inhibitor therapy. AIDS, 2001;15(3):329-34.

vanced human immunodeficiency virus infection. HIV Outpatient Study Investiga.

[53] Lewden C, Chene G, Morlat P, Raffi F, Dupon M, Dellamonica P, Pellegrin JL, Katla‐ ma C, Dabis F, Leport C. HIV-infected adults with a CD4 cell count greater than 500 cells/mm3 on long-term combination antirretroviral therapy reach same mortality

[54] Lima VD, Hogg RS, Harrigan PR, Moore D, Yip B, Wood E, Montaner JS. Continued improvement in survival among HIV-infected individuals with newer forms of high‐

[55] Olalla J, Salas D, de la Torre J, Del Arco A, Prada JL, Martos F, Perea-Milla E, García-

[56] Hajjar LA, Calderaro D, Yu PC, Giuliano I, Lima EMO; Barbaro G, Caramelli B. Man‐ ifestações cardiovasculares em pacientes com infecção pelo vírus da imunodeficiên‐

[57] Hürlimann D, Weber R, Enseleit F, Lüscher TF. HIV infection, antirretroviral thera‐

[58] Kannel WB, Giordano M. Long-term cardiovascular risk with protease inhibitors and

[59] Bernal E, Masiá M, Padilla S, Gutiérrez F. High-density lipoprotein cholesterol in HIV-infected patients: evidence for an association with HIV-1 viral load, antirretrovi‐ ral therapy status, and regimen composition. AIDS Patient Care STDS. 2008;22(7):

[60] Mulligan K, Grunfeld C, Tai VW, Algren H, Pang M, Chernoff DN, Lo JC, Schambe‐ lan M. Hyperlipidemia and insulin resistance are induced by protease inhibitors in‐ dependent of changes in body composition in patients with HIV infection. J Acquir

[61] Murata H, Hruz PW, Mueckler M. The mechanism of insulin resistance caused by

[62] Hsue PY, Hunt PW, Wu Y, Schnell A, Ho JE, Hatano H, Xie Y, Martin JN, Ganz P, Deeks SG. Association of abacavir and HIV disease factors with endothelial function in patients on long-term suppressive ART. In: Program and abstracts of the 16th Con‐ ference on Retroviruses and Opportunistic Infections; February 8-11, 2009; Montreal.

[63] Maggi P, Serio G, Epifani G, Fiorentino G, Saracino A, Fico C, Perilli F, Lillo A, Fer‐ raro S, Gargiulo M, Chirianni A, Angarano G, Regina G, Pastore G. Premature le‐ sions of the carotid vessels in HIV-1-infected patients treated with protease

management of the dyslipidemia. Am J Cardiol. 2004;94(7): 901-6.

HIV protease inhibitor therapy. J Biol Chem. 2000;275(27):20251-4.

rates as the general popul. J Acquir Immune DeficSyndr. 2007, 46(1):72-7.

Alegría J. Ankle-brachial index in HIV infection.AIDS Res Ther. 2009;6:6.

ly active antirretroviral therapy. AIDS. 2007;21(6):685-92.

cia humana. Arq Bras Cardiol. 2005;85(5):363-77.

py, and endothelium. Herz. 2005;30(6):472-80.

Immune DeficSyndr. 2000;23(1):35-43.

inhibitors.AIDS. 2000;14(16):F123-8.

569-75.

Abstract 723.

N Engl J Med. 1998, 338(13): 853-60.

94 Current Trends in Atherogenesis

[77] Leger P, Boccalon H. Bilan d'un artériopathie des membres inférieurs (AMI). In: Boc‐ calon H, editor. Guide Pratique des Maladies Vasculaires, 2a ed. France: Masson; 2001. p.13-18.

**Chapter 5**

**The Evaluation of New Biomarkers of Inflammation and**

Peripheral artery disease is a clinical manifestation of atherosclerosis with significant morbid‐ ity and mortality (Sharma Sharma & Aronow, 2012; Resnick et al. 2004; Diehm et al. 2009). Despite well-recognized significance of traditional risk factors in the initiation and progression of the disease, not all causes and mechanisms leading to disease development have been identified so far. Inflammation, angiogenesis, and endothelial activation are important processes contributing to the pathogenesis of peripheral arterial disease which are related in a complex and interdependent manner (Li et al., 2007; Brevetti et al., 2010; Brevetti Get al.,

Pathophysiologic events in peripheral artery disease are represented by ishaemic tissue damage, and the severity of clinical presentation depends on the site and extent of stenosis and availability of collateral circulation (Meru et al., 2006; Cooke 2008). Angiogenesis and arteriogenesis (collateral growth) are different forms of vessel growth, which contribute to the compensation for an occluded artery. Hypoxia is known to trigger angiogenesis in the setting of ischaemia, whereas fluid shear stress might be the most important stimulus for initiation of collateral growth. Besides these specific initial triggers, angiogenesis and collateral growth share growth factors, chemokines, proteases, and inflammatory cells, which play different

During an tissue ischemia, hypoxia-inducible factor 1 (HIF-1) drives transcriptional acti‐ vation of hundreds of genes involved in vascular reactivity, angiogenesis, arteriogenesis, the mobilization of bone marrow-derived angiogenic cells (Rey & Semenza 2010). The current evidence suggests considerable overlap between the molecular mechanisms and

and reproduction in any medium, provided the original work is properly cited.

© 2013 Perkov et al.; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use,

© 2013 The Author(s). Licensee InTech. 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,

distribution, and reproduction in any medium, provided the original work is properly cited.

roles in promoting and refining these processes ( Silvestre et al., 2008).

**Angiogenesis in Peripheral Arterial Disease**

Sonja Perkov, Mirjana Mariana Kardum Paro,

Additional information is available at the end of the chapter

Vinko Vidjak and Zlata Flegar-Meštrić

2003; Brevetti et al., 2008; Findley et al., 2008).

http://dx.doi.org/10.5772/53341

**1. Introduction**

[78] Spácil J, Spácabilová J. The ankle-brachial blood pressure index as a risk indicator of generalized atherosclerosis.SeminVasc Med. 2002;2(4):441-5.

**Chapter 5**


**1. Introduction**

In order to replace fossil fuels by renewable energy sources, utilization of biofuels and renewable energy sources has been incorporated in the national and international legal standards and the government programs of developed countries. The EU in the Directive 2009*/*28*/*EC has defined a program of replacing 20% of total energy consumption with renewable energy sources and 10% of the consumption of liquid fuels with biofuels by 2020. One possibility of increasing the share of energy from renewable sources is biogas production

© 2016 The Author(s). Licensee InTech. 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. © 2016 The Author(s). Licensee InTech. 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.

from energy crops. This option has gained wide application in particular in connection with government support of the electricity price produced from biogas in many countries of the EU. In addition, growing and utilization of energetic crops for biogas production is one of the alternatives of agriculture production diversification which can significantly improve farm economics. Energy from biogas produced by anaerobic digestion of energetic crops can be utilized to improve the energetic balance of a farm as excess energy can be sold (e.g. to the electric grid). Maize in the form of silage provides high yields (10–30 t of total solids—TS per hectare [1–3]) and is thus a suitable energetic crop for biogas production. More than 17,000 biogas plants, mostly using maize silage as the main substrate, are in operation in Europe; for example, in Germany, more than 8000 biogas plants have been in operation by the end of 2015 with the plant biomass utilization of more than 52 mass% and of livestock excrements of 43 mass% [4]. The rest are industrial and agro- and food processing waste as well as municipal biowaste. Advantages of plant biomass utilization are even pronounced by the fact that 52 mass% of the total substrates processed in biogas plants result in a 79% energy production. Maize silage represents 73 mass% of the plant biomass processed in the biogas plants, while the energy represents 72% of the total energy production. Thus, in 2014, 56.88% of energy produced by biogas plants in Germany originated from maize silage [4]. Even though no precise information on the species composition of the biogas plant substrates in other countries of the European Union is available, it is clear that the main substrate is maize silage. However, only little information on its anaerobic digestion is provided in literature. Generally, it can be stated that studies on the anaerobic digestion of fresh and ensiled materials did not show any significant differences between the biogas production from these materials [5, 6]. Concerning the anaerobic digestion, the main advantage of ensiling is the conservation of plant substrates to enable biogas production for the whole year. Zauner and Kuntzel [7] present anaerobic processing of maize silage in their work achieving methane production of 0.270–0.289 m3 /kg of TS in a laboratory batch reactor. The production was somehow lower, 0.181–0.184 m3 /kg of TS, in continuous laboratory reactors. Amon et al. [2] studied the biogas production from maize and clover grass in more detail. They focused on the biogas production of various species in different stages (milk, wax, and full ripeness). Also the influence of ensiling and drying on the methane production was studied. Various species had different optimal harvesting time in different ripeness stages. Specific methane production was in the range of 0.206–0.283 Nm3 /kg of the volatile solids—VS and the methane yield was in the range of 5300 to 8530 Nm3 /ha of the VS. These results were obtained by the batch tests of the anaerobic digestion in mesophilic conditions (40°C) for 60 days. Some maize varieties showed minimum difference in the methane production considering the ripeness stage and some showed a difference of more than 25% (variety Saxxo, wax ripeness) [2]. Specific methane production of 0.282–0.419 Nm3 /kg of the VS was achieved in the work of Schittenhelm [8], who studied the effect of maize composition and ripeness stage on the methane yield. Specific methane production from hybrids with late ripeness increased with the higher date of sampling more significantly than from climatically adapted "medium-early" hybrids, which reached the maximum methane production more quickly. These results are comparable with those provided by other authors [3, 9–14]. In [13], maximum yield of 9440.6 Nm3 /ha (hybrid maize,

ripeness stage FAO 400—FAO 500) and in [14], 10,401 m3

various plant substrates, or industrial wastes [17–21].

experiences using other co-substrates is presented.

**2.1. Test of maize silage biomethane potential**

of a substrate and the possible biogas production.

To increase the specific methane production from silage, various methods of physical, chemical, or biological pre-treatment or their combination can be used [15, 16]. However, each pretreatment method complicates the biogas production technology and increases the operation cost. Therefore, it is necessary to always consider if a higher amount of biogas produced has a relevant effect. Considering its properties and composition, maize silage is often used in cofermentation with other substrates, for example, with manure, sludge from wastewater plants,

Here, results obtained by anaerobic digestion of maize silage as the single substrate for biogas production in laboratory as well as in full-scale conditions are presented. Start-up of a biogas plant anaerobic reactor for maize silage processing as a single substrate and operation

Within the laboratory experiments on anaerobic processing of maize silage, tests of the maize silage biogas potential were carried out, and a long-term operation of a biogas production model was monitored. The aim of these tests was to determine the specific biogas production.

It is necessary to emphasize that the tests of biomethane potential have only an informational character and the specific methane production reached by long-term operation of anaerobic digestion of biologically degradable substrates can differ considerably. Single biomethane potential test results are significantly affected by the anaerobic sludge used as inoculum. Used anaerobic sludge is not usually adapted to the substrate degradation and during batch test the adaptation is not carried out. Therefore, the biomethane potential test provides a value lower than that obtained by long-term anaerobic digestion, when the adaptation of the anaerobic sludge to the used substrate and thus deeper anaerobic digestion of the substrate can take place. If the substrate contains a toxic or inhibitory substance, its influence might not be demonstrated during the biomethane potential test, due to the sufficient dilution of the substrate by the anaerobic sludge used for inoculation, for example, in substrates with high nitrogen or sulfur content. In long-term anaerobic digestion process, when the substrate is repeatedly supplied to the reactor, nitrogen or sulfur can accumulate in the reactor, and ammonia or sulfide inhibition of anaerobic processes can occur gradually. However, the biomethane potential test is a suitable tool for the primary evaluation of anaerobic digestion

Maize silage produced at the STIFI farm in Hurbanovo was used in the biomethane potential test without particle size adjustment. The particle size was given by the harvesting machine as up to 5 cm in length. Silage was made in the traditional way. Harvesting took place at the

**2. Anaerobic digestion of maize silage in laboratory conditions**

obtained.

/ha (20°C and normal pressure) were

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http://dx.doi.org/10.5772/64378

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ripeness stage FAO 400—FAO 500) and in [14], 10,401 m3 /ha (20°C and normal pressure) were obtained.

To increase the specific methane production from silage, various methods of physical, chemical, or biological pre-treatment or their combination can be used [15, 16]. However, each pretreatment method complicates the biogas production technology and increases the operation cost. Therefore, it is necessary to always consider if a higher amount of biogas produced has a relevant effect. Considering its properties and composition, maize silage is often used in cofermentation with other substrates, for example, with manure, sludge from wastewater plants, various plant substrates, or industrial wastes [17–21].

Here, results obtained by anaerobic digestion of maize silage as the single substrate for biogas production in laboratory as well as in full-scale conditions are presented. Start-up of a biogas plant anaerobic reactor for maize silage processing as a single substrate and operation experiences using other co-substrates is presented.


*Edited by Hamid A. Al-Megren*

Natural gas is a vital component of the world's supply of energy and an important source of many bulk chemicals and speciality chemicals. It is one of the cleanest, safest, and most useful of all energy sources, and helps to meet the world's rising demand for cleaner energy into the future. However, exploring, producing and bringing gas to the user or converting gas into desired chemicals is a systematical engineering project, and every step requires thorough understanding of gas and the surrounding environment. Any advances in the process link could make a step change in gas industry. There have been increasing efforts in gas industry in recent years. With state-of-the-art contributions by leading experts in the field, this book addressed the technology advances in natural gas industry.

ISBN 978-953-51-0507-7

Advances in Natural Gas Technology

Photo by Bet\_Noire / iStock


*Edited by Gary P. Moynihan*

Operations management (OM) is the function concerned with the planning, design, implementation, and control of business operations in the production of goods and services. OM has expanded from its original factory-centric orientation to encompass the service industry and the respective, accompanying supply chains, with a broad, global range of applications, increasing reliance on quantitative analysis, and the development and the use of supporting computer-based information systems and technology. This book highlights some critical aspects and advances in the field of operations management. Topics covered include investigations in the area of sustainable supply chain management; the application of OM principles to the deployment of field laboratories to address epidemics; and novel approaches to applying operations management in response to increasingly diverse requirements, circumstances, and performance criteria.

ISBN 978-1-78923-310-0

Contemporary Issues and Research in Operations Management

Published in London, UK © 2018 IntechOpen © spainter\_vfx / iStock


In a qualitative study, building on interviews and observations, one can experience that the material at hand provides answers to a different research question than the one you set out with. It can then be fruitful to revisit and reformulate the research question and hypotheses. In a quantitative study, based on questionnaires and other forms of factual data, changing the hypothesis after the data are known is considered to be a questionable research practice (Kerr 1998), but with an explorative, qualitative study, it can be both normal and acceptable.

A research question about the communication climate in an organisation can build on concepts and ideas formulated in this book. Here are some examples:

The opening quote from Kjøllesdal's thesis was part of an answer to the last question, specifed in relation to nurses operating at an emergency call centre. She used input from her informants to theorise about communication climate, using concepts outlined in this book, and the concept of high-quality connections at work (Dutton 2003). A list of more specifc research questions from other theses that I have supervised illustrates the variety of possible phenomena to explore:

It is possible to approach a group or organisation with a version of one of these questions or fnd other inroads into the communication climate at work.

The richest and most interesting theses about communication climate build on empirical gold, in the shape of vivid narratives from organisational life. Researchers and students in this feld depend on input from practitioners who share concrete and lively examples. One recurring challenge in interviews is that the conversation may reach a general and overarching level and remain there. People might say that our communication climate is at its best when we are well prepared and agree upon the way forward. Here, the interviewer needs to probe for examples. What happens in a particular situation where one is well prepared and has a common script for what to do next? In one project, researchers had secured an interview with two highly successful tennis coaches, who regularly had been able to turn talents into successful tennis players. During the interview, the coaches explained that their work rested on giving the talents concrete challenges and tasks. This general answer opened an opportunity to investigate further. What could a challenge or task consist of? What would be the concrete steps in how the talents responded? Instead, the interviewers moved on to further general questions about the importance of motivation and support, and so on. Here was a critical quality moment in the research process. The interviewees provided an exciting but general answer about their methods. The interviewers had the opportunity to learn something deeper by probing for examples, but they did not take it.

Rich narratives, then, are the empirical gold one needs to build an interesting thesis about communication climate. Even equipped with this understanding, interviewers return from their conversations with practitioners with their notebooks and recording devices full of generalisations, material that at its best is empirical silver. They have encountered interviewees who talk at length about the general communication challenges, motivations, patterns, and scripts from their working life. The examples are either only briefy mentioned or absent.

Systematic preparation can lower people's barriers for sharing narratives. The interviewer can approach the interviewees in advance and ask them to think about a situation or two at work where the communication climate has been particularly good and bring those examples to the interview. Researchers can be reluctant to share their questions upfront, out of fear that it will make the interview less spontaneous and open. The interviewees can turn up with prepared statements, impeding the process of talking freely about the topic. However, asking them to prepare by thinking about concrete experiences and examples can make it easier to get beyond the generalisations.

The interviewer who is eager for narratives can come equipped with a set of probing questions to make the interviewees say more about the episode or situation they have brought to the interview. There can be various ways of unlocking experiences and getting people to talk about them. I have found the following set of questions useful, and so have my students:

For each of these questions, it is important to probe further and ask: What else? Tell me more. Time and again you can repeat these follow-up phrases. An interviewer should not hesitate to reiterate: What else? Tell me more. During an interview it can turn out that one or two of the questions above are particularly important, and so should get more attention than the others.

When you have a set of narratives to refect from, it is time to look for patterns. When Kjøllesdal fnished her round of interviews with the operators at emergency call centres, she could start to look for common features in them. One of the frst she noticed was that the operators sensed that the most dramatic situations brought out the best in themselves and their colleagues. When the stakes were high, as in the opening example where the operator and the team around her sought to prevent a suicide, people mobilised their best listening capacities and their professionalism in providing adequate input to the operator communicating with the caller. The study also documented how training and debriefng was crucial to create learning among the operators. Before they were handed the responsibility for taking emergency calls, they would work with a mentor, an experienced operator, and see how that person responded to calls. After every dramatic event, there would be a debriefng session with a supervisor to review the call and refect on strengths and room for improvement. Some of the operators explained that they would scan the room at the beginning of the workday, noticing who would be at hand to collaborate and support if a caller reported an emergency. The quality of the communication climate could vary with each shift and depend upon the personal resources of those present. Some colleagues were perceived to be more reliable in such situations than others. Some were more team oriented. Others had an individualistic attitude and preferred to shine alone, blocking them from becoming engaged in collaboration. The study concluded that highquality connections at work (Dutton 2003) serve as a foundation for highquality performances when professionals respond to emergencies.

The fnal point to make about studies of communication climate is that they can provide input to how organisations can improve the ways people communicate and collaborate at work. A process of sharing and dwelling on narratives can create learning. In the tradition of the pragmatist philosopher John Dewey, researchers have noted how experience alone does not create learning (Kolb et al. 2001; Kolb and Yeganeh 2011; Kolb 2014). It is a misunderstanding to think that working together on a project and getting things done in themselves constitute a learning process. People also need to articulate what they have experienced and make collective efforts to understand the various steps in the process. Experience coupled with refection is what can create new insights and understandings of how to move forward and address tasks at work in better ways. Refection on situations when the emergency call operators are at their best can provide learning in their own work environment and inspire similar refections in other organisations. The debriefng sessions they undertake after dramatic events make it possible to process the information and learn together. As argued by Amabile and Kramer (2011) in their work on the progress principle, refections on small accomplishments and breakthroughs can have a particularly powerful effect and guide future efforts.

The executive student theses that I have supervised on these topics typically end with suggestions for small-scale practical improvements. It can be to change the design of meetings to make more people speak up by giving everybody a chance to say something at the beginning. It can be to give the role of devil's advocate during presentations of new ideas to different people every time. It can be to introduce a short debriefng session towards the end of every workday or work process to increase learning. The introduction of these suggestions can be experimental and explorative. It is possible to test their usefulness and see if they are worth pursuing. Strengthening communication can be a process of introducing new ways of doing things through trial and error.

This fnal chapter has zoomed in on how to study and learn more about communication climates at work. The opening narrative was from a study of collaboration among nurses operating in emergency call centres. The nurses were invited to share examples from their own work experience where they had managed to coordinate help in stressful situations. The learning points from that study are relevant in other settings, both with regard to the research design of collecting and interpreting narratives, and with regard to the conclusions about how to create a foundation for collaboration. Similar studies from other practices and organisational contexts can create a better understanding of what constitutes a constructive communication climate.

The motivation for writing this book has been to understand better what it takes to establish and maintain a well-functioning communication climate in groups and organisations. I have theorised and presented concepts that can guide attempts to strengthen the communication between people in organisations. As a practitioner of applied philosophy, I have tried to connect my theorising with how we should cope with current societal challenges. I share with other researchers of human agency and motivation a sense of urgency to make a practical contribution that can strengthen our capacities to address the monumental challenges that humanity currently faces. Human responses to destructive political, social, and environmental developments locally and globally require that we mobilise our most excellent qualities. A well-functioning communication climate is the platform we depend on to conduct small-scale and largescale miracles of collaboration.

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