intoxication due to carbon monoxide ( co ) is one of the most common types of poisoning , and one of the most important toxicological global causes of morbidity and mortality ( 1 ) .
a weak association between carboxyhemoglobin ( cohb ) level and patients clinical picture is documented ( 2 ) .
co binds rapidly to hemoglobin with greater affinity than oxygen ( o2 ) and forms cohb , which leads to a decrease in the o2 carrying capacity of the blood resulting in tissue hypoxia .
therefore , organs with high oxygen demand , such as heart , brain and lungs are most sensitive to hypoxia ( 3 - 6 ) .
cardiac effects of cohb range from simple arrhythmias to myocardial infarction ( 7 - 9 ) . cardiac troponins ( ctn )
the release of ctn into the circulation occurs as a consequence of cardiomyocyte injury ( 10 ) .
highly sensitive - ctn ( hs - ctnt ) assays are developed recently , enabling measurements of concentrations that are 100-fold lower than those of the ones previously measurable ( 11 ) .
the current study aimed to assess whether or not myocardial damage occurs in patients with co poisoning . the study investigated the relationship between blood carboxyhemoglobin and hs - ctnt level with a highly sensitive assay in patients with acute co poisoning .
the current retrospective study was conducted at the sevket yilmaz training and research hospital that is a state tertiary hospital with 1050 beds , located in the eastern bursa , turkey .
the study used the data available in the hospital clinical data warehouse , a centralized data repository integrating information in several databases including the order entry database and the laboratory results database of the hospital .
patients diagnosed with co poisoning were included in the study and their corresponding electronic charts were reviewed for data collection .
prescription data were linked to detailed clinical information including patient demographics , diagnosis , clinical characteristics ( including past medical history , smoking status ) , co source ( charcoal or fire ) , vital signs at presentation , physical examination characteristics , cohb levels , treatment therapy , complications in erectile dysfunction ( ed ) , and laboratory data ; the latter included specimen collection date , time , and location ( for example : intensive care unit ) . two - hundred - seventeen cases admitted to the emergency medicine unit of the hospital in 2012 , ( january 2012 - january 2013 ) with the diagnosis of acute co intoxication
seventy - six patients whose additional diagnoses indicated chronic ischaemic heart disease , heart failure , myocarditis , muscular dystrophy , polymyositis , implanted cardiac resynchronization device , chronic inflammatory disease , and chronic renal failure were excluded .
the overall study population included 141 subjects ( 87 females ( 62% ) and 54 males ( 38% ) ; 70% of the poisonings occurred in the winter , 24% in spring and 6% in autumn .
the study was approved by the sevket yilmaz research and education hospital ethics committee ( no .
2013/7 - 4 ) and was in compliance with the helsinki declaration ; informed consent was not assumed necessary because of the retrospective observational nature of the study and all steps were taken to ensure the anonymity of the data .
blood samples were first collected ( on admission ) in the emergency department and four hours later in the intensive care unit ( icu ) .
routine laboratory data ( cohb , creatine kinase - myocardial band ( ck - mb ) and high - sensitivity cardiac troponin t ( hs - tnt ) were recorded .
cohb levels were measured by a blood gas analyzer ( omni s , roche diagnostics penzberg , germany ) supported by a co - oximetry panel .
hs - ctnt and ck - mb levels were determined by an elecsys 2010 autoanalyzer ( roche diagnostics , penzberg , germany ) using commercial assays . according to the manufacturer of the hs - ctnt stat assay ,
ng / l , and the 99th percentile in healthy volunteers was 14 ng / l . for quality assurance purposes ,
the laboratory participates in an external quality assessment scheme run by labquality , helsinki , finland . at the time of the present study , the qc program reported average values
as part of the treatment , all the patients inhaled high flow normobaric oxygen and were monitored and followed up in icu .
treatment continued until clinical findings stabilized and serum cohb levels decreased to target levels of 5% .
the patients intoxicated with co were divided into three groups depending on cohb levels : group i , mild cohb level < 15% ; group ii , cohb levels < 25% and > 15% ; group iii , severe acute co intoxication cohb levels > 25%
. samples with hs - ctnt below the limit of blank ( i e , 3 ng / l ) were assigned a value of 1 ng / l .
the comparisons between the medians of three groups were performed by the kruskal - wallis test and the post - hoc dunnett tests were used to examine the significance levels between groups .
spearman rank analysis was used to assess associations between cohb , ck - mb and hs - tnt levels
( spss , chicago , il ) and p values of < 0.05 were considered significant .
the patients intoxicated with co were divided into three groups depending on cohb levels : group i , mild cohb level < 15% ; group ii , cohb levels < 25% and > 15% ; group iii , severe acute co intoxication cohb levels > 25%
. samples with hs - ctnt below the limit of blank ( i e , 3 ng / l ) were assigned a value of 1 ng / l .
the comparisons between the medians of three groups were performed by the kruskal - wallis test and the post - hoc dunnett tests were used to examine the significance levels between groups .
spearman rank analysis was used to assess associations between cohb , ck - mb and hs - tnt levels .
( spss , chicago , il ) and p values of < 0.05 were considered significant .
one - hundred - forty of the patients were poisoned at home and only one of the patients was poisoned at work and they used coal or wood for heating .
the predominating symptoms were nausea ( n = 89 ) , headache ( n = 86 ) , dizziness ( n = 47 ) and vomiting ( n = 28 ) .
cohb levels ranged from 8 to 35 ( median 23 , mean 22.0  6.6% ) on admission .
the patients intoxicated with co were divided into three groups depending on their cohb levels : group i , mild cohb level < 15% ( n = 29 ) ; group ii , cohb between 15% and 25% ( n = 67 ) ; group iii , severe acute co intoxication cohb levels > 25% ( n = 45 ) ( table 1 ) ( 12 ) .
abbreviations : ck - mb , creatine kinase - myocardial band ; cohb , carboxyhemoglobin ; hs - tnt , high - sensitivity cardiac troponin t. values are expressed as median ( interquartile range ) or mean  sd .
median hs - ctnt increased with increasing cohb level ( kruskal - wallis p = 0.05 ; table 1 ) .
when the post - hoc dunnett test was performed , hs - ctnt levels were not statistically different between the groups .
ck - mb levels did not differ between the three groups ( kruskal - wallis ; p = 0.48 ) .
cohb levels with hs - tnt values were weakly correlated ( r = 0.173 , p = 0.041 ) ; on the other hand , ck - mb levels were not correlated with those of the cohb ( r = 0.013 , p = 0.883 ) ( table 2 ) . abbreviations :
ck - mb , creatine kinase - myocardial band ; hs - tnt , high - sensitivity cardiac troponin t. on admission , 5 of the 141 patients had elevated serum ck - mb levels and 20 had elevated serum hstnt levels ( > 14 ng / l ) , only three of the patients with cardiac markers were elevated on the follow - up period .
the findings of the cohort current study of patients with cohb intoxication hs - ctnt levels were slightly higher in severe toxicated patients than in mild toxicated patients without significant correlation between cohb and hs - ctnt levels .
cardiac troponins are components of the contractile apparatus of cardiomyocytes and are released during myocardial necrosis .
serum troponin elevation is a specific and well established myocardial necrosis biomarker , and can detect extremely small amounts of myocardial necrosis ( < 1.0 g ) ( 12 , 13 ) . very low , but
detectable amounts of hs - ctnt levels may reflect a normal biological process of myocyte turnover and it may also be associated with an increased cell turnover ( 14 , 15 ) .
the proposed mechanisms of cardiac troponin release include apoptosis , cellular release of proteolytic degradation products , increased cell wall permeability , and formation and release of membranous blebs ( 11 ) .
many acute diseases are associated with elevated ctn in the absence of acute ischemic heart disease that can occur for many reasons ( 16 ) .
direct toxic effects of circulating cytokines and chemotherapies can cause severe myocardial toxicity as severe sepsis and septic shock ( 12 , 16 ) .
recent data showed that one can detect the effects of some toxic chemotherapy by monitoring ctn ( 16 ) .
low levels of co activate soluble guanylate cyclase which in turn exerts beneficial effects such as vasodilatation and inhibition of platelet aggregation ( 7 ) . in the current study ,
hs - ctnt levels were higher in patients with severe co toxicity compared to the ones with mild co intoxication .
although ultramicroscopic changes are reported in cases of co toxicity , its relative effects need to be documented ( 17 ) .
a direct toxic effect of cohb is discussed as a consequence of experimental studies on cytochrome oxidase ( 17 ) .
co binds with cardiac myoglobin causes a rapid decrease in myocardial oxygen reserves ( 18 ) .
when the energy source is blocked , then the function of the myoglobin is diminished ( 19 , 20 ) .
myocardial fiber necrosis and other changes observed with electron microscopy are associated with impaired energy metabolism ( 22 , 23 ) . however
, cardiac troponins are released without electron microscopic changes ( 24 , 25 ) . in this study
ck - mb levels did not differ between the three groups and did not correlate with cohb .
patients with detectable troponin , but no ck - mb , in the blood may exhibit microscopic zones of myocardial necrosis ( microinfarction ) ( 13 ) .
( 26 ) showed that in co poisoning , patients without known underlying significant coronary artery disease with cohb levels of up to 60% do not develop myocardial damage but they used only cardiac biomarkers ck - mb and ctnt .
the current study did not find any significant elevation in ck - mb levels , but in contrast a significant increase in hs - ctnt levels was found , which might be because of the microscopic myocardial necrosis ( 26 ) .
myocardial injury , documented with elevations in cardiac biomarkers , could be present in about one - third of the patients with serious co poisoning and it was associated with mortality ( 7 ) . the severity of myocardial injury depended on the duration and amount of co exposure ( 27 ) . moreover
, the level of co in the tissues may have an equal or greater impact on the clinical status of the patient than does the blood level of co ( 28 ) .
the primary limitation of the current small study group was the method of data collection .
there was no information on the length of co exposure and the timing of the blood cohb levels in relation to the co exposures .
further studies are necessary in this regard . another limitation was the retrospective nature of the study .
the data were reviewed by one researcher who avoided the selection bias ; however , misclassification , may still exist , which can not be verified or validated .
these results apply only to the elecsys hs - ctnt and ck - mb ( roche diagnostics ) assays , and may not be generalized to other high sensitivity assays by other manufacturers . finally , the study design was based on the data available in one hospital , and the obtained results may not necessarily be generalized . in conclusion , in patients without clear signs of myocardial infarction ,
even mild co poisoning is associated with quantifiable circulating levels of hs - ctnt when tnt is measured using a highly sensitive assay and cardiac complications should be considered in such patients .
plasma levels of the hs - tnt and ck - mb assays were not correlated with the cohb levels .
in conclusion , in patients without clear signs of myocardial infarction , even mild co poisoning is associated with quantifiable circulating levels of hs - ctnt when tnt is measured using a highly sensitive assay and cardiac complications should be considered in such patients .
plasma levels of the hs - tnt and ck - mb assays were not correlated with the cohb levels .
 backgroundintoxication due to carbon monoxide ( co ) is one of the most common types of poisoning . 
 cardiac effects of carboxyhemoglobin ( cohb ) range from simple arrhythmias to myocardial infarction.objectivesthe current study aimed to investigate the relationship between blood carboxyhemoglobin and high - sensitivity cardiac troponin t ( hs - ctnt ) level with a highly sensitive assay in patients with acute carbon monoxide poisoning.patients and methodsthis retrospective study was conducted on 141 ( 54 males and 87 females ) patients , with acute co intoxication , admitted to the sevket yilmaz research and education hospital emergency unit during a one - year period ( january 2012 - january 2013 ) . 
 the patients were divided into three groups based on cohb levels : group i , mild cohb level < 15% ; group ii , cohb between 15% and 25% ; group iii , severe acute co intoxication cohb levels > 25% . 
 cohb , hs - ctnt ( stat ) , creatine kinase ( ck ) and creatine kinase - myocardial band ( ck - mb ) levels were measured on admission.resultsthe mean age of the patients was 38  16 years . 
 cohb levels ranged from 8 to 35 . 
 hs - ctnt levels on inclusion in this study were slightly different between the groups ( p = 0.05 ) . 
 cohb levels with hs - ctnt values were weakly correlated ( r = 0.173 , p = 0.041 ) ; on the other hand , ck - mb levels were not correlated with cohb ( r = 0.013 , p = 0.883).conclusionsin patients without clear signs of myocardial infarction , even mild co poisoning was associated with quantifiable circulating levels of hs - ctnt when tnt was measured using a highly sensitive assay in the current study patients . 
 plasma levels of the hs - tnt and ck - mb assays were not correlated with the cohb levels in the current study patients . 
1. Background
2. Objectives
3. Patients and Methods
3.1. Statistics
4. Results
5. Discussion
5.1. Conclusion