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Cardiac Troponin I Level in STEMI and Clinical Correlation with Left Ventricular Dysfunction in Indian Population

Department of Biochemistry1, Department of Medicine2 India Rajnish Singh3, Department of Cardiology4, India M. Imteyaz Ahmad1*
1Department of Biochemistry, PGIMER and Dr. Ram Manohar Lohia Hospital, New Delhi, India Neera Sharma
2Department of Medicine, PGIMER and Dr. Ram Manohar Lohia Hospital, New Delhi, India A.K Varshney
3Department of Medicine, PGIMER and Dr. Ram Manohar Lohia Hospital, New Delhi, India Rajnish Singh
4Department of Cardiology, PGIMER and Dr. Ram Manohar Lohia Hospital, New Delhi, India Ranjit Kumar Nath
Corresponding Author : Dr. M. Imteyaz Ahmad
Department of Biochemistry, Nursing Home Laboratory
Room no.20, Dr. Ram Manohar Lohia Hospital
Baba Kharak Singh Marg, New Delhi, India Pin: 110001
Tel: +919953130525
E-mail: [email protected]
Received June 29, 2013; Accepted July 30, 2013; Published August 06, 2013
Citation: Ahmad MI, Yadaw BK, Sharma N, Varshney AK, Sharma L, et al. (2013) Cardiac Troponin I Level in STEMI and Clinical Correlation with Left Ventricular Dysfunction in Indian Population. J Cardiovasc Dis Diagn 1:116. doi: 10.4172/2329-9517.1000116
Copyright: © 2013 Ahmad MI, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Objective: To determine the relationship of serum troponin I after first acute myocardial infarction with left
ventricular ejection fraction as assessed by echocardiography.

Methods: A total of 40 patients of acute myocardial infarction were included in the study. Troponin I concentration was measured by ELISA method and echocardiographic ejection fraction was calculated by modified Simpson’s rule. Echocardiographic ejection fraction was compared with serum troponin I concentration. Patients with previous myocardial infarction were excluded.

Result: There was strong negative correlation between troponin I concentration and left ventricular ejection fraction, i.e., with an increasing troponin level, there was a fall in ejection fraction. The Pearson’s correlation coefficient was –0.69, which was statistically significant (p<0.0001). In our study, we observed that patients with ejection fraction >50%, though small in number were having cTnI levels at 24 hrs ≤ 8 ng/ml. Patients with ejection fraction <50% (left ventricular systolic dysfunction) were having cTnI levels at 24 hrs ≥ 17 ng/ml. Therefore a presumptive cut off level of cTnI ≤ 8 ng/ml may be taken to consider normal left ventricular systolic function in STEMI. The normal range of Troponin I in apparently health individual without STEMI was observed to be <1.0 ng/ml. The mild increase in Troponin I at 24 hrs of STEMI with preserved EF >50% may be due to peak value of biomarker achieved at 24-36 hrs after myocardial injury as most of troponin I are attached to myofibrils.

Conclusion: Serum troponin I concentration has a strong negative correlation with left ventricular ejection
fraction after first acute myocardial infarction, and hence can be used to assess the LVEF in patients with first myocardial infarction. An observation was made that a cut off level of cTnI ≤ 8 ng/ml was associated with normal left ventricular systolic function.

Keywords
TROP I: Troponin I; LVEF: Left Ventricular Ejection Fraction; IWMI: Inferior Wall Myocardial Infarction; AWMI: Anterior Wall Myocardial Infarction
Introduction
Asian Indians have considerably higher prevalence of premature Coronary Artery Disease (CAD) and standardized mortality rates for CAD compared with Europeans, Chinese and Malays [1-4].
Over the last four decades there has been a 10-fold increase in the prevalence of coronary artery disease in urban area of India. The overall rate of Coronary artery disease was 11.0% in Chennai Urban population [5]. Acute Coronary Syndrome (ACS) refers to the spectrum of clinical presentations ranging from ST-Segment Elevation Myocardial Infarction (STEMI) to non-ST-segment elevation myocardial infarction (NSTEMI) to unstable angina (i.e., acute coronary syndrome without release of enzymes or biomarkers of myocardial necrosis) [6].
As per the Revised Definition of Myocardial Infarction (MI), either of the following satisfies the Criteria for acute, evolving, or recent MI include: 1- Typical rise and gradual fall (troponin) or more rapid rise and fall Creatine Kinase (CK-MB) of biochemical markers of myocardial necrosis with at least one of the following. (a) Ischemic symptoms (b) Development of pathologic Q waves on the ECG reading. (c) ECG changes indicative of ischemia (ST=segment elevation or depression). (d) Coronary artery intervention (e.g. coronary angioplasty). 2- Pathological findings of an acute MI [7]. ECG Criteria for a STEMI is - New ST elevation at the J-point in two contiguous leads with the cut – off points: ≥ 0.2 mV in men or ≥ 0.15 mV in women in leads V2- V3 and / or ≥ 0.1 mV in other leads in the absence of LVH/LBBB [8].
Ventricular function is the best predictor of death after an acute coronary syndrome. It serves as a marker of myocardial damage, provides information on systolic function as well as diagnosis and the prognosis [9,10].
Troponin is a globular protein of muscle that binds to tropomyosin and has a marked affinity for calcium ions, and is thus a central regulatory protein of muscle contraction. The troponin, a proteincomplex, consists of three subunits with different structure and functions (T, I, C) [11-13]. Troponin I is a 23.5 kDa component of Troponin complex that inhibits the interaction of myosin cross-bridges with the actin-tropomysoin complex, and thus regulates the striated muscle contraction [13]. Three isoforms of Tnl have been described, a cardiac (cTnI) and two skeletal muscle [slow twitch (sTnI) and fast twitch (fTnI)] [14]. Each of the three Tnl isoforms is encoded by three different genes located on different chromosomes [15]. The skeletal isoforms show approximately 40% heterogeneity of primary sequence, while the cardiac isoform displays a similar degree of sequence heterogeneity compared to each skeletal isoform. Due to the presence of an additional 31 amino acids at the N-terminal region, cTnI (MW 24,000 Da) is uniquely different than either fTnI or sTnI (MW 19,800 Da). During human development, both sTnI and cTnI are expressed in the myocardium. At birth, however, only cTnI is expressed in the myocardium [16]. cTnI has been shown not to be expressed in any type of skeletal muscle, independent of developmental or disease stimuli [17]. Therefore, knowledge that cTnI is 100% tissue-specific for the myocardium. cTnI has been shown to be a very sensitive and specific marker for acute myocardial infarction (AMI) [18-21]. The early release kinetics for cTnI is similar to those of creatine kinase (CK) MB, in that it takes 4-8h to increase above the upper reference limit. Thus, cTnI does not provide an earlier detection method for AMI than CK MB [22]. The initial cTnI rise is from the release of 3 to 6% cytoplasmic fraction of troponin in the cell following ischemic injury [20]. cTnI peaks between 14 and 36 h after onset of AMI and remains elevated for five to seven days after AMI. The mechanism for the lengthy time for elevations of cTnI is most likely due to the ongoing release of troponin from the 95 to 97% myofibril-bound fraction. The ongoing release and clearance thus gives the impression that cTnI has a long half-life. However, the true half-life of cTnI is less than 2 h [23].
According to international consensus and task force definitions of myocardial infarction (MI), the diagnosis of MI is based mainly on an elevated cardiac troponin level exceeding the 99th percentile and demonstrating an increase or decrease over time [7,8]. The universal definition recommends the use of a more sensitive troponin assay with a coefficient of variation of 10% or less at the diagnostic cutoff concentration representing the 99th percentile of a reference population [8]. The major limitation of standard cardiac troponin assays is their relatively low clinical sensitivity at the time of ED presentation owing to the troponin release kinetics and the time it takes for increased concentrations to reach the circulation. Consequently, the diagnosis of AMI requires prolonged monitoring with serial determination of cardiac biomarkers over 6-9h after ED presentation. This contributes to delays in initiating treatment as well as ED overcrowding and the need for unnecessary admissions to rule out myocardial infarction.
It is now recognized that the major predictor of long-term survival after recovery from acute myocardial infarction is the functional status of the left ventricle. Left ventricular function has usually been described in terms of the ejection fraction (EF), but it is not clear whether EF is the most meaningful index of left ventricular function in the post infarction situation [24-27]. Low EF may, on the one hand, be caused by poor contractile function due to extensive myocardial damage or continuing ischemia or, on the other hand, to left ventricular dilation caused by infarct expansion and stretching of the myocardial scar. Thus End-Systolic Volume (ESV) or End-Diastolic Volume (EDV) might be more meaningful predictors of prognosis than EF, which is merely an arithmetical term based on these two values.
If a sufficient quantity of myocardium undergoes ischemic injury, left ventricular pump function (left ventricular ejection fraction) becomes depressed; cardiac output, stroke volume, blood pressure, and peak dP/dt are reduced and end-systolic volume is increased [28]. The degree to which end-systolic volume is increased perhaps is the most powerful predictor of mortality following STEMI [29].
Left ventricular systolic dysfunction and its myocardial damage can be assessed by 2.D-echocardiography. In acute STEMI troponin I value shows an inverse correlation with left ventricular ejection fraction [7]. The present study plan to analyse the relationship between peak troponin I level after STEMI and left ventricular systolic dysfunction determined by 2.D-echocardiography.
The aim of the study is to measure the troponin I in acute STelevation myocardial infarction, assessment of left ventricular dysfunction by echocardiography in acute ST-elevation myocardial infarction and co-relation between troponin I levels and left ventricular dysfunction in acute ST- elevation myocardial infarction.
Materials and Methods
The study was conducted at PGIMER and Dr RML Hospital. Cases were selected from the patients admitted in Dr. RML Hospital New Delhi. Study group consisted of 40 patients hospitalized for 1st acute ST-Elevation myocardial Infarction. Consent was taken from all the patients prior to inclusion in the study. Inclusion criteria’s are, age 20 to 60 years, both male and female, case of acute onset myocardial infarction as diagnosed by clinical presentation, symptom of ischaemia lasting >30 minute Retrostermal chest pressure, burning, or heaviness; radiating occasionally to neck jaw, epigastrium, shoulders, or left arm. ECG characteristics - New ST elevation at the J-point in two contiguous leads with the cut – off points: ≥ 0.2 mV in men or ≥ 0.15 mV in women leads V2-V3 and / or ≥ 0.1 mV in other leads in the absence of LVH/ LBBB [5]. Biochemical cardiac Marker (Increased CK-MB, TroponinI)
Exclusion criteria are a known case of old myocardial infarction, a patient having pre-existing ECG changes s/o old MI. ECG showing Q wave at the time of admission. Echocardiographic finding of old scar/ previous wall motion abnormalities / structural heart disease / congenital heart disease. All those conditions in which Troponin I also increases without Ischaemic heart disease: significant renal impairement, rheumatoid arthritis, myocarditis (pericarditis), sepsis, acute congestive heart failure, acute pulmonary embolism, or prolonged tachyarrhythmias.
Study design
All admitted patients 40 (forty) of Acute ST-elevation MI were included in the prospective study. The protocol included. Complete history and clinical assessment with investigations with baseline and special investigations including echocardiography.
Blood sample collection
On admission, 10 ml of peripheral venous blood was collected from the antecubital vein by an autoclaved syringe using 20 gauze needles. The blood was allowed to clot at room temperature for at least half an hour. The glass tube with clotted blood was centrifuged at 2000 rpm for 20 minutes and the centrifugation was repeated once more to remove the red cells completely. The supernatant serum, devoid of cellular elements, was separated from the clot and placed in two acid cleaned small test tubes. Samples with any visible haemolysis were discarded, as erythrocytes contain large quantities of enzymes which are known to alter the total CPK, CPK-MB, LDH and Troponin I. Anticoagulants were avoided to circumvent unnecessary variables which might interfere with accurate assays of enzyme activity.
Principle of the assay
The cTnI ELISA test is based on the principle of a solid phase enzyme-linked immunosorbent assay. The assay system utilizes four unique monoclonal antibodies directed against distinct antigenic determinants on the molecule. Three mouse monoclonal anti-troponin I antibodies are used for solid phase immobilization (on the microtiter wells). The fourth antibody is in the antibody-enzyme (horseradish peroxidase) conjugate solution. The test sample is allowed to react simultaneously with the four antibodies, resulting in the troponin I molecules being sandwiched between the solid phase and enzymelinked antibodies. After 90-minute incubation at room temperature, the wells are washed with water to remove unbound-labeled antibodies. A solution of Tetramethylbenzidine (TMB) Reagent is added and incubated for 20 minutes, resulting in the development of a blue color. The color development is stopped with the addition of 1N Hydrochloric Acid (HCl) changing the color to yellow. The concentration of troponin I is directly proportional to the color intensity of the test sample. Absorbance is measured spectrophotometrically at 450 nm.
The routine investigations done are complete haemogram and ESR, Blood Sugar, Blood urea serum creatinine, Lipid profile; Total cholesterol, serum triglyceride, HDL Cardiac enzyme CPK, CK-MB, LDH, SGOT done by chemiluminescence (orthoclinical diagnostics). Troponin I at 6 hrs or at the time of admission and 24 hrs was done by Calbiotech Troponin I ELISA kit with EVOLIS (Biorad) instrument.
The special investigations added are Echocardiography- Left ventricular ejection fraction was assessed by modified Simpson’s method from Apical two chamber and Four chamber views,16 segment regional wall motion abnormalities was determined in Parasternal long axis, Parasternal short axis apical four chambers and apical two chamber views by 2D echocardiography and M-Mode echocardiography [30]. Echocardiograms were obtained using Philips, Sonus echocardiography machine with the subjects lying in the left lateral decubitus position and supine position. The assessment of cardiac valve structures, chamber size evaluation, Left Ventricular features, LVIDd (Left Ventricular Internal dimension in diastole, LVIDs(Left Ventricular Internal dimension in systole), LVEF (Left Ventricular Ejection fraction), Left Ventricular wall motion abnormalities, Fractional Shortening, LVEF (Left Ventricular ejection fraction).
The ejection fraction is defined as the ratio of stroke volume to enddiastolic volume.
EF=EDV-ESV/EDVX100 (%)
Where EF=Ejection fraction, EDV= end-diastolic volume and ESV =end-systolic volume. Normal values of left ventricular ejection fraction are 0.55 to 0.75 when determined by echocardiography and angiocardiography. There are no gender differences, but ejection fraction normally declines with age.
LVEF less than 50% was taken as systolic dysfunction [31]. Left ventricular ejection fraction will be calculated by 2.D-echocardiography at 48 to 72 hours after the onset of clinical symptoms. Left ventricular ejection fraction will be assessed by modified Simpson’s method from apical two chamber and four chamber views [32].16 segment regional wall motion abnormality was determined in parasternal long axis, parasternal short axis apical four chamber and apical two chamber views by 2D echocardiography and M-Mode echocardiography. Echocardiograms will be obtained using Philips, Sonus echocardiography machine with the subjects lying in the left lateral decubitus position and supine position.
Results
The study was carried out in a study group of consecutive 40 inpatients in the department of medicine of PGIMER and Dr.RML Hospital New Delhi satisfying the selection criteria (as per inclusion and exclusion criteria laid down).
Mean age of the patients in present study was 49.15 ± 8.28. Most of the patients in our study were in age group 41-60yrs (82.5%). 92.5% of patients were male and only 7.5% were female. 72% of patients had AWMI and 28% patients had IWMI, 52.5% patients had dyslipidemia. It was found to be most common risk factor. Smoking (47.80%) and Hypertension (24.32%) were other significant risk factors, mainly in male patients. Risk factors were much more common in AWMI as compared to IWMI patients. On comparison of AWMI and IWMI, it was found that mean values of SBP, DBP and PR were significantly lower in IWMI patients as compared to AWMI patients (p value<.05) (Tables 1 and 2).
The mean values of TROP-I at 24 hour was significantly higher as compared to mean value of TROP-I at 6 hour. The mean value of TROP-I at 6 hour and 24 hour were similar in both group AWMI as well as IWMI. The mean values of EF were 37.6%. 37 patients out of 40 patients had LV dysfunction. On comparison of left ventricular echocardiography parameter- LVIDd and LVIDs were significantly lower in IWMI patients as compared to AWMI patients (Tables 3 and 4). All the 37 patients of LV dysfunction had higher value of TROP-I.
The mean value of TROP-I was increasing as EF was decreasing. The mean values of TROP-I was much higher in patients in which EF was less than 30%. An observation was made that a cut off level of cTnI ≤ 8 ng/ml was associated with normal left ventricular systolic function as 3 patients with >50% EF. The normal range of Troponin I in apparently health individual without STEMI was observed to be<1.0 ng/ml. The mild increase in Troponin I at 24 hrs of STEMI with preserved EF >50% may be due to peak value of biomarker achieved at 24-36 hrs after myocardial injury as most of troponinI are attached to myofibrils.
Discussion
The present study entitled Assessment of left ventricular dysfunction by Echocardiography and its correlation with quantitative troponin I level in Acute ST-elevation myocardial infarction’ was conducted in 40 STEMI in-patients in the department of medicine PGIMER and Dr. RML Hospital New Delhi.
CTnI is accepted as a highly reliable biochemical marker for detecting myocardial damage, and its use in the diagnosis of acute myocardial infarction is increasing. Data suggests that cTnI may be related to the amount of myocardial damage and cTnI release inversely correlates with left ventricular ejection fraction and infarct size. However, there are very few studies to substantiate the claim.
In patients with ST segment elevation and in which ejection fraction analysis was delayed, observed that troponin was a good indicator of depressed ejection fraction [33]. The relationship between peak troponin and systolic function in patients without ST segment elevation, however, has received little attention in the literature.
In the present study, mean age of patients was 49.5 yrs. The no. of male patients presenting with chest pain were more than no. of female and M: F ration was 12.3:1. In similar study Vincet et al. observed 3.28:1. This observation was in consonance with the fact that the incidence of myocardial infarction is more in male than in the female and there are certain risk factors which are more commonly seen in males (smoking, alcohol intake) [33].
In the present study most common risk factor in the patients were dyslipidemia (52.4%), similar observation was reported by Deepak et al. (54%) in his study. HTN were observed in 25% of STEMI Patients in the present study; however Deepak et al. found slightly higher percentage at 32% and Vishwanathan et al. 43% [34]. Diabetes Mellitus was present in only 2.5% of patients in present study which was small compared to other studies. Difference might be because of younger patients in the present study and because of small sample size.
In present study 29 patients (72%) out of 40, sustained an anterior wall MI and 11 patients (28%) out of 40 STEMI sustained inferior wall MI. The mean value of EF was 37.63 ± 8.32 (Table 4). In a similar study on 50 patients of first acute myocardial infarction, Sharkey et al observed mean EF 37.6 ± 15.2%. In our study 92.5% patients were thrombolysed and 7.5% patients were non- thrombolysed. Our study shows Troponin I values at 24 hrs is 69.68 ± 43.28 in thrombolysed patients and 19.33 ± 2.0 in non- thrombolysed patients. (Table 5). The higher release of markers due to washout phenomena occurring in patients receiving thrombolytic treatment. Troponin I, as expected, was raised in all cases and the mean cTnI value at 6 hr/admission was 20.21 ± 18.35 and at 24 hr. was 66.94 ± 43.53 (Table 4).
In the present study positive predictive value of TROP-I was 92.5%. However previous worker reported 89% Vincet et al., 100% Deepak et al. This observation was similar to the previous study.
In the present study mean value of TROP-1 in LV Dysfunction patient was 66.94 ± 43.53 (Table 6).
In the present study LV Dysfunction was present in 92.5% of STEMI patients. However Deepak et al. observed LV Dysfunction in only 48% of patient and Vincet et al. observed in only 33.3% of patients [33,34]. Difference was observed because the present study has small number of patients which had, multiple risk factor in most of them and compared to western population Indian population have extensive coronary artery disease. The mean values of TROP-I were much higher in present study as compared to previous study. This could be because large number of our patients had extensive anterior wall myocardial infarction with consequent large infarct size. It has been recognized that the total quantity of cardiac enzyme released correlates with the infarct size.
As most of our patients received thrombolytic treatment, higher Troponin I level in part could be due to washout phenomenon occurring in patient receiving thrombolytic treatment.
In our study, we observed that patients with ejection fraction>50%, though small in number were having cTnI levels at 24 hrs ≤ 8 ng/ ml. Patients with ejection fraction <50% (left ventricular systolic dysfunction) were having cTnI levels at 24 hrs ≥ 17ng/ml. Therfore a cut off level of cTnI ≤ 8 ng/ml may be taken to consider normal left ventricular systolic function in STEMI. We observed strong inverse correlation between peak cTnI concentration and left ventricular ejection fraction. The pearson correlation coeffiecient was -0.628 (P<0.0001).
Our secondary observation in Indian subjects is dyslipidemia was the most common risk factor in STEMI patients. LV dysfunction was present in 37 patients out of 40 patients of STEMI. The mean value of TROP-I at 24 hour was much higher as compared to TROP-I at 6 hour (Figure 1).
On comparison, echocardiographic parameters- LVIDd and LVIDs, as well as, SBP, DBP and PR were significantly lower in IWMI patients as compared to AWMI patients, though there was no difference between cTn-I values between the two groups.
cTnI has practical advantages over other markers in the assessment of left ventricular ejection fraction. After acute infarction, cTnI has a peak value at 12 hours from the onset of pain. The plateau phase of cTnI, however, lasts upto 48 hours, and represents an integrated estimate of myocyte necrosis [35,36]. The peak value will therefore be missed in samples taken 12-48 hours after admission, but there is a large time window. This makes repeated sampling unnecessary, and represents a cost and time-effective method of diagnosis and quantification (Figures 2 and 3). This is in contrast to creatine kinase-MB or myoglobin, for which multiple measurements are required to identify the peak value and whose values are affected by thrombolysis [37,38]. This marker offers a simple, inexpensive, quick noninvasive method of identifying such patients. Estimation of troponin I can also be used to identify those patients who may benefit from other treatments, for example, ACE inhibitors.
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