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Aim of this study was to evaluate the role of Myeloperoxidase (MPO) and high sensitive Troponin T in the early diagnosis of acute coronary syndrome (ACS). This was a cross sectional study that comprised of 120 individuals of which 75 were cases and 45 healthy controls. On the basis of clinical history and 12 lead electrocardiogram initial diagnosis of ACS was made in the cases. MPO and high sensitive Troponin T (hs-cTnT) was measured in all the individuals. Levels of MPO were significantly higher in patients of ACS as compared to those in control group [medians: 15.40 (95 % CI 11.06-20.84) vs 5.84 (95 % CI 5.50-6.44)]. By taking the cut off as >11.87 U/mL for MPO, its sensitivity was 87 % (95 % CI 73.7-95.1), specificity was 97.3 % (95 % CI 90.6-99.7), positive predictive value was 94.6 % and negative predictive value was 92.6 %. Positive likelihood ratio was 33.0 while negative likelihood ratio was 0.13, whereas the corresponding values in case of hs-cTnT were 95.6 % (95 % CI 85.2-99.5), 61.3 % (95 % CI 49.5-72.6), 59.7 %, 95.8 %, 2.47 and 0.07 by taking cut off as >14 pg/ml. The area under the ROC curves (AUC) of MPO and hscTnT at 0-6 h were 0.971 (95 % CI 0.92-0.99, P < 0.001) and 0.797 (95 % CI 0.71-0.86, P < 0.001) respectively. The logistic model combining the two markers yielded sensitivity, specificity, positive predictive value and negative predictive value of 95.7, 97.3, 98.2 and 93.7 % respectively. It was concluded that MPO and hs-cTnT may be useful tools for risk stratification of ACS and can be used together with better accuracy in the early diagnosis of ACS.

Currently employed markers for the detection of acute coronary syndrome are Troponin T, CK (Creatine Kinase) and CKMB activity. CKMB activity measured by immunoinhibition method can give falsely elevated results due to the presence of atypical CK and CKBB and at times lead to the mis-diagnosis of acute coronary syndrome. Hence, CKMB mass (CKMB) measured by electrochemiluminence sandwich principle was employed. In this cross-sectional study 183 samples of 61 patients were analyzed within 6 h of diagnosis of acute coronary syndrome and followed up to 72 h. The correlation coefficient between CKMB activity and CKMBM at 4-6 h was 0.744, while at 12-24 h it was 0.909 and at 48-72 h it was 0.337. Thus there was good association between the two methods at 12-24 h but, statistically for method comparison studies and for replacing one method by another, the two methods need to be in agreement with one another. In this study the two methods are not in agreement with one another and thus analytically not replaceable. Another finding was obtained that CKMBM reached cut off levels prior to CKMB enzyme activity and hence, CKMBM is clinically better than CKMB activity to detect reinfarction.

Laboratory infarction diagnostics are based on the detection of elevated serum activities of creatine kinase (CK) Creatine kinase Isoenzyme MB (CKMB) and Transaminases. Determination of these cardiac marker enzymes permits the diagnosis of transmural myocardial infarction. However in such patients the diagnosis of acute myocardial infarction can be confirmed by the clinical symptoms and changes in the ECG, in addition to the enzyme assays. The 50 AMI patients selected in the present study were those admitted to the ICCU of Shri Krishna Hospital, Karamsad. The blood samples were taken at Zero hours (i.e. at the time of admission of the patient). Within 6 hrs of the starting of chest pain, 1.5 million units of streptokinase were mixed with 100 to 150ml of normal saline and administered by infusion over a period of one hour. The blood samples were further collected at intervals of 6 hrs, 14hrs, 32hrs, 48hrs, 5(th) day and 7(th) day. The blood samples were analyzed for CK, CKMB, SGOT, α HBDH and Cardiac specific Troponin T. By 6hrs the CK and CKMB values had started rising, the rise continuing at 14hrs with peak values at 32hrs. The CK showed a slight decrease by 48 hrs. The cardiac Troponin T showed wide time window from 4 hrs to 7(th) day for detecting myocardial damage. The maximum cardiac Troponin T values were during the first 24hrs. Cardiac Troponin T in serum appears to be a more sensitive and early indicator of myocardial cell injury in comparison to CKMB.

It is well established that smoking increases the risk for cardiovascular disease. From the studies in diabetic subjects it has been shown that smoking induces microalbuminuria and accelerates the progression to end stage renal disease. Little is known whether smoking is also related to microalbuminuria and renal end organ damage in non diabetic subjects. The hypothesis which was put forward that tobacco chewing is related to microalbuminuria and renal functional changes in non diabetic subjects. We therefore performed a population based study in the Anand city of Gujarat in which we studied the relation between tobacco chewing and urinary albumin excretion. Tobacco chewers had a higher urinary albumin excretion (Albumin excretion 373±13.9 mg/day: P<0.01) than those who do not consume tobacco. In conclusion tobacco chewing is associated with albuminuria.

Laboratory infarction diagnostics are based on the detection of elevated serum activities of total Creatine Kinase (CK), Creatine Kinase isoensyme MB, (CKMB), Lactate dehydrogenase (LDH), isoenzyme forms of LDH and transaminases. Determination of these cardiac marker enzymes permits a highly sensitive diagnosis of transmural myocardial infarction. In such patients the diagnosis of acute myocardial infarction can be confirmed by the clinical, symptoms, and changes in the ECG in addition to the enzyme assays. The 50 AMI patients selected in the present study were those admitted to the ICCU of Shri Krishna Hospital, Karamsad. The blood samples were taken at the time of admission (ie. within four hours of the start of chest pain). The samples were analyzed for CK, CKMB, SGOT, (Serum glutamate oxaloactate transaminase) αHBDH α-hydroxybutyrate dehydrogenase and troponin T. The serum CKMB activity in AMI showed an increase only 5-6 hours after the commencement of chest pain. The elevation in SGOT and αHBDH was still delayed. At the same time we could observe that the cardiac Troponin T (cTnT) was elevated at the time of admission of the patient itself. This increase of cTnT in AMI patients was 20 times higher than the normal blood donors. The controls included 25 normal blood donors and 25 patients with polytraumatic injuries with no chest contusion. The study shows that cTnT estimation could serve in the early diagnosis of AMI. The increase of cardiac troponin T in AMI patients was 20 times higher than the normal blood donors in AMI patients at the time of admission. Cardiac troponin T in serum appears to be a more sensitive indicator of myocardial cell injury than CKMB activity and its detection in the circulation may be a useful prognostic indicator in patients with unstable angina as well. When the blood of normal blood donors or that of patients with polytraumatic injury was analysed the troponin T values were well within the normal range in both the above categories showing that cardiac troponin T is highly specific for heart tissue. Although CKMB and cardiac troponin T are released soon after the myocardial injury, the release of cardiac troponin T is much earlier than CKMB thereby invalidating the important role of cardiac troponin T in diagnosing AMI. Cardiac troponin T has been shown to be highly sensitive for cardiac injury and not elevated in any other trauma, heavy exercise or skeletal muscle injury. Cardiac troponin T is ordinarily undetectable in healthy individuals, and so its measurement can serve as a powerful tool in the diagnosis of AMI.