Determination of diagnostic enzymes and analysis of genetic variations in acute myocardial infarction

ABSTRACT DETERMINATION OF DIAGNOSTIC ENZYMES AND ANALYSIS OF GENETIC VARIATIONS IN ACUTE MYOCARDIAL INFARCTION Acute myocardial infarction (AMI) is a disease with multifactorial etiology which has 20 percent of the cases undiagnosed and carries a 25 percent mortality rate. The diagnosis of AMI is based on by clinical findings, ECG and biochemical tests. In our study, we followed 27 patients which were admitted to the emergecy department with chest pains and later diagnosed as AMI with diagnostic enzymes and markers levels for a period of six days. We also analyzed the genetic variations of Factor V Leiden and Prothrombin 20210 G/A in our patients. In the surviving 24 patients between 0 and 5 hours creatinin kinase myocardial band (CKMB), cardiac troponin T (ctnT), cardiac troponin I (ctnl) and LDH isoenzymes levels were increased where as AST and total LDH levels did not change. The total CKMB activity increased nine fold from the initial level (176 + 149 Ü/L) and peaked at 12 hours, ctnT level increased seven fold (3.3+1.2 ng/mL) and peaked at 24 hours, ctnl level increased thirtythree times (629+679 ng/mL) and peaked at 12 hours and LDH1/LDH2 ratio increased two fold (3.1+1.0) and peaked at 24 hours. CKMB activity fell to the normal range after 3 days, but ctnT, ctnl levels and LDH1/LDH2 ratios were still elevated on the 6th day. We have found ALT (2200±800Ü/L), AST (1234+1 41 8Ü/L) and LDH (8905+1 1774Ü/L) levels to be expectionally high in the 3 patients died (%11). Heterozygot Prothrombin 2021 0G/A genetic variation and Factor V Leiden genetic variation were found in 1 patients (%3.7). We have also found that malondialdehyde which is a free oxygen radical metabolite was increased significantly in the immediate 12 hour period after AMI. Key words: AMI, diagnostic tests, factor variations.