Echocardiographic comparison of regional wall motion abnormality between patients with acute anteroseptal and acute extensive anteior ST segment elevation myocardial infarction.

Post myocardial infarction (MI) short and long-term clinical outcome is largely determined by the size of the infarcted area. It is generally assumed that as the lead involvement in electrocardiography (ECG) is less in anteroseptal ST segment elevation myocardial infarction (AS-STEMI), where ST segment elevation (STE) is limited to leads V1 to V3, myocardial damage is likely to be less; and in extensive anterior STEMI (EA-STEMI), as the STE extends further upto V6, the myocardial damage is likely to be more. This study was intended to compare regional wall motion abnormality (RWMA) between acute anteroseptal STEMI and acute extensive anterior STEMI patients. 90 patients with AS-STEMI and 106 patients with EA-STEMI, admitted in between October 2012 and September 2013, were included. For each patient, a transthoracic echocardiogram (TTE) was performed within 24-48 hours of MI and was interpreted by an independent investigator blinded to the patient's ECG data. No differences were observed between the two groups in baseline characteristics; except AS-STEMI group had more patients with diabetes and EA-STEMI group had more patients with family history of coronary artery disease. Distribution, extent of wall motion abnormalities and mean number of total involved segments were similar between patients with AS-STEMI and those with EA-STEMI (p > 0.05). Regarding regional dysfunction, the apical septal (99.1% vs. 92.2%, p < 0.05) and apical (76.4% vs. 60.0%, p < 0.05) segments were the only two segments that were affected significantly more in patients with EA-STEMI than in patients with AS-STEMI. So, the term AS-STEMI may be a misnomer, as it implies that only the anteroseptal segments of the left ventricle are involved. This study shows that regional dysfunction in patients with AS-STEMI extends beyond the anteroseptal region. So, any patients with anterior wall involvement, either anteroseptal or extensive anterior STEMI, should be treated with equal importance.

Elevated serum homocysteine level has a positive correlation with serum cardiac troponin I in patients with acute myocardial infarction.

The objective of the present study is to find out whether the increased serum homocysteine level is associated with the increased serum troponin I as a surrogate marker of extent of myocardial injury in acute myocardial infarction patients. Elevated homocysteine levels are associated with increased thrombosis. In patients presenting with Acute Coronary Syndrome (ACS), it is not known whether this association is reflected in the degree of myocardial injury. This was a cross sectional study conducted among the patients with acute myocardial infarction in the Department of Cardiology, Dhaka Medical College Hospital during the period of October 2009 to September 2010 and which included 194 consecutive patients with acute myocardial infarction. The mean (+/- SD) serum homocysteine level was 20.2 +/- 14.3 micromol/L with range from 7.4 to 129.1 micromol/L. Mean serum troponin-I level was classified according to normal (<15 micromol/L) and high (> or = 15 micromol/L) levels of serum homocysteine values. The mean serum troponin-I level was 8.9 +/- 8.6 ng/ml in the patients having normal serum homocysteine level and 18.4 +/- 6.5 ng/ml in the patients having high serum homocysteine level. A significant positive correlation (r=0.273; p<0.001) was found between serum troponin-I level with homocysteine level. Patients with moderate hyperhomocysteinemia (> or = 15 micromol/L) was found to be 7.09 times more likely to have increased serum troponin-I (a surrogate marker of extent of myocardial injury). The main observation of the present study was that elevated serum homocysteine level has a positive correlation with serum cardiac troponin-I in patients with acute myocardial infarction. So serum homocysteine is associated with increased extent of myocardial injury as measured by serum cardiac troponin-I level, a surrogate marker in patients with acute myocardial infarction.