Resolution of ST-segment elevation after thrombolytic therapy in elderly patients with acute myocardial infarction.

We examined the resolution of ST-segment elevation after thrombolytic therapy in elderly versus younger patients with acute myocardial infarction. Electrocardiograms were recorded before, on completion of, and on day 1 and day 2 post-thrombolytic therapy (streptokinase or tissue thromboplastin activator) in 36 patients older than 65 years and 36 patients younger than 65 years. There was no significant different in the pre-thrombolytic ST-segment elevation per lead in both elderly and younger patients (3.7 +/- 0.7 versus 3.5 +/- 0.8 mm; P = NS). On completion of thrombolytic therapy, both groups demonstrated resolution of ST-segment elevation and, although the ST-segment elevation per lead was higher in elderly patients (3.0 +/- 0.9 versus 2.5 +/- 0.9 mm; P = 0.008), the percentage resolution per lead was not significantly different (19% versus 29%; P = NS). On day 1 post-thrombolytic therapy, there was further resolution of ST-segment elevation in both groups, but at this point, the percentage resolution per lead was significantly less in the elderly than in the younger patients (51% versus 66%; P = 0.03), and the ST-segment elevation per lead remained higher in elderly patients (1.8 +/- 1.0 versus 1.2 +/- 0.6 mm; P = 0.0009). On day 2 post-thrombolytic therapy, although there was further resolution of ST-segment elevation in both groups, the percentage resolution per lead remained significantly less (68% versus 80%; P = 0.05) and ST-segment elevation per lead remained significantly higher in elderly patients (1.2 +/- 0.7 versus 0.7 +/- 0.4 mm; P = 0.0002). Resolution of ST-segment elevation after thrombolytic therapy was less marked in elderly patients, indicating a reduced response to thrombolytic therapy in this patient population.

Effect of thrombolytic therapy on QT dispersion in elderly versus younger patients with acute myocardial infarction.

The objective of this study was to assess the degree of QT dispersion and effect of thrombolytic therapy on QT dispersion in elderly (age > or =65 years) versus younger (age <65 years) patients with acute myocardial infarction. The QT dispersion was measured manually in 10 +/- 2 leads of 12-lead electrocardiograms on admission, at completion of thrombolytic therapy, and at day 2 after thrombolytic therapy in 36 elderly (73 +/- 5.7 years) and 36 younger (59.9 +/- 7.7 years) patients with acute myocardial infarction. Before initiation of thrombolytic therapy, elderly patients had higher absolute and corrected QT dispersion than younger patients (absolute QT dispersion: 76.3 +/- 7.3 versus 69.6 +/- 7.5 milliseconds, respectively, P < 0.0001; corrected QT dispersion: 77.9 +/- 7.6 versus 70.8 +/- 7.4 milliseconds, respectively, P < 0.001). The difference in QT dispersion between elderly and younger patients persisted at the completion of thrombolytic therapy (absolute QT dispersion: 75.1 +/- 7.2 versus 69.1 +/- 8.4 milliseconds, respectively, P = 0.001; corrected QT dispersion: 77.2 +/- 7.2 versus 70.7 +/- 8.0 milliseconds, respectively, P = 0.001) and at day 2 after thrombolytic therapy (absolute QT dispersion: 74.1 +/- 8.2 versus 69 +/- 9.1 milliseconds, respectively, P = 0.01; corrected QT dispersion: 76.0 +/- 7.9 versus 70.5 +/- 8.8 milliseconds, respectively, P = 0.006). Compared with the prethrombolytic values, there was no significant change in absolute and corrected QT dispersion at the completion of thrombolytic therapy or at day 2 after thrombolytic therapy in elderly or younger patients. Elderly patients with acute myocardial infarction have higher QT dispersion than younger patients with acute myocardial infarction, and QT dispersion does not change early after thrombolytic therapy in elderly or younger patients.

Acute coronary syndrome in patients with human immunodeficiency virus disease.

With more effective prophylactic treatment and an increased time of survival, noninfectious conditions associated with human immunodeficiency virus (HIV) disease are being recognized with increasing frequency in HIV patients. Cardiac involvement in HIV-infected patients varies from clinically silent to a fatal disease with a direct cardiac cause of mortality estimated at 1% to 6%. Pericardial effusion, pericarditis, myocarditis, cardiomyopathy, endocarditis, and pulmonary hypertension are known cardiac manifestations associated with HIV infection. Coronary artery disease (CAD) has not been a recognized complication of HIV disease, although some recent case reports have suggested occurrence of premature CAD and accelerated atherogenesis in HIV-infected patients. The role of protease inhibitors have been suggested in the development of this complication. After reviewing records of the last 7 years, the authors found 10 cases of acute coronary syndrome in HIV-infected patients who had no other risk factor for CAD except smoking. The presence of CAD was confirmed by angiography or autopsy. The mean CD4 count was 380 cells/mm3, and the mean duration between the diagnosis of HIV infection and CAD was 7.5 years. Four patients had single-vessel disease, 1 patient had 2-vessel disease, and 5 patients had 3-vessel disease. Three patients underwent coronary bypass surgery and 1 patient died of cardiogenic shock. CAD may be associated with HIV disease.