Early intervention in acute myocardial infarction: significance for myocardial salvage of immediate intravenous streptokinase therapy followed by coronary angioplasty.

Sixteen patients with acute myocardial infarction underwent treatment with streptokinase up to 3 hours after the onset of chest pain. Nine patients (group I) received streptokinase within 1 hour of the onset of pain, and seven patients (group II) received it within 2 to 3 hours. All underwent multigated radionuclide ventriculography after streptokinase therapy and 1 week later. Percutaneous transluminal coronary angioplasty of the infarct artery was performed within 24 hours in all patients. An effort-limited treadmill stress test was performed before discharge. There was no mortality or serious complication. Mean peak total creatine kinase was 521 +/- 289 mU/ml in group I, and 1,614 +/- 709 mU/ml in group II (p less than 0.05). The mean initial left ventricular ejection fraction was 47 +/- 11% in group I and 37 +/- 10% in group II. After early angioplasty (within 24 hours) and at 1 week recovery, left ventricular ejection fraction increased to 53 +/- 9% in group I (p less than 0.05) and to 40 +/- 7% in group II (p = NS). Seven of the nine patients in group I had normal radionuclide ventriculograms at discharge compared with none of the seven patients in group II. Thrombolytic therapy administered less than 1 hour after the onset of symptoms of acute myocardial infarction followed by angioplasty of the infarct artery results in preservation of left ventricular function, whereas therapy given after 2 hours has only a limited effect.

Percutaneous transluminal coronary angioplasty as a cause of isolated right ventricular infarction.

Acute myocardial infarction is a recognized major complication of percutaneous transluminal coronary angioplasty (PTCA). Isolated right ventricular infarction is rare. A 60-year-old patient underwent PTCA 24 h following clinically successful thrombolytic therapy for an acute occlusion of a dominant right coronary artery. Following successful PTCA of this artery, a right ventricular branch was noted to be occluded. This was associated with chest pain, elevated venous pressure, S-T segment elevation in ECG leads V1-3, and a transient rise in serum creatine kinase. The clinical course was uneventful and a week later the right ventricular ejection fraction had increased from 18 to 36%. The long-term effects of right ventricular infarction are benign and occlusion of a right ventricular branch during PTCA is rarely of clinical significance.

Clinical and hemodynamic effects of combined propranolol and nifedipine therapy versus propranolol alone in patients with angina pectoris.

To determine the comparative effectiveness and hemodynamic effects of long-term oral treatment with propranolol alone and combined with nifedipine in patients with stable angina pectoris, 20 patients with coronary disease were studied by equilibrium radionuclide ventriculography. Measurements were performed at rest and during supine bicycle exercise before treatment, after 4 weeks on propranolol, 1 hour after institution of combined propranolol and nifedipine treatment, and after 4 weeks on the combined treatment. The reduction in exercise rate-pressure product induced by the combination (17.2 +/- 2.6 X 10(3)) was significantly greater (p less than 0.001) than that attained by propranolol alone (19.3 +/- 2.8 X 10(3)). In patients at rest, neither propranolol nor the combined therapy altered global left ventricular (LV) ejection fraction (EF). Without drugs and on propranolol, exercise EF decreased significantly. On the combined therapy there was a significant improvement in exercise EF compared both with rest values (p less than 0.01) and with exercise EF on propranolol (p less than 0.001). Exercise tolerance, expressed as total work load, significantly increased on propranolol and further increased on combined therapy. Thus the combined propranolol/nifedipine therapy in patients with stable angina proved to be hemodynamically superior to therapy with propranolol alone and safe even in patients with moderately depressed LV function.

Apical hypertrophic cardiomyopathy: evaluation by noninvasive and invasive techniques in 23 patients.

Over a 3 year period we evaluated 23 patients (16 men, seven women) with apical hypertrophic cardiomyopathy by noninvasive and invasive methods. Sixteen patients had chest pain. In 17, results of cardiovascular examination were normal. The electrocardiogram showed precordial inverted T waves in all patients and these were of mild-to-moderate amplitude (less than 10 mm) in 18 and giant (greater than 10 mm) in five. M mode echocardiography revealed a typical pattern of contraction and relaxation in the apical region of the left ventricle that was associated with significant hypertrophy. These findings were confirmed by two-dimensional echocardiography. Systolic anterior motion of the mitral valve was not observed nor was there any evidence of obstruction of the left ventricular outflow tract. Results of Doppler echocardiographic study of the mitral and aortic flow were normal in all patients but one who had mild mitral insufficiency. Radionuclide studies of 14 patients revealed a mean left ventricular ejection fraction of 66 +/- 6% (range 55% to 79%), with normal left ventricular contraction in all patients but two with apical hypokinesis. In all six patients who underwent catheterization a characteristic appearance of the left ventricle at end-systole as well as abnormal end-diastolic contour were noted on the left ventricular angiogram, but the "ace of spades" configuration was seen in only one. We conclude that the 23 patients studied form a homogeneous group of individuals with nonobstructive apical hypertrophic cardiomyopathy, which differs in many respects from cardiomyopathies reported by other investigators.