Effect of propranolol on postexercise left ventricular ejection time index.

The net delta left ventricular ejection time index 4 minutes after exercise is prolonged in many patients with coronary artery disease. This prolongation is thought to be due to the lack of response of the ischemic myocardium to adrenergic stimulation and has been proposed as a measure of myocardial ischemia. In this study, the effect of beta adrenergic blockade on net delta left ventricular ejection time was studied in nine normal subjects (Group A) and in eight patients with stable angina and coronary artery disease (Group B). In Group A, a treadmill exercise test was performed for 10 minutes before and after administration of propranolol, 160 mg daily, for 2 days. The postexercise net delta left ventricular ejection time was significantly greater after propranolol (mean +/- standard error of the mean 12 +/- 4 versus 35 +/- 4 ms, p less than 0.01). In group B a maximal treadmill exercise test was performed before and after therapy with propranolol. Only patients with a normal net delta left ventricular ejection time before propranolol were selected. The net delta left ventricular ejection time again increased significantly after propranolol (11.5 +/- 4 versus 35.3 +/- 5 ms p less than 0.01). It is concluded that prolongation of postexercise net delta left ventricular ejection time cannot be used to diagnose ischemia in patients who are receiving propranolol therapy. Our data support the hypothesis that prolongation of net delta left ventricular ejection time after exercise is caused by an impaired myocardial response to catecholamines, whether due to ischemia or effective beta adrenergic blockade.

Acute massive (pericardial effusive) pulmonary thromboembolism--pulmonary embolectomy revisited.

The most recent patient in a 13-year experience with 14 patients suffering massive pulmonary thromboembolism requiring pulmonary thromboembolectomy is the focus of this report. This 40-year-old woman not only survived life-threatening acute hypoxemia and right heart failure, but was also found to have developed a unique transudative 700 cc pericardial effusion. Pulmonary artery pressure was 90/30 (mean 50 mmHg), accompanied by 17 mm right ventricular alternans. Systemic alternans and tamponade physiology were absent. This unusual natural model for acute right heart failure illustrates a novel mechanism for pericardial effusion physiology.

Relationship of angiographic and echographic dimensions in chronic left ventricular dilatation.

Recently discrepancies have been reported between echocardiographic (Echo) % delta D and angiocardiographic (Angio) ejection fraction (EF), particularly in valvular regurgitation. One hundred and twelve patients with varying degrees of LV dilatation were studied in the right anterior oblique position with M-mode Echo. None had localized contraction abnormalities. There were 20 normals, 33 with primary myocardial disease, and 59 with mitral and/or aortic regurgitation. Echo end-diastolic diameter (EDD) and end-systolic diameter (ESD) were consistently smaller than Angio calculated EDD and ESD, and the difference was magnified at larger EDDs (p less than 0.01). The result is a relatively poor correlation of Echo % delta D and Angio EF (r = 0.69), compared to r = 0.98 for Angio % delta D and EF, both from Angio visualization. However, if valvular disease patients are excluded, the correlation improves to 0.82. The mechanisms for these disparities include increased sphericity as the ventricle dilates, and in the case of valvular disease where the EF is better for any degree of dilatation, the echo measurement errors for EDD and ESD are different.

Inhibition of water absorption in the intestine by Staphylococcus aureus delta-toxin.

Water absorption in intestinal segments was monitored by measuring the concentration of polyethylene glycol, a nonabsorbable reference marker, in a balanced salt solution continuously perfused through the lumen. Staphylococcus aureus delta-toxin inhibited water absorption in rabbit jejunum and ileum perfused in vivo and in guinea pig ileum perfused in vitro. Cholera toxin also interfered with water absorption in guinea pig ileum maintained in vitro, but S. aureus enterotoxin B had no demonstrable effect on this tissue.