The effect of hypoxia on thallium kinetics in cultured chick myocardial cells.

To assess the effect of hypoxia on cellular thallium-201 (201Tl) uptake and washout independent of coronary flow, we studied thallium kinetics during normoxia and hypoxia in cultured chick ventricular cells. Monolayers of contracting ventricular cells grown on coverslips were placed in a chamber and perfused to asymptote with media containing 201Tl. Perfusates were equilibrated with 5% CO2-95% air or 5% CO2-95% nitrogen for normoxia and hypoxia, respectively. Washout thallium kinetics were then observed during perfusion with unlabeled media. Twenty paired experiments were performed, randomly alternating the sequence of normoxia and hypoxia. Pharmacokinetics for thallium were determined by computer using standard formulae. Thallium uptake and washout were best described by assuming that intracellular thallium was contained within a single compartment. Cellular thallium uptake, as well as transfer rate constants for thallium uptake and for thallium washout during normoxia and hypoxia, were compared using paired t-tests. During normoxia and hypoxia, respectively, thallium uptake was 22 +/- 7% and 19 +/- 7% of asymptote (p less than 0.01); the compartmental rate constant for uptake by the cell was 0.16 +/- 0.07 min-1 and 0.15 +/- 0.06 min-1 (N.S.); and the transfer rate constant for washout from the cell was 0.26 +/- 0.06 min-1 and 0.23 +/- 0.05 min-1 (p less than 0.01). We conclude that there was a small (14%) decrease in thallium uptake during hypoxia. The rate of thallium uptake and washout was slightly less during hypoxia, although only the rate of washout was significantly less. These data show that cellular accumulation of thallium and the rate of washout of thallium were minimally decreased by hypoxia independent of blood flow.

Randomized comparison of intravenous versus intracoronary streptokinase for myocardial infarction.

The efficacy of intravenous (i.v.) thrombolytic therapy has not been firmly established in comparison with the intracoronary (i.c.) route of administration. In a randomized trial of 28 patients who underwent angiography before and during i.v. and i.c. administration of streptokinase (STK), recanalization was achieved in 73% of patients who received the drug by the i.c. route, compared with 62% of patients who received the drug by the i.v. route (difference not significant). Reopening took 28 minutes for i.c. STK and 39 minutes for i.v. STK. Patients in whom recanalization was successful using either route of administration had shorter euglobulin lysis times and lower fibrinogen levels than did patients in whom it was not successful (p less than 0.05). Bleeding complications were closely correlated with heparinization after thrombolysis rather than with STK itself. These results in a limited patient series suggest that early administration of i.v. STK in the emergency department may yield recanalization rates similar to those for the i.c. route and may benefit myocardial preservation by restoring flow much earlier.

Surgical treatment of ventricular septal rupture and mitral regurgitation complicating acute myocardial infarction: report of a case and review of the literature.

Coexisting ventricular septal rupture (VSR) and severe mitral regurgitation following myocardial infarction is rare; only ten cases have been documented in the English literature. Present refinements in myocardial preservation and surgical techniques have markedly improved the results of surgery in this group of desperately ill patients. Early repair of both lesions is advocated and exemplified by a case report.

Methysergide-induced heart disease: a case of multivalvular and myocardial fibrosis.

Methysergide (Sansert) is known to cause mitral and aortic valvular fibrosis and dysfunction, but has generally not been known to damage right heart valves or the myocardium, and cardiac fibrosis has not been considered to be a risk if therapy is intermittently interrupted. The woman who is the subject of this case report developed catheterization-proven severe tricuspid and moderate aortic and mitral regurgitation during noncontinuous therapy with methysergide. In addition, right ventricular endomyocardial biopsy revealed extensive endocardial and intramyocardial fibrosis.

Dose response effectiveness of propranolol for the treatment of angina pectoris.

Seventeen patients received placebo medication during a 12-week run-in period, followed by four double-blind study periods of six weeks each, during which time placebo, 80 mg, 160 mg and 320 mg propranolol dosages were administered. Examination of the frequency of angina episodes and nonprophylactic nitroglycerin consumption revealed significant beneficial clinical responses for both the 160 and 320 mg dosages. Exercise testing also demonstrated increased exercise tolerance (320 mg dose) with a shift of the exercise end point from pain to fatigue in seven of 17 patients. The interrelationships between propranolol daily dosage, clinical response assessed by percent reduction in anginal episodes, beta-adrenergic blockade measured by percent reduction in exercise heart rate and serum levels were examined. In general, serum levels of 30 ng/ml, when drawn 90 to 180 minutes following the last oral dose, were required to achieve a 25% or greater reduction in angina frequency. Serum levels above 30 ng/ml were similarly correlated with a 20% or greater reduction in exercise heart rate at equivalent levels of exercise. Detailed examination of different patterns of clinical response with respect to beta-blockade, serum levels and oral doses are presented.