Quinidine therapy in hospitalized patients with ventricular arrhythmias.

Quinidine serum levels and pharmacokinetic data were assessed during steady state therapy with oral quinidine sulfate in 19 hospitalized patients who were being treated for ventricular arrhythmias. A new high performance liquid chromatography assay was employed. Four patients were studied both after the first dose of quinidine and at steady state, and the initial dose pharmacokinetic values were found not to be predictive of steady state. The mean half-life of quinidine was 4.5 hours, but there was wide individual variation. The elimination rate constant for quinidine was significantly lower in patients with echocardiographic evidence of left ventricular dilatation than in patients with normal echocardiographic left ventricular size. The average urinary excretion of quinidine was only 11.3%. The pharmacokinetic data in seven chronic alcoholic patients without clinical or laboratory evidence of hepatic insufficiency did not differ from the data obtained in nonalcoholic patients. However, with severely impaired liver function, there may be marked prolongation of quinidine half-life predisposing to quinidine toxicity. The possible clinical implications of these findings are discussed.

Systolic time intervals in hypothyroidism: end organ function as a reflection of clinical status.

Systolic time intervals (STI) were determined in 14 hypothyroid patients who did not have congestive heart failure or atrial fibrillation, and who were not taking cardiotropic drugs. Compared to normals, there was a significant decrease in the left ventricular ejection time (LVET) and there were significant increases in the pre-ejection period (PEP) and the PEP/LVET ratio. The prolongation of the PEP primarily reflected lengthening of the isovolumic contraction time. Serial recordings during thyroxine therapy in seven patients showed consistent changes in STI toward normal values. These results in hypothyroid patients complement our earlier data in hyperthyroid patients; they indicate that STI's are a sensitive measure of the heart as an end organ over the entire range of thyroid hormonal activity.

Misleading noninvasive signs of Bjork--Shiley mitral valve dysfunction.

Three months after receiving a Bjork--Shiley mitral valve prosthesis, a patient experienced acute gastronintestinal bleeding associated with heavy alcohol intake and poor compliance with oral anticoagulation therapy. As a result of the gastrointestinal bleeding, treatment with warfarin was discontinued. Ten months later, the patient presented with symptoms of transient cerebral ischemia. Despite demonstrated loss by phonocardiography of the previously well-recorded opening click and echocardiographic suggestion of a thrombosed prosthetic mitral valve, no thrombosis or dysfunction of the prosthetic mitral valve was revealed at reoperation.