To assess the diastolic and systolic performance characteristics of the left ventricle in alcoholism, three patient groups with a history of heavy alcohol consumption were compared with normal subjects. In those with symptoms related to chest pain or palpitations, heart size was normal on x ray. In groups III and IV, dyspnea was associated with varying degrees of cardiomegaly and a high prevalence of absent septal Q on the ECG.Despite substantial differences in physical findings, all three groups exhibited a significant increase in end‐diastolic pressure. Group I was distinguished by the fact that end‐diastolic volume was not increased but actually somewhat diminished. Groups II and III were characterized by a significant increase in end‐diastolic volume and tension. The latter was enhanced to a significantly greater extent in group III and was the most prominent hemodynamic abnormality in this group. A major change in the index of contractility, as well as in the rate of relaxation, occurred in group I. Further moderate depression of these indices was observed in the groups with enhanced diastolic volume. In the patients who had mitral regurgitation a more severe depression of left ventricular function was present in the alcoholic group than in a nonalcoholic control group, and was presumably due to the toxic effects of ethanol on the left ventricle.Thus, in those alcoholic patients who develop cardiac alterations, the earliest abnormality is characterized by diminished left ventricular compliance and a moderate contractility deficit without heart failure. In those who progress, end‐diastolic tension is substantially enhanced and further reduction in contractility indices is observed. The potential for reversibility is discussed.

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To characterize the acute hemodynamic effects of tocainide hydrochloride, a new antiarrhythmic agent, 11 patients undergoing diagnostic cardiac catheterization were given intravenous infusions of the drug for 15 minutes at rates of 0.50 (six patients) or 0.75 (five patients) mg/kg/min. The hemodynamic status of these subjects was determined before, during, and for 15 minutes after treatment, and blood levels of tocainide were followed during and after treatment. Tocainide blood levels at the end of the infusions were 14.9 +/- 1.6 microgram/ml (S.E.) and 15 minutes later were 6.0 +/- 0.7 microgram/ml. In these subjects treatment was not associated with significant changes in Ao or PCW, but it was associated with a statistically significant but small decrease in LV dp/dt. At the same time, LVED was not significantly elevated. Treatment was also accompanied by small increases in PA diastolic and mean pressures, but RA and RV were unchanged. Significant changes were not seen in HR, CO, CI, SV, SVR, or PVR. Thus, the intravenous infusion of 0.50 and 0.75 mg/kg/min of tocainide for 15 minutes produced small but statistically significant depression of left ventricular function without producing changes in CO or clinical evidence of congestive heart failure.