Excessive oxidative stress is considered one of the mechanisms of a decrease in contractile force without concomitant reduction in oxygen cost in failing myocardium. We hypothesized that the antioxidant vitamin C may help reverse hyporesponsiveness to β-adrenergic stimulation and improve myocardial efficiency in patients with heart failure (HF) after myocardial infarction (MI).

Nineteen patients with mild to moderate HF due to previous MI (mean left ventricular [LV] ejection fraction 39%) were instrumented with conductance and coronary sinus thermodilution catheters. Left ventricular contractility, expressed as E_es,, the slope of end-systolic pressure-volume relationship, and mechanical efficiency, expressed as the ratio of LV stroke work (SW) to myocardial oxygen consumption (MV̇o₂), were measured in response to the intravenous infusion of dobutamine (4 μg/kg per min) before (Dob) and during (Dob + Vit C) the infusion of vitamin C (2.0-g bolus injection and subsequent 50-mg/min infusion through the jugular vein) (vitamin C group, n = 10). The infusion of vitamin C augmented the E_es response to dobutamine by 20% ± 8% (Dob 2.1 ± 0.3, Dob + Vit C 2.5 ± 0.4 mm Hg/mL, P < .01) and the SW/MV̇o₂ response by 21% ± 5% (Dob 36% ± 3%, Dob + Vit C 43% ± 4%, P < .01). In the control group (n = 9), E_es and SW/MV̇o₂ were measured in response to dobutamine before (Dob) and during (Dob + vehicle) the infusion of saline. No difference in E_es or SW/MV̇o₂ was observed between Dob and Dob + vehicle (E_es: Dob 2.1 ± 0.2, Dob + vehicle 2.1 ± 0.2 mm Hg/mL per square meter, P = nonsignificant) (SW/MV̇o₂: Dob 35% ± 4%, Dob + vehicle 33% ± 4%, P = nonsignificant).

The administration of the antioxidant vitamin C enhances the contractile response to dobutamine and improves myocardial efficiency in patients with HF.