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).
Methods and Results
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 Ees,, the slope of end-systolic pressure-volume relationship, and mechanical efficiency, expressed as the ratio of LV stroke work (SW) to myocardial oxygen consumption (MV?o2), 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 Ees 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/MV?o2 response by 21% ± 5% (Dob 36% ± 3%, Dob + Vit C 43% ± 4%, P < .01). In the control group (n = 9), Ees and SW/MV?o2 were measured in response to dobutamine before (Dob) and during (Dob + vehicle) the infusion of saline. No difference in Ees or SW/MV?o2 was observed between Dob and Dob + vehicle (Ees: Dob 2.1 ± 0.2, Dob + vehicle 2.1 ± 0.2 mm Hg/mL per square meter, P = nonsignificant) (SW/MV?o2: 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.