Effects of human atrial natriuretic peptide on myocardial performance and energetics in heart failure due to previous myocardial infarction

BackgroundHuman atrial natriuretic peptide (hANP) and spontaneous nitric oxide (NO) donor share cyclic guanosine monophosphate (cGMP) as a second messenger, but their effect on myocardium may differ. We compared the effect of hANP and sodium nitroprusside (SNP) on left ventricular (LV) mechano-energetics in heart failure (HF).MethodsTen patients with HF due to previous myocardial infarction (LV ejection fraction: 45 ± 3%) were instrumented with conductance and coronary sinus thermodilution catheters. LV contractility (Ees: slope of end-systolic pressure–volume relation) and the ratio of LV stroke work (SW) to myocardial oxygen consumption (SW/MVO2 = mechanical efficiency) were measured in response to intravenous infusion of ANP (0.05 μg/kg/min) or SNP (0.3 μg/kg/min) to lower blood pressure by at least 10 mmHg, and changes in plasma cGMP.ResultsSNP had no effect on Ees, SW, or MVO2, thus SW/MVO2 remained unchanged (40.54 ± 5.84% to 36.59 ± 5.72%, p = 0.25). ANP increased Ees, and decreased MVO2 with preserved SW, resulting in improved SW/MVO2 (40.49 ± 6.35% to 50.30 ± 7.96%, p = 0.0073). Infusion of ANP (10.42–34.95 pmol/ml, p = 0.0003) increased cGMP levels, whereas infusion of SNP had no effect (10.42–12.23 pmol/ml, p = 0.75).ConclusionsCompared to SNP, the ANP-dependent increase in cGMP may ameliorate myocardial inotropy and energetics in HF.