Why the study?
Do vasodilators (ISDN, NGO, Pz) improve peripheral and cardiac hemodynamics in patients with heart failure due to acute myocardial infarction?
Do vasodilators (ISDN, NGO, Pz) improve peripheral and cardiac hemodynamics in patients with heart failure due to acute myocardial infarction?
Different vasodilators have distinct hemodynamic profiles in acute MI complicated by heart failure, with ISDN acting primarily on capacitance vessels and prazosin/nitroglycerin ointment acting on both capacitance and resistance vessels.
May inform vasodilator choice in acute MI-HF; leaves open outcome impact pending randomized trials.
Effects of three representative vasodilators on peripheral and cardiac hemodynamics were studied in 20 patients with heart failure due to acute myocardial infarction (PCWP greater than 18 mmHg, C1 greater than 2.20 L/min/m2) using venous occlusion plethysmography and a Swan-Ganz catheter. Sublingual isosorbide dinitrate (ISDN) significantly increased calf venous capacitance (CVC) from 5 to 60 min (p less than 0.01) and calf blood flow (CBF) in the initial 15 min (p less than 0.05), while simultaneously lowering PCWP (p less than 0.05) and central venous pressure (p less than 0.05). Calf vascular resistance (CVR), cardiac index, blood pressure, and total systemic peripheral resistance (TSPR) were not affected significantly. Nitroglycerin ointment (NGO) significantly decreased CVR (p less than 0.05) and increased CVC (p less than 0.05) from 60 to 240 min, simultaneously with lowering of PCWP (p less than 0.01), central venous pressure (p less than 0.05), and TSPR (p less than 0.05). Oral prazosin (Pz) increased CBF (p less than 0.01) and CVC (p less than 0.05) from 60 to 240 min, simultaneously with significant lowering of PCWP (p less than 0.01) and TSPR (p less than 0.05), resulting in increased stroke work index (p less than 0.05). These data confirm that ISDN predominantly causes capacitance vessel dilatation and reduce excessive venous return, while Pz and NGO dilate not only capacitance vessels but also resistance vessels, consequently reducing systemic vascular resistance and resulting in increased peripheral blood flow and cardiac performance. It was observed that the higher the base-line calf vascular resistance rose, the better the response to the vasodilator treatment appeared in terms of a decrease in calf vascular resistance.
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Seino et al. (1982) studied this question.
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