Role of Nitroglycerin in Acute Myocardial Infarction

Abstract

Intravenous nitroglycerin lowers left ventricular filling pressure and systemic vascular resistance in patients with acute myocardial infarction. At lower infusion rates ( < 30 µg/min) nitroglycerin acts principally as a venodilator, while at higher infusion rates a balanced venous and arterial dilating effect is seen. Patients with left ventricular failure demonstrate increased or maintained stroke volumes, while patients without failure will show a decrease in stroke volume. All hemodynamic subgroups will show a reduction in left ventricular filling pressures and in electrocardiographic evidence of regional myocardial ischemia. Longer-term infusions (24–48 h) have been associated with a reduction in short-term mortality and evidence of myocardial preservation, as evidenced by improved left ventricular function or indices of infarct size. Studies comparing intravenous nitroglycerin and sodium nitroprusside have revealed increases in intercoronary collateral flow with nitroglycerin, in contrast to decreases with nitroprusside, suggesting a coronary steal with nitroprusside. Current clinical practice would recommend intravenous nitroglycerin as initial adjunctive therapy for patients receiving intravenous thrombolytic therapy and/or acute percutaneous transluminal angioplasty within 4–6 h of the onset of symptoms of acute myocardial infarction, with the goal of optimizing collateral flow until reperfusion can be accomplished. Patients treated later than 6 but less than 12–14 h after symptom onset should still receive intravenous nitroglycerin for 24–48 h with the hope of reducing infarct size. Likewise, congestive heart failure and arterial hypertension complicating acute infarctions as well as postinfarction unstable angina are additional current indications for the use of intravenous nitroglycerin in patients with acute myocardial infarction.