Intravenous nitroglycerin-infusion in uncomplicated myocardial infarction?

Although nitroglycerin and nitroprusside reduce overall myocardial oxygen consumption in patients with acute myocardial infarction, potentially they may increase hypoxia in some areas of the myocardium. The effects on local coronary perfusion pressure and resultant changes in ischemia injury are unpredictably different from the aortic diastolic pressure. The basic principle which is emerging from both animal experiments and human studies is that the perfusion pressure to the ischemic zone must be maintained. Randomized prospective trials of the effects of intravenous nitroglycerin on survival rate or "infarct size" in acute myocardial infarction are not sufficient and thus inconclusive. In consequence, for the present intravenous nitroglycerin infusion should be limited to patients with elevated left ventricular filling pressure. Careful hemodynamic monitoring is mandatory. In 15 patients with acute myocardial infarction nitroprusside significantly reduced the arterial-coronary sinus oxygen difference most probably by dilating the resistance vessels. Concomitantly, there was a significant decrease in myocardial lactate extraction. Therefore, nitroprusside can result in redistribution of intramyocardial flow and increase ischemic injury by a shift of blood flow to non-ischemic areas. During nitroglycerin infusion neither the mean arterial-coronary sinus oxygen difference nor the average myocardial lactate extraction changed. In individual patients the myocardial lactate extraction may deteriorate.