Hemodynamic effects of nitroglycerin in acute myocardial infarction.

Abstract

Nitroglycerin (NTG) has recently been suggested to decrease myocardial ischemia and enhance cardiac pump function during acute myocardial infarction (AMI). To evaluate the sublingual agnet in this condition, the hemodynamic effects of 0.4 mg NTG administered to 16 supine patients during the first 72 hours of AMI were determined serially 5, 10 to 15, and 20 to 30 minutes post-NTG. Data were evaluated for the entire group, as well as for six patients with normal pulmonary artery wedge pressure (PAW) (less than or equal to 12 mm Hg; mean 7) who formed group I and for ten patients with elevated PAW (greater than 12 MM Hg; mean 19) who comprised group II. In the 16 patients, NTG resulted in significant decreases in PAW (14 TO 7 MM Hg; P less than .01), mean systemic arterial pressure (MAP) (95 TO 82 MM Hg; P less than .01), cardiac index (CI) (1.79 TO 1.46 L/min/m-2; P less than .02), stroke index (SI) (24 TO 18 CC/M-2; P less than .01) and stroke work index (SWI) (27 TO 20 GM TIMES M/M-2; P less than .01). These alterations were significant in both subgroups, with the decline in PAW greater (P less than .05), while there was no change in group II. There was no significant change in total peripheral vascular resistance (TPVR) for the entire group or in the two subgroups. This study demonstrates that, regardless of initial left ventricular filling pressure, sublingual NTG given in the acute phase of AMI results in rapid fall in PAW, concomitant with decreases in systemic blood pressure, cardiac output and SWI, without changes in TPVR and with little or no effect on heart rate. Since TPVR was unaltered, the decline in MAP was due to fall in cardiac output. Thus, the principal action of sublingual NTG in AMI appears to be systemic venodilation with consequent reduction of ventricular preload. This effect is translated into decline ofpump output even in patients with high initial filling pressures. Although NTG may rapidly relieve pulmonary congestion and lower myocardial oxygen consumption, use of the agent sublingually is limited in AMI because these salutary effects are accomppanied by potentially deleterious fall in cardiac output and systemic blood pressure.

Efficacy of ambulatory systemic vasodilator therapy with oral prazosin in chronic refractory heart failure. Concomitant relief of pulmonary congestion and elevation of pump output demonstrated by improvements in symptomatology, exercise tolerance, hemodynamics and echocardiography.

“…Therefore, while pulmonary congestion is relieved by nitrates, cardiac output is only minimally and inconsistently influenced by these agents. '4 16,19,[23][24][25] Although hydralazine recently has been shown to improve ventricular performance by raising cardiac output, it has little to no affect on left ventricular filling pressure.27 28 While the combination of hydralazine with long-acting nitrates has been demonstrated both to improve pulmonary congestion by lowering ventricular preload and to reduce fatigue by increasing cardiac output,29' 30 oral prazosin offers the advantage of a single drug which effectively accomplishes the same therapeutic purposes without the disadvantages of hydralazine side effects.3'3 Further, our clinical experience with prazosin in heart failure therapy has indicated the agent does not cause serious untoward actions; only transient headache and mild nausea were noted in two patients which did not require discontinuance of the drug. Of additional importance is that we have not observed orthostatic hypotension with the careful and individualized use of prazosin in relieving severe heart failure symptomatology, apparently because the agent did not lower left ventricular preload below the upper limits of normal ( fig.…”

“…However, attempts to continue the benefits of such balanced ventricular unloading therapy in ambulatory patients with chronic heart failure have been difficult because of the lack of an oral vasodilator drug with both arteriolar and venous relaxing properties. Thus the nitrates, which principally cause venodilation, are capable of reducing ventricular preload and pulmonary congestion3' 13,14,16,19,[23][24][25][26] but lack consistent effects on systemic impedance and therefore produce minimal alterations of cardiac output …”

Sustained salutary effects of oral controlled‐release nitroglycerin on ventricular function in congestive heart failure

“…Although the major hemodynamic effects of nitroglycerin given sublingually have been established with relative consistency by previous investigations (2,3,6,11,12,15,16,19,26,35,40,41) the efficacy of this agent when administered orally has been a subject of continuing controversy. This study demonstrates significant, prolonged hemodynamic action by controlled-release nitroglycerin.…”

“…Previous evaluation of sublingual nitroglycerin in acute myocardial infarction by our group (40) and others (11,15) has documented certain beneficial hemodynamic effects which are, however, brief in duration. Recent studies have indicated favorable hemodynamic actions for several hours by certain orally administered nitrates (1,3,40). Because of the desirability of an effective long-acting vasodilator that can be readily administered to ambulatory patients, the following study was performed in patients with acute or chronic congestive heart failure of differing etiologies to evaluate the hemodynamic effects of nitroglycerin administered orally (ONTG) in a form to produce sustained action.…”

“…This approach differs from traditional pharmacologic therapy for the failing heart which consists chiefly of positive inotropic agents and diuretics. Vasodilator therapy improves left ventricular function in cardiac failure by reducing afterload and preload without a direct effect on myocardial contractility (8,11,14,15,17,21,28,40). In addition, because these actions diminish myocardial oxygen consumption and may thereby improve the balance between myocardial oxygen demand and supply, this therapy also has the potential, in the acutely ischemic myocardium, of limiting infarct size (4,25,37).…”