The acute haemodynamic effects of intravenous enalaprilic acid (MK422) in patients with left ventricular dysfunction.

Abstract

Intravenous enalaprilic acid (2.5 mg) was given to 11 patients with stable cardiac failure (NYHA functional class II‐IV). Reductions in mean right atrial, pulmonary artery and pulmonary capillary wedge pressure of 25%, 18% and 30% respectively (P less than 0.01), were observed. Cardiac output rose by 13% (NS) and mean blood pressure fell by 20% (P less than 0.01) with a decrease in systemic vascular resistance of 24% (P less than 0.01). Heart rate was unaltered. The haemodynamic effects correlated with control plasma renin activity (r = 0.78, P less than 0.01). Marked hypotension occurred in several subjects but no other side‐effects were noted. The rapid onset of action and mixed venous and arteriolar dilating activity of intravenous enalaprilic acid may be an advantage in some clinical situations where parenteral vasodilating therapy is required.

Hemodynamic and hormonal effects of quinaprilat in patients with congestive heart failure*

“…AI1 of the hemodynamic changes observed in this study are consistent with observations made by others after open-label intravenous administratio,t of ACE inhibitors to patients with congestive heart failure. [15][16][17][18][19][20][21][22][23][24] Effects on enzyme (renin and ACE) activities and hormonal (angiotensin and aldosterone) concentrations after quinaprilat administration are generally consistent with responses observed in previous studies that examined the acute effects of intravenous ACE inhibitors in patients with congestive heart failure 15~17,21-22,23 although none of the other studies examined as extensively the hormonal profiles evaluated here. In this study, predose PRA and plasma concentrations of angiotensin II, aldosterone, norepinephrine, and ANP were in the upper range of or elevated above normal, whereas plasma ACE activity and plasma concentrations of epinephrine and dopamine were within normal ranges.…”

Bolus versus Continuous Low Dose of Enalaprilat in Congestive Heart Failure with Acute Refractory Decompensation

“…We expected CI increase, especially after lowering afterload to the bad left ventricle, accompanied with massive MR [4, 16, 17]. Unchanged CI despite lower left ventricular afterload could be explained by a worsened left ventricular function per se, or possibly by reduced angiotensin II inotropic activation [18], or appearance of silent myocardial ischemia, which could worsen systolic and diastolic heart function.…”

“…It has immediate alleviating effects on increased preload and afterload and lacks unfavorable effects upon myocardial oxygenation [3, 4, 5]. Several reports have described the acute hemodynamic effects of ACE inhibitors in chronic heart failure, but in most studies ACE inhibitor was used only with digoxin and diuretics, without other vasoactive treatment [3, 4, 5].…”

Differential Control of Vascular Tone and Heart Rate by Different Amino Acid Neurotransmitters in the Rostral Ventrolateral Medulla of the Rat

“…However, the precise mechanism of action of CEI on the central nervous system is not yet known. Many studies have reported that CEI have depressor effects, with minimal reflex tachycardia, both clinically and in experimental animal models (Pegram & Frohlich 1982;Daly 1985;Hornung & Hillis 1987). Whether administered chronically or acutely, CEI cause less reflex tachycardia than other vasodilating hypotensive agents (Ueno et al 1980).…”