Haemodynamic effects of enalaprilat and preload in acute severe heart failure complicating myocardial infarction

Abstract

In this study, the acute haemodynamic effects of angiotensin converting enzyme (ACE) inhibition with intravenous enalaprilat alone or in combination with preload restoration were determined in patients with severe heart failure complicating acute myocardial infarction. Ten patients with raised pulmonary arterial wedge pressure (PAWP > or = 18 mmHg) were first studied during constant conventional vasodilation with diuretic and inotropic medication, by monitoring central haemodynamics and arterial blood gases. The same variables were measured before enalaprilat infusion, after preload reduction with enalaprilat (1 mg.h-1, rate doubled every 30 min until PAWP decreased > or = 25% or up to total cumulative dose of 10 mg) and after preload restoration with fluid loading (4% albumin given 15 ml.min-1 to restore PAWP to baseline) during continuous low dose enalaprilat infusion. Enalaprilat alone (median dose 0.9 mg) reduced significantly the PAWP (from 25 to 17 mmHg; P = 0.004), the mean arterial pressure (from 87 to 83 mmHg; P = 0.008), the mean pulmonary arterial pressure and the right atrial pressure. The cardiac index, stroke volume index and systemic vascular resistance index remained unchanged. Preload restoration during continuous enalaprilat infusion (median dose of 4% albumin 230 ml, and enalaprilat 0.2 mg) did not further enhance left ventricular function; rather, there was a nearly significant decrease in myocardial perfusion pressure. Arterial oxygenation remained unchanged throughout the study. In conclusion, adding intravenous enalaprilat to conventional therapy makes it possible to relieve pulmonary congestion while maintaining the cardiac function and arterial oxygenation. Preload restoration during continuous ACE inhibition offers no further advantages, and may have adverse effects, since the myocardial perfusion pressure may fall.

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.…”

Clinical and Research Considerations for Patients With Hypertensive Acute Heart Failure: A Consensus Statement from the Society for Academic Emergency Medicine and the Heart Failure Society of America Acute Heart Failure Working Group

“…The only significantly large investigation evaluated a subset of patients with AHF after acute myocardial infarction in the medical intensive care unit, and this cohort is not representative of the typical ED patients with H‐AHF. While other studies suggest that enalaprilat is safe and well tolerated and may be efficacious in patients with AHF, the studies suffer from small sample sizes, and study designs lack contemporary treatment reflective of standard ED treatment . Such observations make it difficult to translate these prior findings to the ED setting.…”

Evaluation and Management of Acutely Decompensated Chronic Heart Failure in the Emergency Department

“…60 Acutely, ACE inhibition reduces both preload and afterload, improves renal hemodynamics, and maintains or enhances left ventricular function. [61][62][63] In the setting of acute heart failure, drug regimens that include an ACE inhibitor appear to have hemodynamic advantages over those based upon other vasodilators, such as nitrates. [64][65][66] For acutely decompensated heart failure, ACE inhibitors can be administered intravenously (e.g., enalaprilat), orally (e.g., captopril), or sublingually (e.g., emptied captopril capsules).…”

“…Depending on the drug, the dose, and the route of administration, hemodynamic effects may be seen within 10-60 minutes. 61,62,64 The safety of administering an ACE inhibitor in the setting of acutely decompensated heart failure is Positive Inotropic Agents. While the role of longterm positive inotropic therapy for chronic heart failure is controversial, short-term therapy with positive inotropes is likely to benefit selected patients with acutely decompensated heart failure.…”