Related Experiment Video
Updated: Jun 23, 2026

Real-time Pressure-volume Analysis of Acute Myocardial Infarction in Mice
Published on: July 2, 2018
Haemodynamic effects of enalaprilat and preload in acute severe heart failure complicating myocardial infarction
H Tohmo1, M Karanko, K Korpilahti
1Cardiorespiratory Research Unit, University of Turku, Finland.
Insights
Intravenous enalaprilat effectively reduces pulmonary congestion in severe heart failure after myocardial infarction. However, restoring preload during ACE inhibition offers no additional benefit and may decrease myocardial perfusion.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Severe heart failure post-myocardial infarction presents significant hemodynamic challenges.
- Pulmonary congestion is a critical issue requiring effective management.
Purpose of the Study:
- To evaluate the acute hemodynamic effects of angiotensin converting enzyme (ACE) inhibition with enalaprilat.
- To assess the impact of preload restoration in combination with enalaprilat.
Main Methods:
- Ten patients with severe heart failure and elevated pulmonary arterial wedge pressure (PAWP) were studied.
- Hemodynamic variables were monitored before and after enalaprilat infusion, with and without preload restoration using fluid loading.
Main Results:
- Enalaprilat significantly reduced PAWP, mean arterial pressure, mean pulmonary arterial pressure, and right atrial pressure.
- Cardiac index, stroke volume index, and systemic vascular resistance index remained unchanged.
- Preload restoration did not improve left ventricular function and led to a decrease in myocardial perfusion pressure.
Conclusions:
- Intravenous enalaprilat effectively relieves pulmonary congestion in severe heart failure post-myocardial infarction while maintaining cardiac function.
- Preload restoration during ACE inhibition provides no additional benefits and may be detrimental.
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.
More Related Videos
Related Concept Videos
Heart Failure Drugs: Diuretics
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
Heart Failure Drugs: β-Blockers
Imbalances in Cardiac Output
CHF can occur due to the failure of either side of the heart. Left-side failure leads to pulmonary congestion—the right side continues to send blood...
Heart Failure II: Pathophysiology
Heart Failure V: Medical Management

