Angiotensin-converting enzyme inhibitors and calcium antagonists after acute myocardial infarction

P A Poole-Wilson1

  • 1Department of Cardiac Medicine, National Heart and Lung Institute, London, United Kingdom.

Insights

Angiotensin-converting enzyme (ACE) inhibitors reduce mortality after myocardial infarction, especially in patients with reduced ejection fraction or heart failure. Calcium antagonists show limited benefit and potential harm, with long-acting forms under investigation.

Area of Science:

  • Cardiology
  • Pharmacology

Background:

  • Myocardial infarction (MI) treatment involves managing hypertension and heart failure.
  • Angiotensin-converting enzyme (ACE) inhibitors and calcium antagonists are drug classes with cardiovascular applications.

Purpose of the Study:

  • To review the efficacy of ACE inhibitors and calcium antagonists in treating myocardial infarction.
  • To assess the impact of these drugs on mortality and cardiac function post-MI.

Main Methods:

  • Analysis of six large clinical trials involving ACE inhibitors post-MI.
  • Review of studies on calcium antagonists, including a placebo-controlled trial (DEFIANT I) for long-acting formulations.

Main Results:

  • ACE inhibitors significantly reduced mortality by 17-27% in specific MI patient subgroups (low ejection fraction, heart failure).
  • Other ACE inhibitor studies showed only marginal benefits in unselected populations.
  • Calcium antagonists yielded discouraging results in heart failure patients, with some evidence of harm. Long-acting versions are being explored for potential benefits.

Conclusions:

  • ACE inhibitors are beneficial for specific myocardial infarction patient populations.
  • Widespread use of calcium antagonists post-myocardial infarction is currently not recommended due to safety and efficacy concerns.

Related Concept Videos

Antihypertensive Drugs: Action of Calcium Channel Blockers01:18

Antihypertensive Drugs: Action of Calcium Channel Blockers

Calcium ions are essential to contract smooth muscle cells in blood vessels. They enter these cells through voltage-dependent calcium channels, specifically L-type calcium channels in the cell membrane. These L-type calcium channels are integral to the excitation-contraction coupling process in smooth muscle. When a stimulus is received by smooth muscle cells, their membrane depolarizes. This alteration in membrane potential instigates the opening of L-type calcium channels. As a result,...
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
Antianginal Drugs: Calcium Channel Blockers and Ranolazine01:25

Antianginal Drugs: Calcium Channel Blockers and Ranolazine

Angina pectoris, a primary symptom of ischemic heart disease, requires careful pharmacological interventions. In this context, calcium channel blockers (CCBs) and ranolazine have emerged as crucial pharmacotherapeutic agents, providing deep insights into the complexities of angina management.
CCBs, a diverse class that includes dihydropyridines (nifedipine) and diphenylalkylamines (verapamil and diltiazem), exert their effect by blocking calcium channels in cardiac and smooth muscle cells. This...