Angiotensin receptor blockers and risk of myocardial infarction: systematic review

Michael A McDonald1, Scot H Simpson, Justin A Ezekowitz

  • 1Division of Cardiology, University of Alberta, 2C2 WMC, University of Alberta Hospital, 8440-112 Street, Edmonton, AB, Canada T6G 2B7.

BMJ (Clinical Research Ed.)
|September 27, 2005
PubMed
Abstract

Insights

Angiotensin receptor blockers (ARBs) do not increase the risk of myocardial infarction in high-risk patients. This systematic review found no significant increase in heart attack risk compared to placebo or ACE inhibitors.

Area of Science:

  • Cardiology
  • Pharmacology
  • Clinical Trials

Background:

  • Cardiovascular disease remains a leading cause of mortality worldwide.
  • Angiotensin receptor blockers (ARBs) are a class of drugs used to treat hypertension and heart failure.
  • Concerns have been raised regarding the potential cardiovascular safety of ARBs, specifically their effect on myocardial infarction (MI).

Purpose of the Study:

  • To systematically evaluate the risk of myocardial infarction (MI) associated with the use of angiotensin receptor blockers (ARBs).
  • To compare the risk of MI between ARBs and placebo.
  • To compare the risk of MI between ARBs and angiotensin-converting enzyme (ACE) inhibitors.

Main Methods:

  • A systematic review and meta-analysis of controlled clinical trials.
  • Searches of major databases including Medline, Embase, and the Cochrane central register of controlled trials.
  • Inclusion of 19 studies with 31,569 patients, comparing ARBs with placebo or ACE inhibitors in patients at risk for cardiovascular events.

Main Results:

  • Across 11 studies (21,062 patients), ARBs were not associated with an increased risk of MI compared to placebo (OR 0.94, 95% CI 0.75-1.16).
  • In nine studies (10,625 patients), ARBs did not show an increased risk of MI compared to ACE inhibitors (OR 1.01, 95% CI 0.87-1.16).
  • The confidence intervals did not exclude a potential increase of up to 16% or a reduction of up to 25% in MI risk.

Conclusions:

  • Treatment with angiotensin receptor blockers is not significantly associated with an increased risk of myocardial infarction.
  • While current findings alleviate safety concerns, larger prospective trials are needed for definitive conclusions.
  • The results suggest ARBs can be safely used in patients at risk for cardiovascular events, pending further evidence.

Related Concept Videos

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...
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,...
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...
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...
Aortic Regurgitation III: Medical Management01:25

Aortic Regurgitation III: Medical Management

Aortic regurgitation (AR) is when the aortic valve does not close or seal properly, leading to backward blood circulation from the aorta into the left ventricle during diastole. Common causes of AR include rheumatic heart disease, congenital valve defects, and aortic root dilation. Managing AR requires a multifaceted approach to alleviate symptoms, preserve left ventricular function, and address the underlying cause of the regurgitation. Patients with symptomatic AR or significant left...