Do angiotensin II receptor blockers increase the risk of myocardial infarction?

Paolo Verdecchia1, Fabio Angeli, Roberto Gattobigio

  • 1Dipartimento Malattie Cardiovascolari, Ospedale R. Silvestrini, 06100 Perugia, Italy. verdec@tin.it

European Heart Journal
|August 6, 2005
PubMed

Insights

Angiotensin receptor blockers (ARBs) do not increase the risk of myocardial infarction (MI). A meta-analysis found no excess MI risk with ARBs compared to placebo or ACE-inhibitors, supporting their safety profile.

Area of Science:

  • Cardiovascular Medicine
  • Pharmacology
  • Clinical Trials

Background:

  • Safety concerns regarding Angiotensin Receptor Blockers (ARBs) emerged due to studies suggesting an increased risk of myocardial infarction (MI).
  • Existing evidence created uncertainty about the cardiovascular safety of ARBs.

Purpose of the Study:

  • To evaluate the association between Angiotensin Receptor Blockers (ARBs) and the risk of myocardial infarction (MI).
  • To clarify the safety profile of ARBs in cardiovascular outcomes.

Main Methods:

  • A meta-analysis of randomized clinical trials was conducted.
  • Trials compared ARBs against placebo or other active drugs, excluding ARBs.
  • Subgroup analyses were performed to assess MI incidence and cardiovascular mortality.

Main Results:

  • Overall, ARBs were not associated with an excess risk of MI compared to placebo or ACE-inhibitors.
  • MI incidence did not significantly differ between ARBs and placebo (OR: 0.96) or ACE-inhibitors (OR: 0.99).
  • Cardiovascular mortality was not different between ARBs and other drug classes, and was slightly lower than placebo (OR: 0.91).

Conclusions:

  • The study findings do not support the hypothesis that ARBs increase the risk of MI.
  • ARBs appear to have a favorable safety profile regarding myocardial infarction.
  • Further investigation into specific drug classes compared to ARBs may be warranted.
Abstract

Related Concept Videos

Antihypertensive Drugs: Action of β1 Blockers01:17

Antihypertensive Drugs: Action of β1 Blockers

β1-receptors are primarily located in the heart and kidneys. In cardiac myocytes, these receptors interact with neurotransmitters released by the sympathetic nervous system during heightened activity or danger. As a result, β1-receptors get activated, initiating a series of biochemical processes. Excessive activation of beta receptors due to chronic stress can abnormally increase heart rate and contractility, resulting in high blood pressure or hypertension. To counteract this,...
2.2K
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...
2.7K
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...
2.9K
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,...
1.9K
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...
1.9K
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...
1.9K