Angiotensin II receptor blockers and isolated left bundle branch block: A retrospective cohort analysis

Nada Said1, Ramzi Ibrahim1, Hoang Nhat Pham2,3

  • 1Division of Cardiovascular Medicine, Mayo Clinic, Phoenix, AZ, USA.

Insights

Angiotensin II receptor blockers (ARBs) did not reduce heart failure events in patients with isolated left bundle branch block (LBBB). However, ARB therapy was linked to a significant decrease in all-cause mortality for this patient group.

Area of Science:

  • Cardiology
  • Pharmacology
  • Clinical Research

Background:

  • Chronic left bundle branch block (LBBB) is linked to adverse cardiac remodeling and cardiomyopathy.
  • The impact of angiotensin II receptor blocker (ARB) therapy on cardiovascular outcomes in isolated LBBB patients without prior heart failure (HF) or cardiomyopathy is not well understood.

Purpose of the Study:

  • To evaluate the effect of ARB therapy on cardiovascular outcomes in adults with isolated LBBB.
  • To determine if ARBs can prevent new-onset acute HF events or reduce mortality in this population.

Main Methods:

  • Retrospective cohort study using the TriNetX global research network.
  • Included adults with isolated LBBB and no history of HF, cardiomyopathy, or ischemic heart disease.
  • Propensity score matching was used to compare outcomes between ARB users and non-users over 5 years.

Main Results:

  • ARB therapy was not associated with a reduction in new-onset acute HF events (HR 1.05).
  • No significant differences were observed in rates of all-cause hospitalizations, cardiac arrest, or ventricular tachycardia.
  • ARB use was associated with a significantly lower all-cause mortality rate (HR 0.67).

Conclusions:

  • ARB therapy does not appear to prevent LBBB-induced cardiomyopathy or reduce acute HF risk.
  • A significant survival advantage was observed in patients with isolated LBBB treated with ARBs.
  • Further prospective studies are needed to confirm these findings and explore the mechanisms behind the mortality benefit.

Related Concept Videos

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...
2.5K
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,...
1.3K
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...
942
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...
2.3K
Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers01:24

Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

Adrenergic stimulation generally impacts cardiac rate and rhythm. Specifically, stimulation of the β-adrenoceptors triggers an increase in intracellular calcium ion influx and pacemaker currents, which may cause arrhythmias. Catecholamines like adrenaline also demonstrate β2-adrenoceptor-mediated hypokalemia, impacting cardiac action potential and disrupting the normal cardiac rhythm. Class II antiarrhythmic drugs are β-adrenoceptor antagonists or β-blockers, which...
1.4K
Adrenergic Antagonists: Chemistry and Classification of β-Receptor Blockers01:25

Adrenergic Antagonists: Chemistry and Classification of β-Receptor Blockers

β-adrenergic antagonists, or β-blockers, modulate the sympathetic nervous system by targeting β-adrenoceptors and inhibiting catecholamine-mediated sympathetic responses. β-blockers differ in their adrenoceptor subtype affinity, lipophilicity, and α-blocking capabilities. The history of β-blocker development began with the prototype, dichloroisoprenaline, which exhibited partial agonist activity. As a result, propranolol was developed as a pure antagonist but...
1.3K