Related Experiment Video

Updated: Jun 1, 2025

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
05:26

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction

Published on: May 28, 2019

9.2K

Beta-Blockers After PCI for Stable Coronary Artery Disease and Preserved Left Ventricular Ejection Fraction

Safi U Khan1, Usman Ali Akbar2, Muhammad Shahzeb Khan3

  • 1Department of Cardiology, Houston Methodist DeBakey Heart & Vascular Center, Houston, Texas, USA. Electronic address: https://twitter.com/safinmc.

JACC. Advances
|January 18, 2025
PubMed

Insights

Early beta-blocker use after percutaneous coronary intervention (PCI) in stable coronary artery disease (CAD) with preserved ejection fraction (LVEF) was linked to increased mortality. This therapy did not significantly impact major cardiovascular events over five years.

Area of Science:

  • Cardiology
  • Pharmacology
  • Clinical Research

Background:

  • Limited long-term data on beta-blockers post-percutaneous coronary intervention (PCI) for stable coronary artery disease (CAD) with preserved left ventricular ejection fraction (LVEF).
  • Need to evaluate early beta-blocker initiation's impact in this specific patient population.

Purpose of the Study:

  • To assess the long-term effects of early beta-blocker initiation versus no initiation after PCI in stable CAD patients with preserved LVEF.
  • To determine the association between early beta-blockers and mortality, cardiovascular events, and safety endpoints.

Main Methods:

  • Retrospective cohort study using TriNetx database (2009-2024) with target trial emulation.
  • 1:1 greedy propensity score matching comparing early beta-blocker initiation (within 7 days) vs. no initiation.
  • 5-year intention-to-treat analysis of all-cause mortality, myocardial infarction, heart failure, stroke, and safety outcomes, with falsification endpoints.

Main Results:

  • Beta-blocker therapy was associated with increased all-cause mortality (HR: 1.11).
  • No significant differences observed in myocardial infarction, stroke, heart failure, or atrial fibrillation/flutter hospitalizations.
  • Higher hospitalization for hypotension noted with beta-blockers (HR: 1.10); no significant association with bone fracture or appendicitis hospitalizations.

Conclusions:

  • Early beta-blocker initiation after PCI in stable CAD with preserved LVEF is associated with increased mortality.
  • No significant impact on major cardiovascular events was found.
  • Findings suggest a need for careful consideration of early beta-blocker use in this patient group.
Abstract

Keywords:
beta-blockerpercutaneous coronary interventionstable ischemic heart diseasetarget-trial emulation

More Related Videos

Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs14:35

Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs

Published on: April 17, 2021

8.4K
Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing12:45

Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing

Published on: December 11, 2017

10.4K

Related Concept Videos

Heart Failure Drugs: β-Blockers01:22

Heart Failure Drugs: β-Blockers

β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation,...
314
Adrenergic Antagonists: ɑ and β-Receptor Blockers01:31

Adrenergic Antagonists: ɑ and β-Receptor Blockers

Third-generation β-blockers, such as labetalol and carvedilol, represent a significant advancement in managing cardiovascular conditions. Unlike conventional β-blockers, which can induce peripheral vasoconstriction, third-generation drugs block α1 adrenoceptors. This promotes vasodilation through several mechanisms, such as increased nitric oxide production, inhibition of calcium ion entry, opening of potassium ion channels, and antioxidant action. Labetalol, for instance, is...
405
Adrenergic Antagonists: Pharmacological Actions of β-Receptor Blockers01:27

Adrenergic Antagonists: Pharmacological Actions of β-Receptor Blockers

β-receptor blockers significantly impact the cardiovascular system by counteracting catecholamine-induced sympathetic responses. These medications decrease heart rate, contractility, and cardiac output, potentially leading to cardiac depression, life-threatening bradycardia, and death. Therapeutically, β-blockers function as mild antihypertensives and are utilized in treating angina pectoris and cardiac arrhythmias. However, nonselective β-blockers inhibit β2-receptors in...
528
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...
517
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...
707
Antianginal Drugs: Nitrates and β-Blockers01:16

Antianginal Drugs: Nitrates and β-Blockers

In cardiovascular health, antianginal drugs combat angina pectoris — a condition marked by chest pain owing to diminished blood flow to the heart.
Organic nitrates,  such as nitroglycerin, play a pivotal role. Once metabolized, they liberate nitric oxide, a molecular marvel. Nitric oxide triggers guanylyl cyclase and augments cGMP production. This biochemical cascade orchestrates the relaxation of vascular smooth muscles, ushering in vasodilation and enhancing coronary blood flow....
512