Background: Perioperative myocardial ischemia occurs in 20-40% of patients at risk for cardiac complications and is associated with a ninefold increase in risk for perioperative cardiac death, myocardial infarction, or unstable angina, and a twofold long-term risk. Perioperative atenolol administration reduces the risk of death for as long as 2 yr after surgery. This randomized, placebo-controlled, double-blinded trial tested the hypothesis that perioperative atenolol administration reduces the incidence and severity of perioperative myocardial ischemia, potentially explaining the observed reduction in the risk for death.

Methods: Two-hundred patients with, or at risk for, coronary artery disease were randomized to two study groups (atenolol and placebo). Monitoring included a preoperative history and physical examination and daily assessment of any adverse events. Twelve-lead electrocardiography (ECG), three-lead Holter ECG, and creatinine phosphokinase with myocardial banding (CPK with MB) data were collected 24 h before until 7 days after surgery. Atenolol (0, 5, or 10 mg) or placebo was administered intravenously before induction of anesthesia and every 12 h after operation until the patient could take oral medications. Atenolol (0, 50, or 100 mg) was administered orally once a day as specified by blood pressure and heart rate.

Results: During the postoperative period, the incidence of myocardial ischemia was significantly reduced in the atenolol group: days 0-2 (atenolol 17 of 99 patients; placebo, 34 of 101 patients; P = 0.008) and days 0-7 (atenolol, 24 of 99 patients; placebo, 39 of 101 patients; P = 0.029). Patients with episodes of myocardial ischemia were more likely to die in the next 2 yr (P = 0.025).

Conclusions: Perioperative administration of atenolol for 1 week to patients at high risk for coronary artery disease significantly reduces the incidence of postoperative myocardial ischemia. Reductions in perioperative myocardial ischemia are associated with reductions in the risk for death at 2 yr.

Download full-text PDF

Source
http://dx.doi.org/10.1097/00000542-199801000-00005DOI Listing

Publication Analysis

Top Keywords

myocardial ischemia
28
perioperative myocardial
12
myocardial
9
atenolol
9
postoperative myocardial
8
patients
8
risk
8
patients risk
8
risk perioperative
8
perioperative atenolol
8

Similar Publications

Initial therapy in patients with pulmonary arterial hypertension and cardiovascular comorbidities.

Eur Respir J

January 2025

INSERM UMR_S 999 « Pulmonary Hypertension: Pathophysiology and Novel Therapies », Hôpital Marie Lannelongue, Le Plessis-Robinson, France

Background: European guidelines recommend initial monotherapy in PAH patients with cardiovascular (CV) comorbidities based on the limited of evidence for combination therapy in this growing population.

Methods: A retrospective analysis was conducted on incident PAH patients enrolled in the French Pulmonary Hypertension Registry between 2009 and 2020. Propensity score matching was used to investigate initial dual oral combination therapy oral monotherapy in patients with at least one CV comorbidity (, hypertension, obesity, diabetes and coronary artery disease).

View Article and Find Full Text PDF

Severe pulmonary arterial hypertension and cardiogenic shock in acute systemic lupus erythematosus.

BMJ Case Rep

January 2025

Department of Allergy, Immunology and Respiratory Medicine, Alfred Hospital, Melbourne, Victoria, Australia.

We describe a woman in her late 20s with newly diagnosed systemic lupus erythematosus (SLE), who presented with fulminant pulmonary arterial hypertension (PAH) requiring inotropic and extracorporeal support. She was established on triple pulmonary vasodilator therapy with concurrent aggressive immunosuppression; however, treatment was complicated by infection and diffuse alveolar haemorrhage, necessitating delays in immunosuppression and withdrawal of epoprostenol. Despite this, with ongoing suppression of her SLE, her pulmonary haemodynamics improved, with normal pressures on right heart catheterisation several months later allowing stepdown to sildenafil monotherapy.

View Article and Find Full Text PDF

Background: Training in complex high-risk indicated percutaneous coronary intervention (CHIP-PCI) has frequently been reserved for established operators (consultants/attending) with trainees (fellows-in-training or FIT) being often discouraged from carrying out such procedures as a primary operator due to their high-risk nature. Whether the outcomes of these cases differ if the primary operator is a supervised FIT compared with a consultant is unknown.

Methods: Using multicentre PCI data from three cardiac centres in South Wales, UK (2018-2022), we identified 2295 CHIP-PCI cases with a UK-BCIS CHIP Score of 3 or more.

View Article and Find Full Text PDF

Stress Cardiac Magnetic Resonance Imaging in Intermediate-Risk Emergency Department Patients with Abnormal High-Sensitivity Troponin.

J Cardiovasc Magn Reson

January 2025

Duke University School of Medicine, Department of Medicine, 2301 Erwin Road, Durham, NC 27710 Durham, NC; Duke University Cardiovascular Magnetic Resonance Center, 2301 Erwin Road, Durham, NC 27710 Durham, NC. Electronic address:

Background: Patients presenting to the emergency department (ED) with chest pain often have abnormal high-sensitivity troponin (hsTn). However, only about 5% have an acute coronary syndrome. We aimed to assess the safety, feasibility and utility of a clinical disposition protocol including outpatient observation with stress cardiac-magnetic-resonance (CMR) in intermediate-risk patients with abnormal hsTn of unclear etiology.

View Article and Find Full Text PDF

P2 purinergic receptors at the heart of pathological left ventricular remodeling following acute myocardial infarction.

Am J Physiol Heart Circ Physiol

January 2025

Université de Tours, Inserm UMR1327 ISCHEMIA Membrane Signalling and Inflammation in reperfusion injuries, Tours, France.

Pathological left ventricular remodeling is a complex process following an acute myocardial infarction, leading to architectural disorganization of the cardiac tissue. This phenomenon is characterized by sterile inflammation and the exaggerated development of fibrotic tissue, which is non-contractile and poorly conductive, responsible for organ dysfunction and heart failure. At present, specific therapies are lacking for both prevention and treatment of this condition, and no biomarkers are currently validated to identify at-risk patients.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!