Pharmacological treatment of chronic stable angina pectoris

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Abstract

<p class="first" id="d1541941e90">Chronic stable angina is the most common manifestation of ischaemic heart disease in the developed world and is associated with impaired quality of life and increased mortality. The pathogenesis of stable angina is complex and often, albeit not always, involves flow-limiting epicardial coronary artery stenoses (atheromatous plaques) that reduce the ability of the coronary circulation to deliver appropriate blood supply to the myocardium. The coronary microcirculation can also play an important role. An imbalance between myocardial oxygen supply and metabolic oxygen demand causes the symptoms of angina pectoris and represents a major therapeutic target. Rational treatment requires a multi-faceted approach combining lifestyle changes, aggressive management of modifiable coronary artery disease risk factors, pharmacological therapy and myocardial revascularisation when appropriate. Despite modern therapies, many patients continue to suffer from angina. Several new anti-anginal drugs have been introduced that might allow more effective symptom control. These novel agents have specific mechanisms of action and fewer side effects compared to conventional drugs. The combined use of traditional and novel treatments is likely to increase the proportion of patients who are managed successfully with medical therapy alone. This article briefly reviews recent advances in the pharmacological management of chronic stable angina pectoris, highlighting how an understanding of the prevailing pathogenic mechanisms in the individual patient can aid appropriate selection of therapeutic strategies and improve clinical outcome. </p>

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Ivabradine for patients with stable coronary artery disease and left-ventricular systolic dysfunction (BEAUTIFUL): a randomised, double-blind, placebo-controlled trial.

Kim Fox, Ian Ford, P Gabriel Steg … (2008)

Ivabradine specifically inhibits the I(f) current in the sinoatrial node to lower heart rate, without affecting other aspects of cardiac function. We aimed to test whether lowering the heart rate with ivabradine reduces cardiovascular death and morbidity in patients with coronary artery disease and left-ventricular systolic dysfunction. Between December, 2004, and December, 2006, we screened 12 473 patients at 781 centres in 33 countries. We enrolled 10 917 eligible patients who had coronary artery disease and a left-ventricular ejection fraction of less than 40% in a randomised, double-blind, placebo-controlled, parallel-group trial. 5479 patients received 5 mg ivabradine, with the intention of increasing to the target dose of 7.5 mg twice a day, and 5438 received matched placebo in addition to appropriate cardiovascular medication. The primary endpoint was a composite of cardiovascular death, admission to hospital for acute myocardial infarction, and admission to hospital for new onset or worsening heart failure. We analysed patients by intention to treat. The study is registered with ClinicalTrials.gov, number NCT00143507. Mean heart rate at baseline was 71.6 (SD 9.9) beats per minute (bpm). Median follow-up was 19 months (IQR 16-24). Ivabradine reduced heart rate by 6 bpm (SE 0.2) at 12 months, corrected for placebo. Most (87%) patients were receiving beta blockers in addition to study drugs, and no safety concerns were identified. Ivabradine did not affect the primary composite endpoint (hazard ratio 1.00, 95% CI 0.91-1.1, p=0.94). 1233 (22.5%) patients in the ivabradine group had serious adverse events, compared with 1239 (22.8%) controls (p=0.70). In a prespecified subgroup of patients with heart rate of 70 bpm or greater, ivabradine treatment did not affect the primary composite outcome (hazard ratio 0.91, 95% CI 0.81-1.04, p=0.17), cardiovascular death, or admission to hospital for new-onset or worsening heart failure. However, it did reduce secondary endpoints: admission to hospital for fatal and non-fatal myocardial infarction (0.64, 95% CI 0.49-0.84, p=0.001) and coronary revascularisation (0.70, 95% CI 0.52-0.93, p=0.016). Reduction in heart rate with ivabradine does not improve cardiac outcomes in all patients with stable coronary artery disease and left-ventricular systolic dysfunction, but could be used to reduce the incidence of coronary artery disease outcomes in a subgroup of patients who have heart rates of 70 bpm or greater.

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Guidelines on the management of stable angina pectoris: executive summary: The Task Force on the Management of Stable Angina Pectoris of the European Society of Cardiology.

Kim Fox, Maria Garcia, Diego Ardissino … (2006)

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High prevalence of a pathological response to acetylcholine testing in patients with stable angina pectoris and unobstructed coronary arteries. The ACOVA Study (Abnormal COronary VAsomotion in patients with stable angina and unobstructed coronary arteries).

Peter Ong, Anastasios Athanasiadis, Gábor Borgulya … (2012)

This study aimed at determining the prevalence of epicardial and microvascular coronary spasm in patients with anginal symptoms, despite angiographically normal coronary arteries. Despite a typical clinical presentation with exercise-related anginal symptoms (chest pain or dyspnea) with or without occasional attacks of resting chest pain suggestive of coronary artery disease, 40% of patients undergoing diagnostic angiography have normal or "near" normal coronary arteriograms. Many of these patients are given a diagnosis of noncardiac chest pain, and some are considered to have microvascular angina. However, we speculate that abnormal coronary vasomotion (reduced vasodilatation with exercise = reduced coronary flow reserve and/or vasospasm at rest) might also represent a plausible explanation for the symptoms of the patient. This was a prospective study in 304 consecutive patients (50% men, mean age 66 ± 10 years) with exertional anginal symptoms undergoing diagnostic angiography. A total of 139 patients (46%) had ≥50% coronary artery disease in at least 1 coronary artery, 21 patients (7%) had luminal narrowings ranging from >20% to 49%, and 144 patients (47%) had normal coronary arteries or only minimal irregularities (<20% diameter reduction). One hundred twenty-four patients of the latter (86%) underwent intracoronary acetylcholine (ACH) testing, which elicited coronary spasm in 77 patients (62%), 35 patients (45%) with epicardial spasm (≥75% diameter reduction with reproduction of the symptoms of the patient) and 42 patients (55%) with microvascular spasm (reproduction of symptoms, ischemic electrocardiographic changes, and no epicardial spasm). Nearly 50% of patients undergoing diagnostic angiography for assessment of stable angina had angiographically normal or near normal coronary arteriograms. The ACH test triggered epicardial or microvascular coronary spasm in nearly two-thirds of these patients. Our results suggest that abnormal coronary vasomotion plays a pathogenic role in this setting and that the ACH test might be useful to identify patients with cardiac symptoms, despite normal coronaries. (Abnormal Coronary Vasomotion in Patients With Suspected CAD But Normal Coronary Arteries; NCT00921856). Copyright © 2012 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.