Acute and stable coronary heart disease: different risk factors

Abstract

Coronary heart disease (CHD) continues to be a worldwide leading cause of death for both men and women. When coronary atherosclerosis progresses, there is deposition of plaque external to the lumen of the artery, thus the plaque may extend eccentrically and outward without compromising the lumen initially. As atherosclerosis worsens the plaque mass may later on bulge into the lumen and may therefore result in a haemodynamic obstruction and angina pectoris symptoms. Typically, angina pectoris develops when an atherosclerotic plaque obstructs at least 70% of the arterial lumen. Thus, stable angina pectoris is a condition in which there is regional myocardial ischaemia caused by inadequate coronary perfusion and is usually induced by increases in myocardial oxygen requirements. Chest pain that can be characterized as chronic stable angina typically is produced with physical exertion and relieved by rest and/or nitroglycerin. In contrast, chest pain that occurs at rest usually is indicative of unstable disease, such as acute coronary syndrome (ACS) that usually is caused by a coronary plaque rupture and subsequent intracoronary thrombosis formation. Prognosis of patients with stable angina is in general very good, with an incidence of death or non-fatal myocardial infarction not exceeding 2% per year.1 On the other hand, patients with an ACS without ST elevation [non-ST-segment elevation myocardial infarction (NSTEMI)] have a much worse prognosis since 10–15% experience death or non-fatal myocardial infarction within 1 year after admission.2 Despite a similar anatomical background, there are differences between stable angina pectoris and ACS. Thus, vulnerable plaques are typically defined by a large lipid pool, and a high percentage of inflammatory cells, as well as a thin fibrous cap separating the lipid core from the blood pool. In contrast to collagen-rich hard plaques, which may progress in severity and result in … *Corresponding author. Tel: + 47 228 94655, Fax: + 47 228 94259, Email: stefan.agewall{at}medisin.uio.no