Clinical Review ABC of interventional cardiology

Pathophysiology and investigation of coronary artery disease

BMJ 2003; 326 doi: (Published 10 May 2003) Cite this as: BMJ 2003;326:1027
  1. Ever D Grech

    In affluent societies, coronary artery disease causes severe disability and more death than any other disease, including cancer. It manifests as angina, silent ischaemia, unstable angina, myocardial infarction, arrhythmias, heart failure, and sudden death.


    Coronary artery disease is almost always due to atheromatous narrowing and subsequent occlusion of the vessel. Early atheroma (from the Greek athera (porridge) and oma (lump)) is present from young adulthood onwards. A mature plaque is composed of two constituents, each associated with a particular cell population. The lipid core is mainly released from necrotic “foam cells”—monocyte derived macrophages, which migrate into the intima and ingest lipids. The connective tissue matrix is derived from smooth muscle cells, which migrate from the media into the intima, where they proliferate and change their phenotype to form a fibrous capsule around the lipid core.

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    Progression of atheromatous plaque from initial lesion to complex and ruptured plaque

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    Schematic representation of normal coronary artery wall (top) and development of atheroma (bottom)

    When a plaque produces a >50% diameter stenosis (or >75% reduction in cross sectional area), reduced blood flow through the coronary artery during exertion may lead to angina. Acute coronary events usually arise when thrombus formation follows disruption of a plaque. Intimal injury causes denudation of the thrombogenic matrix or lipid pool and triggers thrombus formation. In acute myocardial infarction, occlusion is more complete than in unstable angina, where arterial occlusion is usually subtotal. Downstream embolism of thrombus may also produce microinfarcts.

    Priorities for cardiology referral

    • Recent onset of symptoms

    • Rapidly progressive symptoms

    • Possible aortic stenosis

    • Threatened employment

    • Severe symptoms (minimal exertion or nocturnal angina)

    • Angina refractory to medical treatment

    Cardiovascular risk factors

    Non-modifiable risk factors
    • Positive family history

    Modifiable risk factors
    • Hypercholesterolaemia

    • Left ventricular hypertrophy

    • Overweight and obesity

    Uncertain risk factors
    • Hypertriglyceridaemia

    • Microalbuminuria

    • Hyperhomocysteinaemia

    • Age

    • Hypertension

    • Sedentary lifestyle

    • Excessive alcohol intake

    • Lp(a) lipoprotein

    • Fibrinogen

    • C reactive protein

    • Male sex

    • Smoking

    • Diabetes

    • Uric acid

    • Renin


    Patients …

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