Minggu, 26 April 2009

Pathophysiology and investigation of coronary artery disease


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.
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.
Patients presenting with chest pain may be identified as having
definite or possible angina from their history alone. In the
former group, risk factor assessment should be undertaken,
both to guide diagnosis and because modification of some
associated risk factors can reduce cardiovascular events and
mortality. A blood count, biochemical screen, and thyroid
function tests may identify extra factors underlying the onset of
angina. Initial drug treatment should include aspirin, a
 blocker, and a nitrate. Antihypertensive and lipid lowering
drugs may also be given, in conjunction with advice on lifestyle
and risk factor modification.
All patients should be referred to a cardiologist to clarify the
diagnosis, optimise drug treatment, and assess the need and
suitability for revascularisation (which can improve both
symptoms and prognosis). Patients should be advised to seek
urgent medical help if their symptoms occur at rest or on
minimal exertion and if they persist for more than 10 minutes
after sublingual nitrate has been taken, as these may herald the
onset of an acute coronary syndrome