SPONTANEOUS CORONARY MICROEMBOLISATION

The development of coronary atherosclerosis can be subdivided into five stages according to the American Heart Association.¹ Atheroma and fibroatheroma, stage IV and V lesions, are characterised by lipid core formation. When the ratio of the lipid core to total plaque size increases and the fibrous cap thickness decreases < 60 μm, the risk of rupture is enhanced particularly if an infiltration of macrophages indicates signs of inflammation.² As these lesions are prone to rupture, they are regarded as vulnerable or plaques at risk.³ Plaques which are vulnerable are showing more vascular compensatory remodelling than non-vulnerable plaques.⁴ Clinical events occur when plaques ulcerate (VIa lesions), show intramural bleeding (VIb lesions), and form mural or occlusive thrombus based on erosion or plaque rupture (VIc lesions).^5,6

Apparently healthy subjects undergoing necropsy have experienced plaque rupture in 9% of cases, and patients with diabetes and hypertension in 17%.^7,8 Rupture ( fig 1) accounts for > 60% of all thrombi associated with sudden coronary death and acutemyocardial infarction, plaque erosion for 35%, and calcified noduli for 2–6 %.² Signs of plaque rupture are found in 85% of patients with unstable angina, but also in 15–25% with stable angina.⁵ Pathological and clinical studies have revealed multiple lesions, not only limited to a single coronary vessel but also in more than one vessel in unstable angina in mean (SD) 1.3 (1.4) hearts and in stable angina in 1.1 (1.3) hearts.² Clinically 2.1–2.6 complicated lesions per patient were found in acute coronary syndromes with …