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Spontaneous and interventional coronary microembolisation

During recent years new imaging techniques have significantly improved the option to study in vivo coronary macro- and microvascular morphology and perfusion, including intracoronary ultrasound and Doppler, positron emission computed tomography as well as magnetic resonance imaging and high frequency transthoracic echocardiography.

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 …