Effects of temperature and histopathologic preparation on the size and morphology of atherosclerotic carotid arteries as imaged by MRI.

Using magnetic resonance imaging the effects of temperature, formalin fixation, and decalcification on the size and morphology of atherosclerotic arteries were evaluated. Ten ex vivo carotid arteries were scanned fresh at body and room temperature and formalin-fixed and decalcified at room temperature. Different spin-echo pulse sequences were used and absolute T2 values calculated. During processing for histopathology, the contrast between the arterial layers increased. From body to room temperature there were significant increases in size (4%-7%), T2 of media (60--> 68 msec), and fibrous plaque component (95--> 110 msec). Formalin fixation caused significant increases in size (2%-3%) and media T2 (68--> 74 msec). Decalcification caused significant shrinkage (2%-5%) and decrease in T2 of media (74--> 53 msec) and fibrous plaque component (118--> 76 msec). Thus temperature and preparation have profound effects on contrast, size, and T2 of atherosclerotic arteries. Ex vivo experiments should be performed on fresh specimens at body temperature. J. Magn. Reson. Imaging 1999;10:876-885.

Atherosclerosis and acute coronary events.

Without thrombosis, coronary atherosclerosis is generally benign. It is plaque disruption, or fissuring, and subsequent thrombosis that make coronary atherosclerosis dangerous. Small ruptures often remain clinically silent, whereas more extensive plaque rupture may cause the development of unstable angina, myocardial infarction, and sudden death. The risk of plaque disruption depends more on plaque type (composition) than on plaque size and stenosis severity. Both plaque vulnerability (intrinsic disease) and rupture triggers (extrinsic forces) are important for plaque disruption. The resultant thrombotic response, which affects the clinical presentation and outcome, is partly determined by the reactivity of the circulating platelets and the balance between the coagulation and fibrinolytic systems. To prevent and treat life-threatening coronary thrombosis, the medical community should seek new ways to identify and treat dangerous, vulnerable plaques and to optimize antithrombotic treatment.

Coronary atherosclerosis: determinants of plaque rupture.

The most important mechanism responsible for the sudden and unpredictable onset of acute coronary syndromes is coronary plaque rupture with thrombosis and vasospasm superimposed. The risk of plaque rupture depends on plaque type (composition) rather than plaque size (volume); most ruptures occur in plaques containing a soft, lipid-rich core that is covered by a thin and inflamed cap of fibrous tissue. Compared with intact caps, the ruptured ones usually are thinner and contain less collagen (responsible for tensile strength), fewer smooth muscle cells (smc; collagen synthesizing cells), and many more macrophages (collagen degrading cells). Therefore, major determinants of plaque vulnerability and rupture are progressive lipid accumulation (core formation) and cap weakening due to ongoing inflammation with collagen degradation (macrophage-related) and impaired healing and repair (smc-related). These intrinsic plaque changes predispose plaques to rupture whereas extrinsic forces imposed on plaques, such as biomechanical and haemodynamic stresses, may determine the actual time of rupture by precipitating or 'triggering' it. Luckily, recent research in patients with coronary artery disease indicates that both plaque vulnerability and rupture triggers may be modified beneficially by treatment.