[2] These characteristics together with the usual hemodynamic pulsating expansion during systole and elastic recoil contraction during diastole contribute to a high mechanical stress zone on the fibrous cap of the atheroma, making it prone to rupture.
Generally an atheroma becomes vulnerable if it grows more rapidly and has a thin cover separating it from the bloodstream inside the arterial lumen.
[5] The sticky cytokines on the artery wall capture blood cells (mainly platelets) that accumulate at the site of injury.
The tests most commonly performed clinically with the goal of testing susceptibility to future heart attack include several medical research efforts, starting in the early to mid-1990s, using intravascular ultrasound (IVUS), thermography, near-infrared spectroscopy, careful clinical follow-up, and other methods, to predict these lesions and the individuals most prone to future heart attacks.
While stability vs. vulnerability cannot be readily distinguished in this way, quantitative baseline measurements of the thickest portions of the arterial wall (locations with the most plaque accumulation).
Concerning stable plaques, the thick fibrous cap avoids the breaking risks, however, it reduces significantly the artery diameter which causes the cardiovascular problems related to the decreasing of vessel's diameter (this is determined by the Hagen–Poiseuille equation which explains how flow-rate is related to the radius of the vessel to the fourth power).
Patients can lower their risk for vulnerable plaque rupture in the same ways that they can cut their heart attack risk: Optimize lipoprotein patterns, keep blood glucose levels low normal (see HbA1c), stay slender, eat a proper diet, quit smoking, and maintain a regular exercise program.