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This work explores for the first time the effects of temperature increments on the development of high shear stresses between plaque and arterial wall due to their different dilatational properties. Data from the literature report febrile reactions prior to myocardial infarction in patients with normal coronary arteries and that coronary syndromes seem to be triggered by bacterial and viral infections, being fever the common symptom. Methods The thermo-mechanical behavior of thoracic aortas of New Zealand White rabbits with different degrees of atherosclerosis was measured by means of pressure–diameter tests at different temperatures. In addition, specific measurements of the thermal dilatation coefficient of atheroma plaques and of healthy arterial walls were performed by means of tensile tests at different temperatures. Results Results show a different thermo-mechanical behavior, the dilatation coefficient of atheroma plaque being at least twice that of the arterial wall. The calculation of temperature-induced mechanical stress at the plaque–vessel interface yielded shear stress levels enough to promote plaque rupture. Conclusions Increases of corporal temperature either local—produced by the inflammatory processes associated with atherosclerosis—or systemic—by febrile reactions—can play a role in increasing the risk of acute coronary syndromes, and they deserve a more comprehensive study.

This work explores for the first time the effects of temperature increments on the development of high shear stresses between plaque and arterial wall due to their different dilatational properties. Data from the literature report febrile reactions prior to myocardial infarction in patients with normal coronary arteries and that coronary syndromes seem to be triggered by bacterial and viral infections, being fever the common symptom. Methods The thermo-mechanical behavior of thoracic aortas of New Zealand White rabbits with different degrees of atherosclerosis was measured by means of pressure–diameter tests at different temperatures. In addition, specific measurements of the thermal dilatation coefficient of atheroma plaques and of healthy arterial walls were performed by means of tensile tests at different temperatures. Results Results show a different thermo-mechanical behavior, the dilatation coefficient of atheroma plaque being at least twice that of the arterial wall. The calculation of temperature-induced mechanical stress at the plaque–vessel interface yielded shear stress levels enough to promote plaque rupture. Conclusions Increases of corporal temperature either local—produced by the inflammatory processes associated with atherosclerosis—or systemic—by febrile reactions—can play a role in increasing the risk of acute coronary syndromes, and they deserve a more comprehensive study.