Ischemic heart disease: clinical and pathological mismatch.

Disagreements between dynamic and postmortem morphology arise mainly from different imaging and selection of study population. The high frequency of severe and multivessel atherosclerotic stenosis in non cardiac patients and healthy subjects dying accidentally questions the direct cause-effect relationship between stenosis and ischemic heart disease; supports the view the dramatically enlarged collaterals always found in this condition may have an adequate compensatory role; and suggests the ineffectiveness of occlusion at the site of severe stenosis already bypassed by collaterals. The degree and number of severe stenoses in ischemic heart disease do not predict onset, course, complications, infarct size or death. On the other hand, the presence in this disease of three different types of morpho-functional myocardial damage indicate that different pathogenic mechanisms exist. Complications and death appear related more to metabolic disorders linked with adrenergic unbalance than to ischemia and subsequent expansion of primary infarct necrosis. Finally, postmortem findings show that lympho-plasmacellular inflammation of coronary atherosclerotic plaques is significantly more frequent (100% acute infarct, 88% chronic ischemia, 83% sudden coronary death, 64% healthy controls), severe and diffuse in all plaques in single patients compared to controls. Its preferential location around pericoronary nerves suggests the working hypothesis that it may be the cause of spasm and/or regional alterations of cardiac contractility with extravascular compression of the intramyocardial vasculature. These functional mechanisms could explain the cineangio imaging of coronary cut off rather than thrombus.