Postinfarction cardiac rupture is the result of thrombotic occlusion of a functional end artery with no previous myocardial damage in the perfusion area of the occluded artery. The pre-existing atherosclerotic stenosis at the site of thrombosis is thus"non-critical" in relation to development of collateral vessels and/or irreversible myocardial damage. Eleven cases of postinfarction cardiac rupture were studied by microscopy of cross-sections of the thrombosed segments. At the site of the thrombosis, pre-existing atherosclerosis had narrowed the lumen to 11% or less of its normal cross-sectional area. Maximal pre-existing narrowing of the proximal left anterior descending artery was found in a case with 97% stenosis (histologically measured cross-sectional area reduction) and an estimated residual lumen of 0.71 mm2. The prestenotic luminal area which is usually considered angiographically as "normal" was in all cases shown histologically to be severely narrowed by a diffuse intimal thickening. It is concluded that organic coronary stenosis must be far greater than 75% to be responsible for the development of collateral vessels and/or irreversible myocardial damage.
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