摘要：

Guidelines for clinical care are derived most commonly from large clinical trials involving thousands of patients. These trials are usually conducted to test hypotheses that have been developed from interesting clinical observations and innovative pilot trials. In this issue of iJACC , Prati et al. ( 1 ) describe interesting hypothesis-generating observations in patients with ST-segment elevation myocardial infarction (STEMI). For almost a half-century, cardiac pathologists have focused on the atherosclerotic lesions underlying the thrombotic coronary occlusions responsible for STEMI. Postmortem examination of patients who died early after acute STEMI have revealed principally 2 kinds of abnormalities. The more common, described by Constantinides ( 2 ), Davies et al. ( 3 ), and Falk ( 4 ) is the rupture of a thin fibrous cap overlying a lipid-rich atherosclerotic plaque, a so-called vulnerable plaque . In many instances, there is evidence of inflammation in the walls of the plaque, with macrophages and T lymphocytes that secrete inhibitors of collagen synthesis, and of proteases that digest the thin fibrous cap. As a consequence of plaque rupture, tissue factor is exposed to the flowing blood, and this in turn causes activation of platelets and the coagulation cascade. The coronary obstruction is caused in part by the plaque that encroaches on the arterial lumen and by the overlying thrombosis that delivers the coup de grace and usually results in total luminal occlusion. Prompt percutaneous coronary intervention (PCI), with stent insertion, is the centerpiece of therapy of these patients. Plaque erosion, a second pathological lesion underlying coronary thrombosis, has been studied by van der Wal et al. ( 5 ) as well as Virmani et al. ( 6 ) (Dr. Virmani is one of the coauthors of the paper by Prati et al. [ 1 ] ). Plaque erosion is responsible for the development of STEMI and/or sudden cardiac death in most of the patients who do not exhibit plaque rupture. These erosions are characterized by an absent or disrupted endothelium overlying a plaque that is characterized by greater proliferation of smooth muscle than inflammatory cells and by the presence of abundant proteoglycans. Plaques with superficial erosions do not, by themselves, cause critical obstruction. In such cases, the coronary obstructions are precipitated largely by the thrombi that develop on the dysfunctional intima. Based on autopsy findings in patients who died suddenly, endothelial plaque erosion may occur in as many as 40% of patients with fatal coronary thrombi ( 5,6 ). Plaque erosions appear to be more common in younger women (younger than 50 years of age) and in premenopausal smokers. Kubo et al. ( 7 ) characterized these lesions by optical coherence tomography (OCT) and reported that they are characterized by loss of endothelial lining with intimal tears. The 31 patients described in the report by Prati et al. ( 1 ) were studied relatively early in the development of STEMI. After arteriography, which revealed total coronary occlusion in 60% of these patients, the investigators removed the offending thrombi by aspiration thrombectomy and/or thrombolysis. They then performed OCT, which showed no evidence of residual, critically obstructive plaques. The decision of how these patients would be treated was left to the interventional cardiologists. Nineteen patients received the recommended treatment of STEMI (i.e., stents were deployed after aspiration thrombectomy). In the other 12 patients, the operators apparently reasoned that nothing might be gained by stenting an artery without a severely obstructing plaque. Indeed, such a procedure might even damage the arterial wall unnecessarily and expose it to a stent, which carries its own, albeit small, risk. Instead, they treated these patients with aspirin, heparin, a thienopyridine, and in some instances a glycoprotein IIb/IIIa inhibitor. The residual coronary stenosis was similar in the 2 groups. Remarkably, after a follow-up of > 2 years, none of the 12 patients treated by thrombectomy alone and only 1

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