Relation of the site of acute myocardial infarction to the most severe coronary arterial stenosis at prior angiography. Am J Cardiol
ABSTRACT To determine whether the site of acute myocardial infarction (AMI) can be predicted on the basis of a previous coronary angiogram, 184 consecutive angiograms obtained between March 1972 and August 1990 in 92 patients who had undergone coronary angiography both before and after AMI without intervening bypass surgery or angioplasty were evaluated. Median time between the first coronary angiography and AMI was 26 months (range 1 to 144). On the first angiogram, most patients (89%) had 1- or 2-vessel disease, and 56 (61%) had an abnormal ventriculography. Seventy-two segments (78%) responsible for a future AMI were not significantly stenosed. On the second angiogram, AMI was related to the previously most stenotic segments in only 29 patients (32%). For these patients, median time between first coronary angiography and AMI was slightly shorter (22 vs 28 months; p = 0.04). The severity of the narrowing on the first angiogram was a poor predictor of subsequent AMI. It is concluded that in a selected, medically treated cohort, AMI is frequently related to a segment that was not the most stenotic one or was not even significantly stenosed at previous angiography, particularly with a long interval between the first angiogram and AMI.
- SourceAvailable from: Jan Václavík
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- "According to a new myocardial infarction definition, type 1 myocardial infarction (thrombotic)  is due to the rupture of an unstable plaque followed by thrombosis, resulting in the partial or complete occlusion of a coronary artery. It develops in the arterial territory areas, usually without severe stenosis N60% and these lesions do not cause ischemia during a stress test  . It occurs early, within 36 h postoperatively , and it manifests more often as an acute myocardial infarction with ST segment elevations and with the subsequent appearance of pathological Q waves on ECG. "
ABSTRACT: The current practice of withdrawing aspirin 7-10 days preoperatively may be dangerous in certain groups of patients. The risk of cardiovascular events increases 3-fold after aspirin withdrawal. The average time between aspirin withdrawal and the manifestation of acute coronary syndrome is 8 to 11 days. The withdrawal of clopidogrel earlier than 4-6 weeks after bare metal stent implantation or less than 12 months after drug-eluting stent implantation is very risky and poses a high risk of stent thrombosis and high perioperative mortality. Continuing aspirin perioperatively leads to a 1.5-fold increase in perioperative bleeding complications but it does not lead to a higher severity of bleeding complications or higher mortality. The article analyzes current European and American guidelines for perioperative antiplatelet treatment and suggests an algorithm based on the guidelines to help make clinical decisions.European Journal of Internal Medicine 02/2011; 22(1):26-31. DOI:10.1016/j.ejim.2010.10.007 · 2.30 Impact Factor
European Heart Journal Supplements 02/2002; 4. DOI:10.1016/S1520-765X(02)90028-3 · 5.64 Impact Factor
- "Ambrose 1986 > 70% 5 0–70% < 50% 0 20 40 60 80 100 0 40 80 120 160 200 Little et al 1986 Nobuyoshi 1991 Giroud 1992 All MI patients (n) "
- "Worthy of note is that coronary occlusion and myocardial infarction frequently take place in the presence of mild or moderate stenosis     ; the smallest plaques may also lead to acute coronary events in the event of abrupt occlusion because they are less frequently associated with protective "
Article: The unstable plaque[Show abstract] [Hide abstract]
ABSTRACT: Acute thrombosis, which frequently complicates the evolution of atherosclerosis, leads to cardiovascular, cerebrovascular and peripheral events. Thrombosis occurs over plaques because of a disruption or tear in the cap of a lipid-rich plaque that leads to exposure of blood to highly thrombogenic plaque components because of denudation and erosion of the endothelial surface. Therefore, the crucial question is why atherosclerosis suddenly becomes complicated by life-threatening thrombosis. Plaque stabilization could be a crucial therapeutic intervention to combat the harmful consequences of coronary atherosclerosis through agents that can favourably impact on plaque pathobiology.