Evidence of Multifocal Activity of Coronary Disease in Patients With Acute Myocardial Infarction

• DOI: 10.1161/01.cir.96.4.1145
• Publication Date: 2012-06-12T00:41:02Z
• Authors: Maurizio D. Guazzi; Maurizio Bussotti; Luca Grancini; Nicoletta De Cesare; Marco Guazzi; Isidoro L. Pera; Alessandro Loaldi
• Keywords: Male; Analysis of Variance; plaque; angina; myocardial infarction; remodeling; Myocardial Infarction; Coronary Artery Disease; Middle Aged; Coronary Angiography; Angina Pectoris; 3. Good health; 03 medical and health sciences; 0302 clinical medicine; Case-Control Studies; Disease Progression; Humans; Female; Prospective Studies

Background Destabilization of the fibrous cap facilitates plaque rupture, thrombus formation, and myocardial infarction. Because systemic stimuli, such as lipoproteins, infectious agents, autoantigens, may incite this reaction, one wonder whether disruption mechanisms are only local or infarction is caused by an arbitrary event a systemic, acute activity coronary disease. Methods Results Early (3 to 5 days) late (1 month) peri-infarction angiographic data in 23 patients with first were compared that similar patients, angiography performed because stable angina repeated after 1 month before angioplasty. Nonculprit lesion changes at narrowest point defined progression regression when exceeding 0.27 mm. In recent we found 16 had progression, 4 regression, both, 2 steady (values being [ P <.001], [NS], 0 20 <.001]); 27 lesions infarct related; 17 45 nonculprit progressed regressed <.001] <.05] out 78); minimal diameter reduction progressing stenoses averaged 0.39 mm; lumen increase regressing 0.30 3 developed interim rest associated lesion. Conclusions A greater proportion subjects (in versus angina) supports hypothesis hallmark disease activity. Changes might vary according “maturation” stage atheroma, maximal expression would be level offending plaque. Shrinkage, thrombolysis, vascular remodeling determine residual morphology.