Evidence of Multifocal Activity of Coronary Disease in Patients With Acute Myocardial Infarction
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
DOI:
10.1161/01.cir.96.4.1145
Publication Date:
2012-06-12T00:41:02Z
AUTHORS (7)
ABSTRACT
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.
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