The role of atherosclerotic plaque stability and inflammation in the pathogenesis of acute coronary syndrome
LI Gui-shuan
Abstract
LI Gui-shuan
Abstract
Objective To elucidate the effect of inflammation and coronary atherosclerotic plaque destabilization in the pathogenesis of acute coronary syndromes (ACS).Methods Twenty-eight patients with ACS and 13 patients with stable angina pectoris (SA) were examined by intravascular ultrasound (IVUS). Coronary plaque morphology and areas in culprit lesions were analyzed. The serum levels of hs-CRP,MMP-9,TIMP-1,sCD40L were also measured.Results Soft plaques were dominant in culprit lesions of ACS patients (71.4%,20/28),and hard plaques were dominant in culprit lesions of SA patients [76.9% (10/13),P=0.004].At the culprit site,plaque area,plaque burden and remodeling index were all significantly larger in culprit lesions of ACS patients than those of SA patients (all P0.05). Positive remodeling was more frequent in ACS patients than in SA patients,whereas negative remodeling was more frequent in SA patients (P0.05). The serum levels of hs-CRP,MMP-9,sCD40L were higher in ACS group compared with SA group (P0.05,respectively). Moreover,hs-CRP level was positively correlated with MMP-9 (r=0.671,P=0.000) and sCD40L (r=0.494,P=0.008),respectively,in ACS patients. There was no difference in TIMP-1 between two groups (P=0.234). Conclusions These results suggest that structurally vulnerable plaques are essential element in the pathogenesis of ACS and inflammation might play an important role in plaque vulnerability.
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Objective To elucidate the effect of inflammation and coronary atherosclerotic plaque destabilization in the pathogenesis of acute coronary syndromes (ACS).Methods Twenty-eight patients with ACS and 13 patients with stable angina pectoris (SA) were examined by intravascular ultrasound (IVUS). Coronary plaque morphology and areas in culprit lesions were analyzed. The serum levels of hs-CRP,MMP-9,TIMP-1,sCD40L were also measured.Results Soft plaques were dominant in culprit lesions of ACS patients (71.4%,20/28),and hard plaques were dominant in culprit lesions of SA patients [76.9% (10/13),P=0.004].At the culprit site,plaque area,plaque burden and remodeling index were all significantly larger in culprit lesions of ACS patients than those of SA patients (all P0.05). Positive remodeling was more frequent in ACS patients than in SA patients,whereas negative remodeling was more frequent in SA patients (P0.05). The serum levels of hs-CRP,MMP-9,sCD40L were higher in ACS group compared with SA group (P0.05,respectively). Moreover,hs-CRP level was positively correlated with MMP-9 (r=0.671,P=0.000) and sCD40L (r=0.494,P=0.008),respectively,in ACS patients. There was no difference in TIMP-1 between two groups (P=0.234). Conclusions These results suggest that structurally vulnerable plaques are essential element in the pathogenesis of ACS and inflammation might play an important role in plaque vulnerability.
Key concepts: Culprit, Pathogenesis, Acute coronary syndrome, Medicine, Internal medicine, Inflammation, Intravascular ultrasound, Fibrous cap