Clinical & Experimental Cardiology

Clinical & Experimental Cardiology
Open Access

ISSN: 2155-9880

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Adventitial Inflammation of the Coronary Arteries in Patients, with and without Diabetes Mellitus, Who Died of Acute Coronary Disease: A Reliable Marker of Active, Progressive, Atherosclerotic Disease

Richard J. Frink

Background: Atherosclerosis is a progressive, chronic inflammatory disease, but it is not yet possible to identify specific plaques with active, progressive, disease. Adventitial inflammation (AI) is a component of the chronic inflammatory response and may be useful in identifying the actively growing, vulnerable plaque, with impending disruption. Methods: The hearts of 61 patients who died of acute coronary disease (ACD), 18 diabetic and 43 non-diabetic, and 22 control patients were obtained fresh and uncut at the autopsy table. The coronary arteries were injected with a colored barium-gelatin mass and the heart fixed in formalin. After fixation, the coronary arteries were dissected intact, decalcified, cut at 2-3 mm intervals, and all segments mounted for microscopic study to determine the frequency of AI and its relationship to the overall plaque burden (PB), the PB in the proximal and distal segments of each coronary artery, and all plaque disruptions (PD). Results: AI was present in 50% of 5,466 coronary segments in these 61 patients compared to 16% in the control patients. Patients with diabetes had a greater PB, P=<0.02, and more extensive AI than non-diabetics, p<0.001, in both proximal and distal segments. There was a direct relationship between PB and AI in both diabetic and nondiabetic patients, but was significantly greater in diabetic patients, p=<0.001. Multiple PD’s, 148, were present in these 61 patients and 95% were associated with AI, but there was no significant difference in the frequency of PD’s in diabetic compared to non-diabetic patients. Conclusions: AI appears to be a reliable histologic marker of active, progressive, atherosclerotic disease and may be helpful in identifying the vulnerable plaque with impending disruption. Diabetes accelerates atherosclerotic disease, but does not accelerate PD