Differences in intravascular ultrasound and histological findings in culprit coronary plaques between ST-segment elevation myocardial infarction and stable angina
A comprehensive evaluation of culprit coronary lesions may help to understand vulnerable plaques responsible for ST-segment elevation myocardial infarction (STEMI). We compared intravascular ultrasound (IVUS) and histological findings in culprit coronary plaques from 94 patients with STEMI (n = 54) or stable angina (n = 40). Tissue specimens were obtained by directional coronary atherectomy and IVUS was performed before percutaneous coronary intervention. IVUS and histological data were analyzed. Clinical characteristics were largely similar between the two groups. Plaque rupture and thrombi were more frequently found in the STEMI group than in the stable angina group. There were no significant differences between plaque types or proximal and distal reference measurements in the two groups. However, the site of minimal lumen area had a greater vessel area, remodeling index, and plaque burden with lesser lumen area in the STEMI group than in the stable angina group. Plaque areas immunopositive for CD68 and CD31 were significantly larger in the STEMI group, while the area immunopositive for α-smooth muscle actin was larger in the stable angina group. In conclusion, culprit lesions in STEMI patients showed a greater plaque burden, remodeling index, and more frequent thrombi with increased inflammation and neovascularization compared to the stable angina group, supporting the current concept of vulnerable plaques being responsible for STEMI.
KeywordsHistology Intravascular ultrasound Myocardial infarction
This study was supported by a grant from the CardioVascular Research Foundation, and the Korea Health 21 R&D Project, Ministry of Health & Welfare, Republic of Korea (H13C1371).
Conflict of interest
- 1.Schaar JA, Muller JE, Falk E, Virmani R, Fuster V, Serruys PW, Colombo A, Stefanadis C, Ward Casscells S, Moreno PR, Maseri A, van der Steen AF (2003) Terminology for high-risk and vulnerable coronary artery plaques: report of a meeting on the vulnerable plaque, June 17 and 18, Santorini Greece. Eur Heart J 2004(25):1077–1082Google Scholar
- 7.Kotani J, Mintz GS, Castagna MT, Pinnow E, Berzingi CO, Bui AB, Pichard AD, Satler LF, Suddath WO, Waksman R, Laird JR Jr, Kent KM, Weissman NJ (2003) Intravascular ultrasound analysis of infarct-related and non-infarct-related arteries in patients who presented with an acute myocardial infarction. Circulation 107:2889–2893PubMedCrossRefGoogle Scholar
- 8.Fujii K, Kobayashi Y, Mintz GS, Takebayashi H, Dangas G, Moussa I, Mehran R, Lansky AJ, Kreps E, Collins M, Colombo A, Stone GW, Leon MB, Moses JW (2003) Intravascular ultrasound assessment of ulcerated ruptured plaques: a comparison of culprit and nonculprit lesions of patients with acute coronary syndromes and lesions in patients without acute coronary syndromes. Circulation 108:2473–2478PubMedCrossRefGoogle Scholar
- 11.Tunstall-Pedoe H, Morrison C, Woodward M, Fitzpatrick B, Watt G (1991) Sex differences in myocardial infarction and coronary deaths in the Scottish MONICA population of Glasgow 1985 to 1991. Presentation, diagnosis, treatment, and 28-day case fatality of 3991 events in men and 1551 events in women. Circulation 1996(93):1981–1992Google Scholar