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Journal Article
Research Support, Non-U.S. Gov't
Significance of intraplaque neovascularisation for vulnerability: optical coherence tomography study.
Heart 2012 October
OBJECTIVES: This study aimed to investigate the role of intraplaque neovascularisation (NV) in culprit lesions and non-culprit lesions of unstable angina pectoris (UAP) and in lesions of stable angina pectoris (SAP) using optical coherence tomography (OCT).
DESIGN: This study was a retrospective study.
SETTING: The significance of NV for culprit and non-culprit plaques remains unclear.
PARTICIPANTS: A total of 356 plaques from 92 UAP patients and 25 SAP patients who underwent OCT imaging were divided into three groups: culprit lesions in UAP (92), non-culprit lesions in UAP (203) and lesions of SAP (61).
MAIN OUTCOME MEASURES: NV and plaque characteristics were examined by OCT and plaques with and without NV were compared.
RESULTS: Among UAP culprit lesions, plaques with NV had significantly higher incidence of thin cap fibroatheroma (81% vs 47%, p=0.002) compared with those without NV. In addition, the fibrous cap was thinner (56±20 μm vs 75±30 μm, p<0.001), lipid arc was greater (254±66° vs 222±65°, p=0.024) and lipid core length was longer (13±5 mm vs 10±6 mm, p=0.007). No significant difference was observed between non-culprit lesions of UAP with and without NV, and between lesions of SAP with and without NV.
CONCLUSION: In patients with UAP, the culprit plaques with NV had vulnerable features such as thinner fibrous cap, greater lipid arc, longer lipid core length and more frequent thin cap fibroatheroma compared with those without NV. In both non-culprit lesions of UAP patients and in lesions of SAP patients NV was not associated with vulnerable plaque characteristics.
DESIGN: This study was a retrospective study.
SETTING: The significance of NV for culprit and non-culprit plaques remains unclear.
PARTICIPANTS: A total of 356 plaques from 92 UAP patients and 25 SAP patients who underwent OCT imaging were divided into three groups: culprit lesions in UAP (92), non-culprit lesions in UAP (203) and lesions of SAP (61).
MAIN OUTCOME MEASURES: NV and plaque characteristics were examined by OCT and plaques with and without NV were compared.
RESULTS: Among UAP culprit lesions, plaques with NV had significantly higher incidence of thin cap fibroatheroma (81% vs 47%, p=0.002) compared with those without NV. In addition, the fibrous cap was thinner (56±20 μm vs 75±30 μm, p<0.001), lipid arc was greater (254±66° vs 222±65°, p=0.024) and lipid core length was longer (13±5 mm vs 10±6 mm, p=0.007). No significant difference was observed between non-culprit lesions of UAP with and without NV, and between lesions of SAP with and without NV.
CONCLUSION: In patients with UAP, the culprit plaques with NV had vulnerable features such as thinner fibrous cap, greater lipid arc, longer lipid core length and more frequent thin cap fibroatheroma compared with those without NV. In both non-culprit lesions of UAP patients and in lesions of SAP patients NV was not associated with vulnerable plaque characteristics.
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