BMC cardiovascular disorders · 2016
In Vivo optical coherence tomography visualization of intraplaque neovascularization at the site of coronary vasospasm: a case report.
Клинический случайСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Tsujita Kenichi, Kaikita Koichi, Araki Satoshi, Yamada Toshihiro, Nagamatsu Suguru, Yamanaga Kenshi, Sakamoto Kenji, Kojima Sunao, Hokimoto Seiji, Ogawa Hisao
Аннотация
BACKGROUND: Coronary plaques in patients with coronary vasospastic angina have been characterized by diffuse intima-media thickening with homogeneous fibrous tissue, without confluent necrotic tissue. However, coronary vasospasm can trigger coronary thrombosis, and may play an important role in the pathogenesis of acute coronary syndromes, though the precise morphological mechanisms underlying this process remain unclear.
CASE PRESENTATION: A 43-year-old man with a history of multivessel coronary vasospastic angina had been treated with long-acting diltiazem and fluvastatin since 2004. Eleven years later, following 1 month of medication nonadherence, he experienced recurrence of rest angina and myocardial infarction, with elevated high-sensitivity troponin T. An emergency coronary angiogram demonstrated no de novo lesions, and the current episode was diagnosed as intractable sustained coronary spasm-induced anterior myocardial infarction. Optical coherence tomography imaging revealed the coronary plaque with homogeneous high-intensity signal, and a clearly visualized intraplaque neovascular microchannel (NVMC) network.
CONCLUSIONS: Neovascularization within a coronary atheroma is known to accelerate coronary atherosclerosis. The current case with coronary vasospastic angina highlights the role of NVMC formation in this process.
CASE PRESENTATION: A 43-year-old man with a history of multivessel coronary vasospastic angina had been treated with long-acting diltiazem and fluvastatin since 2004. Eleven years later, following 1 month of medication nonadherence, he experienced recurrence of rest angina and myocardial infarction, with elevated high-sensitivity troponin T. An emergency coronary angiogram demonstrated no de novo lesions, and the current episode was diagnosed as intractable sustained coronary spasm-induced anterior myocardial infarction. Optical coherence tomography imaging revealed the coronary plaque with homogeneous high-intensity signal, and a clearly visualized intraplaque neovascular microchannel (NVMC) network.
CONCLUSIONS: Neovascularization within a coronary atheroma is known to accelerate coronary atherosclerosis. The current case with coronary vasospastic angina highlights the role of NVMC formation in this process.