Caracterização tecidual e fenotípica in vivo da placa aterosclerótica em pacientes com infarto agudo do miocárdio: análise pelo ultrassom intravascular utilizando o mapeamento tecidual iMAP®

• Ano de defesa: 2016
• Autor(a) principal: Souza, Cristiano Freitas de [UNIFESP]
• Tipo de documento: Tese
• Tipo de acesso: Acesso aberto
• dARK ID: ark:/48912/00130000299mw
• Idioma: por
• Instituição de defesa: Universidade Federal de São Paulo (UNIFESP)
• Palavras-chave em Português: Coronary disease; Myocardial infarction; Ultrassonography; Coronary vessel; Plaque; Atherosclerotic; Computer-assisted image processing; Doença das coronárias; Infarto do miocárdio; Vasos coronários/ultrassonografia; Placa aterosclerótica; Processamento de imagem assistida por computador
• Link de acesso: https://sucupira.capes.gov.br/sucupira/public/consultas/coleta/trabalhoConclusao/viewTrabalhoConclusao.jsf?popup=true&id_trabalho=3816175; https://repositorio.unifesp.br/handle/11600/47129

Background: There is limited data on plaque tissue characterization and phenotype classification using radiofrequency iMAP-IVUS?. Methods: In the iWonder study patients presenting with non-ST-elevation myocardial infarction (STEMI) or STEMI underwent 3-vessel grayscale IVUS and iMAP-IVUS? tissue characterization prior to percutaneous intervention. In total, 385 lesions from 100 patients were divided into culprit (n=100) and non-culprit (n=285) lesions. Lesion phenotype was classified in a hierarchical fashion into: (1) TCFA (thin-cap fibroatheroma ? at least 1 frame with >30° of necrotic core [NC] abutting to the lumen); (2) ThCFA (NC >10%, confluent dense calcium [DC] >10%, well-defined fibrous cap); (3) PIT (pathological intimal thickening ? mainly fibrofatty tissue, <10% confluent NC); (4) fibrotic plaque (mainly fibrous tissue, <10% confluent NC, <10% confluent DC) and (5) fibrocalcific plaque (mainly fibrous tissue, >10% confluent DC and <10% confluent NC). Results: Culprit lesions had smaller minimum lumen area with greater plaque burden compared to non-culprit lesions. Volumetric analysis showed that culprit lesions had longer length and larger vessel and plaque volumes compared to non-culprit lesions. iMAP-IVUS? revealed that culprit lesions presented more NC and fibrofatty volume, both at lesion level and at the minimum lumen area (MLA) site (all p<0.001). Any fibroatheroma was more frequently identified in the culprit lesions compared to non-culprit lesions (93% vs. 78.9%, p=0.001). Also, a TCFA was more prevalent within culprit vs. non-culprit lesions (39.0% vs. 19.0%, p<0.001) anywhere within the lesion as well as at the MLA site (18.0% vs. 9.5%, p=0.07). Conclusion: Three-vessel radiofrequency iMAP-IVUS? study demonstrated a greater plaque burden and higher prevalence of any fibroatheroma as well as TCFAs in culprit vs non-culprit lesions in patients presenting with STEMI or non-STEMI and undergoing percutaneous intervention.