RESUMEN
BACKGROUND: Prospective data on the associations of adiponectin with in-vivo measurements of degree, phenotype and vulnerability of coronary atherosclerosis are currently lacking. OBJECTIVE: To investigate the association of plasma adiponectin with virtual histology intravascular ultrasound (VH-IVUS)-derived measures of atherosclerosis and with major adverse cardiac events (MACE) in patients with established coronary artery disease. METHODS: In 2008-2011, VH-IVUS of a non-culprit non-stenotic coronary segment was performed in 581 patients undergoing coronary angiography for acute coronary syndrome (ACS, n = 318) or stable angina pectoris (SAP, n = 263) from the atherosclerosis-intravascular ultrasound (ATHEROREMO-IVUS) study. Blood was sampled prior to coronary angiography. Coronary plaque burden, tissue composition, high-risk lesions, including VH-IVUS-derived thin-cap fibroatheroma (TCFA), were assessed. All-cause mortality, ACS, unplanned coronary revascularization were registered during a 1-year-follow-up. All statistical tests were two-tailed and p-values < 0.05 were considered statistically significant. RESULTS: In the full cohort, adiponectin levels were not associated with plaque burden, nor with the various VH-tissue types. In SAP patients, adiponectin levels (median[IQR]: 2.9(1.9-3.9) µg/mL) were positively associated with VH-IVUS derived TCFA lesions, (OR[95%CI]: 1.78[1.06-3.00], p = 0.030), and inversely associated with lesions with minimal luminal area (MLA) ≤ 4.0 mm2 (OR[95%CI]: 0.55[0.32-0.92], p = 0.025). In ACS patients, adiponectin levels (median[IQR]: 2.9 [1.8-4.1] µg/mL)were not associated with plaque burden, nor with tissue components. Positive association of adiponectin with death was present in the full cohort (HR[95%CI]: 2.52[1.02-6.23], p = 0.045) and (borderline) in SAP patients (HR[95%CI]: 8.48[0.92-78.0], p = 0.058). In ACS patients, this association lost statistical significance after multivariable adjustment (HR[95%CI]: 1.87[0.67-5.19], p = 0.23). CONCLUSION: In the full cohort, adiponectin levels were associated with death but not with VH-IVUS atherosclerosis measures. In SAP patients, adiponectin levels were associated with VH-IVUS-derived TCFA lesions. Altogether, substantial role for adiponectin in plaque vulnerability remains unconfirmed.
Asunto(s)
Adiponectina/sangre , Enfermedad de la Arteria Coronaria/diagnóstico por imagen , Placa Aterosclerótica/diagnóstico por imagen , Ultrasonografía Intervencional/métodos , Anciano , Biomarcadores/sangre , Angiografía Coronaria/métodos , Enfermedad de la Arteria Coronaria/sangre , Enfermedad de la Arteria Coronaria/complicaciones , Femenino , Humanos , Modelos Logísticos , Masculino , Persona de Mediana Edad , Análisis Multivariante , Placa Aterosclerótica/sangre , Placa Aterosclerótica/complicaciones , Estudios Prospectivos , Valores de Referencia , Factores de RiesgoRESUMEN
Abstract Background: Prospective data on the associations of adiponectin with in-vivo measurements of degree, phenotype and vulnerability of coronary atherosclerosis are currently lacking. Objective: To investigate the association of plasma adiponectin with virtual histology intravascular ultrasound (VH-IVUS)-derived measures of atherosclerosis and with major adverse cardiac events (MACE) in patients with established coronary artery disease. Methods: In 2008-2011, VH-IVUS of a non-culprit non-stenotic coronary segment was performed in 581 patients undergoing coronary angiography for acute coronary syndrome (ACS, n = 318) or stable angina pectoris (SAP, n = 263) from the atherosclerosis-intravascular ultrasound (ATHEROREMO-IVUS) study. Blood was sampled prior to coronary angiography. Coronary plaque burden, tissue composition, high-risk lesions, including VH-IVUS-derived thin-cap fibroatheroma (TCFA), were assessed. All-cause mortality, ACS, unplanned coronary revascularization were registered during a 1-year-follow-up. All statistical tests were two-tailed and p-values < 0.05 were considered statistically significant. Results: In the full cohort, adiponectin levels were not associated with plaque burden, nor with the various VH-tissue types. In SAP patients, adiponectin levels (median[IQR]: 2.9(1.9-3.9) µg/mL) were positively associated with VH-IVUS derived TCFA lesions, (OR[95%CI]: 1.78[1.06-3.00], p = 0.030), and inversely associated with lesions with minimal luminal area (MLA) ≤ 4.0 mm2 (OR[95%CI]: 0.55[0.32-0.92], p = 0.025). In ACS patients, adiponectin levels (median[IQR]: 2.9 [1.8-4.1] µg/mL)were not associated with plaque burden, nor with tissue components. Positive association of adiponectin with death was present in the full cohort (HR[95%CI]: 2.52[1.02-6.23], p = 0.045) and (borderline) in SAP patients (HR[95%CI]: 8.48[0.92-78.0], p = 0.058). In ACS patients, this association lost statistical significance after multivariable adjustment (HR[95%CI]: 1.87[0.67-5.19], p = 0.23). Conclusion: In the full cohort, adiponectin levels were associated with death but not with VH-IVUS atherosclerosis measures. In SAP patients, adiponectin levels were associated with VH-IVUS-derived TCFA lesions. Altogether, substantial role for adiponectin in plaque vulnerability remains unconfirmed.
Resumo Fundamento: Faltam dados prospectivos sobre as associações de adiponectina com medidas in-vivo de grau, fenótipo e vulnerabilidade da aterosclerose coronariana. Objetivo: Investigar a associação da adiponectina plasmática com medidas de aterosclerose derivadas de ultrassonografia virtual intravascular (VH-IVUS) e eventos cardíacos adversos importantes (major adverse cardiac events - MACE) em pacientes com doença arterial coronariana estabelecida. Métodos: Em 2008-2011, a VH-IVUS de um segmento coronariano não estenótico não culpado foi realizado em 581 pacientes submetidos à angiografia coronariana para síndrome coronariana aguda (SCA, n = 318) ou angina pectoris estável (APE, n = 263) a partir do estudo de ultrassonografia aterosclerótica-intravascular (ATHEROREMO-IVUS). Sangue foi amostrado antes da angiografia coronária. Foram avaliados a carga de placa coronária, a composição tecidual, as lesões de alto risco, incluindo fibroateroma de capa fina (FCF) derivado de VH-IVUS. Mortalidade por todas as causas, SCA, e revascularização coronária não planejada foram registradas durante um ano de acompanhamento. Todos os testes estatísticos foram bicaudais e os valores de p < 0,05 foram considerados estatisticamente significativos. Resultados: Na coorte completa, os níveis de adiponectina não foram associados à carga de placa, nem a vários tipos de tecido virtual histológico. Entre os pacientes com APE, os níveis de adiponectina (mediana[IIQ]: 2,9(1,9-3,9) µg/mL) foram associados positivamente às lesões FCF derivadas de VH-IVUS, (OR[IC 95%]: 1,78[1,06-3,00], p = 0,030), e inversamente associados a lesões com área luminal mínima (ALM) ≤4,0 mm2 (OR[IC 95%]: 0,55[0,32-0,92], p = 0,025). Em pacientes com SCA, os níveis de adiponectina (mediana[IIQ]: 2,9 [1,8-4,1] µg/mL) não foram associados à carga de placa nem a componentes teciduais. A associação positive de adiponectina ao óbito esteve presente na coorte completa (HR[IC 95%]: 2,52[1,02-6,23], p = 0,045) e (limítrofe) em pacientes com APE (HR[IC 95%]: 8,48[0,92-78,0], p = 0,058). Entre pacientes com SCA, essa associação perdeu significância estatística após ajuste multivariado (HR[IC 95%]: 1,87[0,67-5,19], p = 0,23). Conclusão: Na coorte completa, os níveis de adiponectina foram associados à obito, mas não a medidas de aterosclerose por VH-IVUS. Em pacientes com APE, os níveis de adiponectina foram associados a lesões FCF derivadas de VH-IVUS. Em geral, o papel da adiponectina na vulnerabilidade da placa permanece não confirmado.