According to post-mortem studies, luminal thrombosis occurs from plaque rupture, erosion and calcified nodules. In vivo studies have found thin cap fibroatheroma (TCFA) as the main vulnerable lesion, prone to rupture. Few data about other post-mortem lesions have been reported in vivo. Our main objective is to characterize in vivo the coronary plaques with intravascular ultrasound-virtual histology (IVUS-VH) and optical coherence tomography (OCT), in order to detect not only thin cap fibroatheroma (TCFA), but also other possible vulnerable lesions. The secondary objective is to correlate these findings with clinical and analytical data. Twenty-five patients (18 stable) submitted to coronary angiography were included in this pilot study. After angiography, the three vessels were studied (when possible) with IVUS-VH and OCT. Plaque characteristics were correlated with clinical and analytical data. Forty-six lesions were analyzed. IVUS-VH detected significant necrotic core in 15 (3 were definite TCFA). OCT detected TCFA in 10 lesions, erosion in 6, thrombus in 5 and calcified nodule in 8. Possible vulnerable lesion was found in 61% of stable and 57% of unstable patients. Erosions and calcified nodules were only found in stable patients. Those with significant necrotic core had higher body mass index (P=0.016), higher levels of hs-CRP (P=0.019) and triglycerides (P=0.040). The higher the levels of hs-CRP, the larger the size of the necrotic core (r=0.69, P=0.003). Lesions with characteristics of vulnerability were detected by IVUS-VH and OCT in more than 50% of stable and unstable coronary patients. A significant necrotic core was mainly correlated with higher hs-CRP.
Introducción y objetivos. La reserva de flujo coronario (RFC) se reduce no sólo en la cardiopatía isquémica, sino también en otras cardiopatías, con o sin insuficiencia cardíaca. El objetivo del estudio fue comprobar si la gravedad de la insuficiencia cardíaca influye en el deterioro de la RFC.Métodos. Se estudió a 40 pacientes diagnosticados de cardiopatía no isquémica e insuficiencia cardíaca, en 41 ocasiones distintas. Fueron repartidos en 4 grupos: 1. 10 pacientes en grado funcional III-IV; 2. 10 pacientes en grado funcional II sin tratamiento con bloqueadores beta; 3. 11 pacientes en grado funcional II tratados con carvedilol, y 4. 10 pacientes en grado funcional I, que previamente habían tenido insuficiencia cardíaca por disfunción sistólica. El flujo miocárdico (FM) se midió mediante tomografía por emisión de positrones (PET) y N-13 amonio: en condiciones basales y durante la infusión de trifosfato de adenosina (ATP).Resultados. El FM máximo y la RFC fueron significativamente más altos en el grupo 4 (1,95 ± 0,58 y 2,40 ± 0,95 ml/min/g) que en el grupo 1 (1,02 ± 0,52 y 1,46 ± 0,48 ml/min/g). La RFC tuvo tendencia a ser mayor en los grupos 2 (1,73 ± 0,72) y 3 (1,89 ± 0,75) que en el grupo 1. No hubo correlación significativa entre la RFC y las siguientes variables: edad, presión arterial sistólica, índice de masa ventricular, índices de volumen y fracción de eyección de ventrículo izquierdo.Conclusiones. La función microvascular coronaria está alterada en la insuficiencia cardíaca no isquémica, y dicha alteración se relaciona con la situación funcional, cualquiera que sea la cardiopatía subyacente.
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