Microscopic analysis of the myocardial bridges and their relationship with atheromatous plaque / Análisis microscópico de los puentes miocárdicos y su relación con la placa ateromatosa

SUMMARY: Most histopathological studies have reported that the segment of the coronary artery below the myocardial bridge does not present atheromatous plaque, while the segment proximal to the myocardial bridge may have it. The aim of this study was to evaluate the microscopic environment of myocardial bridges. This descriptive study was carried out with 60 hearts of individuals who underwent autopsy at the National Institute of Legal Medicine and Forensic Sciences in Bucaramanga-Colombia. For each specimen, the coronary arteries and their branches were dissected, removing the subepicardial adipose tissue to identify the myocardial bridges and obtain histological sections of the compromised arterial branches. The presence of myocardial bridges was observed in 22 hearts (36.7%) with a length of 17.31 + 4.41 mm and a thickness of 904.57 + 312.27 mm. The coronary vessel caliber at the prepontine level was 246.57 + 49.33 mm and was significantly higher than in the pontine (188.92 + 60.55 mm) and postpontin (190.40 + 47 mm) segments (p=0.001 for both values). Atheromatous plaque was observed in the prepontine segment in 12 cases (46.15 %) and in 8 samples (30.76%) at the pontine level, but in this segment, there was slight damage to the vascular endothelium, or phase I level. The thickness of the tunica intima in the cases with atheromatous plaque was 15.68 + 13.39 mm and that of the plaque-free segments was 5.10 + 4.40 mm (p=0.005), and in the pontine segment the overlying periarterial adipose tissue had a thickness of 72.01 + 69.44 mm, which was higher than the other three locations (p=0.005). The morphometry of the perivascular fat pad and the presence of phase I atheromatous plaque are the main contributions of this study to the histology of myocardial bridges.

RESUMEN: La mayoría de los estudios histopatológicos han reportado que el segmento de la arteria coronaria debajo del puente miocárdico no presenta placa ateromatosa, mientras que el segmento proximal al puente miocárdico puede tenerla. El objetivo de este estudio fue evaluar el entorno microscópico de los puentes miocárdico. Este estudio descriptivo se realizó con 60 corazones de individuos a quienes se les práctico autopsia en el Instituto Nacional de Medicina Legal y Ciencias Forenses de Bucaramanga-Colombia. Para cada espécimen se realizó disección de las arterias coronarias y sus ramas, eliminando el tejido adiposo subepicárdico para identificar los puentes miocárdicos y obtener secciones histológicas de las ramas arteriales comprometidas. Se observó presencia de puentes miocárdicos en 22 corazones (36,7 %) con una longitud de 17.31 + 4.41 mm y un espesor de 904.57 + 312.27 mm. El calibre del vaso coronario a nivel prepontino fue 246.57 + 49.33 mm y fue significativamente mayor que en el segmento pontino (188.92 + 60.55 mm) y pospontino (190.40 + 47 mm) (p=0.001 para ambos valores). Se observó placa ateromatosa en el segmento prepontino en 12 casos (46.15 %) y en 8 muestras (30.76%) al nivel pontino, pero en este segmento, correspondieron a fase I, con ligero daño en el endotelio vascular. El espesor de la túnica íntima en los casos con placa ateromatosa fue de 15.68 + 13.39 mm y de los segmentos libres de placa fue 5.10 + 4.40 mm (p=0.005) y en el segmento pontino el tejido adiposo periarterial suprayacente presento un espesor de 72.01 + 69.44 mm, el cual fue mayor a las otras tres ubicaciones (p=0.005). La morfometría de la almohadilla adiposa perivascular y la presencia de placa ateromatosa en fase I son los principales aportes de este estudio a la histología de los puentes miocárdicos.

Progress of residual inflammatory cardiovascular risk / 医学研究生学报

Coronary artery disease (CAD) remains a leading cause of morbidity and mortality in the world. Although the comprehensive control of cardiovascular disease risk factors has achieved remarkable progress in recent years, the incidence of cardiovascular events is still high after the control of traditional risk factors such as low density lipoprotein cholesterol, blood pressure and blood glucose, collectively referred to as cardiovascular residual risk. Inflammation is a central driver of atherosclerosis and the ultimate rupture of plaque, as well as an important cause of residual cardiovascular risk. Therefore, this article reviews the formation, assessment and treatment of residual inflammatory cardiovascular risk.