El Shahawy Mahfouz, Tucker Susan, Izadi Lillee, Sabatini Antonella, Mohan Sukanya
Cardiovascular Center of Sarasota, 1950 Arlington Street, Suite 300, Sarasota, FL, 34239, USA.
Lake Erie College of Osteopathic Medicine, Bradenton, FL, USA.
Egypt Heart J. 2021 Apr 13;73(1):37. doi: 10.1186/s43044-021-00159-4.
Excess epicardial fat volume (EFV) has been recently implicated in cardiovascular structural and functional abnormalities. It has been associated with abnormal microvascular stiffness (as reflected by radial artery waveform; C2), which may result in microvascular dysfunction and contribute to the atypical chest pain syndrome without obstructive coronary artery disease (CAD). Women have been statistically shown to present with atypical chest pain more often than men and specifically without obstructive CAD. The aim of this study is to assess whether excess EFV in female subjects is associated with significant microvascular dysfunction (i.e., C2), in subjects without obstructive CAD.
We screened 596 asymptomatic subjects, ages 20-79, using the Early Cardiovascular Health Risk Scoring System (ECVHRS), which has been reported. Out of the 596 total subjects, 230 subjects had a CACS. Out of these 230 subjects, 77 subjects (45 females; 32 males) had a 0 CACS. The 45 females from this cohort were the subjects of this study, and they were further categorized into 3 groups: group 1 (normal EFV, non-obese female subjects; n=16), females with ECVHRS < 3 and ACC/AHA risk score < 5%; group 2 (n = 9), females with elevated EFV and no abdominal visceral obesity; and group 3 (n=20), females with elevated EFV and abdominal visceral obesity. The average EFV was determined to be 72±20 cm among group 1, which indicates the values for normal EFV. The results in group 2 indicate that excess EFV is contributing to the development of microvascular dysfunction, resulting in abnormal micro-arterial (C2) elasticity (p< 0.00001), increase in resting blood pressure (p =0.0001), an abnormal rise in blood pressure (BP) at rest and post-mild protocol exercise (PME) (p = < 0.00001), and abnormal increase in carotid intima-media thickness (CIMT) (p = 0.000164).
Excess EFV appears to be not only a novel cardiovascular risk marker, but also the culprit for other cardiovascular risk markers. Based on these findings, elevated EFV may contribute to the development of the atypical chest pain syndrome in females without obstructive CAD. Additionally, EFV is emerging as a potential clinically relevant significant cardiovascular risk biomarker and may become a target to reduce cardiovascular morbidity and mortality.
近期研究表明，心外膜脂肪体积（EFV）超标与心血管结构和功能异常有关。它与微血管僵硬度异常（通过桡动脉波形反映；C2）相关，这可能导致微血管功能障碍，并引发无阻塞性冠状动脉疾病（CAD）的非典型胸痛综合征。统计学显示，女性比男性更常出现非典型胸痛，尤其是无阻塞性CAD的情况。本研究旨在评估无阻塞性CAD的女性受试者中，EFV超标是否与显著的微血管功能障碍（即C2）相关。
我们使用已报道的早期心血管健康风险评分系统（ECVHRS）对596名年龄在20 - 79岁的无症状受试者进行了筛查。在596名受试者中，230名受试者有冠状动脉钙化评分（CACS）。在这230名受试者中，77名受试者（45名女性；32名男性）的CACS为0。该队列中的45名女性成为本研究的对象，她们被进一步分为3组：第1组（正常EFV，非肥胖女性受试者；n = 16），ECVHRS < 3且ACC/AHA风险评分 < 5%的女性；第2组（n = 9），EFV升高且无腹部内脏肥胖的女性；第3组（n = 20），EFV升高且有腹部内脏肥胖的女性。第1组的平均EFV被确定为72±20 cm，表明为正常EFV值。第2组的结果表明，EFV超标导致微血管功能障碍的发展，导致微动脉（C2）弹性异常（p < 0.00001）、静息血压升高（p = 0.0001）、静息和轻度方案运动后（PME）血压异常升高（p = < 0.00001）以及颈动脉内膜中层厚度（CIMT）异常增加（p = 0.000164）。
EFV超标似乎不仅是一种新的心血管风险标志物，也是其他心血管风险标志物的罪魁祸首。基于这些发现，EFV升高可能导致无阻塞性CAD的女性发生非典型胸痛综合征。此外，EFV正在成为一种潜在的临床相关重要心血管风险生物标志物，并可能成为降低心血管发病率和死亡率的靶点。
