Department of Internal Diseases, Hypertension and Vascular Diseases, Medical University of Warsaw, Warsaw, Poland.
Department of General, Transplant and Liver Surgery, Medical University of Warsaw, Warsaw, Poland.
Cardiology. 2024;149(1):23-27. doi: 10.1159/000534645. Epub 2023 Oct 19.
Obesity is one of the major risk factors for the development of heart failure (HF), although the exact underlying mechanism remains unclear. In the clinical setting, assessing the impact of obesity on the cardiovascular system is difficult due to comorbidities.
The purpose of this study was to evaluate an independent influence of obesity on the left ventricular (LV) morphology and function. To eliminate hemodynamic and metabolic confounders, we performed an echocardiographic evaluation of severely obese but normotensive and metabolically healthy patients without fatty liver disease.
The patients were retrospectively selected from the cohort of 180 consecutive obese patients systematically evaluated with transthoracic echocardiography before bariatric surgery. Finally, 25 obese subjects, predominantly females, were evaluated with transthoracic echocardiography. Inclusion criteria were defined as absence of diabetes, hypertension, and hyperlipidemia, no use of medications and no hepatic steatosis on liver biopsy. They were matched with a control group of healthy subjects with normal body mass index.
In obese patients, LV hypertrophy (LVH) (expressed as LV mass indexed for height in meters2.7) was significantly more frequent in the obese group (48 vs. 0%, p < 0.001). LV longitudinal systolic function measured by mitral annular systolic velocity was significantly lower in the obese group (S' 8.5 vs. 9.7 cm/s, p = 0.002). All studied indices of the LV diastolic function (E/A, mean E' and E/E' ratio) were impaired in obese subjects, even after adjustment for systolic blood pressure and heart rate (E/A 1.31 vs. 1.64, p < 0.001, E' mean 11 vs. 14.8 cm/s, p < 0.001, E/E' 7.5 vs. 6.4, p = 0.002 for obese vs. controls, respectively).
LVH is significantly more common, and LV diastolic and longitudinal systolic function is significantly impaired in young, metabolically healthy, normotensive, severely obese individuals without fatty liver disease when compared to age and sex-matched lean subjects. These abnormalities may represent the independent effect of the obesity on the heart, which may contribute to the development the obesity-related HF in later life.
肥胖是心力衰竭（HF）发展的主要危险因素之一，尽管其确切的潜在机制仍不清楚。在临床环境中，由于合并症的存在，评估肥胖对心血管系统的影响较为困难。
本研究旨在评估肥胖对左心室（LV）形态和功能的独立影响。为了消除血流动力学和代谢混杂因素，我们对非脂肪肝且血压正常和代谢健康的重度肥胖患者进行了超声心动图评估。
从接受过减重手术的 180 例连续肥胖患者的队列中回顾性选择患者。最终，对 25 名主要为女性的肥胖患者进行了经胸超声心动图评估。纳入标准定义为无糖尿病、高血压和高血脂，无药物使用且肝活检无肝脂肪变性。将这些患者与具有正常体重指数的健康对照组进行匹配。
在肥胖患者中，LV 肥厚（LVH）（表示为以米为单位的身高 2.7 指数化的 LV 质量）在肥胖组中更为常见（48%比 0%，p < 0.001）。LV 纵向收缩功能通过二尖瓣环收缩速度测量，在肥胖组中明显较低（S' 8.5 比 9.7cm/s，p = 0.002）。即使在调整了收缩压和心率后，肥胖患者的所有 LV 舒张功能研究指标（E/A、平均 E' 和 E/E' 比值）均受损（E/A 1.31 比 1.64，p < 0.001，E' mean 11 比 14.8cm/s，p < 0.001，E/E' 7.5 比 6.4，p = 0.002 为肥胖组与对照组）。
与年龄和性别匹配的瘦对照组相比，在无脂肪肝的年轻、代谢健康、血压正常、重度肥胖个体中，LVH 更为常见，LV 舒张和纵向收缩功能明显受损。这些异常可能代表肥胖对心脏的独立影响，可能导致肥胖相关 HF 在以后的生活中发生。
