Is There an Obesity Paradox in Cardiogenic Shock?

C. Lavie, A. daSilva-deAbreu, H. Ventura, M. Mehra
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引用次数: 1

Abstract

Obesity has reached epidemic levels in the United States and in much of the Westernized world.1– 3 The majority of the US population is now either overweight or obese (75%), and 42% meet the current body mass index criteria (BMI ≥30 kg/m2) for obesity, with 9% meeting criteria for severe, class III obesity (formerly called morbid obesity with a BMI ≥40 kg/ m2 or a BMI of 35 kg/m2 or higher and experiencing obesityrelated health conditions).1 Obesity adversely influences cardiovascular diseases (CVD) by its intersection with major CVD risk factors, including worsening of arterial pressure and glucose intolerance, thus leading to metabolic syndrome and diabetes and worsening lipids, especially triglyceride levels. Not only is obesity associated with worsening inflammation, but it also increases the prevalence of hypertension and coronary heart disease, all of which conspire to cause heart failure (HF). Thus, obesity increases the risk of HF, especially HF with preserved ejection fraction (EF) more so than HF with reduced EF. As reviewed elsewhere3,4 obesity is associated with development of atrial fibrillation, worsened renal function, venous thromboembolism, and respiratory illness, all of which alone and together can worsen HF prognosis. Despite the increased health risks associated with obesity, considerable focus has centered on the “obesity paradox” (wherein individuals with overweight or obesity and CVD have a better shortand mediumterm prognosis than do leaner patients with the same degree of disease) among patients with CVD, endstage renal disease, pulmonary diseases (including chronic obstructive pulmonary disease), and complications from infections.2,3,5– 8 Particularly, an obesity paradox has been noted with both HF with reduced EF and HF with preserved EF, manifest by a lower overall and CVDmortality in people who are overweight or mildly obese, whereas hospitalizations seem to be increased as obesity progresses to severe.9,10 In advanced stages of HF and especially in states of therapy for such a condition such as use of left ventricular assist devices or heart transplantation, the presence of obesity perpetuates complications and worsens survival.11,12 Similarly, an obesity paradox has not been demonstrated in cardiogenic shock. Recently, Sreenivasan and colleagues13 did not find an obesity paradox in a large US population of cardiogenic shock (CS) compared with those who were nonobese, and moderate and severe obesity had progressively higher mortality.13,14 In this issue of the Journal of the American Heart Association (JAHA), Kwon and colleagues15 studied 1227 patients with CS from a South Korean registry and classified patients as obese (BMI ≥25 kg/m2 based
心源性休克是否存在肥胖悖论?
肥胖在美国和大部分西化国家已经达到了流行病的程度。1 - 3目前,大多数美国人口要么超重,要么肥胖(75%),42%符合当前肥胖的体重指数标准(BMI≥30 kg/m2), 9%符合严重的III类肥胖标准(以前称为病态肥胖,BMI≥40 kg/m2或BMI为35 kg/m2或更高,并经历与肥胖相关的健康状况)肥胖通过与主要心血管疾病危险因素(包括动脉压恶化和葡萄糖耐受不良)的交叉对心血管疾病(CVD)产生不利影响,从而导致代谢综合征和糖尿病,并导致血脂,特别是甘油三酯水平恶化。肥胖不仅与炎症恶化有关,而且还会增加高血压和冠心病的患病率,所有这些都会导致心力衰竭(HF)。因此,肥胖增加HF的风险,尤其是保留射血分数(EF)的HF比射血分数降低的HF更明显。如其他文献所述3,4肥胖与房颤、肾功能恶化、静脉血栓栓塞和呼吸系统疾病的发生有关,所有这些单独或共同可使心衰预后恶化。尽管与肥胖相关的健康风险增加,但在患有心血管疾病、终末期肾病、肺部疾病(包括慢性阻塞性肺病)和感染并发症的患者中,相当多的焦点集中在“肥胖悖论”上(超重或肥胖合并心血管疾病的个体比患有相同疾病程度的苗条患者有更好的短期和中期预后)。2,3,5 - 8特别值得一提的是,对于心力衰竭降低的心衰和心力衰竭保留的心衰,肥胖悖论已经被注意到,表现为超重或轻度肥胖患者的总体和心血管死亡率较低,而随着肥胖进展到严重,住院治疗似乎增加。9,10在心衰晚期,特别是在使用左心室辅助装置或心脏移植等治疗阶段,肥胖的存在使并发症持续存在并恶化生存。11,12同样,肥胖悖论在心源性休克中也未得到证实。最近,Sreenivasan和他的同事们在美国的心源性休克(CS)人群中与非肥胖者相比,并没有发现肥胖悖论,而且中度和重度肥胖的死亡率逐渐升高。13,14在本期的《美国心脏协会杂志》(JAHA)上,Kwon及其同事研究了1227名来自韩国的CS患者,并将患者分类为肥胖(BMI≥25 kg/m2)
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