BackgroundObesity and hypertension are risk factors for myocardial infarction (MI); however, their potential interactions on post‐MI outcomes are unclear. We examined interactions of obesity and hypertensionon post‐MI function, remodeling, metabolic changes, and recovery.Methods and ResultsMale and female C57BL/6J mice were provided standard chow or high‐fat/fructose diet for 8 weeks and then infused with angiotensin II for 2 weeks to induce hypertension. MI was then induced by surgical ligation of the left coronary artery for 7 days. Obesity alone did not cause cardiac injury or exacerbate hypertension‐induced cardiac dysfunction. After MI, however, obese‐normotensive mice had lower survival rates compared with chow‐fed mice (56% versus 89% males; 54% versus 75% females), which were further decreased by hypertension (29% males; and 35% females). Surviving obese‐normotensive males displayed less left ventricular dilation and pulmonary congestion compared with chow‐fed males after MI; hypertension reversed left ventricular dilation because of high‐fat/fructose diet and promoted significant pulmonary congestion compared with chow‐fed controls. Obese‐normotensive males displayed higher left ventricular α‐MHC (alpha‐myosin heavy chain) protein, phosphorylated Akt (protein kinase B) and AMPK (adenosine‐monophosphate activated kinase), PPAR‐γ (peroxisome proliferator activated receptor gamma), and plasma adiponectin levels after MI, indicating favorable contractile and metabolic changes. However, these favorable contractile and metabolic changes were attenuated by hypertension. Obese‐hypertensive males also had lower levels of collagen in the infarcted region, indicating decreased ability to promote an adaptive wound healing response to MI.ConclusionsObesity reduces post‐MI survival but is associated with improved post‐MI cardiac function and metabolism in surviving normotensive mice. When hypertension accompanies obesity, favorable metabolic pathways associated with obesity are attenuated and post‐MI cardiac function and remodeling are adversely impacted.

中文翻译：

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肥胖和高血压对心肌梗死后心脏代谢重构和存活的相互作用

背景肥胖和高血压是心肌梗死 (MI) 的危险因素；然而，它们对 MI 后结果的潜在相互作用尚不清楚。我们检查了肥胖和高血压对 MI 后功能、重塑、代谢变化和恢复的相互作用。 2周诱发高血压。然后通过手术结扎左冠状动脉 7 天诱导 MI。肥胖本身不会导致心脏损伤或加剧高血压引起的心脏功能障碍。然而，在 MI 后，与饲料喂养的小鼠相比，肥胖正常血压小鼠的存活率较低（雄性为 56% 对 89%；雌性为 54% 对 75%），而高血压进一步降低了存活率（雄性为 29%；雌性为 35%） ）。与 MI 后进食食物的男性相比，存活的肥胖正常血压男性表现出较少的左心室扩张和肺充血；与饲料喂养的对照组相比，高血压逆转了高脂肪/果糖饮食引起的左心室扩张，并促进了显着的肺充血。肥胖正常血压男性显示出较高的左心室 α-MHC（α-肌球蛋白重链）蛋白、磷酸化 Akt（蛋白激酶 B）和 AMPK（腺苷单磷酸激活激酶）、PPAR-γ（过氧化物酶体增殖物激活受体 γ）和血浆MI 后脂联素水平，表明有利的收缩和代谢变化。然而，这些有利的收缩和代谢变化因高血压而减弱。肥胖高血压男性梗塞区域的胶原蛋白水平也较低，表明促进对 MI 的适应性伤口愈合反应的能力降低。结论肥胖会降低 MI 后的存活率，但与存活的正常血压小鼠的 MI 后心脏功能和新陈代谢的改善有关。当高血压伴随肥胖时，与肥胖相关的有利代谢途径减弱，MI 后心脏功能和重塑受到不利影响。