Key result
Obesity combined with hypertension reduces post-MI survival to ~29% in mice.
Why the study?
Obesity and hypertension are risk factors for myocardial infarction, but their potential interactions on post-MI outcomes remain unclear.
Does the combination of obesity and hypertension worsen post-MI survival and cardiac remodeling compared to obesity alone or lean controls in mice?
Does the combination of obesity and hypertension worsen post-MI survival and cardiac remodeling compared to obesity alone or lean controls in mice?
In a mouse model of MI, obesity reduces survival but improves cardiac function and metabolism in survivors, whereas concurrent hypertension attenuates these favorable metabolic pathways and worsens remodeling.
Answers are grounded in this paper and cite their sources.
Should not alter post-MI care in obese-hypertensive patients; leaves open translation of mouse survival effects to humans.
Background Obesity 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 Results Male 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. Conclusions Obesity 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.
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Mouton et al. (2021) studied Myocardial Infarction. High-fat/fructose diet and angiotensin II infusion vs. Standard chow and saline was evaluated on 7-day survival rate post-myocardial infarction (males) (p=<0.05). In mice, obesity alone reduced 7-day post-myocardial infarction survival compared to a normal diet, and the presence of hypertension further decreased survival to 29% in males and 35% in females.
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