The Association Between a Second Course of Cardiac Rehabilitation and Cardiovascular Outcomes Following Repeat Percutaneous Coronary Intervention Events

Zhang, Wenliang; Supervía, Marta; Dun, Yaoshan; Lennon, Ryan J.; Ding, Rongjing; Sandhu, Gurpreet S.; Tilbury, Thomas; Squires, Ray W.; Vardar, Ufuk; Tabatabaei, Niloufar; Thomas, Randal J.

doi:10.1097/hcr.0000000000000717

Cited by 3 publications

(1 citation statement)

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“…Our recent clinical study showed that exercise-based cardiac rehabilitation significantly prevented cardiovascular death and recurrent heart attack ( 10 ). In addition, recent preclinical studies from our team investigated drug ( 11 , 12 ) and non-drug ( 11 – 13 ) preconditioning strategies to ameliorate muscle damage caused by fatal stress induced by exhaustive exercise in non-obese mice.…”

Section: Introductionmentioning

confidence: 99%

Exercise prevents fatal stress-induced myocardial injury in obese mice

Dun,

Hu,

You

et al. 2023

Front. Endocrinol.

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IntroductionThis study aimed to explore whether aerobic exercise (AE) can prevent fatal stress-induced myocardial injury.MethodsThirty C57BL/6J mice were divided into either a normal diet, high-fat diet, or high-fat diet plus AE (n=10 per group). The AE protocol consisted of eight weeks of swimming. At the end of the diet and AE interventions, the mice were stimulated with fatal stress caused by exhaustive exercise (forced weight-loaded swimming until exhaustion), after which cardiac function was evaluated using echocardiography, myocardial ultrastructure was examined using transmission electron microscopy, and myocardial apoptosis was assessed using western blotting and TUNEL. Mitophagy, mitochondrial biogenesis and dynamics, and activation of the macrophage migration inhibitor factor (MIF)/AMP-activated protein kinase (AMPK) pathway were evaluated using quantitative PCR and western blotting. Obesity phenotypes were assessed once per week.ResultsAE reversed high-fat diet-induced obesity as evidenced by reductions in body weight and visceral fat compared to obese mice without AE. Obesity exacerbated fatal stress-induced myocardial damage, as demonstrated by impaired left ventricular ejection fraction and myocardial structure. The apoptotic rate was also elevated upon fatal stress, and AE ameliorated this damage. Obesity suppressed mitophagy, mitochondrial fission and fusion, and mitochondrial biogenesis, and these effects were accompanied by suppression of the MIF/AMPK pathway in the myocardium of mice subjected to fatal stress. AE alleviated or reversed these effects.ConclusionThis study provides evidence that AE ameliorated fatal stress-induced myocardial injury in obese mice. The cardioprotective effect of AE in obese mice might be attributed to improved mitochondrial quality.

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