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Obesity as a risk factor for cardiac arrhythmias.

ABSTRACT: Obesity is global health problem with an estimated three billion people worldwide being classified as overweight or obese. In addition to being associated with a range of adverse health outcomes, obesity is linked to higher risks of atrial and ventricular arrhythmias, as well as sudden cardiac death. Obesity is a multifactorial disease that often co-exists with hypertension, diabetes, and sleep apnoea, which are also independent risk factors for cardiac arrhythmias. Nevertheless, compelling evidence suggests that increasing adiposity is an independent proarrhythmic risk factor and that weight loss can be a mitigating and preventative intervention to reduce arrhythmia incidence. This review briefly outlines the economic and social burden of obesity and summarises evidence for the direct and indirect effects of increasing adiposity on risk of atrial and ventricular arrhythmias. The paper also summarises the evidence for electrocardiographic changes indicative of obesity-related atrial and ventricular remodelling and how weight reduction and management of comorbidity might reduce arrhythmic burden.

SUBMITTER: Patel KHK

PROVIDER: S-EPMC9951386 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature

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Obesity as a risk factor for cardiac arrhythmias.

Patel Kiran Haresh Kumar KHK Reddy Rohin K RK Sau Arunashis A Sivanandarajah Pavidra P Ardissino Maddalena M Ng Fu Siong FS

BMJ medicine 20221019 1

Obesity is global health problem with an estimated three billion people worldwide being classified as overweight or obese. In addition to being associated with a range of adverse health outcomes, obesity is linked to higher risks of atrial and ventricular arrhythmias, as well as sudden cardiac death. Obesity is a multifactorial disease that often co-exists with hypertension, diabetes, and sleep apnoea, which are also independent risk factors for cardiac arrhythmias. Nevertheless, compelling evid ...[more]

PMID: 36936556

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Project description:Heart repair by stem cell treatment may involve life-threatening arrhythmias. Cardiac progenitor cells (CPCs) appear best suited for reconstituting lost myocardium without posing arrhythmic risks, being commissioned towards cardiac phenotype. In this study we tested the hypothesis that mobilization of CPCs through locally delivered Hepatocyte Growth Factor and Insulin-Like Growth Factor-1 to heal chronic myocardial infarction (MI), lowers the proneness to arrhythmias. We used 133 adult male Wistar rats either with one-month old MI and treated with growth factors (GFs, n?=?60) or vehicle (V, n?=?55), or sham operated (n?=?18). In selected groups of animals, prior to and two weeks after GF/V delivery, we evaluated stress-induced ventricular arrhythmias by telemetry-ECG, cardiac mechanics by echocardiography, and ventricular excitability, conduction velocity and refractoriness by epicardial multiple-lead recording. Invasive hemodynamic measurements were performed before sacrifice and eventually the hearts were subjected to anatomical, morphometric, immunohistochemical, and molecular biology analyses. When compared with untreated MI, GFs decreased stress-induced arrhythmias and concurrently prolonged the effective refractory period (ERP) without affecting neither the duration of ventricular repolarization, as suggested by measurements of QTc interval and mRNA levels for K-channel ?-subunits Kv4.2 and Kv4.3, nor the dispersion of refractoriness. Further, markers of cardiomyocyte reactive hypertrophy, including mRNA levels for K-channel ?-subunit Kv1.4 and ?-subunit KChIP2, interstitial fibrosis and negative structural remodeling were significantly reduced in peri-infarcted/remote ventricular myocardium. Finally, analyses of BrdU incorporation and distribution of connexin43 and N-cadherin indicated that cytokines generated new vessels and electromechanically-connected myocytes and abolished the correlation of infarct size with deterioration of mechanical function. In conclusion, local injection of GFs ameliorates electromechanical competence in chronic MI. Reduced arrhythmogenesis is attributable to prolongation of ERP resulting from improved intercellular coupling via increased expression of connexin43, and attenuation of unfavorable remodeling.

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Obesity as a risk factor for cardiac arrhythmias.

Publications

Obesity as a risk factor for cardiac arrhythmias.

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