Abstract

Chronic heart failure and obesity are two conditions which despite all the advances made in the recent years, still represent two of the leading causes of morbidity and mortality worldwide. Moreover, a well-known fact is that the risk of sudden cardiac death, mostly related to malignant arrhythmias is higher in apparently healthy obese individuals in comparison with lean subjects. On the other hand, obese heart failure patients bring unique challenges in the diagnosis of heart failure, having a better prognosis than their normal or underweight counterparts. Taking into account the above-mentioned existing data, there are questions regarding whether cardiac arrhythmias such as atrial fibrillation or ventricular arrhythmias in this population have certain evolutive particularities. This paper describes various mechanisms of cardiac arrhythmias found in obese heart failure patients, such as myocardial architectural changes, neurohormonal and paracrine modifications.

Highlights

  • Chronic heart failure and obesity are two conditions which despite all the advances made in the recent years, still represent two of the leading causes of morbidity and mortality worldwide

  • Heart failure and obesity represent major public health problems with extremely high mortality rates, the mortality due to heart failure being evaluated by up to 50 % at 5 years of evolution, despite the data provided by important studies such as Framingham Heart and Olmsted County Studies, which showed significant improvements in the survival of the patients with heart failure in the last years[1,2]

  • We summarize below some of the possible mechanisms involved in the development and progression of these arrhythmias

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Summary

Introduction

Chronic heart failure and obesity are two conditions which despite all the advances made in the recent years, still represent two of the leading causes of morbidity and mortality worldwide. The Framingham study showed an increase in the risk of developing heart failure by 5% for males and 7% for women for every one-point increase in BMI over 25.

Results
Conclusion

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