Impact of comorbidities on myocardial remodeling and dysfunction in heart failure with preserved ejection fraction.

Abstract

Aim. The generalization of the modern data on the influence of comorbidities on cardiac remodeling and heart dysfunction in chronic heart failure (CHF) with preserved ejection fraction (EF). The objectives of the study included the analysis of the pathogenesis of CHF with preserved ejection fraction. Material and methods. Analyzed all Russian and English literature, submitted to the search engines. Results. Analysis of scientific literature showed that the increase in systemic vascular inflammation, endothelial dysfunction and oxidative stress lead to reduced bioavailability of nitric oxide , which leads to increased stiffness of the left ventricle and adverse remodeling of the heart in CHF with preserved ejection fraction. Comorbidities such as overweight /obesity, diabetes, hypertension, chronic obstructive pulmonary disease, anaemia and chronic renal dysfunction leads to coronary remodeling in microvascular endothelial inflammation. The negative contribution is also made by demographic factors such as older age and female gender. In the present review substantiates the crucial role of comorbidities in the pathophysiology of CHF with preserved ejection fraction. Conclusion. Summarizing the analysis of literature sources, devoted to the pathogenesis of CHF with comorbidity, the findings that, in addition to diastolic dysfunction of the left ventricle, there are other patofiziologiia mechanisms: the violation of backup functions, the violation of jeludochno-blood relationship, the energy deficit of the myocardium, pulmonary hypertension, chronotropic imbalance, inflammation, oxidative stress and endothelial dysfunction. With CHF with preserved ejection fraction comorbidities contribute to systemic inflammation which causes oxidative stress in the coronary microvascular endothelium. This reduces the bioavailability of nitric oxide in the myocardium and leads to reduced activity of protein kinase G in cardiomyocytes, which therefore become stiff and hypertrophied. In addition, with increasing age and postmenopausal hormonal changes may lead to additional structural and functional changes.