Key result
Chronic kidney disease facilitates the development and progression of left ventricular diastolic dysfunction in patients with HFpEF by affecting intracellular signaling pathways.
Understanding the mechanisms by which chronic kidney disease contributes to diastolic dysfunction in HFpEF may help identify novel cellular targets for drug therapy.
Chronic kidney disease is observed in most patients with CHF with preserved ejection fraction (HFpEF) and presents a major risk factor facilitating development and progression of LV diastolic dysfunction. The review focused on the effect of chronic kidney disease on intracellular signaling pathways affecting stiffness and diastolic relaxation of cardiomyocytes in response to inflammation and endothelial dysfunction of coronary capillaries, excessive sympathetic activation, and dysregulation of natriuretic peptides, which directly participate in the development of CHF. Elucidation of these mechanisms allows to identify new cell targets for new approaches to drug therapy for patients with HFpEF.
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Ob et al. (2018) conducted a review in Heart failure with preserved ejection fraction (HFpEF) and chronic kidney disease. Chronic kidney disease was evaluated. Chronic kidney disease facilitates the development and progression of left ventricular diastolic dysfunction in patients with HFpEF by affecting intracellular signaling pathways.
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