Key result
Chronic low-grade microvascular inflammation, primarily driven by macrophages and lymphocytes, plays a key role in the pathogenesis of heart failure with preserved ejection fraction.
Why the study?
Effective treatment options for HFpEF remain elusive, and suppressing microvascular inflammation driven by a chronic pro-inflammatory state may represent a novel therapeutic strategy.
Microvascular inflammation and immune cell activation (macrophages, T-cells, B-cells) play a central role in the pathogenesis of HFpEF, highlighting potential novel anti-inflammatory therapeutic targets.
Answers are grounded in this paper and cite their sources.
Supports microvascular inflammation as a therapeutic target in HFpEF; hypothesis-generating pending randomized trials.
Heart failure with preserved ejection fraction (HFpEF) is a severe disease with an often unfavorable outcome. The prevalence of HFpEF continues to increase, while effective treatment options remain elusive. All the medical strategies used to improve the outcome in a heart failure with reduced ejection fraction proved ineffective in HFpEF, which was probably due to the different mechanisms of development of these two types of heart failure and the diversity of the HFpEF phenotypes. According to the current paradigm of HFpEF development, a chronic mild pro-inflammatory state causes a coronary microvascular endothelial inflammation, with further myocardial fibrosis and diastolic dysfunction progression. This inflammatory paradigm of HFpEF has been confirmed with some evidence, and suppressing the inflammation may become a novel strategy for treating and managing HFpEF. This review summarizes current concepts about a microvascular inflammation in hypertrophied myocardium and provides a translational perspective of the anti-inflammatory and immunomodulatory approaches in HFpEF.
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Овчинников et al. (2020) conducted a review in Heart failure with preserved ejection fraction (HFpEF). Anti-inflammatory and immunomodulatory therapies was evaluated. Chronic low-grade microvascular inflammation, primarily driven by macrophages and lymphocytes, plays a key role in the pathogenesis of heart failure with preserved ejection fraction.
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