Microvascular Dysfunction across the Spectrum of Heart Failure Pathology: Pathophysiology, Clinical Features and Therapeutic Implications
Coronary microvascular dysfunction (CMD) plays a crucial role across the spectrum of heart failure (HF) pathology, contributing to disease development, progression, and outcomes. The pathophysiological mechanisms linking CMD to HF are complex and still not completely understood and include chronic i...
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Veröffentlicht in: | International journal of molecular sciences 2024-07, Vol.25 (14), p.7628 |
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creator | La Vecchia, Giulia Fumarulo, Isabella Caffè, Andrea Chiatto, Mario Montone, Rocco A Aspromonte, Nadia |
description | Coronary microvascular dysfunction (CMD) plays a crucial role across the spectrum of heart failure (HF) pathology, contributing to disease development, progression, and outcomes. The pathophysiological mechanisms linking CMD to HF are complex and still not completely understood and include chronic inflammation, oxidative stress, and neurohormonal activation. Despite the diagnostic and prognostic relevance in patients with HF, there is no specific therapeutic strategy targeting CMD to date. Moreover, the diagnosis of this clinical condition is challenging. In this review article, we aim to discuss the different clinical pathogenetic mechanisms linking CMD to HF across the different spectra of these diseases, their prognostic relevance, and the possible therapeutic targets along with the remaining knowledge gaps in the field. |
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The pathophysiological mechanisms linking CMD to HF are complex and still not completely understood and include chronic inflammation, oxidative stress, and neurohormonal activation. Despite the diagnostic and prognostic relevance in patients with HF, there is no specific therapeutic strategy targeting CMD to date. Moreover, the diagnosis of this clinical condition is challenging. In this review article, we aim to discuss the different clinical pathogenetic mechanisms linking CMD to HF across the different spectra of these diseases, their prognostic relevance, and the possible therapeutic targets along with the remaining knowledge gaps in the field.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms25147628</identifier><identifier>PMID: 39062871</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Animals ; Blood vessels ; Cardiovascular disease ; Dapagliflozin ; Development and progression ; Diabetes ; Diagnosis ; Ejection fraction ; Endothelium ; Health aspects ; Heart failure ; Heart Failure - etiology ; Heart Failure - pathology ; Heart Failure - physiopathology ; Heart Failure - therapy ; Humans ; Hypertension ; Inflammation ; Ischemia ; Ivabradine ; Kidney diseases ; Kinases ; Liraglutide ; Microcirculation ; Microvessels - pathology ; Microvessels - physiopathology ; Nitric oxide ; Oxidative Stress ; Pathology ; Pathophysiology ; Prognosis ; Smooth muscle ; Systemic diseases ; Trimetazidine ; Valsartan</subject><ispartof>International journal of molecular sciences, 2024-07, Vol.25 (14), p.7628</ispartof><rights>COPYRIGHT 2024 MDPI AG</rights><rights>2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). 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The pathophysiological mechanisms linking CMD to HF are complex and still not completely understood and include chronic inflammation, oxidative stress, and neurohormonal activation. Despite the diagnostic and prognostic relevance in patients with HF, there is no specific therapeutic strategy targeting CMD to date. Moreover, the diagnosis of this clinical condition is challenging. 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The pathophysiological mechanisms linking CMD to HF are complex and still not completely understood and include chronic inflammation, oxidative stress, and neurohormonal activation. Despite the diagnostic and prognostic relevance in patients with HF, there is no specific therapeutic strategy targeting CMD to date. Moreover, the diagnosis of this clinical condition is challenging. In this review article, we aim to discuss the different clinical pathogenetic mechanisms linking CMD to HF across the different spectra of these diseases, their prognostic relevance, and the possible therapeutic targets along with the remaining knowledge gaps in the field.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>39062871</pmid><doi>10.3390/ijms25147628</doi><orcidid>https://orcid.org/0009-0006-9800-0480</orcidid><orcidid>https://orcid.org/0000-0001-5264-1043</orcidid><orcidid>https://orcid.org/0000-0002-6439-1018</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Animals Blood vessels Cardiovascular disease Dapagliflozin Development and progression Diabetes Diagnosis Ejection fraction Endothelium Health aspects Heart failure Heart Failure - etiology Heart Failure - pathology Heart Failure - physiopathology Heart Failure - therapy Humans Hypertension Inflammation Ischemia Ivabradine Kidney diseases Kinases Liraglutide Microcirculation Microvessels - pathology Microvessels - physiopathology Nitric oxide Oxidative Stress Pathology Pathophysiology Prognosis Smooth muscle Systemic diseases Trimetazidine Valsartan |
title | Microvascular Dysfunction across the Spectrum of Heart Failure Pathology: Pathophysiology, Clinical Features and Therapeutic Implications |
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