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A Novel Paradigm for Heart Failure With Preserved Ejection Fraction: Comorbidities Drive Myocardial Dysfunction and Remodeling Through Coronary Microvascular Endothelial Inflammation

Journal of the American College of Cardiology, 2013-07, Vol.62 (4), p.263-271 [Peer Reviewed Journal]

2014 INIST-CNRS ;Copyright © 2013 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved. ;ISSN: 0735-1097 ;EISSN: 1558-3597 ;DOI: 10.1016/j.jacc.2013.02.092 ;PMID: 23684677 ;CODEN: JACCDI

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Title:
A Novel Paradigm for Heart Failure With Preserved Ejection Fraction: Comorbidities Drive Myocardial Dysfunction and Remodeling Through Coronary Microvascular Endothelial Inflammation
Author: PAULUS, Walter J ; TSCHÖPE, Carsten
Subjects: Animals ; Biological and medical sciences ; Cardiology. Vascular system ; Cardiovascular system ; Comorbidity ; Coronary Circulation - physiology ; Coronary heart disease ; Endothelium, Vascular - metabolism ; Endothelium, Vascular - pathology ; Heart ; Heart Failure - metabolism ; Heart Failure - pathology ; Heart Failure - physiopathology ; Heart failure, cardiogenic pulmonary edema, cardiac enlargement ; Humans ; Inflammation - pathology ; Inflammation - physiopathology ; Investigative techniques of hemodynamics ; Investigative techniques, diagnostic techniques (general aspects) ; Medical sciences ; Microcirculation - physiology ; Myocardium - metabolism ; Myocardium - pathology ; Stroke Volume - physiology ; Ventricular Remodeling - physiology
Is Part Of: Journal of the American College of Cardiology, 2013-07, Vol.62 (4), p.263-271
Description: Over the past decade, myocardial structure, cardiomyocyte function, and intramyocardial signaling were shown to be specifically altered in heart failure with preserved ejection fraction (HFPEF). A new paradigm for HFPEF development is therefore proposed, which identifies a systemic proinflammatory state induced by comorbidities as the cause of myocardial structural and functional alterations. The new paradigm presumes the following sequence of events in HFPEF: 1) a high prevalence of comorbidities such as overweight/obesity, diabetes mellitus, chronic obstructive pulmonary disease, and salt-sensitive hypertension induce a systemic proinflammatory state; 2) a systemic proinflammatory state causes coronary microvascular endothelial inflammation; 3) coronary microvascular endothelial inflammation reduces nitric oxide bioavailability, cyclic guanosine monophosphate content, and protein kinase G (PKG) activity in adjacent cardiomyocytes; 4) low PKG activity favors hypertrophy development and increases resting tension because of hypophosphorylation of titin; and 5) both stiff cardiomyocytes and interstitial fibrosis contribute to high diastolic left ventricular (LV) stiffness and heart failure development. The new HFPEF paradigm shifts emphasis from LV afterload excess to coronary microvascular inflammation. This shift is supported by a favorable Laplace relationship in concentric LV hypertrophy and by all cardiac chambers showing similar remodeling and dysfunction. Myocardial remodeling in HFPEF differs from heart failure with reduced ejection fraction, in which remodeling is driven by loss of cardiomyocytes. The new HFPEF paradigm proposes comorbidities, plasma markers of inflammation, or vascular hyperemic responses to be included in diagnostic algorithms and aims at restoring myocardial PKG activity.
Publisher: New York, NY: Elsevier
Language: English
Identifier: ISSN: 0735-1097
EISSN: 1558-3597
DOI: 10.1016/j.jacc.2013.02.092
PMID: 23684677
CODEN: JACCDI
Source: Geneva Foundation Free Medical Journals at publisher websites
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A Novel Paradigm for Heart Failure With Preserved Ejection Fraction: Comorbidities Drive Myocardial Dysfunction and Remodeling Through Coronary Microvascular Endothelial Inflammation

2014 INIST-CNRS ;Copyright © 2013 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved. ;ISSN: 0735-1097 ;EISSN: 1558-3597 ;DOI: 10.1016/j.jacc.2013.02.092 ;PMID: 23684677 ;CODEN: JACCDI

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