Left ventricular diastolic dysfunction represents a frequent clinical condition and is associated with increased cardiovascular morbidity and mortality. Diastolic dysfunction is the most common cause of HF-PSF (heart failure with preserved ejection fraction). Therefore it becomes important to understand the pathophysiological mechanisms underlying diastolic dysfunction, as well as the effective therapeutic strategies able to antagonize its development and progression. Among the complex pathophysiological factors that may contribute to the development of diastolic dysfunction, the RAAS (renin–angiotensin–aldosterone system) has been shown to play a significant role. Paracrine and autocrine signals of the RAAS promote structural and functional changes in the heart largely linked to increased myocardial fibrosis. Enhanced and dysregulated activity of the RAAS also contributes to the development of volume overload and vasoconstriction with subsequent increases in left ventricular diastolic filling pressures and a higher susceptibility of developing CHF (congestive heart failure). More recently, it has also been suggested that the RAAS may play a role in triggering myocardial and vascular inflammation through the activation of different cell types and the secretion of cytokines and chemokines. RAAS-induced myocardial inflammation leads to perivascular myocardial fibrosis and to the development or progression of diastolic dysfunction. For these reasons pharmacological blockade of the RAAS has been proposed as a rational approach for the treatment of diastolic dysfunction. In fact, ACEIs (angiotensin-converting enzyme inhibitors), ARBs (angiotensin II receptor blockers) and AAs (aldosterone antagonists) have been demonstrated to delay the development and progression from pre-clinical diastolic dysfunction towards CHF, as well as to reduce the morbidity and mortality associated with this condition.
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March 2009
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Review Article|
February 12 2009
Role of the renin–angiotensin–aldosterone system and inflammatory processes in the development and progression of diastolic dysfunction
Sebastiano Sciarretta;
Sebastiano Sciarretta
*Department of Cardiology, II Faculty of Medicine, University of Rome “La Sapienza”, S. Andrea Hospital, Via di Grottarossa 1035-1039, 00100 Rome, Italy
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Francesco Paneni;
Francesco Paneni
*Department of Cardiology, II Faculty of Medicine, University of Rome “La Sapienza”, S. Andrea Hospital, Via di Grottarossa 1035-1039, 00100 Rome, Italy
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Francesca Palano;
Francesca Palano
*Department of Cardiology, II Faculty of Medicine, University of Rome “La Sapienza”, S. Andrea Hospital, Via di Grottarossa 1035-1039, 00100 Rome, Italy
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Diana Chin;
Diana Chin
*Department of Cardiology, II Faculty of Medicine, University of Rome “La Sapienza”, S. Andrea Hospital, Via di Grottarossa 1035-1039, 00100 Rome, Italy
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Giuliano Tocci;
Giuliano Tocci
*Department of Cardiology, II Faculty of Medicine, University of Rome “La Sapienza”, S. Andrea Hospital, Via di Grottarossa 1035-1039, 00100 Rome, Italy
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Speranza Rubattu;
Speranza Rubattu
*Department of Cardiology, II Faculty of Medicine, University of Rome “La Sapienza”, S. Andrea Hospital, Via di Grottarossa 1035-1039, 00100 Rome, Italy
†Istituto Di Ricovero e Cura a Carattere Scientifico Neuromed, Via Atinense 18, 86077 Pozzilli (IS), Italy
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Massimo Volpe
*Department of Cardiology, II Faculty of Medicine, University of Rome “La Sapienza”, S. Andrea Hospital, Via di Grottarossa 1035-1039, 00100 Rome, Italy
†Istituto Di Ricovero e Cura a Carattere Scientifico Neuromed, Via Atinense 18, 86077 Pozzilli (IS), Italy
Correspondence: Professor Massimo Volpe (email [email protected]).
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Publisher: Portland Press Ltd
Received:
August 07 2008
Revision Received:
October 10 2008
Accepted:
October 21 2008
Online ISSN: 1470-8736
Print ISSN: 0143-5221
© The Authors Journal compilation © 2009 Biochemical Society
2009
Clin Sci (Lond) (2009) 116 (6): 467–477.
Article history
Received:
August 07 2008
Revision Received:
October 10 2008
Accepted:
October 21 2008
Citation
Sebastiano Sciarretta, Francesco Paneni, Francesca Palano, Diana Chin, Giuliano Tocci, Speranza Rubattu, Massimo Volpe; Role of the renin–angiotensin–aldosterone system and inflammatory processes in the development and progression of diastolic dysfunction. Clin Sci (Lond) 1 March 2009; 116 (6): 467–477. doi: https://doi.org/10.1042/CS20080390
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