Abnormal regulation of renin angiotensin aldosterone system is associated with right ventricular dysfunction in hypertension.
BACKGROUND
Right ventricular dysfunction (RVD) is a major predictor of cardiovascular mortality. Inadequate suppression of the renin-angiotensin-aldosterone system (RAAS) after postural manoeuvres favours alterations of left ventricular (LV) function. The effects of RAAS dysregulation on RV performance remain elusive. The present study investigated RV function in hypertensive patients with or without altered RAAS activation.


METHODS
Plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were measured in 104 newly diagnosed hypertensive patients after both supine and upright positioning to assess dynamic changes of RAAS induced by antigravitational stress. Twenty-four-hour ambulatory blood pressure monitoring and echocardiographic evaluation of the right ventricle including tissue Doppler imaging (TDI) were performed. Patients were divided as follows: (1) normal PRA and PAC (N group [n = 58]), (2) suppressible RAAS after supine positioning (SR group [n = 24]), and (3), nonsuppressible RAAS (NSR group [n = 22]). RVD was identified by the TDI-derived myocardial performance index (MPI) calculated with a multisegmental approach.


RESULTS
Patients in the NSR group had reduced indices of RV function compared with patients in the N and SR groups. MPI of the right ventricle as well as prevalence of RVD were also significantly higher in the NSR group. Regression models showed that inadequate RAAS suppression was independently associated with RVD, regardless of blood pressure values and LV dysfunction (LVD).


CONCLUSIONS
Patients without supine normalization of RAAS display a significant impairment of RV function. Our findings suggest that a dynamic RAAS evaluation may help to identify hypertensive patients at higher risk of RVD.
Division of Cardiology, Department of Clinical and Molecular Medicine, University of Rome "Sapienza", Rome, Italy. Electronic address: gremao@libero.it.
Mario
M
Gregori
Division of Cardiology, Department of Clinical and Molecular Medicine, University of Rome "Sapienza", Rome, Italy; Istituto di Ricerca a Carattere Scientifico (IRCCS) Neuromed, Pozzilli, Italy.
Giuliano
G
Tocci
Division of Cardiology, Department of Clinical and Molecular Medicine, University of Rome "Sapienza", Rome, Italy.
Benedetta
B
Giammarioli
Division of Cardiology, Department of Clinical and Molecular Medicine, University of Rome "Sapienza", Rome, Italy.
Alberto
A
Befani
Division of Cardiology, Department of Clinical and Molecular Medicine, University of Rome "Sapienza", Rome, Italy.
Giuseppino Massimo
GM
Ciavarella
Division of Cardiology, Department of Clinical and Molecular Medicine, University of Rome "Sapienza", Rome, Italy.
Andrea
A
Ferrucci
Division of Cardiology, Department of Clinical and Molecular Medicine, University of Rome "Sapienza", Rome, Italy; Istituto di Ricerca a Carattere Scientifico (IRCCS) Neuromed, Pozzilli, Italy.
Francesco
F
Paneni
D000328:Adult; D000450:Aldosterone / Q000097:blood*; D001794:Blood Pressure / Q000502:physiology*; D015150:Echocardiography, Doppler; D005260:Female; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D008297:Male; D012083:Renin / Q000097:blood*; D012084:Renin-Angiotensin System / Q000502:physiology*; D018497:Ventricular Dysfunction, Right / Q000097:blood / Q000209:etiology* / Q000503:physiopathology; D016278:Ventricular Function, Right
D000450:Aldosterone; D012083:Renin