Maurizio Cesari1, Claudio Letizia1, Paolo Angeli1, Susanna Sciomer1, Silvia Rosi1, Gian Paolo Rossi2. 1. From the Department of Internal Medicine and Medical Specialties (C.L.), and Department of Cardiovascular, Respiratory, Nephrology, Anesthetic, and Geriatric Sciences (S.S.), University La Sapienza, Rome, Italy; Unit of Internal Medicine and Hepatology, Department of Medicine, University of Padova, Italy (P.A., S.R.); and Hypertension Clinic, Department of Medicine-DIMED, University of Padova, Italy (M.C., G.P.R.). 2. From the Department of Internal Medicine and Medical Specialties (C.L.), and Department of Cardiovascular, Respiratory, Nephrology, Anesthetic, and Geriatric Sciences (S.S.), University La Sapienza, Rome, Italy; Unit of Internal Medicine and Hepatology, Department of Medicine, University of Padova, Italy (P.A., S.R.); and Hypertension Clinic, Department of Medicine-DIMED, University of Padova, Italy (M.C., G.P.R.). gianpaolo.rossi@unipd.it.
Abstract
BACKGROUND: Primary aldosteronism (PA) causes excess left ventricular (LV) hypertrophy and diastolic dysfunction; whether this occurs also in secondary aldosteronism (SA) without hypertension is unknown. We investigated the cardiac modifications in patients with preserved LV ejection fraction who had PA or SA. METHODS AND RESULTS: We measured several Doppler echocardiography-derived variables, including tissue Doppler imaging (TDI) parameters and strain rate analysis, in 262 patients with PA, 117 with SA because of liver cirrhosis, and in 61 control healthy subjects. SA and PA patients showed markedly elevated aldosterone levels (67 versus 39 ng/dL, respectively; normal values <15 ng/dL) but contrasting values of plasma renin activity (15.00 versus 0.56 ng/mL/h; P<0.001). Compared with PA, SA patients showed higher heart rate, and lower blood pressure and vascular resistance values. Both PA and SA showed increased LV diameters, LV volumes, stroke volume, stroke work, and septal peak systolic tissue velocity, and had more LV hypertrophy (61% and 39%, respectively) and diastolic dysfunction (35% and 36%, respectively) than healthy subjects. Peak systolic septal strain (20% versus 23%; P=<0.001) and midwall fractional shortening (15.9% versus 16.7%; P=0.001) were lower in PA than in SA patients. CONCLUSIONS: Primary and secondary hyperaldosteronism correlate with LV enlargement and high prevalence of LV hypertrophy and diastolic dysfunction; a subclinical systolic dysfunction is evident only in PA. In SA, the high rate of LV hypertrophy, in spite of low peripheral resistances and low-to-normal blood pressure, could be accounted for the high renin and aldosterone values, and the work overload associated with a hyperdynamic circulatory state.
BACKGROUND: Primary aldosteronism (PA) causes excess left ventricular (LV) hypertrophy and diastolic dysfunction; whether this occurs also in secondary aldosteronism (SA) without hypertension is unknown. We investigated the cardiac modifications in patients with preserved LV ejection fraction who had PA or SA. METHODS AND RESULTS: We measured several Doppler echocardiography-derived variables, including tissue Doppler imaging (TDI) parameters and strain rate analysis, in 262 patients with PA, 117 with SA because of liver cirrhosis, and in 61 control healthy subjects. SA and PA patients showed markedly elevated aldosterone levels (67 versus 39 ng/dL, respectively; normal values <15 ng/dL) but contrasting values of plasma renin activity (15.00 versus 0.56 ng/mL/h; P<0.001). Compared with PA, SApatients showed higher heart rate, and lower blood pressure and vascular resistance values. Both PA and SA showed increased LV diameters, LV volumes, stroke volume, stroke work, and septal peak systolic tissue velocity, and had more LV hypertrophy (61% and 39%, respectively) and diastolic dysfunction (35% and 36%, respectively) than healthy subjects. Peak systolic septal strain (20% versus 23%; P=<0.001) and midwall fractional shortening (15.9% versus 16.7%; P=0.001) were lower in PA than in SApatients. CONCLUSIONS: Primary and secondary hyperaldosteronism correlate with LV enlargement and high prevalence of LV hypertrophy and diastolic dysfunction; a subclinical systolic dysfunction is evident only in PA. In SA, the high rate of LV hypertrophy, in spite of low peripheral resistances and low-to-normal blood pressure, could be accounted for the high renin and aldosterone values, and the work overload associated with a hyperdynamic circulatory state.
Authors: Teresa M Seccia; Brasilina Caroccia; Gail K Adler; Giuseppe Maiolino; Maurizio Cesari; Gian Paolo Rossi Journal: Hypertension Date: 2017-04 Impact factor: 10.190
Authors: Paul Erne; Andrea Müller; Gian Paolo Rossi; Burkhardt Seifert; Fabrice Stehlin; Maurice Redondo; Peter T Bauer; Richard Kobza; Therese J Resink; Dragana Radovanovic Journal: Medicine (Baltimore) Date: 2017-06 Impact factor: 1.889
Authors: Gian Paolo Rossi; Valeria Bisogni; Alessandra Violet Bacca; Anna Belfiore; Maurizio Cesari; Antonio Concistrè; Rita Del Pinto; Bruno Fabris; Francesco Fallo; Cristiano Fava; Claudio Ferri; Gilberta Giacchetti; Guido Grassi; Claudio Letizia; Mauro Maccario; Francesca Mallamaci; Giuseppe Maiolino; Dario Manfellotto; Pietro Minuz; Silvia Monticone; Alberto Morganti; Maria Lorenza Muiesan; Paolo Mulatero; Aurelio Negro; Gianfranco Parati; Martino F Pengo; Luigi Petramala; Francesca Pizzolo; Damiano Rizzoni; Giacomo Rossitto; Franco Veglio; Teresa Maria Seccia Journal: Int J Cardiol Hypertens Date: 2020-04-15