Myocardial and aortic stiffening in the early course of primary aldosteronism
- PMID: 18781603
- PMCID: PMC6653704
- DOI: 10.1002/clc.20270
Myocardial and aortic stiffening in the early course of primary aldosteronism
Abstract
Background: Primary aldosteronism (PA) has been experimentally and clinically linked to myocardial and vascular fibrosis, and it has been further associated with left ventricular (LV) structural adaptations.
Hypothesis: Functional cardiovascular adaptations in hypertensive patients with PA precede structural alterations in the early stages of the disease.
Methods: We studied 17 hypertensive subjects with a recent diagnosis of PA (10 male patients, aged approximately 55 y, with office blood pressure [BP] of 137/88 mm Hg), and 30 essential hypertensives matched for age, sex, office BP levels, treatment status, and LV mass index (LVMI). Apart from standard 2-Dimensional (2-D) and conventional Doppler parameters, tissue Doppler imaging (TDI) methodology was used to assess LV diastolic function; averaging early and late diastolic mitral annular peak velocities (Emav/, Amav, Emav/Amav ratio) from 4 separate sites of measurement (septal, lateral, anterior, and inferior walls). Aortic stiffness was evaluated by means of carotid-femoral pulse wave velocity (cf-PWV) measurements.
Results: Although transmitral E/A ratio was similar in both groups (0.95+/-0.26 versus 0.98+/-0.24, p=0.66), hypertensive subjects with PA compared with essential hypertensives are characterized by significantly higher relative wall thickness (0.50+/-0.07 versus 0.41+/-0.06, p<or=0.001), decreased values of Emav (7+/-1.7 versus 8.1+/-1.8 cm/s, p=0.048), and Emav/Amav ratio (0.63+/-0.16 versus 0.77+/-0.17, p=0.015). The higher PWV in the PA population failed to reach statistical significance (8.5+/-1.6 versus 7.9+/-0.9 msec, p=0.19).
Conclusion: Our study demonstrates altered LV geometry and TDI-revealed diastolic dysfunction in hypertensives with PA compared with demographically- and LVMI-matched essential hypertensives. Furthermore, the increased aortic stiffening in PA patients failed to reach statistical significance.
Copyright (c) 2008 Wiley Periodicals, Inc.
References
-
- Ganguly A: Primary aldosteronism. N Eng J Med 1998; 339: 1828–1834. - PubMed
-
- Rossi GP, Bernini G, Caliumi C, Desideri G, Fabris B, et al.: PAPY Study Investigators: A prospective study of the prevalence of primary aldosteronism in 1,125 hypertensive patients. J Am Coll Cardiol 2006; 48(11): 2293–3000. - PubMed
-
- Milliez P, Girerd X, Plouin PF, Blacher J, Safar ME, et al.: Evidence for an increased rate of cardiovascular events in patients with primary aldosteronism. J Am Coll Cardiol 2005; 45: 1243–1248. - PubMed
-
- Rossi GP: Cardiac consequences of aldosterone excess in human hypertension. Am J Hypertens 2006; 19: 10–12. - PubMed
-
- Matsumura K, Fujii K, Oniki H, Oka M, Iida M: Role of aldosterone in left ventricular hypertrophy in hypertension. Am J Hypertens 2006; 19: 13–18. - PubMed
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