Role of Aldosterone in Left Ventricular Hypertroph

Authors: Matsumura Kiyoshi Fujii Koji Oniki Hideyuki Oka Masayo Iida Mitsuo

Publish Date: 2006/01/01

Volume: 19, Issue: 1, Pages: 13-18

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Abstract

Kiyoshi Matsumura Koji Fujii Hideyuki Oniki Masayo Oka Mitsuo Iida Role of Aldosterone in Left Ventricular Hypertrophy in Hypertension American Journal of Hypertension Volume 19 Issue 1 January 2006 Pages 13–18 https//doiorg/101016/jamjhyper200505013Aldosterone induces cardiac fibrosis in experimental animal models but only limited information is available on the association between aldosterone and left ventricular LV hypertrophy in human beings The aim of the present study was to determine the role of aldosterone in LV geometry and to investigate other types of target organ damage in hypertensive patientsA total of 25 patients with primary aldosteronism caused by Conn’s adenoma 29 patients with renovascular hypertension and 29 patients with essential hypertension EHT were included in the present study Echocardiographic examinations and 24h ambulatory blood pressure BP monitoring were conducted in all subjectsThe mean 24h systolic and diastolic BP in primary aldosteronism and renovascular hypertension were found to be comparable to those in EHT However LV mass index adjusted by age sex mean 24h systolic BP mean 24h pulse rate body mass index and duration of hypertension was significantly increased in the patients with primary aldosteronism and renovascular hypertension compared with values in patients with EHT 1502 ± 77 1423 ± 72 and 1152 ± 72 g/m2 respectively Hypertensive organ damages such as proteinuria and hypertensive retinopathy were more pronounced in the patients with renovascular hypertension however LV hypertrophy was especially exaggerated in patients with primary aldosteronismLeft ventricular LV hypertrophy is the most common cardiac complication caused by hypertension1 However it has been shown that LV hypertrophy is not only attributable to the pressure overload but also to humoral factors such as angiotensin II and aldosterone2–4 In animal models both cardiac load and high circulating aldosterone levels stimulate fibrosis within the myocardium leading to LV hypertrophy56 Aldosterone has been demonstrated to influence LV remodeling independent of its impact on systemic BP as this cardiac fibrosis was prevented by treatment with nonantihypertensive doses of spironolactone the aldosterone receptor antagonist56 These findings in experimental studies are supported by clinical findings demonstrating that serum aldosterone levels are elevated in patients with heart failure which denote an adverse prognosis7Primary aldosteronism PA is the syndrome caused by the autonomous hypersecretion of aldosterone resulting in a decrease in plasma renin activity PRA and an increase in BP Hypertension with low PRA has been considered to result in fewer cardiovascular complications than other types of hypertension with normal or high PRA8 although some previous studies have shown that cardiovascular complications and LV hypertrophy were common even in patients with PA910 Patients with renovascular hypertension RVHT showed increases in PRA and in their plasma aldosterone concentration PAC and plasma angiotensin II concentration although the PAC is usually higher in patients with PA than in those with RVHT Previous experimental findings indicate that both angiotensin II and aldosterone participate in the development of hypertensive target organ damage2–4 however the differential roles of these peptides in hypertensive target organ damage have not yet been well determined especially in human beings Accordingly the aim of the present study was to determine the change in LV geometry and the development of target organ damage in patients with hypertension with different etiologies namely essential hypertension EHT RVHT or PA To keep the BP levels adjusted correctly 24h ambulatory BP monitoring was conducted in all subjectsThe study group consisted of hypertensive patients admitted to the Kyushu University Hospital in Fukuoka Japan A total of 25 patients with PA caused by Conn’s adenoma 29 patients with RVHT and 29 patients with EHT were included In all cases Conn’s adenoma was identified using computed tomography and adrenal vein sampling of the PAC Surgical treatment was carried out in all patients with PA Histologic analysis was conducted to confirm Conn’s adenoma and the PAC was normalized in all patients after adrenalectomy The presence of RVHT was identified with renal scintigraphy renal angiography and renal vein sampling of PRA Of the 29 patients with RVHT 14 were treated with percutaneous transluminal angioplasty and their BP was confirmed to have decreased to the normal range All patients were in sinus rhythm and none had any valvular or ischemic heart diseaseOf the 25 patients with PA 12 were treated with antihypertensive agents 10 of these patients were treated with calcium Ca antagonists one patient with a combination of a Ca antagonist and an αblocker and one patient with spironolactone Oral potassium supplementation was used in eight patients Of the 29 patients with RVHT 17 were treated with antihypertensive agents such as Ca antagonists angiotensinconverting enzyme inhibitors αblockers or βblockers A total of 29 patients with EHT in whom all possible causes of secondary hypertension had been excluded were studied as control subjects All patients with EHT were free of antihypertensive agents The details of the study protocol were explained to the subjects and their informed consent was obtained before participation

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