Abstract-Hyperaldosteronism has been causally linked to myocardial interstitial fibrosis experimentally, but it remains unclear if this link also applies to humans. Thus, we investigated the effects of excess aldosterone due to primary aldosteronism (PA) on collagen deposition in the heart. We used echocardiography to estimate left ventricular (LV) wall thickness and dimensions and for videodensitometric analysis of myocardial texture in 17 consecutive patients with PA and 10 patients with primary (essential) hypertension who were matched for demographics, casual blood pressure, and known duration of hypertension. The groups differed in serum K ϩ , ECG PQ interval duration, plasma renin activity, and aldosterone levels (all PՅ0.002) but not for casual blood pressure values, demographics, and duration of hypertension. Compared with hypertensive patients, PA patients showed a higher LV mass index (53.7Ϯ1.8 versus 45.5Ϯ2.0 g/m 2.7 ; Pϭ0.008) and lower values of the cyclic variation index of the myocardial mean gray level of septum (CVI s ; Ϫ12.02Ϯ5.84% versus 6.06Ϯ3.08%; Pϭ0.012) and posterior wall (Ϫ11.13Ϯ6.42% versus 8.63Ϯ9.62%; Pϭ0.012). A regression analysis showed that CVI s was predicted by the PQ duration, supine plasma renin activity, plasma aldosterone, and age, which collectively accounted for Ϸ36% of CVI s variance. PA is associated with alterations of myocardial textures that suggest increased collagen deposition and that can explain both the dependence of LV diastolic filling from presystole and the prolongation of the PQ interval. Key Words: hypertension, endocrine Ⅲ aldosterone Ⅲ myocardial Ⅲ hypertrophy Ⅲ fibrosis Ⅲ echocardiography L eft ventricular hypertrophy (LVH) is commonly associated with arterial hypertension and represents an important independent predictor of cardiovascular events, 1 including congestive heart failure. Extracellular matrix and collagen deposition are invariable findings of LVH and lead to cardiac fibrosis (CF), which occurs particularly in the perivascular areas and correlates directly with the severity of LVH. 2 CF is a major cause of cardiac dysfunction because an excessive deposition of collagen may be responsible for abnormal tissue stiffness and diastolic dysfunction. The latter is an early marker of heart involvement in hypertension (for review, see Agabiti-Rosei and Muiesan 3 ) and is associated with CF more closely than with LVH. 4,5 Fibroblasts constitute the vast majority (Ͼ90%) of nonmyocyte cells in the heart; they can increase the production of extracellular matrix on exposure to a variety of injuries, including pressure overload. The latter seems to be only one of the determinants of CF, because it was experimentally shown, both in vitro and in vivo, that CF in both ventricles was linked to activation of the renin-angiotensin-aldosterone system 6 and that it could be prevented by nonantihypertensive dosages of spironolactone. 7 Thus, angiotensin II and aldosterone play important roles in the heart (for review, see Swynghedauw 8 ). Angiotensin II induces cardi...

Subclinical hypothyroidism (sHT) affects 5-15% of the general population; however, the need of lifelong L-T(4) therapy is still controversial. As myocardium is a main target of thyroid hormone action, we investigated whether sHT induces cardiovascular alterations. Twenty sHT patients were randomly assigned to receive placebo or L-T(4) therapy and were followed for 1 yr. Twenty sex- and age-matched normal subjects served as controls. Doppler echocardiography and videodensitometric analysis were performed in all subjects. Myocardium textural parameters were obtained as mean gray levels, which were then used to calculate the cyclic variation index (CVI; percent systolic/diastolic change in mean gray levels). Patients had a significantly higher isovolumic relaxation time (3.1 +/- 0.5 vs. 2.6 +/- 0.6; P < 0.03), peak A (0.77 +/- 0.16 vs. 0.56 +/- 0.13 m/s; P < 0.01), and preejection/ejection time (PEP/ET) ratio (0.72 +/- 0.05 vs. 0.57 +/- 0.06; P < 0.03) and a lower CVI (P < 0.0001) than controls. CVI was inversely related to TSH level (P < 0.0001) and PEP/ET ratio (P < 0.01). L-T(4)-treated patients showed a significant reduction of the PEP/ET ratio (P < 0.05), peak A (P < 0.05), and isovolumic relaxation time (P < 0.05) along with a normalization of CVI. Conversely, no changes were observed in the placebo-treated group. In conclusion, sHT affects both myocardial structure and contractility. These alterations may be reversed by L-T(4) therapy.

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