Changes in Left Ventricular Anatomy and Function in Hypertension and Primary Aldosteronism

TLDR

The study examined how primary aldosteronism‑induced excess aldosterone and renin‑angiotensin suppression affect cardiac structure and function using echocardiography and Doppler flow measurements. The authors compared 34 primary aldosteronism patients with 34 matched essential hypertension patients, assessing cardiac parameters via echocardiography and Doppler. Patients with primary aldosteronism exhibited higher left ventricular mass, LV hypertrophy, impaired diastolic filling, and prolonged PQ interval, all of which improved after surgical removal of the aldosterone‑producing tumor but not with medical therapy.

Abstract

Abstract We investigated the effects on the heart of hypertension due to the excess of aldosterone and suppression of the renin-angiotensin system caused by primary aldosteronism with M-mode echocardiography and transmitral Doppler flow velocity measurements. We studied 34 consecutive patients with primary aldosteronism and 34 with essential hypertension individually matched for age, gender, race, body mass index, blood pressure values, and duration of hypertension. The groups were similar in age, body mass index, blood pressure, and duration of hypertension. However, lower serum potassium levels (3.5±0.6 versus 4.1±0.2 mmol/L, P <.0001) and plasma renin activity (0.53±0.45 versus 1.82±1.59 ng Ang I·mL −1 ·h −1 , P <.0001) and higher plasma aldosterone levels (1107±774 versus 206±99 pmol/L, P <.0001), left ventricular wall thickness, and left ventricular mass index (112±4.7 versus 98±3.7 g/m 2 , P =.029) were found in patients with primary aldosteronism compared with those with essential hypertension. Similarly, the PQ interval was longer (173±20 versus 141±14 milliseconds, P <.001) in primary aldosteronism than in essential hypertension patients. Significantly more primary aldosteronism than essential hypertension patients had left ventricular hypertrophy or left ventricular concentric remodeling (50% versus 15%, χ 2 =11.97, P =.007). Both the E wave flow velocity integral (1063±65 versus 1323±78, P =.013) and the E/A integral ratio (0.91±0.05 versus 1.25±0.08, P <.001) were lower, and atrial contribution to left ventricular filling was higher (53.3±1.5% versus 45.5±1.3%, P <.001) in patients with primary aldosteronism compared with essential hypertension patients. After 1 year of follow-up, highly significant decreases of left ventricular wall thickness and mass were observed in patients treated with surgical excision of an aldosterone-producing tumor, but not in those treated with medical therapy. Thus, in patients with primary aldosteronism, the excess aldosterone with suppression of the renin-angiotensin system is associated with both increased left ventricular mass and significant changes of left ventricular diastolic filling. The former changes appear to be reversible on removal of the cause of excessive aldosterone production.