Primary aldosteronism (PA) is a common cause of secondary hypertension due to unilateral adrenocortical adenoma (APA) or idiopathic hyperplasia.1 There is increased awareness of the possible cardiac sequelae of aldosterone excess, including cardiac hypertrophy, fibrosis, and vascular endothelium injury.2,3
A 54-year-old woman was referred for rest and nighttime worsening dyspnea and palpitations. One year earlier she was admitted to another hospital with the same symptoms and discharged with a diagnosis of idiopathic dilated cardiomiopathy.
At admission, physical examination revealed a body mass index of 21 kg/m2 and blood pressure (BP) of 210/105 mm Hg. Chest auscultation revealed mild expiratory wheezes and rales in both lower lobes. Electrocardiography showed signs of left ventricular (LV) overloading and hypertrophy. Laboratory analysis showed severe hypokalemia (1.8 mEq/L; normal range 3.5–5 mEq/L) and metabolic alkalosis (pH 7.51; partial pressure of carbon dioxide 41 mm Hg; partial pressure of oxygen 86 mm Hg; 32.6 mmol/L; excess bases 10 mmol/L) (Table I). Chest radiography revealed an enlarged cardiac silhouette, congested pulmonary hilum, and bilateral pleural effusion (Figure 1A). Echocardiography showed an increase in LV end-diastolic diameter (58 mm) and left atrial volume (46 mm) and a signficant decrease in global LV performance (ejection fraction [EF] 30%) (Table II). The 24-hour ambulatory BP monitoring (ABPM) revealed severe systo-diastolic hypertension without physiological nocturnal fall (nondipper pattern).
|Red blood cell count, 106/mm3||4.99|
|White blood cell count, 103/mm3||4.65|
|Platelet count, 103/mm3||205|
|Blood fasting glucose, mg/dL||71|
|Potassium, mEq/L||1.8 L|
|Blood gas analysis|
|Partial pressure of carbon dioxide, mm Hg||40.8|
|Partial pressure of oxygen, mm Hg||86|
|Excess bases, mmol/L||10|
|Oxygen saturation, %||92|
|Urinary sodium excretion, mEq/24 h||108|
|Urinary potassium excretion, mEq/24 h||107.3|
|Urinary chloride excretion, mEq/24 h||131.4|
|Follow-Up, y||EF, %||IVS, mm||PW, mm||LVEDD, mm||LA, mm||BP, mm Hg||PAC, ng/mL||PRA, ng/mL/h||PAC/PRA||K+, mEq/L|
Subsequent investigation showed suppressed plasma renin activity (PRA) (0.08 ng/mL/h; normal range 0.2–2.7 ng/mL/h), high plasma aldosterone (PAC 16.17 ng/dL; normal range 7.5–15 ng/dL), and PAC/PRA ratio (202.17 ng/dL: ng/ml/h; normal value<30 ng/dL: ng/mL/h). Because of suspicion of PA, we performed a captopril test. After 60 minutes of captopril 50 mg, the PAC/PRA ratio was still elevated (529.93 ng/dL: ng/mL/h). Magnetic resonance imaging of the superior abdomen demonstrated a 20-mm nodule in the left adrenal gland (Figure 2). The patient underwent laparoscopy adrenalectomy, and histopathology revealed an APA. Subsequently, her BP was normalized at 140/90 mm Hg with amlodipine, ramipril, and serum potassium. After 6 months of follow-up, BP was 110/80 mm Hg, with normal serum potassium. Chest radiography showed resolution of congestive heart pulmonary imaging with a decreased cardiac silhouette (Figure 1B). Repeat echocardiography demonstrated a significant improvement in LV hypertrophy and EF (50%).
Recently, the Primary Aldosteronism Prevalence in Italy Study (PAPY)1 reported a PA prevalence of 11.2% in patients with new-onset hypertension. The potential comorbidity and prevention of excessive cardiovascular events and organ damage led to development of accurate strategies for diagnosis of PA.3 PA patients display an unfavorable cardiovascular profile, suggesting a role of aldosterone beyond its well-known hypertensive effects.
The successful outcome was possible with surgical removal of APA. This case provides interesting information to assess the pathophysiologic roles of aldosterone in cardiac damage. Considerable experimental animal work has demonstrated that aldosterone can stimulate an abnormal accumulation of collagen (type I and type III), which can be reversed by spironolactone.4 In particular, an animal study by Brilla and colleagues5 demonstrated that aldosterone infusion with high salt intake induces cardiac hypertrophy and myocardial interstitial fibrosis. In clinical studies, Rossi and associates6 have reported that PA patients exhibit significant changes of myocardial texture compared with essential hypertensive patients that may be due to cardiac fibrosis, which is an important determinant of myocardial remodeling and impaired tissue stiffness. Lin and coworkers7 performed a clinical study to investigate LV structure and myocardial fibrosis (cyclic variation of integrated backscatter echocardiography method) in 11 patients with unilateral PA and their change after adrenelectomy, showing that adrenelectomy reverses LV geometry and alters myocardial texture in PA patients. Finally, Gaddam and colleagues8 demonstrated in patients with resistant hypertension a dichotomous effect that depended on the underlying aldosterone status: in patients with high aldosterone levels, intravascular and intracardiac overload is evident; in patients with normal or low aldosterone levels, volume overload is less prominent, suggesting that hypertension is more dependent on vascular stiffness.