Aldosterone Producing Adenoma Associated with Takotsubo Cardiomyopathy
Presentation Number: SAT 373
Date of Presentation: April 1st, 2017
Jamila Benmoussa*1 and James Desemone2
1Albany Medical College, Albany, NY, 2Albany Medical College, Albany
Takotsubo cardiomyopathy is believed to be induced by excess catecholamine release and is frequently associated with emotional stress. We report a case of this condition associated with an Aldosterone Producing Adenoma (APA).
A 47-year-old African American female with hypertension since age 28 presented with an acute MI. Her history was significant for right renal artery fibromuscular dysplasia which was treated with angioplasty. Her blood pressure had been controlled with calcium channel blockers until age 45 when an ARB was added. Four months prior to presentation she had chest pain and was diagnosed clinically with perimyocarditis. A cardiac catheterization showed normal coronary and a chest CT revealed a 1.6 x 1.8 cm left adrenal incidentaloma (0 Hounsfield units). Subsequent laboratory evaluation showed a serum aldosterone of 42 ng/dl (normal <3.0 – 23.2 ng/dl), and a renin <0.15 mg/ml/hr. Epleronone therapy was started, and four days later she presented with rapidly escalating chest pain associated with headache, high blood pressure, and diapherosis. The ECG showed an acute inferior wall MI and the troponin level rose to 16 ng/dl. she denied emotional stress. A cardiac catheterization showed apical hypokinesis, no evidence of ASCVD, and normal renal arteries. The ejection fraction was 55%. An adrenal MRI showed a 2.0 x 1.3 x 1.8 cm left adrenal nodule which was consistent with a lipid rich adenoma. A 24 hour urine collection for catecholamines, metanephrenes , normetanephrines, and cortisol was normal. The epleronone dose was adjusted and surgical consultation was obtained.
The effect of hypealdosteronism on cardiac morbidity could be from HTN alone and/or the direct effects of aldosterone on myocardial and vascular cells. It is known that high levels of aldosterone stimulate renal sodium retention by increasing expression of the thiazide-sensitive sodium-chloride cotransporter and the amiloride-sensitive epithelial sodium channel (ENaC) leading to plasma volume expansion and HTN. The role of aldosterone in eliciting acute vascular effects through nongenomic signaling pathways has been increasingly recognized. High levels of aldosterone increase markers of oxidative stress in plasma and heart tissue and alter intracellular Mg and Ca concentrations in smooth muscle cells and lead to coronary artery dysfunction. Acute aldosterone exposure causes dose-dependent myosin light-chain phosphorylation, a mechanism by which it can mediate vasoconstriction. These rapid effects of aldosterone can be inhibited by both spironolactone and eplerenone.
To our knowledge, this is the first report of Takotsubo’s cardiomyopathy associated with an APA. It suggests that non-genomic effects of aldosterone may enhance the risk of acute coronary vasoconstriction and can lead to myocardial ischemia in susceptible patients.
Nothing to Disclose: JB, JD