An unusual case of dilated cardiomyopathy associated with partial hypopituitarism

Abstract

Dilated cardiomyopathy (DCM) secondary to endocrinologic disease occurs rarely. In a large clinicopathological review of 673 patients, only 1.5% fall in the metabolic category, mostly due to thyroid disorders [1]. Sporadic reports of DCM associated with other endocrinopathies have been subsequently published including acromegaly, GH deficiency, pheochromocytoma, hypoparathyroidism, Sheehan syndrome, and Addison’s disease. We herein describe a rare case of DCM secondary to partial hypopituitarism, in turn related to a previous intracranial surgery, promptly responding to multiple hormonal replacement therapy. A 55-year-old woman was admitted to our Intensive Coronary Unit in February 2008 because of a communityacquired pneumonia complicated by acute heart failure. Her chief complaint was shortness of breath, which had become progressively worse during the prior 4–5 days. She had a productive yellow cough and blood-tinged sputum. Examination revealed a tachycardia (115 bpm), tachypnea 22 breaths/min, BP 90/50 mmHg, a raised venous pressure, fine bilateral basal crepitations, right-sided crackles, and dullness to percussion. She was treated conventionally in a territorial hospital for acute pulmonary edema with partial initial symptomatic recovery. The patient was also started on a ‘‘pneumonia protocol’’ with cefotaxime and azithromycin, and oxygen. Notwithstanding standard therapy for acute heart failure including nitrates, furosemide and digoxin, and the introduction of inotropic support, the patient was still hypotensive, and for this reason she was admitted to the intensive care unit of our tertiary care hospital. The past medical history revealed systemic hypertension, chronic kidney disease (GFR of 25 ml/min), subclinical hypothyroidism (TSH 6.3 lU/mL with normal FT3 and FT4), and surgical intervention for aneurysmectomy of the left middle cerebral artery, which had been performed in 2006. She never smoked or used alcohol EtOH or drugs. She lived with her family. A complete mono-two-dimensional and Doppler echocardiographic examination was performed. The ultrasound analysis displayed a very enlarged poorly contracting left ventricle (EF 13%) with moderate-to-severe mitral regurgitation (see Fig. 1; Table 1). Diastolic function was moderately impaired. Interestingly, a previous echocardiogram obtained in 2006 was reviewed, and only displayed mild LV hypertrophy with normal cavity diameters and a preserved systolic function (EF 55–60%). After resolving the decompensated HF and the right pneumonia, the patient was still in class IV of the NYHA, and could not undergo a cardiopulmonary stress test that we routinely perform in CHF patients. To rule out ischemic etiology, a coronary angiography was performed that revealed no significant coronary stenosis. An endomyocardial biopsy was suggested but not performed since the patient refused the procedure. A complete hormonal panel showed low levels of earlymorning serum cortisol and undetectable levels of serum IGF1 without evidence of secondary gonadal failure (Table 1). Thyroid failure was partial insofar as TSH increased up to 10.9 lU/mL, indicating residual pituitary secretion. We next performed a GHRH ? arginine stimulation test for diagnosis A.M. Marra and M. Arcopinto contributed equally to this work.