Metabolic cardiomyopathy with heart failure: a late, reversible complication of bariatric surgery

Introduction: Dilated cardiomyopathy (DCM) is characterized by cardiac enlargement and impaired left ventricular systolic function, mostly caused by coronary artery disease, which may be effectively treated with myocardial revascularization techniques. However, besides other generally progressive aetiologies of DCM, such as the idiopathic form, there are also reversible causes of DCM, including those secondary to arterial hypertension and alcoholism or to metabolic-nutritional imbalances, such those operating in the present case. Case presentation: We report the case of a 74 years old woman, referred to the University Hospital of Parma because of progressive dyspnoea and peripheral oedema lasting from three months. In her clinical history, almost 30 years before the onset of the symptoms, she underwent a jejuno-ileal bypass surgery for severe obesity, with consequent 40 Kg weight loss. First clinical examination showed an undernourished (body mass index 16 Kg/m2), symptomatic subject with marked peripheral oedema and resting dyspnoea. Blood pressure levels were low (82/59 mmHg). ECG showed a sinus tachycardia with non-specific intraventricular conduction delay and flattened T-waves in the left precordial leads (Fig.1). An early echocardiogram demonstrated a left ventricular dilation with severe systolic dysfunction (end-diastolic diameter 60 mm, ejection fraction 22 %) and severe functional mitral regurgitation (MR) (Fig. 2). Coronary angiogram excluded significant coronary artery disease. Laboratory blood tests showed: normal renal function, markedly reduced values of the main serum electrolytes (2.1 mEq/L potassium; 0.76 mEq/L ionized calcium; 0.6 mg/dL magnesium; 1.4 mg/dL inorganic phosphorus) and of the albumin (1.9 g/dL); significant anaemia (8.7 g/dL haemoglobin) and depletion of iron, folate and Vitamin D; a 346 pg/mL serum concentration of PTH indicated secondary hyperparathyroidism; BNP was elevated (1647 pg/mL), while enzymes of myocardial injury were negative. On the assumption of a malabsorption syndrome as the cause of dilated cardiomyopathy resulting in congestive heart failure, the patient received transfusion of 3 red blood cell units and a three-weeks’ lasting intravenous supplementation of potassium, magnesium, calcium, phosphorus, iron and vitamins, with early clinical and laboratory improvement. Then a sustained oral supplementation was initiated and continued after discharge from the Hospital. She also received pharmacological therapy with beta-blocker and angiotensin-receptor blocker (ARB), while loop diuretic treatment, initially needed to control oedema and dyspnoea, was permanently discontinued. At the follow-up the patient felt progressively better with significant improvement of the functional class ( NYHA – from IV to I). Serial echocardiographic exams showed a left ventricular ejection fraction rising to 35% within one month, with downgrading of MR to a moderate degree, and to 65% after eight months, with complete regression of left ventricular dilation (51 mm end-diastolic diameter) and a further recovery of MR to a mild degree (Fig. 3). Conclusions: This observation reports a rare case of bariatric surgery induced metabolic cardiomyopathy, which completely regressed after correction of nutritional abnormalities.