Tacrolimus
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Dilated cardiomyopathy leading to heart failure: case report A 66-year-old woman developed dilated cardiomyopathy leading to heart failure during immunosuppressive treatment with tacrolimus. The woman, who had a history of asthma, chronic subdural haemorrhage, osteoarthritis, microcytic anaemia and end-stage renal failure secondary to hypertensive nephropathy, had been receiving intermittent unit-based haemodialysis between 2011 and 2018. Her medications included candesartan-cilexetil [candesartan], aspirin, alfacalcidol and furosemide. Transthoracic echocardiogram performed in September 2016 showed normal left ventricular (LV) size with mildly impaired systolic function and mildly dilated left atrium. In August 2017, she underwent an uneventful deceased donor kidney transplant, with immediate graft function. She received low immunologic risk immunosuppression protocol with basiliximab as induction. Additionally, she started receiving immunosuppressive therapy with tacrolimus 9mg twice a day [0.1 mg/kg twice a day; route not stated] along with mycophenolate mofetil and prednisolone (stopped on day 7). The dose of tacrolimus was progressively decreased to achieve a target concentration of 8–12 micg/L (first 3m) and 6–8 micg/L (after 3m). She was discharged on day 5 after transplant, without any symptoms and signs of cardiac failure. In January 2018, she presented with signs and symptoms of decompensated heart failure, which included orthopnoea, exertional dyspnoea and pitting oedema. Also, she had pulmonary oedema, which needed admission for IV diuretics. The woman was admitted, and an echocardiogram revealed a dilated LV with severe global LV dysfunction. The EF was noted to have declined to 20–25%. Based on the rapidity of the onset of the heart failure, viral myocarditis was suspected; however, a panel of serologies and viral PCRs were negative. Then, the adverse impact of the AV fistula on cardiac function was considered and ligated in March 2018. However, no improvement was observed in the cardiac function. She had been receiving treatment with maximum tolerated doses of spironolactone, loop diuretic and ramipril; however, she had short of breath on minimal exertion, and she experienced New York Heart Association class 3/4 heart failure. Tacrolimus levels were noted to be within the target range of 5–8 mcg/L. She experienced progression of deterioration. By April 2018, a transthoracic echocardiogram revealed a dilated left ventricle (mildly dilated by diameter and severely dilated by volume-modified biplane) with severely impaired global systolic function. An evidence of restrictive filling pattern of the left ventricle was observed. The right ventricle (RV) was basally dilated, with impaired systolic function. Also, she had evidence of mild mitral regurgitation. Subsequently, she underwent further investigations for the cause of heart failure. A coronary angiogram revealed calcified unobstructed coronaries. A cardiac MRI scan demonstrated a severely dilated LV cavity with severe global LV systolic impairm
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