Steroid-induced cardiomyopathy

Clinical record

In December 2012, a 30-year-old man was admitted via the emergency department of our tertiary hospital with atrial fibrillation (AF), new-onset biventricular cardiac failure, acute renal failure and elevated liver function test results.

He presented with a 2-week history of dyspnoea, palpitations and epigastric discomfort. An electrocardiogram confirmed AF with a rapid ventricular response, and he was subsequently admitted to hospital. His initial heart rate varied between 120 and 140 beats/min and his blood pressure was 140/90 mmHg. He had distended jugular veins and cardiac examination revealed a gallop rhythm and an apical pansystolic murmur. His lungs were clear to auscultation and he had no peripheral oedema.

The patient was a successful bodybuilder and strongman. Over the past 12 months, he had taken testosterone 1.5 g per week, trenbolone 500 mg per week, methandrostenolone 40 mg daily, anastrozole 0.5 mg daily and naproxen 1.1 g daily in preparation for a national championship competition. The products were obtained through other users at the gym where the patient trained. He had ceased all the above supplements about 6 weeks before his admission. He was 141 kg at the time of presentation.

Further questioning elicited that he had taken anabolic steroids for about 7 years leading up to his presentation. He stated that he had only recently started taking trenbolone. Further examination did not reveal any evidence of gynaecomastia, testicular atrophy or acne.

His social history was otherwise unremarkable. There was no history of heavy alcohol use, smoking or illicit drugs. There was no family history of cardiomyopathy. There were no signs and symptoms of a viral illness.

Fifteen months before presentation, he had a transthoracic echocardiogram for hypertension, which revealed normal biventricular size and systolic function, normal biatrial size, normal diastolic function and normal valve function. At the time, he also underwent a treadmill stress echocardiogram, for which he exercised for 8 min 50 s on a 2-minute Bruce protocol, achieving 100% maximum predicted heart rate and 14.5 metabolic equivalents. There was no evidence of inducible ischaemia.

Initial laboratory tests showed an increased haemoglobin level (192 g/L [reference interval (RI), 130–180 g/L]) with a normal haematocrit level (0.54 L/L [RI, 0.40–0.54 L/L]); renal dysfunction (creatinine level, 138 μmol/L [RI, 62–106 μmol/L]) with normal electrolytes; a mildly increased level of high-sensitivity troponin T (26 ng/L [RI, < 15 ng/L]) with no subsequent increase; and increased liver enzyme levels (alanine aminotransferase [ALT], 207 U/L [RI, < 41 U/L]; aspartate aminotransferase [AST], 116 U/L [RI, < 40 U/L]). However, his albumin and bilirubin levels and international normalised ratio were normal. Initial therapy included metoprolol and anticoagulation with low molecular weight heparin.

The patient underwent transoesophageal echocardiography on Day 3 of his admission. This showed severe global biventricular dysfunction, moderate to severe mitral regurgitation as a result of annular dilatation, biatrial enlargement, and the presence of spontaneous echo contrast in the left atrial appendage without thrombus. Electrical cardioversion was performed, resulting in sinus tachycardia; however, AF recurred within 24 hours. Pharmacological therapy to promote sinus rhythm included intravenous amiodarone (300 mg immediately, followed by 1200 mg over 24 hours) followed by oral loading (400 mg three times a day).

Our patient was given carvedilol and ramipril. However, he deteriorated on Day 4, developing hypotension (blood pressure, 80/50 mmHg) and renal dysfunction (creatinine level, 267 μmol/L), and a worsening of his liver function (ALT, 1857 U/L; AST, 1697 U/L). Low-dose dobutamine infusion was started and continued for 72 hours, resulting in excellent diuresis and improvement in his clinical condition with recovery of liver and kidney function.

Investigations to exclude a secondary cause of cardiomyopathy included thyroid function tests, iron studies and plasma metanephrine tests, which all returned normal results.

• angiotensin-converting enzyme inhibitor: ramipril 5 mg daily;
• β-blocker: carvedilol uptitrated to 50 mg twice daily;
• aldosterone antagonist: initially spironolactone 25 mg daily, subsequently changed to eplerenone 25 mg daily because of gynaecomastia;
• amiodarone to maintain sinus rhythm: initially 200 mg daily, reduced to 100 mg daily, and eventually stopped because of hyperthyroidism;
• anticoagulation for AF: initial warfarin therapy now changed to aspirin; and
• testosterone replacement (125 mg per week) for rebound low serum testosterone.

He had serial transthoracic echocardiograms, with improvement documented in left ventricular structure and function (Box).

Our patient was treated for a dilated cardiomyopathy as a result of anabolic steroid use. He has now stopped taking anabolic steroids for 18 months. He weighs 122 kg; however, through a different training regimen, he can lift the same weight as he did when he was 141 kg.

Lessons from practice

• Anabolic steroid use and misuse is an important issue in the bodybuilding community.
• Anabolic steroid use and misuse is an important potential cause of dilated cardiomyopathy.
• The mainstay of treatment involves abstinence from the offending agent, as well as initiation of conventional heart failure therapy.
• The recent addition of trenbolone to the patient’s steroid regimen potentially contributed to his presentation.