An 18-year-old male was diagnosed with attention-deficit hyperactivity disorder (ADHD) in 2005.

He was overweight with a body mass index (BMI) of 40.

He was started on quetiapine fumarate (Seroquel®) 900 mg daily in April 2005 and methylphenidate (Concerta®) 54 mg daily in September 2005.

In the beginning of August 2006 he was admitted to his local hospital with severe dyspnoea, tachypnea, tachycardia, and cyanosis.

On admission the blood pressure was 120/80 mmHg, and the arterial blood gas revealed a pH of 7.45, pCO2 of 3.55 kPa, paO2 of 7.76 kPa, and BE of −5.1 mmol/l.

C-reactive protein was not elevated.

The chest X-ray showed an enlarged heart.

He developed hemoptysis and was treated with unfractionated heparin in suspicion of pulmonary embolism.

He subsequently developed cardiogenic shock and was treated with vasoactive drugs.

In spite of the treatment he became oliguric and his liver enzymes were rising.

He was referred to our hospital for further treatment.

On admission the blood pressure was 90/60 mmHg, despite infusion with noradrenaline.

His heart rate was 130/minute and his temperature was 38.4 °C.

A thoracic computed tomography scan did not show pulmonary embolism.

Echocardiography revealed biventricular failure and left ventricular end diastolic diameter was 7 cm.

The left ventricle was severely hypokinetic with an ejection fraction (EF) of 20%–25%.

The left ventricular end diastolic pressure was markedly elevated, and there was a moderate mitral regurgitation.

Intermittent hemodialysis was initiated.

His liver function improved slightly, but despite dialysis the renal function deteriorated with increasing creatinine values.

After three days there was a further worsening of the left ventricular systolic function with an ejection fraction of 10%–12% and marked pulmonary hypertension with systolic pulmonary pressure estimated to 30 mmHg.

The clinical picture resembled dilated cardiomyopathy with low output failure causing renal and liver failure.

We suspected drug-induced cardiomyopathy and methylphenidate and quetiapine fumarate were discontinued.

Screening for infectious pathogens, immunological markers, and iron or amyloid deposition were all negative.

After three days he was transferred to the National Hospital (Rikshospitalet, Oslo) with ongoing noradrenaline and dobutamine infusions.

Shortly after admission an intraaortic balloon pump (IABP) was inserted and noradrenaline was replaced by nitroprusside.

Coronary angiography was normal.

Endomyocardial biopsy from the right ventricle did not reveal any distinct myocardial pathology.

On treatment with IABP, nitroprusside, and dialysis, the clinical situation gradually improved and the liver function returned to normal.

His renal function also improved with increasing diuresis and creatinine fell from 798 to 98 μmol/l.

His EF was still markedly reduced (15%).

Because of behavioral problems and adipose stature, he was denied a heart transplant.

He was treated with IABP for 26 days, and after 28 days he was transferred back to our hospital.

At that time his liver and renal functions were normal.

He was treated with an angiotensin-converting enzyme (ACE)-inhibitor, a beta-blocker, and diuretics.

During the following two weeks his clinical status improved and he was subsequently discharged to his home.

The echocardiography still showed markedly dilated left ventricle with EF of 20%.

In March 2007, his clinical status was improved and he was in function class II (New York Heart Association) with an EF estimated by echocardiography to 30%–35%.