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Reduction in temperature magnifies the cycle length dependent changes in action potential duration both during abrupt changes in cycle length, as with an extra stimulus, and during changes of steady state cycle length. This may indicate a greater dispersion of premature action potential durations during hypothermia, and hence predispose to hypothermia induced arrhythmias.

Although based upon a limited number of patients, this report indicates that CRT reduces peripheral markers of immune activation in patients with CHF. Further large scale studies are warranted to verify these findings.

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An 18-year-old obese man with a body mass index of 40, diagnosed with attention-defi cit hyperactivity disorder and treated with methylphenidate (Concerta ® ) was acutely admitted to hospital with hypoxia and dyspnoea. On investigation signs of liver-, renal-, and heart-failure were found. Noradrenalin infusion was started. Echocardiography showed dilated left ventricle and an ejection fraction (EF) of 25%. Liver function improved, noradrenalin and dobutamine were tapered, but three days after admission a new echocardiography showed an EF of 10%. The patient was transferred to the National Hospital (Rikshospitalet, Oslo), where intensifi ed treatment including intra aortic balloon pump (IABP) was instituted. Cardiac function improved, and 3 weeks later the IABP was disconnected. EF at this point was 15%. The patient was denied heart transplantation due to various cofactors. The investigation concluded with a probable relationship between his cardiomyopathy and the use of methylphenidate (Concerta). Keywords: cardiomyopathy, heart failure, ADHD, methylphenidate Heart failure due to idiopathic dilated cardiomyopathy (DCM) is rare in young people. Case descriptionAn 18-year-old male was diagnosed with attention-defi cit 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