In March 2003, a 23-year-old Arab ethnicity Kuwaiti male with a strong family history of dilated cardiomyopathy presented to a specialized neurology hospital with dizzy spells and feet parasthesia. He was given intravenous methylprednisolone for 3 days for probable multiple sclerosis and was booked electively for a magnetic resonance imaging (MRI) of the brain. On March 23rd 2003, he had a witnessed sudden cardiac arrest and suddenly collapsed when he was at an automated banking teller machine. The paramedic personnel were at the scene within 5 minutes of the call, endotracheal intubation was carried out as well as an intra-tracheal atropine and adrenalin was given at the scene. A cardiac monitor was attached and revealed ventricular fibrillation, and thus was electrically cardioverted 3 times (200 J, 300 J and 360 J) until reverted to sinus rhythm. The resuscitation procedure including the transit time to hospital was around 30 minutes. On arrival to intensive care unit (ICU), he had a heart rate of 150 beats per minute and a blood pressure of 110/70 mm/Hg. Electrocardiography (ECG) revealed sinus rhythm with incomplete Left bundle branch block (LBBB) and non-specific ST-T wave changes. A transthoracic echocardiography showed a mildly dilated left ventricular (LV) with severe global LV systolic dysfunction with an estimated Left Ventricular Ejection Fraction (LVEF) of 20 to 25%. An echocardiogram was done 6 months prior to the hospital admission and LV systolic function reported to be normal. During his ICU stay, he had recurrent convulsions, which were controlled with epanutin and clonazepam. Computed tomography scan (CTS) of the head showed a small infarct (probably embolic) in the right centrum semiovale adjacent to the body of the right lateral ventricle. An electroencephalograph (EEG) was performed and this revealed diffuse cortical dysfunction with no epileptic discharge. He had a battery of laboratory investigations including liver function test, renal function test, complete blood count and thyroid function test and these were all within normal limits. Later on, he had a transient rise in liver enzymes and this was found to be secondary to hepatic hypo-perfusion (hepatitis viral screening, auto-immune screening and serum copper tests were all normal). Eventually a tracheostomy was performed and a nasogastric tube fed him. His neurological condition showed a slow but steady improvement over a course of 3 months and regained consciousness, with spontaneous breathing and thus the tracheostomy was closed. However, he was left mentally handicapped with sphincteric incontinence and was referred to the rehabilitation hospital for aggressive physiotherapy. During his follow up, he was treated medically with anti-failure and antiepileptic drugs (digoxin, revotril, epanutin, zestril, lasix, zantac and amiodarone). However, he continued to show non-sustained ventricular tachycardia on a 24-hour holter monitor. Eventually, he had an automated implantable cardioverter-defibrillator (AICD) inserted in 2004 and his functional status significantly improved and he is still alive. He developed amiodarone induced thyroiditis with hyperthyroidism, Thyroid test, FT4 = 15.29 (Normal = 5.69-13.44) and Thyroid stimulating hormone, TSH = 0.03 (Normal = 0.43-4.1) which was proven by a positive thyroid scan. His thyroid function normalized following the discontinuation of amiodarone. Investigations of his family history revealed that his father was known to have dilated cardiomyopathy (DCM) and was treated with AICD, but had a sudden cardiac death a few years ago while he was waiting for cardiac transplantation. In addition, two of his sisters had pacemakers inserted, and one of his paternal uncles died suddenly at the age of 25 years. Family pedigree is shown in.