Introduction: Sudden cardiac death (SD) remains the main cause of mortality worldwide. Patients with cardiac ischemic disease and those with heart failure have the highest risk. Nevertheless sudden cardiac arrest by ventricular malignant arrhythmia can appear in young population without cardio-vascular risk factors and risk stratification remains a delicate issue. We present the case of a nineteen years old female patient, with resuscitated sudden cardiac arrest by ventricular fibrillation. Medical history include episodes of recurrent syncope (the last one 4 years ago), ventricular premature beats (VPB) -ventricular bigeminy- prolapsed mitral valve (PMV) with mild mitral regurgitation. She had an episode of upper airway respiratory tract infection three weeks prior the event. Methods: Case report: Under mechanical ventilation and antiarrhythmic treatment (betablocker, lidocaine) the vital parameters rapidly improves. The ECG shows ST segment elevation in lateral territory and the markers for myocardial necrosis are elevated. An acute coronary syndrome is excluded by coronary angiography which reveals normal coronary arteries. Echocardiography shows moderate systolic dysfunction with ejection fraction 35% of the left ventricle (LV) with hypokinetic segments in the antero-lateral wall and the apex, mild mitral regurgitation and no pericardial effusion. Laboratory tests demonstrates infl ammatory syndrome C – reactive protein (CRP) = 62.5 mg/dl; we could not identify any acute viral infection with serum specific tests. We did not perform endomyocardial biopsy (EMB). Results: Cardiac MRI ten days aft er the arrhythmic episode shows normal dimensions and function of the LV, trabeculation and areas of fibrosis of the left lateral free wall, with normal morphology of the right ventricle. With anti-arrhythmic treatment (beta-blocker and lidocaine) sinus rhythm alternates with ventricular bigeminy and there were repeated episodes of nonsustained ventricular polymorphic tachycardia. In this context: arrhythmic substrate (myocardial fibrosis), trigger (VPB) and an episode of SD we decide to implant an internal cardiac defibrillator (ICD) as secondary prevention. At three months evaluation – with beta-blocker and aldosterone antagonist treatment, the patient is asymptomatic, with normal LV function and no arrhythmic episodes to require defibrillation; the VPB persists. Conclusions: This data are with high probability sustaining postmyocarditis cardiomyopathy; the certain diagnosis even with EMB with immunohistochimic and biomolecular techniques is difficult to be done in current clinical practice. The presence of PMV and VPB prior to SD was not considered significant. This case illustrates the difficulties in establishing the diagnosis in young patients with no cardiovascular risk factors who suffer sudden cardiac arrest and also highlights the importance of SD secondary preventions with ICD.
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