Abstract

After excluding cardiac genetic and structural abnormalities, idiopathic VF is estimated to account for ∼5% of cases of sudden cardiac death. In these cases, it may be difficult to identify an etiology for VF. We present a case of idiopathic polymorphic VT/VF (pVT/VF) with the diagnosis made in the EP lab. N/A A 47-year-old man had a witnessed cardiac arrest and was found to be in VF. A work-up including coronary angiography was unrevealing; MRI was largely normal, though suggestive of an inferolateral area of subepicardial scar. A subcutaneous ICD (SICD) was placed. He presented to us with recurrent pVT/VF on sotalol resulting in multiple ICD shocks, some of which failed to immediately defibrillate. At EP study, stimulation did not induce sustained ventricular arrhythmias. Standard pericardial access was obtained to permit epi/endo mapping to identify arrhythmogenic substrate. But immediately upon onset of pericardial mapping, ST segment elevation occurred, and the patient developed non-sustained pVT (Figure). Immediate coronary angiography revealed diffuse coronary spasm, most strikingly in the proximal LAD. With administration of intracoronary nitroglycerin, the LAD spasm and pVT/VF resolved; ST segment abnormalities resolved within minutes. DFT testing revealed a normal functioning SICD. He was discharged on long-acting nifedipine and nitrates for coronary vasospasm. Severe coronary vasospasm may cause idiopathic polymorphic VT/VF. Medical therapy with calcium-channel blockers and oral nitrates are the first-line therapy as ICD therapies alone may be ineffective in the setting of on-going spasm and ischemia.

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