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A 50-year-old man who had previously been in good general health was admitted to our department after an out-of-hospital cardiac arrest, with documented ventricular fibrillation. Normal sinus rhythm was restored by defibrillation and our patient experienced an uneventful neurological recovery. The baseline ECG was normal (figure 1). Apparent underlying heart disease, including myocardial ischaemia, was excluded by echocardiography, bicycle ergometry, coronary angiography and Holter monitoring. Flecainide drug challenge did not demonstrate Brugada ECG patterns. Electrophysiological study did not reveal any inducible ventricular arrhythmia. An implantable cardioverter defibrillator was inserted, which delivered therapy on two separate occasions during follow-up due to ventricular tachycardia. These events occurred two years after the index episode, six-months apart and on both occasions not related to exercise or other specific activity. Outpatient follow-up Holter monitoring demonstrated transient ST-segment elevation in the inferolateral ECG leads, during which the patient suffered from atypical chest discomfort in the early morning hours, not related to physical exertion (figure 2). Subsequently repeated coronary angiography, including fractional flow velocity reserve measurements, was normal. However, an extended and diffuse coronary spasm of the left descending coronary artery, occluding the first diagonal branch, was found following intracoronary administration of acetylcholine (figure 3). The spasm resolved and the flow was restored after administration of nitroglycerin. A calcium channel blocker, angiotensin-converting enzyme inhibitor, aspirin and statin therapy were started before discharge. Neither symptoms nor ICD therapy recurred during the following 18 months of follow-up.
Figure 1
Baseline 12-lead electrocardiogram.
Figure 2
Holter recording during transient anginal chest pain in the morning hours, not related to physical exertion. ST-segment elevation is recorded.
Figure 3
Selective contrast injection into the left coronary artery before the administration of acetylcholine (right panel). A fractional flow reserve (FFR) wire was introduced into the left anterior descending artery before acetylcholine provocation and not manipulated following FFR measurement, which appeared to be normal. Vessel diameter is reduced significantly due to coronary spasm after coronary administration of acetylcholine (left panel).