CASE REPORT
A 48-year old Caucasian male presented to our hospital following a witnessed out-of-hospital cardiac arrest. Bystander cardiopulmonary resuscitation (CPR) was initiated swiftly. On arrival of the ambulance crew the initial arrest rhythm was found to be ventricular fibrillation VF for which he received CPR with two DC shocks. Return of spontaneous circulation (ROSC) was established within ten minutes of the initial collapse. The post-ROSC ECG showed ST segment elevation in leads II, III and aVF (see figure 1), in keeping with a right coronary artery occlusion. The patient was intubated on scene and brought immediately to the William Harvey Hospital with a view to primary percutaneous coronary intervention (pPCI).
Figure 1. Presentation ECG showing Inferior STEMI
Collateral history revealed that the patient had experienced several episodes of left-sided chest and shoulder pain in the preceding two days. These episodes were not associated with physical exertion and had been attributed by the patient to work-related stress. On further questioning it transpired that two years previously, the patient had presented to the emergency department with chest, arm and shoulder pain following a one-week history of diarrhoea, fever and night sweats. ECG had shown mild ST segment elevation in leads V2-V5 associated with a significant troponin rise leading to an initial diagnosis of Non-ST Elevation Myocardial Infarction (NSTEMI). Coronary angiography had subsequently been normal. Echocardiography had showed a left ventricular ejection fraction of 35-40 per cent with an 0.7cm pericardial effusion and mild hypokinesia of the septum and anterior wall. He had been given a diagnosis of viral myopericarditis and discharged home on Ramipril. Repeat echocardiography some months later had shown resolution of the pericardial effusion, improved ejection fraction of 55-60 per cent and residual mild anteroseptal and apical hypokinesia. He had subsequently returned to work, suffering no further symptoms.
On arrival at the emergency department, the initial inferior ST segment elevation reported on the post-ROSC ECG had resolved. Bedside echocardiography revealed mild infero-basal hypokinesia with a left ventricular ejection fraction of 55 per cent. The patient was immediately transferred to the cardiac catheter suite where, once again, coronary angiography showed no clinically significant disease in the major coronary arteries (see figure 2).
Figure 2. Normal right coronary artery at angiography
The patient was subsequently transferred to the intensive care unit for post cardiac arrest care including therapeutic hypothermia. During the first 48 hours on intensive care there were multiple episodes of ST elevation in the inferior leads. On each occasion this ST elevation would be followed shortly thereafter by significant bradycardia (with rates as low as 30 beats per minute) with first-degree heart block and associated haemodynamic compromise. The bradycardia would, in turn, be followed predictably by ventricular tachycardia (VT) requiring emergency DC cardioversion. On two occasions the VT degenerated to VF requiring brief cardiopulmonary resuscitation and DC cardioversion.
A clinical diagnosis of coronary artery vasospasm or Prinzmetal’s angina was made. Treatment was commenced with an infusion of glyceryl trinitrate (GTN), followed by initiation of calcium channel blockade with nifedipine. The potassium channel activator nicorandil was also added. His rapid response to medical treatment obviated the need to place temporary pacing wires.
After 24 hours free from dysrhythmia or ECG changes, periods of sedation hold were trialled. To facilitate weaning from sedation and mechanical ventilation, a percutaneous tracheostomy was inserted on day four. Weaning was successfully achieved over the following few days and the patient was decannulated uneventfully on day nine. He was subsequently transferred to the coronary care unit on day 10, fully alert and orientated.
A dual chamber implantable cardioverter-defibrillator (ICD) device was later i