By: 5 September 2016
Case Report: ST Elevation Myocardial Infarction in a patient with a normal coronary angiogram


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).

Screen Shot 2016-09-02 at 09.54.47

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).

Screen Shot 2016-09-02 at 09.55.08

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 inserted on day 12 and the patient was ultimately discharged home 14 days after his acute presentation.



Prinzmetal’s Angina

Coronary artery vasospasm comprises a spectrum of vasospastic syndromes that are now well recognised in the aetiology of ischaemic heart disease. Prinzmetal’s or variant angina, an extreme manifestation of this phenomenon, was first described in a seminal paper by Prinzmetal et al in 19591. This form of angina is different from typical angina pectoris in that chest pain is not predictably induced by exercise. ECGs captured during these periods show transient but marked ST segment elevation in a territory specific manner. This observation led Prinzmetal et al to propose increased “tonus” within the coronary artery as an explanation for this phenomenon1. Endothelial dysfunction, coronary smooth vessel hyperactivity and autonomic imbalance have all been proposed as mechanisms underlying the vasospasm (reviewed by MacAlpin, 2015 2), though their individual contribution and interplay remains elusive.

Typically, patients with variant angina report recurrent episodes of chest pain, that come on during rest and which resolve spontaneously. Diagnosis of coronary artery spasm is made based on a history of non-exertional chest pain, with associated ST segment changes (elevation or depression) and subsequent “normal” coronary angiography.

The transient nature of the vasospasm makes ECG documentation difficult. In addition, intra-arteriographic findings of obstructive disease (albeit at a sub-critical level) frequently co-exist making the diagnosis of vasospasm yet more challenging. Interestingly, it has previously been proposed that pathological “eddies” surrounding areas of atherosclerosis may in fact be a trigger for vasospasm. This is supported by the fact that coronary artery vasospasm rarely occurs in pristine coronary arteries, is relatively rare in young people and smoking is a major aetiological risk factor in the development of both.

The Task Force on the Management of Stable Angina Pectoris of the European Society of Cardiology 2006 guideline 3,4 makes the following recommendations for diagnosis and management of vasospastic angina:

  • ECG during angina
  • Coronary angiography to determine the extent of underlying coronary artery disease
  • Intracoronary provocation testing in patients with normal or non-obstructive lesions on coronary angiography and the clinical picture of coronary spasm3. Provoked ST segment elevation with intracoronary administration of acetylcholine or ergonovine has been shown 5.

Nitrates and calcium channel antagonists are the mainstay of pharmacological management of coronary artery vasospasm. It is suggested that nitrates are effective in abolishing acute vasospasm, however prevention of these attacks is better achieved through the use of high doses of calcium channel blockers such as verapamil, diltiazem or nifedipine. Nicorandil, a potassium channel activator, may also be useful in refractory vasospastic angina6. Beta-blockers should be avoided in vasospastic angina due to the possible blockade of vasodilatory B2 activity.

In patients, such as in the case described above, where life-threatening arrhythmias have occurred, or those where syncope is associated with angina episodes, insertion of an implantable cardiac defibrillator (ICD) device is advised as the degree of success with pharmacological treatment alone in such cases is currently unknown.

Finally, as described above, our patient was found to have presented to hospital with angina and ECG changes two years prior to admission. Coronary angiography was normal at this time and he was given a diagnosis of myopericarditis. In a small observational study by Yilmaz and colleagues of biopsy positive parvovirus B19 myocarditis patients, intracoronary acetylcholine provocation testing suggested that the cause of chest pain in the absence of significant coronary artery disease may actually be coronary artery vasospasm7.



  1. Prinzmetal M, Kennamer R, Merliss R, Wada T, Bor N. Angina pectoris. I. A variant form of angina pectoris; preliminary report. The American journal of medicine. Sep 1959;27:375-388.
  2. MacAlpin RN. Some observations on and controversies about coronary arterial spasm. International journal of cardiology. Dec 23 2014;181c:389-398.
  3. Messerli FH, Mancia G, Conti CR, Pepine CJ. Guidelines on the management of stable angina pectoris: executive summary: the task force on the management of stable angina pectoris of the European society of cardiology. European heart journal. Dec 2006;27(23):2902-2903; author reply 2903.
  4. Fox K, Garcia MA, Ardissino D, et al. Guidelines on the management of stable angina pectoris: executive summary: The Task Force on the Management of Stable Angina Pectoris of the European Society of Cardiology. European heart journal. Jun 2006;27(11):1341-1381.
  5. Ong P, Athanasiadis A, Sechtem U. Patterns of coronary vasomotor responses to intracoronary acetylcholine provocation. Heart (British Cardiac Society). Sep 2013;99(17):1288-1295.
  6. Lablanche JM, Bauters C, McFadden EP, Quandalle P, Bertrand ME. Potassium channel activators in vasospastic angina. European heart journal. Jul 1993;14 Suppl B:22-24.
  7. Yilmaz A, Mahrholdt H, Athanasiadis A, et al. Coronary vasospasm as the underlying cause for chest pain in patients with PVB19 myocarditis. Heart (British Cardiac Society). Nov 2008;94(11):1456-1463.


Authors: Roochi Trikha1, Rebekah Rodgers2, Mark Snazelle3 & Kayvan Kamalvand4

1,2, Core trainees in intensive care medicine. 3 Consultant intensivist and anaesthetist. 4 Consultant cardiologist

William Harvey Hospital, East Kent Hospitals University Foundation Trust