Coronary plaque instability in severe acute respiratory syndrome.

In his second week of severe acute respiratory syndrome (SARS) illness, a patient developed an unusually complicated course of acute coronary syndrome. One day after initial stabilization of a non-ST-elevated anterior myocardial infarction (MI), he sustained an ST-elevated anterior MI. Eight hours after emergency coronary intervention to the culprit lesion, he developed another ST-elevated MI in the inferior territory. Acute inflammation and cytokine storm in the immunopathological phase of SARS may play a role in coronary plaque instability. Physicians should be alert to this potentially fatal complication and adopt appropriate vigilant and aggressive management strategies.

Case report

A 66-year-old man presented in April 2003 with fever, cough, and dyspnoea for 3 days. He showed bilateral lung base infiltrates on chest radiograph, and fulfilled the World Health Organization case definition of probable severe acute respiratory syndrome (SARS).

He had diabetes mellitus and hypertension, but no known history of coronary artery disease. On admission, he was in mild respiratory distress. Intravenous ribavirin, methylprednisolone, and levofloxacin were started according to our protocol for SARS. However, he had progressively deteriorating respiratory status necessitating pulsed intravenous methylprednisolone and non-invasive ventilatory support initiated on Day 3, and then was subsequently stabilized. On Day 7, he developed acute non-ST-elevated anterior myocardial infarction (MI), which responded to medical therapy. On Day 8, chest pain recurred with extensive ST-elevated MI in the same territory. Intravenous streptokinase was given. The patient had persistent symptoms and developed frequent ventricular tachycardia with hypotension. Urgent coronary angiography revealed 3-vessel disease Fig. 1, Fig. 2 . A critical stenosis with thrombus was present in the culprit left anterior descending (LAD) artery. The right coronary artery (RCA) could not be selectively cannulated. Angioplasty and stenting was successfully performed to the left circumflex (LCx) artery and the culprit LAD artery, respectively, with symptom abolition and haemodynamic stabilization. However, sudden retrosternal pain and hypotension recurred 8 h later. ECG showed acute ST-elevated inferior MI attributable to the RCA territory. In view of the gross haemodynamic instability, and difficulty in cannulating the RCA, further intervention was not contemplated. Intravenous alteplase was administered. The patient continued to deteriorate and succumbed on the same day.

Fig. 1

Coronary angiogram of left coronary artery in right anterior oblique cranial projection, showing a stenosis with thrombus in the mid segment of the left anterior descending artery.

Fig. 2

Non-selective coronary angiogram of right coronary artery in left anterior oblique projection, showing multiple stenoses in the proximal and distal segments of the vessel.

Discussion

The patient had several provoking causes for acute coronary syndrome. Diabetes mellitus and hypertension predisposed him to chronic obstructive coronary atherosclerosis. Hypoxaemia and stress from the acute respiratory illness could aggravate existing imbalance between myocardial oxygen supply and demand. Whether the use of ribavirin can be incriminated is unclear. Acute MI had been reported in a patient receiving ribavirin and interferon for active hepatitis C, in whom a reduction in haemoglobin was an alternative explanation of myocardial ischaemia [1].

A systemic cause of plague instability could be implicated in view of the patient's recurrent acute coronary syndromes involving more than one coronary territory. Vascular inflammatory response, raised inflammatory cytokines and acute phase proteins such as fibrinogen have been linked to acute coronary syndrome and plague instability [2], [3]. Murphy et al. [4] recently demonstrated elevated markers of circulatory monocytes and endothelial activation, providing evidence that a systemic rather than local inflammation is implicated in acute coronary events. Endothelial activation and inflammation has also been shown to be associated with failure of thrombolyis in acute MI [5]. In the context of SARS, a tri-phasic clinical course has been observed: viral replication phase, immunopathological phase and phase of end-organ damage [6]. The immunopathological phase is characterized by clinical progression in respiratory distress and radiological deterioration which could be due to immune-mediated damage from excessive host response. The resultant proinflammatory cytokine “storm” may have contributed to coronary plague instability and a catastrophic series of cardiac events in our patient. Acute MI did account for two of the seven deaths among 75 SARS patients in another report [6]. Physicians should be alert to potentially fatal cardiac problems in SARS and adopt vigilant and aggressive treatment strategies as appropriate.