Double vessel acute myocardial infarction showing simultaneous thrombotic occlusion of the distal right coronary artery and a marginal branch in a patient with persistent foramen ovale

Background: Simultaneous occlusion of two epicardial coronary arteries is an uncommon finding in patients presenting with ST-segment elevation acute myocardial infarction (AMI). We report the case of a 36-year-old man who had simultaneous thrombotic occlusion of the distal right coronary artery and a marginal branch of the left coronary artery.

Case Report: The 36-year-old male patient was admitted to a peripheral hospital with sudden central chest pain. There where no neurologic abnormalities. The patient was a cigarette smoker.  Electrocardiography revealed ST-segment elevation in leads II, III, aVF, and V4–V6 (Figure 1A). The patient received 500 mg aspirin und unfractionated heparin and was hemodynamic stable.
He was referred for urgent cardiac catheterization. Coronary angiography showed a flow limiting thrombus of the distal posterior descending branch of the right coronary artery (RCA) und a thrombotic occlusion of the distal marginal branch of the left coronary artery (LCA) (Figure 1B, arrows). Percutaneous balloon angioplasty and placement of two stents in the RCA resulted in TIMI III flow. The lesion in the distal LCA was consideres to be to small for stent implantation and no invasive therapy was delivered.
The maximal creatininkinase was 1695 U/l und ejection fraction was 43% in echocardiography. For further differentiation a cardiac magnetic resonance imaging was performes after 10 days. The short axis views showed two areals of wall motion abnormalies, cardiac edema and late enhancement. One areal was posterolateral in the perfusion territory of the marginal branch and the other was inferior corresponding to the distal RCA perfusion territory.
Assuming one cause of the simultaneous thrombotic occlusion of two coronary arteries a transesophageal echocardiography was performed. It showed a small, but repeatedly demonstrable persistent open foramen ovale (PFO). We consider this as the possible cause of the simultaneous thrombotic occlusion and PFO closure with a device is scheduled. Antithrombotic and heart insufficiency therapy was prescribed.

Conclusion:  Myocardial infarction of simultaneous total occlusion of two coronary arteries is a rare constellation and has usually with a poor prognosis. Our 36-year-old patient was fortune that only distal branches where occluded. Nevertheless myocardial function was impaired with a creatininkinase was 1695 U/l und an ejection fraction was 43%.
Atheromatous plaque rupture with subsequent thrombus formation and resulting vessel occlusion is the most common cause of AMI, but myocardial infarction may occur with non-obstructive coronary arteries (MINOCA). Patent foramen ovale (PFO) is a risk factor for systemic embolic events such as cryptogenic stroke. Far less commonly patent foramen ovale is associated with non-cerebral systemic embolic events such as coronary artery embolism. Our young patient had a small PFO and a simultaneous thrombotic occlusion of two small epicardial coronary arteries. We suggest the PFO as the cause of the MINOCA. In such a constellation it should be searched for a PFO with the option of device closure.



Figure 1: Medical findings of an 36-year-old patient with MINOCA and PFO. A: electrocardiogramm with ST segment elevation, B: thrombotic occlusion of the distal RCA and distal marginal branch (arrows), C und D: Cardiac magnetic resonance imaging showing edema and late enhancement in two different areas, E: transesophageal echocardiography with PFO.