Myocardial Infarction Due to Paradoxical Embolism in a Patient with Large Atrial Septal Defect
- Volume 21 - Issue 10 - October, 2009
- Posted on: 10/13/09
- 0 Comments
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From the Department of Cardiology, University Hospital Bern, Switzerland.
Disclosure: Bernhard Meier has received a research grant and is on the speakers bureau for AGA Medical, Corporation.
Manuscript submitted April 6, 2009, provisional acceptance given June 4, 2009, and final version accepted June 9, 2009/Address for correspondence: Bernhard Meier, MD, Professor and Chairman of Cardiology, Swiss Cardiovascular Centre Bern, University Hospital, CH-3010 Bern, Switzerland. E-mail: firstname.lastname@example.org
ABSTRACT: We present the case of a patient who presented with acute inferior myocardial infarction and embolic occlusion of the distal left anterior descending and proximal right coronary artery. A large atrial septal defect (ASD) was seen on transesophageal echocardiography and the ASD was closed during the same session as coronary angiography and percutaneous coronary intervention. The presence of embolic or thrombotic occlusions of coronary arteries should prompt interventional cardiologists to look for a patent foramen ovale or ASD and perform percutaneous closure right away.
J INVASIVE CARDIOL 2009;21:E184–E186
Case Report. A 52-year-old male, heavy smoker, visited his general practitioner (GP) because of dyspnea and a cough lasting for about 3 weeks. The patient reported having a swollen leg and subsequent chest pain 3 weeks previously. The GP found a dyspneic, cyanotic patient with markedly reduced transcutaneous oxygen saturation (72%) while the patient was breathing room air. The electrocardiogram revealed third-degree atrio-ventricular block with ST elevations in the inferior leads (Figure 1). The qualitative troponin test was positive and the C-reactive protein (CRP) was elevated at 246 mg/l. Medical treatment for acute coronary syndrome (ACS) was initiated and the patient was referred to our emergency department.
The patient was tachydyspneic (35/minute); his blood pressure was 130/72 mmHg and his pulse was 70/minute. There was no pulmonary congestion and no murmur was heard during cardiac auscultation. The partial O2 pressure while breathing 15 liters of O2 through a facemask was 47 mmHg (normal range: 71–100 mmHg), and his O2 saturation was 79%. Laboratory analysis showed that the patient’s creatine-kinase was 693 U/l (normal value < 190), his troponin-T was 3.39 ug/l (< 0.01), and he had an elevated BNP of 425 pg/ml (< 80).
The patient was admitted to the intensive care unit where endotracheal intubation was performed and a provisory pacemaker was inserted. Transesophageal echocardiography was performed and showed a large atrial septal defect (ASD) with a bidirectional shunt and a dilated right ventricle with severely impaired systolic function. Left ventricular systolic function was only slightly reduced with inferior hypokinesia.
The clinical status of the patient worsened over the subsequent hours, necessitating vasoactive support with dobutamine and noradrenalin. Cardiac catheterization was carried out under general anesthesia 24 hours after admission and coronary angiography showed an occlusion of the proximal right coronary artery (RCA) (Figure 2A) and an occluded distal left anterior descending artery (LAD) (Figure 2B). Recanalization of the RCA was successful and 2 everolimus-eluting stents were deployed (Figure 2C). After this, the ASD was crossed with a 0.035 inch wire and sized with an AGA 34 mm balloon (AGA Medical Corp., Minneapolis, Minnesota). A 40 mm Amplatzer septal occluder was successfully deployed to close the defect under fluoroscopic guidance (Figure 2D).
The patient improved and was extubated 3 days later. He remained dyspneic on heavy exertion. Echocardiographic control before discharge (13 days after admission) showed a correctly placed occluder (Figure 3) with no right-to-left shunting, a dilated right ventricle with markedly improved systolic function, no pulmonary hypertension and a slightly reduced systolic function of the left ventricle. Computed tomography (CT) of the lung to look for pulmonary embolism showed a lack of perfusion in a segmental artery of the right upper lobe suggestive of pulmonary embolism (Figure 4).
Discussion. Acute myocardial infarction (AMI) is usually the consequence of plaque rupture, resulting in complete occlusion of an epicardial coronary artery.1,2 Paradoxical embolism due to a patent foramen ovale (PFO) or ASD, resulting in AMI has been reported in the literature,3–5 but is rarely considered in clinical practice. Our patient had right ventricular infarction and a large ASD, which resulted in rapid hemodynamic deterioration due to increased right-to-left shunting (minimal oxygen saturation was 69% while receiving 100% oxygen). Coronary angiography revealed mild, diffuse coronary artery disease with an obviously embolic occlusion of the distal LAD and a likely embolic occlusion of the proximal RCA. This, along with patient’s history of a swollen leg made paradoxical embolism very likely. The confirmation of a pulmonary embolism with CT strongly supported this hypothesis. Emergency percutaneous closure of the ASD resulted in rapid improvement of the clinical situation.
This case demonstrates that an ASD can be responsible for multiple quasi-simultaneous myocardial infarctions. Its ad hoc closure can improve the physical state dramatically, particularly in the realm of right ventricular infarction.
The presence of an embolic or thrombotic coronary occlusion should prompt interventional cardiologists to consider paradoxical embolism and to actively look for a PFO or ASD during the initial workup or cardiac catheterization. Transcatheter closure is a safe and feasible alternative to surgical closure6 and can be performed during the same session as coronary angiography and angioplasty.