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: email@example.com
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.