A 40-year-old woman presented with an extensive anterior myocardial infarction. After initial thrombolytic therapy, coronary angiography was performed a few days later revealing normal coronaries with severe left ventricular dysfunction secondary to anterior wall akinesia. Echocardiography showed severe left ventricular systolic dysfunction and a patent foramen ovale (PFO). The patient had a history of long-term oral contraceptive consumption. A paradoxical embolus into the left coronary artery via a large PFO was suspected and was successfully treated with PFO closure.
A 40-year-old woman presented to the emergency room with severe substernal chest pressure and ST segment elevation in I, AVL, and precordial leads with reciprocal ST depression in the inferior leads. She was treated with streptokinase on the diagnosis of extensive anterior wall myocardial infarction (MI), with symptomatic relief. A few days later she was referred to a tertiary center for further evaluation. A coronary angiogram was performed on arrival revealing normal coronaries (see Figure 1) with anterior akinesia and apical aneurysm.
She had no history of venous thrombosis or smoking and a negative family history for coronary artery disease. She had a history of fetal abortion twice (one was induced and the other one was spontaneous). She had been on an oral contraceptive agent for at least the last 14 years. Physical examination revealed fixed splitting of her second heart sound and systolic II/VI murmur at the base of her heart with no sign of deep vein thrombosis. Transthoracic echocardiography (TTE) revealed moderate left ventricular (LV) enlargement and severe LV systolic dysfunction (LV ejection fraction [LVEF] 35 %) with apical aneurysm and anteroseptal and anteroapical wall akinesia. She also had mild mitral and tricuspid regurgitation with estimated systolic pulmonary arterial pressure of 35 mmHg.
Her laboratory tests, except her cardiac enzymes, were normal. Her further tests for hypercoagulability six months later were normal (normal antiphospholipid antibody, antinuclear antibody [ANA], cytoplasmic antineutrophil cytoplasmic antibody [C.ANCA], perinuclear antineutrophil cytoplasmic antibody [P.ANCA], erythrocyte sedimentation rate [ESR], C-reactive protein [CRP], anti ds.DNA, serum homocysteine, factor V Leiden, serum proteins C and S, lupus anticoagulant, anticardiolipin antibody, and thyroid function test). Ultrasound studies of her pelvic and leg veins were also normal. Her anterior wall motion abnormalities did not change significantly at six-month follow-up. Due to localized wall motion abnormalities with persistent electrocardiogram (ECG) changes and presence of wall motion abnormalities on follow-up echocardiogram, diagnosis of stress cardiomyopathy was deemed to be unlikely. Paradoxical embolism into her left anterior descending artery was suspected. Transesophageal echocardiography (TEE) was performed revealing a tunnel-shaped 8 mm patent foramen ovale (PFO) with significant right-to-left shunt seen on her bubble study (see Figure 2). After discussion with the patient about different treatment options including aspirin and anticoagulation, the patient opted for PFO closure which was successfully performed using an amplatzer closure device (see Figure 3). The patient remains stable at six-month follow-up and is off contraceptive medication. Her wall motion abnormalities remained unchanged on follow-up echocardiographic examination.
Extensive MI in the setting of normal coronary arteries in young adults can have a variety of non-atherosclerotic causes, including vasculitis, trauma, vasospasm, spontaneous dissection, congenital coronary anomalies, Takotsubo (or stress-induced) cardiomyopathy, or embolization into the coronary arteries (infectious endocarditis, mitral valve prolapse, cardiac myxoma, atrial fibrillation, paradoxical emboli, etc.).1 In this case, paradoxical embolism was the most likely cause of her extensive MI. Stress-induced cardiomyopathy was unlikely due to persistent localized wall motion abnormalities and lack of emotional or physical stress. She had hypercoagulable state due to long-term consumption of oral contraceptives, together with the presence of a PFO.2–4
Her PFO was a tunnel-like space between the overlying septum secundum and septum primum1 which is found in 25–30 % of autopsies and in community based TEE studies.5,6 The prevalence and size of PFOs are similar between the genders.5 A PFO can serve as a pathway for passage of emboli from the venous to the arterial system via right-to-left shunting when the pressure in the right atrium is higher than in the left atrium during the Valsalva maneuver. PFO is much more common than other lesions as a cause of intracardiac right-to-left shunting.6 Most patients with PFO are asymptomatic but many may present with cryptogenic stroke, MI, possible migraine and vascular headache, decompression sickness, or platypnea.7–10
Further evaluation of patients with suspected paradoxical emboli and PFO includes TTE or TEE with bubble study.6,11,12 Transcranial Doppler is another method for documenting right-to-left shunting.12–14 TEE is more sensitive than TTE for detection of potential sources of cardiac emboli.12,15,16 In patients with PFO, agitated saline injected during TEE or TTE examination should appear in the left-sided cardiac chambers within three beats after contrast opacification of the right atrium, suggesting the presence of an intracardiac shunt, as opposed to the late appearance of bubble, suggesting shunting at the pulmonary level.1 However, in many patients with PFO, bubble studies could remain negative if right-to-left shunting only occurs intermittently. Treatment of the first-time occurrence of suspected paradoxical embolism in young patients without anticoagulation abnormalities is controversial. Based on the guidelines, aspirin therapy should be the first treatment choice in low-risk patients. However, closure of PFO in young patients is a viable option that should be discussed with each patient individually based on their risk factor and preference.
- Libby P, Bonow RO, Mann DL, Zipes DP (eds), Braunwald’s Heart Disease, eighth edition, Philadelphia: Elsevier Saunders, 2008.
- Hara H, Virmani R, Ladich E, et al., Patent foramen ovale: current pathology, pathophysiology, and clinical status, J Am Coll Cardiol, 2005;46:1768–76.
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- Hagen PT, Scholz DG, Edwards WD, Incidence and size of patent foramen ovale during the first 10 decades of life: an autopsy study of 965 normal hearts, Mayo Clin Proc, 1984;59:17–20.
- Meissner I, Whisnant JP, Khandheria BK, et al., Prevalence of potential risk factors for stroke assessed by transesophageal echocardiography and carotid ultrasonography: the SPARC study. Stroke Prevention: Assessment of Risk in a Community, Mayo Clin Proc, 1999;74:862–9.
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- Di Tullio M, Sacco RL, Venketasubramanian N, et al., Comparison of diagnostic techniques for the detection of a patent foramen ovale in stroke patients, Stroke, 1993;24:1020–4.
- Droste DW, Schmidt-Rimpler C, Wichter T, et al., Right-to-leftshunts detected by transesophageal echocardiography and transcranial Doppler sonography, Cerebrovasc Dis, 2004;17:191–6.
- Kerr AJ, Buck T, Chia K, et al., Transmitral Doppler: a new transthoracic contrast method for patent foramen ovale detection and quantification, J Am Coll Cardiol, 2000;36:1959–66.
- Pearson AC, Labovitz AJ, Tatineni S, Gomez CR, Superiority of transesophageal echocardiography in detecting cardiac source of embolism in patients with cerebral ischemia of uncertain etiology, J Am Coll Cardiol, 1991;17:66–72.
- Rahmouni HW, Keane MG, Silvestry FE, et al., Failure of digital echocardiography to accurately diagnose intracardiac shunts, Am Heart J, 2008;155:161–5.