Coronary embolism is one of the less common causes of myocardial infarction. In this case, we describe a patient who sustained a myocardial infarction due to coronary embolism which was successfully treated using a thrombus aspiration device, thereby obviating the need for any further coronary intervention.

       Case Report. A 48-year-old African American female presented to the emergency department with complaint of intermittent chest pressure for the past 10–12 hours. The patient had a history of hypertension, current tobacco abuse, past cerebrovascular accident without residual deficit, and had undergone mitral valve replacement 15 years earlier secondary to rheumatic mitral valve disease. Her presenting electrocardiogram (ECG) revealed sinus rhythm with T-wave inversion in leads V5–V6. Her initial cardiac enzymes were positive: CPK 822, CK-MB 87.2, CK index 10.6, troponin I 12.8 (abnormal > 0.5). The patient’s chest discomfort was relieved with therapy given in the emergency department, which included 325 mg aspirin, 300 mg clopidogrel, intravenous (IV) heparin, IV eptifibatide, IV nitroglycerin and 50 mg p.o. metoprolol. After the diagnosis of non-ST-elevation myocardial infarction was established, the patient was taken for diagnostic cardiac catheterization.

Figure 1. Selective coronary angiogram revealing a tubular, intraluminal defect in the second obtuse marginal branch of the circumflex artery (circled).

       Diagnostic catheterization revealed a tubular intraluminal defect (Figures 1 and 2) in the second obtuse marginal branch of the circumflex artery (2.5 mm vessel), with TIMI III flow. Otherwise, the left anterior descending and right coronary arteries were free of significant atherosclerotic coronary vascular disease. The

Figure 2. Tubular, intraluminal defect in the second obtuse marginal branch (zoom view).

estimated ejection fraction was 45% without significant wall motion abnormalities. The lesion was thought to be consistent with a cardiac embolus. Therefore, intervention was not undertaken at the time of diagnostic catheterization. Instead, IV eptifibatide was continued for 24 hours in an attempt to dissolve the thrombotic material. A repeat catheterization was planned for the next day to reevaluate the lesion. Intravenous heparin was initiated 4 hours post-sheath removal while transitioning to long-term oral anticoagulation.
Since the findings at diagnostic catheterization were thought to be embolic in nature, the patient was scheduled for transesophageal echocardiography (TEE) for inspection of her mitral valve prosthesis. Thepatient had a history of rheumatic mitral valve disease, with surgical implantation of a St. Jude mechanical prosthesis. The patient’s International Normalized Ratio on admission was subtherapeutic at 1.5 (therapeutic range: 2.5–3.5).
       TEE revealed a normal-functioning St. Jude mechanical prosthesis. No evidence of thrombus was observed. The left atrial appendage was without thrombus. There was no evidence of intra-atrial shunting by

Figure 3. Extracted specimen revealed a tubular, red-tan, tissue consistent with thrombus.

color-flow Doppler or agitated saline study. No significant regurgitant lesions were identified. After the TEE, the patient underwent a repeat catheterization to reevaluate the lesion. The intraluminal defect had not changed with 24 hours of antiplatelet therapy, and a decision was made to intervene on the second obtuse marginal lesion.
Coronary intervention proceeded utilizing a 6 Fr Voda guiding catheter via the right femoral approach. A 0.014 mm BMW guidewire (Guidant Corp., Indianapolis, Indiana) was introduced into the second obtuse

Figure 4. Selective coronary angiogram after thrombus extraction revealing no significant atherosclerotic lesion.

marginal branch. A Pronto® V3 thrombus extraction catheter (Vascular Solutions, Inc, Minneapolis, Minnesota) was introduced under fluoroscopy and advanced to the second obtuse marginal branch. Thrombectomy was performed, and a tubular structure was recovered which resembled thrombus (Figure 3). Repeat angiography revealed no atherosclerotic stenosis with TIMI III flow (Figure 4). No further intervention was undertaken. Pathologic analysis revealed a tubular, 8 x 2 mm, red-tan, firm, rubbery tissue consistent with thrombus (Figure 5).
       The patient had an uncomplicated hospital course and was discharged after her warfarin was in the therapeutic range. The patient was maintained on a daily 81 mg enteric-coated aspirin. The clopidogrel was discontinued.

       Discussion. Atherosclerotic coronary vascular disease is not the etiology of an acute coronary syndrome in as many as 1–7% of cases.¹ Within this subset, coronary embolism remains an important cause of myocardial infarction. Risk factors for coronary embolism include arrhythmias (e.g., atrial fibrillation), cardiac tumors, dilated cardiomyopathy, endocarditis, iatrogenic (during catheterization or cardiac surgery), intracardiac prosthesis, left ventricular aneurysm, or paradoxical embolism (e.g., pulmonary embolus with an associated intracardiac shunt).^2–10 The left anterior descending coronary artery is the most common site of embolism due to its takeoff from the left main artery.¹¹ The consequences of the embolic event depend on the size of the embolus and the size and distribution

Figure 5. Histology of the aspirated materials revealed thrombus.

of the artery receiving the embolus.
       To date, there is no consensus on the correct interventional technique to employ when treating myocardial infarction caused by coronary embolism. Modalities used include the percutaneous Fogarty maneuver,^12–13 primary angioplasty¹⁴ and thrombectomy with an aspiration catheter.²
       We utilized a Pronto catheter system to effectively diagnose and treat coronary embolism. Although other modalities could be utilized, we sought to avoid the potential disadvantages of the other treatment modalities. The Fogarty maneuver or advancing a guiding catheter to the site of embolism could potentially cause intimal dissection of the vessel, which could contribute to the development of thrombosis. Primary angioplasty could result in distal embolization and the no-reflow phenomenon. Kotooka et al reported three cases of coronary embolism caused by atrial fibrillation. In these cases, the rescue percutaneous thrombectomy system (Boston Scientific, Natick, Massachusetts) and the Thrombuster system (Kaneka Medics, Osaka, Japan) were used without complication and two of the three cases did not require balloon angioplasty or stent placement.
       Use of the Pronto^® catheter (Vascular Solutions, Inc., Minneapolis, Minnesota) was reported previously in acute myocardial infarction.15 The Pronto thrombus aspiration catheter is a monorail extraction system with a large diameter lumen (0.056 inch). It employs suction with a syringe allowing aspiration of thrombotic material during passage of the flexible catheter tip across the arterial segment. The Pronto extraction catheter is indicated for the removal of fresh, soft emboli and thrombi from arterial vessels. The Pronto catheter is contraindicated in vessels < 2 mm in diameter.
       We present a report of the Pronto catheter used to treat coronary embolism. Also, we believe this is the first reported case in which a thrombus extraction catheter was used to treat a coronary embolism after mitral valve replacement. This case demonstrates that embolectomy with a thrombus extraction catheter can be a feasible and safe approach for treating coronary embolism.