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This manuscript received a double-blind review from members of the Cath Lab Digest editorial board. Disclosure: The authors report no conflicts of interest regarding the content herein.
The authors can be contacted via Dr. Aditya Kapoor at email@example.com.
Coronary embolism leading to acute myocardial infarction (MI) is a rare occurrence in patients with mechanical and tissue prosthetic valves and has been reported usually in patients with a single valve prosthesis.1-5 The usual therapeutic strategy has been thrombosuction with or without plain balloon angioplasty and experience with coronary stenting in such cases is limited.6 A young female with mechanical aortic and mitral prosthetic valves discontinued oral anticoagulation (OAC) 3 months prior and sustained an acute ST-elevation anterior MI. The patient stopped OAC voluntarily (a not infrequent occurrence in the developing world, primarily due to lack of knowledge and ignorance on part of the patients). Although she had been advised to obtain regular follow-up in the valve clinic, she discontinued these visits, also of her own volition. While both prosthetic valves were functioning normally, coronary angiography revealed a mid 100% occluded left anterior descending artery (LAD) that was successfully stented.
A 35-year-old premenopausal female with no coronary risk factors presented with sudden chest pain and a 12-lead electrocardiogram (ECG) revealed acute anterior ST-elevation MI (Figure 1). She had undergone double valve replacement 10 years ago for regurgitant lesions at both aortic and mitral valves (a St. Jude Medical bileaflet 27 mm at the mitral valve and 21 mm at the aortic valve) due to underlying chronic rheumatic heart disease. The patient had discontinued OAC 3 months prior and was not on any oral contraceptives. At admission, the pulse rate was 75/min, blood pressure 135/85 mm Hg, and prosthetic valve clicks were well audible. Echocardiography demonstrated normally functioning mitral and aortic prostheses, severely hypokinetic LAD territory, and a left ventricular (LV) ejection fraction of 45%. No thrombus was demonstrable either at the valves, in the LV, or left atrial cavity (Figures 2-3, Video 1).
The admission international normalized ratio (INR) was 1.0, while a work up for hypercoagulable state was normal (normal lupus anti-coagulant and protein C/S levels). After loading with oral aspirin (325 mg) and clopidogrel (600 mg), the patient underwent coronary angiography via the right radial route, which revealed total occlusion of the mid LAD with grade 5 thrombus (Figure 4, Videos 2-3). On fluoroscopy, a normal opening of both mechanical valves was documented (Videos 2-3). Intravenous tirofiban was administered, the lesion crossed using a 0.014-inch floppy wire, and manual aspiration of the thrombus was attempted with an aspiration catheter (Thrombuster, Medtronic). Since no significant improvement in thrombus burden was noted, balloon angioplasty using a 1.5 mm x 10 mm and 2.5 mm x 10 mm balloon was performed, resulting in TIMI-2 flow in the LAD. A residual lesion was evident in the mid LAD, which was stented using a sirolimus drug-eluting stent (Pronova-XR, 2.75 x 16 mm, Vascular Concepts), resulting in TIMI-3 flow (Figure 5, Videos 4-5). Post-procedure unfractionated heparin was continued and oral warfarin initiated. After achieving a target INR of 2-3, the patient was discharged on the fifth day. The patient remained on aspirin, clopidogrel, and OAC for 3 months, followed by continuation of clopidogrel and OAC on follow-up, with omission of aspirin from the therapeutic regimen. She remains asymptomatic at the last follow-up of nearly 8 months and her ejection fraction has improved from 45% to 58%.
Coronary embolization and acute MI in patients with both mechanical and tissue heart valves has been reported, for the most part, in patients with single prosthetic valves.4-6 Most of these cases present with anterior MI with embolic obstruction of the left coronary system, postulated to be due to the preferential flow into the LAD during cardiac diastole. Sub-therapeutic anticoagulation is an important pre-disposing factor, as happened in our case. Prosthetic valve function in many of these cases has been reported to be normal and the occurrence of associated thrombus on the prosthetic valve is quite rare. We also did not document any thrombus on the valves, or in the LV or left atrial cavity.
Small micro-thrombi may have formed on the valves due to the sub-therapeutic anti-coagulation; these thrombi, while insufficient to cause acute prosthesis dysfunction, could have embolized in toto to the coronary vasculature, leaving the valve surface devoid of any residual thrombus. It was quite fortuitous that despite having two mechanical prosthetic valves, both valves were devoid of any thrombus. Although coronary embolism remains a presumptive diagnosis, the patient’s age, lack of any coronary risk factors, and discontinuation of OAC, along with the angiographic appearance of the culprit artery, suggest an embolic etiology.
The optimal management strategy for such patients has varied, and thrombosuction with or without balloon angioplasty has been performed in most cases.5-6 Since following thrombosuction and balloon angioplasty, only TIMI-2 flow could be achieved due to the presence of a residual stenosis and the risk of possible re-occlusion at this site, a stent was deployed.
Coronary embolization leading to acute MI is a rare entity in patients with prosthetic valves. We report the case of a young female who presented with acute anterior MI resulting from possible acute coronary embolism in the setting of a double valve replacement performed 10 years earlier. Clinicians should bear in mind that coronary embolism with acute MI can occur even without prosthetic valve thrombosis, especially in the setting of sub-optimal INR.
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