Thrombectomy and Fibrinolytic Therapy of Prosthetic Valve Thrombosis Complicated by Coronary Embolism

ABSTRACT: Prosthetic valve thrombosis is rare; its complication by coronary embolism is even more uncommon and when present, often fatal. Here, we present a rare case of mechanical aortic valve thrombosis with coronary emboli presenting in cardiogenic shock, managed successfully using a hybrid approach of mechanical thrombectomy and intravenous fibrinolytic therapy. J INVASIVE CARDIOL 2011;23:E243–E245 ———————————————————— Prosthetic valve thrombosis (PVT) is an uncommon but serious and potentially life-threatening complication of heart valve replacement.¹ Coronary embolism (CE) is a further catastrophic sequelae of PVT that is rare and often fatal.² Surgical thrombectomy and valve replacement are usually required for PVT,³ in addition to coronary artery bypass grafting or percutaneous coronary intervention (PCI) for CE.² However, in high-risk subsets, intravenous fibrinolytic therapy has been used as an alternative due to high operative mortality.³ We present herein a rare case of PVT complicated by CE in cardiogenic shock that was treated successfully with percutaneous coronary thrombectomy and intravenous fibrinolytic therapy. Case Report. A 55-year-old, morbidly obese male with a known history of mechanical aortic valve replacement (25 mm Top Hat, Carbomedics, Austin, Texas) 2 years prior, presented with sudden onset of left-sided chest pain and shortness of breath. Physical examination was remarkable for moderate respiratory distress, tachycardia (heart rate, 122 beats/minute), mild hypotension (systolic blood pressure, 91 mmHg), hypoxia with diminished pulse oximetry on room air (requiring 4 liters supplemental oxygen), and cardiac auscultation with distant heart sounds and no prosthetic valve clicks. Electrocardiogram on admission revealed sinus rhythm with right bundle branch block and left posterior fascicular block, which was unchanged from previous exam. Laboratory analysis was pertinent for elevated troponin at 156.8 and subtherapeutic INR of 1.2. A technically limited transthoracic echocardiogram revealed severe regional hypokinesis of the anterior, anteroseptal and apical myocardium. Although the mechanical valve prosthesis could not be adequately visualized, Doppler velocities through the aortic valve were elevated at 4.5 m/s (Figure 1). Meanwhile, the patient was initiated on argatroban due to a history of heparin-induced thrombocytopenia (HIT) and amiodarone infusion since he began demonstrating brief runs of ventricular tachycardia. Due to worsening respiratory status and signs of myocardial infarction, the patient was taken emergently to the cardiac catheterization laboratory for fluoroscopy of the mechanical valve and coronary angiography. Fluoroscopy of the mechanical aortic valve in orthogonal views confirmed severely restricted valve leaflets. Coronary angiogram revealed normal, right-dominant coronary anatomy with a thrombotic subtotal occlusion of the left anterior descending (LAD) artery and first diagonal branch bifurcation with Thrombolysis in Myocardial Infarction (TIMI) 2 flow into both territories (Figure 2). Thrombectomy of the LAD was performed using an Export catheter (Medtronic, Minneapolis, Minnesota) with 3 passes followed by thrombectomy of the diagonal branch with 5 passes, retrieving large pieces of thrombi (Figure 3). Final angiograms revealed a small residual thrombus in the mid-segment of the diagonal branch with TIMI 3 flow to both LAD and diagonal territories (Figure 2). Right heart catheterization revealed elevated pressures with a pulmonary artery pressure of 70/25 mmHg and a mean pulmonary capillary wedge pressure of 30 mmHg. Surgical consultation was obtained for replacement of the thrombosed aortic valve, but the patient was deemed to be a poor surgical candidate due to his comorbidities of acute myocardial infarction, left ventricular dysfunction with decompensated congestive heart failure, and possible HIT on argatroban. In a palliative effort, thrombolysis of the mechanical aortic valve was attempted by intravenous infusion of 100 mg tissue plasminogen activator (tPA) over 3 hours (6 mg bolus followed by 54 mg/hr for 1 hour, and then 20 mg/hr for 2 hours). Thrombolysis was tolerated well without hemodynamic or neurologic complications. Following thrombolysis, there was dramatic clinical improvement in respiratory status corroborated by improved pulmonary artery diastolic pressure of 24 mmHg. Repeat echocardiogram showed significant reduction of Doppler velocities across the aortic valve (Figure 1) and fluoroscopy revealed dramatic improvement in leaflet mobility. Transesophageal echocardiogram the following day confirmed normal appearing prosthetic aortic valve without evidence of residual thrombus. The remainder of the hospital course was unremarkable, with steady clinical improvement until discharge on hospital day 9 after therapeutic anticoagulation on warfarin. Discussion. The incidence of PVT and CE is dependent on valve type, location and adequacy of anticoagulation.⁴ PVT has been reported to occur in 0.5–8% of left-sided mechanical prosthetic valves.^3,5 Symptoms may be mild or non-specific, yet the condition may rapidly deteriorate to death, making a prompt diagnosis crucial.¹ Therefore, a high index of suspicion for PVT is warranted within a clinical presentation of unexplained hemodynamic instability, or systemic embolism. Auscultatory findings of muffled prosthetic valve sounds or murmurs can be valuable in making a diagnosis, since careful cardiac auscultation of a normal prosthetic valve should reveal the opening and closing clicks of the valve; however, auscultation may be unreliable if the obstruction is partial, in low cardiac output states, or in the presence of another normally functional mechanical valve.⁴ Fluoroscopy has been long established as an effective, non-invasive diagnostic method for evaluating heart valve prostheses,¹ but its role as a first-line diagnostic tool has progressively declined since the introduction of transesophageal echocardiography, which has now become the most commonly used technique for diagnosis of PVT.⁶ However, in scenarios where patients are unable to undergo transesophageal echocardiography rapidly and efficiently, fluoroscopy can yield adequate information in up to 90% of patients.¹ Surgery has been the traditional treatment for PVT, although reported operative mortality rates have ranged from 0–69% depending on risk factors and clinical functional class.⁴ Fibrinolytic therapy is an alternative treatment that is reserved for high-risk surgical candidates due to the increased risk of cerebral thromboembolism with left-sided PVT.⁴ A review of almost 200 published reports of thrombolytic therapy for left-sided PVT yielded an initial success rate of 82% with an overall thromboembolism rate of 12%, recurrent thrombosis rate of 11%, stroke rates of 5–10%, death rate of 6%, and major bleeding rate of 5%.⁴ Therefore, the American College of Cardiology/American Heart Association guidelines on management of patients with valvular heart disease⁷ currently recommend fibrinolytic therapy for left-sided PVT only when the clot burden is small and the patient is at high surgical risk due to the concern for cerebral thromboembolism. CE, although rare, can be a fatal complication of PVT. The majority of emboli involve the left coronary system due to preferential flow into that artery related to aortic valve morphology.² Treatment options include surgery and thrombolysis as discussed previously for PVT, in addition to PCI for CE. PCI for CE can include rheolytic or mechanical thrombectomy with or without placement of distal embolization protection devices. Although PCI with adjunctive anticoagulation and glycoprotein IIb/IIIa inhibitors is a reasonable therapeutic option for CE,² it only serves as a bridge to definitive therapy for the source of the embolus from PVT. As in patients who have undergone surgical mechanical prosthetic valve replacement, management of patients after successful thrombolytic treatment involves anticoagulation with a target INR of 2.5–3.5 in addition to aspirin 81–100 mg daily,^4,7 since the incidence of PVT is primarily related to inadequacy of anticoagulation, as in our patient. In these patients, regular close follow-up of prothrombin time and INR is critical in addition to Doppler echocardiography at least monthly during the first 6 months, then every 6 months.⁴ Our case is unique as the first published report of a rare presentation of PVT, complicated by coronary embolism and cardiogenic shock, treated successfully with a hybrid approach of thrombectomy and intravenous fibrinolytic therapy, with reperfusion and thrombolysis documented by angiography, fluoroscopy, and echocardiography.

References

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———————————————————— From the Division of Cardiovascular Medicine, Deborah Heart and Lung Center, Browns Mills, New Jersey. The authors report no conflicts of interest regarding the content herein. Manuscript submitted March 5, 2010, provisional acceptance given April 16, 2010, final version accepted June 14, 2010. Address for correspondence: Jon C. George, MD, Director of Clinical Research, Interventional Cardiology and Endovascular Medicine, Deborah Heart & Lung Center, 200 Trenton Road, Browns Mills, NJ 08015. E-mail: jcgeorgemd@hotmail.com