PVT is defined as any obstruction of prosthesis by non-infective thrombotic material. It has an estimated incidence of 0.03% - 4.3% per year  and is reported to occur in 0.5% - 8% of the left-sided prosthetic valves and in up to 20% of tricuspid prostheses [3, 4]. The most common cause of PVT is inadequate anticoagulant therapy (in up to 82% of cases) . Other pathogenic factors include: mitral position of the prosthesis; type of prosthesis; atrial fibrillation; left atrial enlargement; ventricular dysfunction; and multiple valve replacements . Diagnosis of prosthetic heart valve thrombosis is made by a combination of clinical data (heart failure, absence of prosthetic sounds, cardiogenic shock), fluoroscopic examination (abnormal mobility of tilting disks) and echocardiographic (both transthoracic and transoesophageal ) abnormalities (high prosthetic gradient, reduction of effective valve orifice area, lack of disk mobility and detection of thrombotic mass adherent to the prosthesis ) [3, 6].
Management of PVT remains controversial. There are currently no randomized controlled trials favoring surgery over thrombolysis and vice versa. Surgery, in the form of thrombectomy or valve replacement, remains the treatment of choice but carries a significant mortality ranging from 4.7% to 20% [2, 3, 7]. Thrombolysis, on the other hand, has emerged as an attractive alternative with reported success rates in the region of 75%-88% for PVT . Our patient had stable hemodynamics which gave us a window of opportunity to use thrombolysis therapy. If this had been unsuccessful we would have proceeded with surgery. In addition, the patient had received his first MV replacement six months previously and we felt that, by giving him a trial of thrombolysis, we would have spared him the added burden of undergoing surgery twice in a short time period. The current treatment algorithms suggested by some authors include using thrombolysis for right sided PVT while using surgery for left-sided PVT [8, 9]. They also recommend using thrombolytic therapy in left-sided PVT if surgery is contraindicated or if the patient is critically ill . Others have reported that patients in the New York Heart Association functional classes I and II achieve the best results with thrombolytic therapy with the lowest incidence of peripheral embolism . In our case, the use of tenecteplase proved useful in a stable patient with no increased risk. Following thrombolysis, he was placed on oral anticoagulant only. We have not started him on low-dose aspirin because there was no evidence of concomitant coronary artery disease and his thrombosed valve was caused solely by his discontinuation of warfarin. However, recent guidelines have suggested that in such cases the use of low-dose aspirin, in addition to oral anticoagulant, may decrease the chance of recurrence .
Thrombolytics reported in the literature are streptokinase, urokinase and recombinant t-PA (alteplase) . There are no studies comparing these different thrombolytic agents in PVT [3, 7]. The most important complications of thrombolytic therapy are thromboembolic events and cerebral hemorrhage. Thromboembolism is more frequent in left-sided prosthesis with an incidence of 9%-20%. Embolic complications occur in two forms: peripheral embolism and cerebral. Cerebral embolism has an overall incidence 3%-10% (more in the presence of atrial fibrillation). Cerebral hemorrhage rates fluctuate between 0%-3% [3, 7]. Tenecteplase is a synthetically engineered variant of alteplase designed to have increased fibrin specificity, greater efficacy, increased resistance to plasminogen activator inhibitor-1 (PAI-1) and a longer half-life. It has been used extensively in acute myocardial infarction (including in our institute) but its use in PVT treatment has rarely been reported [1, 3]. One advantage of tenecteplase is that its dosing is based on actual body weight which enhances both safety and efficacy outcomes by avoiding wider fluctuations in the drug plasma concentration. Compared to recombinant t-PA (for example, alteplase), tenecteplase use leads to lower rates of bleeding complications and a decreased risk of cerebral hemorrhage among high risk patients . Tenecteplase, contrary to recombinant tissue plasminogen activators, has been synthetically modified which in turn has important clinical applications. The increased fibrin specificity theoretically enhances the enzymatic activity at the clot and reduces systemic fibrinolysis. Furthermore, the increased resistance to PAI-1, an enzyme secreted by platelets that inhibit thrombolytics, may enhance the efficacy of tenecteplase. This drug proved useful in our case where successful thrombolysis was achieved for mitral PVT with no increased risk to the patient. We elected to use it in a slow infusion rate rather than a bolus in order to potentially reduce the risk of breaking up the thrombus into large emboli and to potentially reduce the risk of cerebral bleed.