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- ↵*Reprint requests and correspondence:
Dr. Joseph S. Alpert, Robert S. and Irene P. Flinn Professor of Medicine and Head, Department of Medicine, University of Arizona Health Science Center, 1501 North Campbell Avenue, Tucson, Arizona 85724, USA.
The four most dreaded complications following mechanical prosthetic valve replacement are dehiscence/disruption/dysfunction, infection, embolism, and thrombosis (mnemonic). Thrombosis of a mechanical prosthetic valve (TPV) is a particularly pernicious complication because it is often associated with embolism and/or life-threatening deterioration in the patient’s clinical status (1). In this issue of the Journal, Roudaut et al. (2)from Bordeaux review their institution’s 23-year experience with thrombosed mechanical prosthetic valves. The catchment area for their hospital includes three million inhabitants. They observed 127 instances of TPV in 110 patients during their study. The overwhelming majority of individuals with TPV were managed medically with thrombolytic therapy followed by antithrombotic therapy. The results were encouraging and not dissimilar from previously reported large series (3–9).
Most patients with TPV in this series, as in others, presented with embolism, dyspnea, or other symptoms of heart failure including pulmonary edema with or without hypotension. Patients with massive valve thrombosis more often presented with severe symptoms. Mitral prosthetic valves were affected more commonly than aortic valves; the most frequent underlying reason for TPV was inadequate anticoagulant therapy with warfarin. The diagnosis of TPV was confirmed by either transthoracic or transesophageal echocardiographic study. During medical therapy, serial echocardiographic studies were employed to document the success or failure of thrombolytic/antithrombotic therapy.
Thrombolytic therapy was not administered to patients with large left atrial thrombi in addition to TPV (2). In these individuals, it was felt that thrombolytic therapy would be associated with an inordinately high risk for systemic embolism secondary to dissolution of the left atrial thrombus. Tissue plasminogen activator (tPA) and streptokinase (SK) were more effective than urokinase in dissolving prosthetic valve thrombi. This is a particularly fortunate finding because urokinase is currently unavailable in the U.S. Repeated courses of intravenous thrombolytic therapy were necessary for complete resolution of prosthetic valve thrombosis in nearly one-third of the patients in this series (2). This is an important finding because U.S. clinicians are more likely to employ surgical intervention in patients with TPV, particularly if the initial infusion of thrombolytic therapy has not resulted in complete clearing of valve-associated thrombus.
Valve replacement was employed in only 23% of the patients in the current series (2). In each of these patients, surgical intervention followed unsuccessful or partially successful intravenous thrombolytic therapy. Medical therapy resulted in total dissolution of prosthetic valve-associated thrombus in 71% of patients and partial dissolution of thrombus in an additional 17%. Medical therapy failed in 12% of individuals with TPV. Thrombolytic therapy was more commonly successful in patients with aortic prosthetic valves (80%) as compared with mitral prostheses (65%). Thrombolytic therapy was associated with severe hemorrhagic complications in 5% of patients and with systemic embolism in 15%. However, systemic embolism resulted in cerebral infarction in only 7% of treated patients (n = 8), although all but one of these individuals died. Other systemic embolic complications included transient ischemic attacks and peripheral embolism that were successfully managed with further medical therapy. Mortality in this series was only 12%. Recurrent valve thrombosis necessitating repeat thrombolytic therapy and/or surgery was observed in nearly 20% of patients treated (2).
The authors argue that medical therapy can and should be employed for most patients with TPVs on the basis of the results observed in their institution over a 23-year period. Moreover, they suggest that thrombosed right-sided prosthetic valves should almost always be treated medically, whereas left-sided valves should undergo surgical intervention if the patient’s symptoms are mild-to-moderate and general physical condition is good. They support these recommendations with their own data as well as with citations from earlier collected series and meta-analyses that report an 8% to 20% mortality when surgical intervention is employed as the primary modality for patients with an “urgent” need for therapy (2–10). These same published series report surgical mortalities in excess of 35% when patients are deemed to be “critically ill.” Mortality is lower and apparently comparable with both medical and surgical therapy when patients present in New York Heart Association (NYHA) clinical class I or II.
In 1997, a consensus conference of clinicians and investigators working in this area proposed that surgical intervention should be the preferred treatment modality for most patients with TPV (10). Thrombolytic therapy was recommended only for individuals who were poor surgical candidates or critically ill, that is, in NYHA clinical classes III or IV. These authors were concerned by the high rate of systemic embolism associated with thrombolytic therapy (10). However, the series of Roudaut et al. (2)in this issue of the Journaldemonstrates that embolic events following medical therapy are more often of a benign nature than previously thought. Thus, the present series of patients should cause us to pause and reconsider the earlier recommendations of Lengyel et al. (10).
Fortunately, thrombosis of a prosthetic valve is not a common occurrence. However, this makes it very unlikely that a study will ever be done randomly comparing medical to surgical therapy. Recommendations for the management of these patients, therefore, will need to be based on series such as the one presented in this issue of the Journal, together with previously reported clinical experience and consensus conference recommendations from the medical literature. The recently published American College of Cardiology/American Heart Association (ACC/AHA) guidelines for patients with valvular heart disease mentioned TPV briefly, but suggested no firm recommendations for the management of these individuals (11). In an effort to further discussion in this area, I have listed a series of tentative recommendations for managing these seriously ill patients. The recommendations are couched in the style of ACC/AHA guideline documents. However, these are my own personal recommendations. They should not be construed in any way as reflecting the opinion of the ACC/AHA Task Force on Practice Guidelines or any of its writing committees. This caveat is particularly important because I am currently a member of this task force. Therefore, it would be distressing to me as well as to the committee if the recommendations included in this editorial were misconstrued as having any official imprimatur from the ACC/AHA Task Force on Practice Guidelines.
In conclusion, my proposed recommendations for patients who present with a thrombosed prosthetic valve are listed here. These recommendations are based on my own personal reading of the medical literature, including the excellent article by Roudaut et al.(2)from this issue of the Journal:
1. All patients with suspected TPVs should undergo echocardiographic study. If adequate visualization of the prosthetic valve is not obtained by a transthoracic study, then a transesophageal echocardiographic study should be undertaken (level of evidence I).
2. Patients with right-sided TPVs should be treated with intravenous rtPA (100 mg administered as 10 mg immediate intravenous bolus followed by 90 mg infused over 90 min) or SK (500,000 IU over 20 min followed by 1.5 million IU infused over 10 h). Reduced doses should be employed in children and very small adults (level of evidence IIa).
3. Patients who are critically ill on presentation with TPV (pulmonary edema, hypotension, NYHA class III/IV symptoms) should receive immediate intravenous thrombolytic therapy as outlined earlier following appropriate echocardiographic confirmation of TPV (level of evidence IIa).
a. Serial echocardiographic studies should be performed in these individuals, and repeated infusions of thrombolytic therapy should be administered if complete resolution of prosthetic valve thrombus is not achieved (level of evidence IIa).
b. Concomitant intravenous unfractionated heparin should be administered along with thrombolytic therapy to achieve an activated partial thromboplastin time that is 1.5 to 2.0 times control (level of evidence IIb).
c. Cardiac surgical consultation should be sought urgently. Valve replacement should be seriously considered if repeated infusions of thrombolytic therapy fail to adequately dissolve the thrombus on the prosthetic valve (level of evidence IIa).
4. Patients with TPV who are clinically stable, that is, in NYHA clinical class I or II, may be managed medically with thrombolytic/antithrombotic therapy or surgically with valve replacement depending on physician/patient preference (level of evidence IIa).
↵* Editorials published in the Journal of the American College of Cardiologyreflect the views of the authors and do not necessarily represent the views of JACCor the American College of Cardiology.
- American College of Cardiology Foundation
- ↵Roudaut R, Lafitte S, Roudaut M-F, et al. Fibrinolysis of mechanical prosthetic valve thrombosis: a single-center study of 127 cases. J Am Coll Cardiol 2003;41:653–8
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