Ann Thorac Surg 2001;71:1180
© 2001 The Society of Thoracic Surgeons
Invited commentary
Endre Bodnar, MD, PhDa
a The Journal of Heart Valve Disease, Crispin House, 12A South Approach, Moor Park, Northwood HA6 2ET, United Kingdom
e-mail: bodnarendre{at}cs.com
This study confirms the findings of Starr and Grunkemeier (reference 17 in the article) that the probability of suffering a repeat embolism after the first event is higher than that of having a first embolic event. The generally accepted explanation of this phenomenon is that patient-related factors would cause or promote thromboembolism in a certain subgroup of the patient population. While in the majority of cases this assumption is probably true, a device-related etiology cannot be ruled out completely. Due to accepted—and inevitable—tolerances in the design and the manufacturing process, replacement valves coming off the same production line are not necessarily and completely identical. There are bioprostheses of identical design which are less durable than others, and it may well be that some mechanical valves of the same design and make are more thrombogenic than others. The actual rate of repeat embolism is perhaps the result of these two factors. There is now good clinical evidence to pinpoint certain patient-related risk factors, like atrial fibrillation, atherosclerosis, hypertension and others. Further research is necessary to reveal additional, but so far unknown risk factors. Equally important is the recent emergence in Atlanta of a nondestructive laboratory methodology pursued by Ajit Yoganathan and his team to assess valve thrombogenicity. Currently, they are comparing different valve designs. It may well be possible that with further refinements those delicate flow assessments might become a routine step in the quality assurance and comparison of individual mechanical valves of the same make and design.
Another important finding of the study by Dr Casselman and associates is that the implant date is an independent predictor of the thromboembolic risk. Again, this is in concordance with the prior results of Starr and Grunkemeier, and adds to the number of etiological factors by proving that in addition to valve-related and patient-related events we must accept the actual, real-life existence of treatment-related thromboembolism. One must regret however that this 36-year follow-up study, due to its retrospective nature, cannot provide any information on the beneficial or detrimental effect of adding platelet inhibitors to warfarin, although about half of the patients was and the other half was not on combined warfarin plus antiplatelet treatment. Scientifically valid results coming from this larger and otherwise well documented study could have been significant in the future structuring of anticoagulation management. Nonetheless, this article remains one of the very few providing data on truly long-term outcome after aortic valve replacement with mechanical prostheses.
Related Article
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Repeated thromboembolic and bleeding events after mechanical aortic valve replacement
- Filip P. Casselman, Michiel L. Bots, Willem Van Lommel, Paul J. Knaepen, Ruud Lensen, and Freddy E.E. Vermeulen
Ann. Thorac. Surg. 2001 71: 1172-1180.
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