Non sono disponibili, per quello che so, trial controllati sul tema. Poiché spesso questi pazienti hanno FA parossistiche l'ASA potrebbe in qualche modo ridurre il possibile rischio trombolico legato all'aritmia (SIC).
Unfortunately there are no guidelines available at that time and also no concrete data. I personally have no idea why to introduce an antiplatelet therapy in a patient after a mitral valve repair. The artificial chords are no reason at all and the annuloplasty ring is initially thrombogenic, so that some kind of oral anticoagulation, usually with coumadine or warfarin is indicated. Most centers recommend a period of 3 months but again, evidence based data are lacking.
What should Aspirin be good for or, in other words, a prophylaxis against what? Does the patient have a CAD or a carotid stenosis, which both would be an indication for a prophylactic antiplatelet therapy, whereas a valvular repair or reconstruction is not.
Vittorio Dall'Aglio! Anyway, I think, you need not in aspirin after this procedure. You need in agressive antihypertesive therapy! If you have sinus rhytm and normal size of LA, the patient can not take any antiplatelet drags. I do not see any difference between artificial cords and native ones.
Thank you for your answers, but i think that the problem is more complex (maybe also for this reason there is not again clear guidelines in literature). I agree with the first 3 months after the surgery (mandatory, in my opinion) but as far as i’m concerned the period of ASA prophylaxis shoul be prolonged indefinitely, if ASA is well tolerated by the pt.. Sure enough, if is considered conceivable that a markedly myxomatous mitral valve (like that of my case) in a young 32 y.o. with severe mitral regurgitation could be considered for antithromboembolic ASA prophylaxis (i obviously don’t mean the possibility of atrial fibrillation, because in a.f. ASA is little more than a placebo in the thromboembolic prevention, but i refer to the markedly irregular and rough structure of the valve), why do not consider for ASA prophylaxis a valve that, although well functioning and with optimal surgical result, was stretched, plicated and stitch-up sutured, undergo to fusion togheter of P2 – P3, knots, sutures and apposition of annular ring, besides conserving his previous myxomatous structure? In literature there is a report of Ring thrombosis following mitral valve repair ) (http://ejcts.oxfordjournals.org/content/45/4/762.long), four cases of prosthetic heart valve ring thrombosis (one of these at one year after the surgery)( http://imaging.onlinejacc.org/article.aspx?articleid=1097024) as well as two cases of Thrombosis after mitral valvuloplasty (one of these 8 months after the surgery) http://www.journalofcardiologycases.com/article/S1878-5409(11)00024-7/fulltext)
In a survey [4] of cardiac surgeons in Great Britain, 64% use warfarin after mitral repair with an annuloplasty ring and 54% used only aspirin in the long-term . Vaughan P, Waterworth PD. An audit of anticoagulation practice among UK cardiothoracic consultant surgeons following valve replacement/ repair. J Heart Valve Dis 2005;14(5):576—82. At Cleveland Clinic, Aspirin is favoured against Warfarin after mitral valve repair (http://my.clevelandclinic.org/services/heart/patient-education/webchats/cardiovascular-surgery/1338_ask-the-heart-surgeon)
MV repair does not cure the underlying degenerative process and patients who had MV repair had a small but constant risk of thromboembolic events (http://circ.ahajournals.org/content/127/14/1485.long)
The mild reduction in left ventricular function and increased left atrial size (like in my case) can contribute to facilitate thrombus formation.
Even in the bioprosthetic valves, that traditionally are considere free from necessity of antithrombotic therapy after the firts three months from surgery, there is the possibility of thrombosis (http://www.nejm.org/doi/full/10.1056/NEJMoa1509233?rss=searchAndBrowset=article) (http://www.medscape.com/viewarticle/855166)
At the moment, there is no clear answer to the question of which antithrombotic therapy should be prescribed after mitral valve repair (MVr) and how long the prophylaxis must be continued. Further prospective, randomized and long term (some years, preferably) studies on this problem are needed. Waiting them, I think that it could not be incorrect to propose ASA indefinetly , if tollerate, after MVR.
I personally keep my patients on aspirin 75mg daily indefinitely provided it is tolerated. There is no research showing for how long this anti platelet should be given post mitral valve repair. My idea is that the sutures, the ring and the neochordae are thrombogenic so anticoagulants may be more appropriate. I think the risks out way the benefits with regards to anticoagulants and anti platelets may prevent embolic phenomena. I will change my practice if research shows otherwise.
Thank You very much Vittorio for the literature survey, which shows again, that there is no clear evidence for any of these anticoagulatory approaches. Just to add one more aspect, most of us are used to recommend an oral anticoagulation after biological heart valve replacement, some for 3 or some for 6 months, just until we would expect an endothelial coverage of the ring, struts etc. . The same biological valves are now used during the TAVI procedures, additionally surrounded by a metal cage, which is even more procoagulatory. The recommendation after these implants is a dual antiplatelet therapy, without any scientific evidence. In consequence, we read more and more reports about early thrombus formation on these implants. Who wonders? And - who cares?
I agree with Joseph. Also if, at the moment, there is no clear answer to the question of which and how long antithrombotic therapy should be prescribed after mitral valve repair (MVr) (http://www.jtcvsonline.org/article/S0022-5223(16)00005-2/fulltext), i think that , when we have to decide which shoud be the best therapeutic or prophylactic option for a patient, we cannot only and “blindly”-strictly base our decision on the absence of clear guidelines in the field (and so often do nothing or the minimum)(moreover, the guidelines can also change with time), but we must reason on the case considering our science, experience and the full clinical, anatomical and pathophysiological aspects of the case.
I think that we can consider a reasonable, if not total at least partial, analogy in prevention of arterial thromboembolic events for MVRepair between my case and two other cases: mitral valve prolapse with severe degenerative mixomatous valve structure and MV substitution with bioprosthetic valves, in sinus rhytm and with CHA2DS2-VASC score of 0 like my patient.
The optimal antithrombotic regimen and duration after placement of a bioprosthetic device is not fully clear. - See more at: http://www.acc.org/latest-in- Cardiology/articles/2015/05/18/09/58/anticoagulation-for-valvular-heart-disease#sthash.YMv8kzGe.dpuf
Here reported is a part of “ACCP Recommendations for Antithrombotic Therapy in Patients With Bioprosthetic Heart Valves “- See more at: http://www.acc.org/latest-in-cardiology/articles/2015/05/18/09/58/anticoagulation-for-valvular-heart-disease#sthash.YMv8kzGe.dpuf
Antiplatelet Therapy
Aspirin (50 to 100 mg/day) is suggested over VKA therapy for the first three months after bioprosthetic aortic valve replacement in patients who are in sinus rhythm and have no other indication for VKA therapy (Grade 2C recommendation)
Aspirin is suggested over no aspirin therapy after the first three months following bioprosthetic valve replacement in patient in sinus rhythm (Grade 2C recommendation
- See more at: http://www.acc.org/latest-in-cardiology/articles/2015/05/18/09/58/anticoagulation-for-valvular-heart-disease#sthash.YMv8kzGe.dpuf
Here reported is a part of “ACC/AHA Recommendations for Antithrombotic Therapy in Patients With Bioprosthetic Heart Valves” - See more at: http://www.acc.org/latest-in-cardiology/articles/2015/05/18/09/58/anticoagulation-for-valvular-heart-disease#sthash.YMv8kzGe.dpuf
Antiplatelet Therapy
After bioprosthetic aortic or mitral valve replacement at a dose of 75 to 100 mg/day (Class IIa recommendation; Level of evidence: B)
- See more at: http://www.acc.org/latest-in-cardiology/articles/2015/05/18/09/58/anticoagulation-for-valvular-heart-disease#sthash.YMv8kzGe.dpuf
Recommendations from the ACC/AHA largely leave the choice of antithrombotic regimen in the setting of bioprosthetic valve replacement up to individual clinicians. Several factors that may influence a clinician's decision include institutionally-specific outcomes, likelihood for patient adherence to medication regimen, prior personal experience, regional convention, and personal preference. The duration and intensity of treatment with aspirin is also left up to the individual clinician's discretion. This lack of a clear consensus on optimal antithrombotic therapy after bioprosthetic valve replacement is reflected in the ACTION® Registry –GWTG™ survey results, which demonstrate a high degree of variability in postoperative treatment regimens across a variety of centers. - See more at: http://www.acc.org/latest-in-cardiology/articles/2015/05/18/09/58/anticoagulation-for-valvular-heart-disease#sthash.YMv8kzGe.dpuf
In the absence of other thromboembolic risk factors, practicing clinicians commonly treat bioprosthetic valve patients with only antiplatelet therapy following implantation, a strategy supported by prospective observational data (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3699194/) and considering, as Joseph highlights, that the risk/benefit ratio, at the moment, favours the ASA strategy over the AVK.
In patients with bioprosthetic valves without AF, long-term therapy with aspirin (75–100 mg/d) is recommended (Stroke Research and Treatment Volume 2011 (2011), Article ID 607852, 23 pages http://dx.doi.org/10.4061/2011/607852
Platelets adhere to the sites of endothelial injury, starting the process leading to formation of white thrombus.Are we sure that at the end of the first three months after surgery the re-endothelization of repaired MV (included ring and knots) be complete? According some surgeon (http://www.jtcvsonline.org/article/S0022-5223(16)00005-2/fulltext) probably we must consider more than the prevention of arterial embolism during the first 6 months after surgery.
In mixomatous MV disease there is a disruption of collagen and infiltration of the valve by a mixomatous substance rich in mucopolysaccharide; the mitral valve is thickened, with irregolare surface and often fibrosis of the endocardial surface of the leaflets; chordae tendineae and mitral annulus can also contain myxomatous deposits.Patients with important MVP sometimes have abnormal left ventricular contractions; at necropsy, thrombi have been found, especially in the angle between the posterior ML and the left atrial wall or in the retro-mitral basal recess.Transformation of the normal rigid valve in the loose myxomatous tissue results in stretching of the valve leaflets, loss of endothelial continuity and rupture of subendothelial connective tissue fibers; these changes could promote the formation of platelet-fibrin thrombi on the valve surface ( Caplan Stroke: A Clinical Approach (https://elsevier.ca/product.jsp?isbn=9781416047216)
Abnormalities of platelet function have been shown in patients with MVP and thromboembolism.Shortened platelet survival time, an increase in circulating platelet aggregates and increate levels of beta-thromboglobulin and platelet factor IV were found in patients with MVP.Interaction of circulating platelets with abnormal endocardial and valve structures in pts. with myxomatous valve degeneration causes increate platelet aggregation, adhesion and secretion. Platelet-Fibrin aggregates adhere to abnormal valve surfaces and can later embolize or promote formation of erythrocyte-fibrin clots (
Caplan's Stroke: A Clinical Approach)( https://elsevier.ca/product.jsp?isbn=9781416047216)
Cardioembolically-related cerebrovascular events represent an especially serious accompaniment of mixomatous MVP. In patients under 45 years of age about 30% of transient ischemic attacks (TIAs) and cerebral infarctions are reported to be due to an MVP . Disturbed platelet function in the form of enhanced platelet adhesion and aggregation, which is generally regarded as a risk factor for cerebrovascular complications, has been observed in MVP patients as well (http://link.springer.com/chapter/10.1007%2F978-3-642-88581-5_23) Thrombus may arise on left ventricular surface and native or prosthetic mitral www.ncbi.nlm.nih.gov/pubmed/2677086
Platelet deposition has been demonstrated on bioprosthetic surfaces using the technique of indium-111 labeled autologous platelets and gamma-camera imaging. Indium- 111 platelet-labeled thrombi have been demonstrated to ebolize in various anatomical districts, brain included; mosto f emboli are small and therefore not clinically detected. Thus, the reported frequency of thromboembolism in patients is undoubtely an under estimate of the true frequency of events
(Recent Progress in Mitral Valve Disease Carlos Duran,William W. Angell,Allen D. Johnson- (http://www.sciencedirect.com/science/book/9780407002944).
So, in conclusion, this discussion could continue indefinitely and , of course, i don’t wish that… But i’m happy to have stimulated a very interesting discussion with my peers on a difficult and controversial matter. Thank you all .
We prescribe an anti-vitamin K treatment for 3 months because of the risk of fibrin deposits and thrombi on the mitral ring that may embolize and also episodes of transient postoperative arrhythmia