Dr.S.Venkatesan MD

Clinical sense

• First and fore most  dictum  is  not  every  prosthetic valve obstruction  is  thrombotic (Most cardiologists are tuned to think that way )
• Pannus, Mechanical failure  and  vegetations can increase the gradient across prosthetic valve.
• If the clinical presentation is acute (< 48 hours ) it is  more likely to be a thrombotic event .
• History of  recent discontinuation of oral anticoagulants /sub optimal INR will favor thrombosis.

A meticulous Echocardiography is vital (TEE though gives more information in an emergency TEE is suffice )

• Thrombolysis is to be considered in all .
• For right sided prosthetic obstruction thrombolysis is the  initial modality of choice.
• For left sided valve thrombosis   surgery is the preferred option .However a trial of  thrombolysis for 24 hours may be tried .
• For a high risk mobile thrombus , thromolysis is contrandicated.

The success rate is less with Mitral than Aortic valve  . Success depend upon more on the  location / Freshness of thrombus than the type of the lytic agent used.

Is there a time window for prosthetic valve thrombolysis ?

Thrombus organisation takes 2 weeks at- least.Hence , it better not to attempt thrombolysis in documented late prosthetic valve thrombosis.

Thrombolysis of left-sided valves has inherent risk of  stroke .

Heparin controversy

Simultaneous usage of heparin along with streptokinase or TPA is  perceived as risky (No good evidence for this perception )It is logical to expect even as the thrombus  lyses the clot lots of pro-coagulant debri  are released . Concomitant usage of heparin  will definitely help accelerate thrombus dissolution. (I am glad  Joseph S   Alpert also feels the same ! )

Assessing successful  thrombolysis

• Can be a tough task .
• Relying purely on gradient is vested with risk of huge error.
• In a patient with shock or LV dysfunction gradients are not reliable as low flow status masks the gradient.
• A accelerated thrombolytic  protocol 15lakhs streptokinsae in 60 minute may be tries in unstable patient .
• It is wiser to rapidly asses for clinical improvement in high risk subsets  and refer the  patient for early surgery .

Surgery

Prohibitive mortality reported in many centres.

It need to be remembered no surgeon will operate on a  sick patient in  shock  exposed to  cocktail of heparin and streptokinase.

Valve replacement is required in most case. Simple valve debridement  (servicing the  valve ) and releasing  discs  from the  sticky thrombus is  also possible in an occasional patient.( Do not ask reference for this !)

Reference (Surprisingly most of the good papers in the topic appeared  in JACC)

http://content.onlinejacc.org/cgi/reprint/41/4/653.pdf

http://content.onlinejacc.org/cgi/reprint/41/4/659.pdf

http://content.onlinejacc.org/cgi/reprint/35/7/1881.pdf

http://content.onlinejacc.org/cgi/reprint/35/7/1874.pdf

After thought

I have not seen a single case of acute prothetic valve thrombosis involving Starr Edwards valve  in the  last  20 years of  of clinical cardiology practice.

Is it true   . . . the new age valves  with more mechanical stress points  are proving more injurious to our patients. Our  pursuit  towards a  perfect artificial  valve need some introspection .

Read a related article in my site :  Who killed Starr Edwards valve ?