Feeds:
Posts
Comments

Posts Tagged ‘prosthetic valve thrombosis’

 

A 40 year old  women came  with acute dyspnea who had a prosthetic mitral valve implanted 2 years ago for RHD  .

An emergency  echo showed  a peak gradient of 35mmhg across the valve .She was on warfarin regularly and her last INR was 2.2.Heart rate  was 138/minute, lungs showed congestion .LA,LV were dilated. LV function appeared mildly compromised  but could not be accurately quantified as the  patient  was in distress.

 

The fellow on duty had no hesitation  in diagnosing prosthetic valve thrombus .He Initiated Inj streptokinse bolus followed by infusion  along with diuretics . After few hours the gradient regressed .Patient felt better .Every one was happy . The consultant congratulated the fellow for  the good job done .To recognize prosthetic valve obstruction early and  successfully lysing it too !  The fellow  felt gratified .

prosthetic valve obstruction thrombus 002

Since I  was hanging around the CCU , watching the proceedings , I Initiated  a debate which was  curious to the team that handled the  patient !

Was it really thrombotic obstruction that caused his symptoms ?

  • No one has visualized the thrombus
  • TEE was not done
  • Fluroscopic evaluation of disk motion was not performed
  • There was no documentation of raising FDP that would Indicate clot lysis.

All  we have  is an unexplained  tachycardia with raised  trans prosthetic gradient . . .

Why we are tuned to think  raised gradients  to be  synonymous with thrombus ?

There has  been lot of assumption here . Subsequent analysis of history and  clinical presentation revealed the patient had a febrile illness which triggered an  atrial tachycardia  that possibly  resulted in transient  LV dilatation and dysfunction.

Once the failure is controlled the gradient has come down , I argued !

Of course, this again could be  a guess work , How can you  still rule out a thrombus ? They wondered !

I told them ,  question here is not ruling in or ruling out prosthetic valve thrombus.

It is an important  lesson to learn , raised  prosthetic gradient is not equal to thrombus  in many  acute hemodynamic situations* .

Many factors other than prosthetic valve obstruction  can elevate the gradient.

After all ,  prosthetic valve orifice is inherently stenosed  .(MVO is  never >2.5sqcm in any prosthetic mitral valve) . So at times of tachycardia the gradient is bound to be elevated .

Other factors that can elevate trans – mitral gradient includes

  • LV dysfunction
  • Acute diastolic dysfunction
  • Acute peri-valvular MR
  • Loss of LA compliance

 *One of the  commonest (yet not recognised) cause for elevation of trans mitral prosthetic gradient is acute left ventricular failure due to any cause.It  can be either acute diastolic dysfunction or a sudden raise in  blood pressure that result in  after load mismatch.

Final message

Please remember flow across prosthetic valve is governed by  delicate  local hemodynamic rules .The gradient  is  critically dependent on heart rate, LA  size and compliance , LVEDP and after-load mismatch if any !

Transient raise can occur at times of tachycardia and falling LV function (Mitral valve has to push hard, in the process elevating the gradient)

Simple raise in trans-valvular gradient should be carefully interpreted. Since visualising thrombus in routine TTE is  difficult  in an acutely  dyspnic  patient  many of us have taken this  granted !

Nothing wrong in playing  guess games in medicine . . . but we  need to acknowledge it!

*Note:Other causes for chronically elevated gradients like pannus formation, mechanical defects of valve, degenerated prosthesis  should be addressed separately.

 

 

Read Full Post »

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 ?

Read Full Post »