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 .
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.
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.