Valve Prosthesis–Patient Mismatch

The concept/phenomenon of valve prosthesis/patient mismatch (VP–PM) was first described in 1978.  All prosthetic heart valves have some degree of VP–PM.

The original paper (in 1978) that described valve prosthesis–patient mismatch (VP–PM) stated that “Mismatch can be considered to be present when the effective prosthetic heart valve area, after insertion into the patient, is less than that of a normal human valve”. It must be noted that all prosthetic heart valves (PHVs) are smaller than normal and thus are inherently stenotic.  The PHV mismatch was stated to be “usually mild to moderate in severity and often of no immediate clinical significance.” However, severe mismatch may lead to significant symptomatic and hemodynamic deterioration and increased mortality.

With the publication of VP–PM, surgeons were more careful and inserted the largest PHV that could be safely inserted. PHVs with improved hemodynamic profile have also been developed. As a result severe VP–PM has become a much less common clinical problem. The overwhelming majority of a large number of scientific publications have related to the aortic valve and not to mitral valve VP–PM.

How should VP–PM be measured?

Different parameters have been evaluated to assess for the severity of VP–PM. The most commonly used measures of valve size is the EOAi.

The EOA is a physiological parameter analogous to the native AVA. The EOA can be measured both invasively and noninvasively using echocardiography/Doppler or magnetic resonance imaging. The most readily and widely available method is echocardiography/Doppler. The accuracy of EOA echocardiographic measurement in the bioprosthetic valve is limited by the same pitfalls that are present in the measurement of the AVA; in particular, the LV outflow tract diameter may be more difficult to measure because of reverberation artifact caused by the prosthetic heart valve, but in these instances, the sewing ring diameter may be a sufficient surrogate. In the bileaflet mechanical valve, the central orifice may produce a high-velocity jet, causing an underestimation of the EOA. Pressure recovery occurs with both bioprosthetic and mechanical heart valves, although the implications of pressure recovery in PHVs have not yet been clarified. The EOAi has a complex relationship with the mean gradient across the aortic valve and PHV.

Assessment of severity of VP–PM

With aortic VP–PM the obstruction to the LV outflow tract is similar to that seen with native AS. Thus, the severity of aortic VP–PM should be assessed by the same criteria as for severe AS. Severe aortic stenosis is defined as mean aortic valve gradient, measured after energy recovery (also called pressure recovery), of ≥50 mm Hg and an AVA index of ≤ 0.6 cm²/m². ); it would be reasonable that this criterion should also be applied to severe VP–PM.

 

 

Grading

AVA and EOA, cm2

AVA Index and EOAi, cm2/m2

Mild

>1.5

>0.9

Moderate

>1.0–1.5

>0.6–0.9

Severe

≤1.0

≤0.6

Very severe/critical

≤0.7

≤0.4

 

When should the severity of VP–PM be determined?

4 phases of physiological healing of mechanical and bioprosthetic PHVs have been described; they are “platelet and fibrin deposition, inflammation, granulation tissue, and finally encapsulation. Long-term device fibrous encapsulation with extension to adjacent tissues adds to structural stability.” Bioprosthetic valves undergo morphological changes of both the tissue material as well as the supporting structures, which may contribute to VP–PM. Valve leaflets become covered by fibrin, platelets, and other cellular material. The matrix of the leaflets undergoes microcalcification as well insulation with plasma materials, causing changes in the matrix structure. These changes may change the resistive properties of leaflet materials. In both mechanical and bioprosthetic valves, a fibrous sheath may also encapsulate the supporting structure of the valve, encroaching on the PHV orifice and also possibly causing valve leaflet or disk immobilization.

For PHVs of the same size, there was a wide range of EOAs. Two echocardiographic/Doppler studies from the Mayo Clinic of patients studied within 1 week of mitral porcine mitral bioprosthesis and of tricuspid mechanical prostheses showed a wide range of gradients and EOAs with the same size of PHV, even in the same brand of PHV.

There are at least several explanations for these findings. 1) PHVs of the same labeled size are not necessarily of precisely the same size. Bioprostheses and other biological valves may also have differences in tissue materials. 2) There are variations from patient to patient with regard to healing changes, hemodynamic conditions, and pressure recovery.

It is best to measure VP–PM early (at 1 week after PHV implantation or at time of hospital discharge) to determine the variations in actual size of the PHV that was implanted in an individual patient. Importantly, VP–PM should also be assessed at 6 to 12 months when the physiological and other morphological changes in the PHV are mostly complete. The severity of VP–PM determined at this time can be expected to determine the long-term impact of VP–PM on patients’ outcomes.

Conclusions:

It must be noted that all prosthetic heart valves (PHVs) are smaller than normal and thus are inherently stenotic.

1) – EOAi should be measured at 1 to 4 weeks or at hospital discharge to evaluate the actual valve size that was implanted. This should also be done at 6 to 12 months to evaluate the severity of VP–PM that will affect long-term outcomes.

2) – The grading of severity of VP–PM should be similar to another common LV outflow tract obstruction, namely, valvular AS. VP–PM can be mild (EOAi >0.9 cm2/m2), moderate (EOAi >0.6 to 0.9 cm2/m2), or severe (EOAi ≤0.6 cm2/m2).

3) – Mild VP–PM, like mild AS, is unlikely to have clinically significant untoward effects. Outcomes with moderate and severe VP–PM should be evaluated separately. Moderate VP–PM is unlikely to reduce survival unless there is progression of valve obstruction, for example, with pannus formation. Severe VP–PM has negative effects on outcomes, but its effect on mortality is still unproven.

4) – Prediction of severity of VP–PM is problematic. The primary goal should be not to prevent VP–PM but rather to prevent severe VP–PM.

5) – Use of the EOAi as a continuous variable may help to define the level of severe VP–PM that results in increased mortality, and this may occur at a critical level of obstruction (≤0.4 cm2/m2).

 

References:
1)- Rahimtoola S, The problem of valve prosthesis-patient mismatch, Circulation 1978; 58:20-24.                                                                                                                                                                                                                                                                                                                  2)- Daneshuar S.A.; Rahimtoola S.H. Valve Prosthesis-Patient Mismatch (VP-PM): Long-Term Prespective. J AM Coll Cardiol 2012;60(13):1123-1135.

About Dr. Hassan Gargoum

Clinical Professor of Medicine, University of Saskatchewan Consultant, Cardiovascular Diseases

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