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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 30, No 4, July/August 2019
220
AFRICA
dependence, unlike traditional echocardiographic parameters, it
is able to detect subclinical longitudinal RV dysfunction.
The decreased RV free-wall PSS with preserved traditional
markers of RV systolic function in this study implies subclinical
RV dysfunction. The mechanism of reduced RV strain in this
study may be related to the elevated PASP, as the RV is known
to be extremely sensitive to afterload.
26,28
Even small increases
in pulmonary vascular resistance can markedly decrease
RV contractile function. Prior studies have noted a similar
relationship between RV systolic performance and pulmonary
hypertension in degenerative MR.
5,6
Le Torneau
et al
. have shown in their study that, even though
increased RV afterload secondary to PHT was an important
cause of RV dysfunction in MR, LV dysfunction also contributed
significantly to RV dysfunction, due to their interdependent
relationship.
5
In this study PASP was only modestly elevated
but the markers of LV remodelling and systolic function such
as LVGLS, LVEDD and S
′
velocity were markedly abnormal.
Therefore, in agreement with Le Torneau
et al
.,
5
LV remodelling
and LV dysfunction, in addition to the modest elevation in
PASP, may be important causes of RV functional impairment
in CRMR.
This is supported by the finding of reduced RV free-wall PSS
in patients with LVEF
<
60% and reduced LVGLS. Additionally,
most patients had abnormal RV free-wall PSS in the presence of
abnormal LVGLS, and those with normal RV free-wall PSS also
had normal LVGLS. However, conventional RV systolic function
parameters were still preserved even in the presence of LV
systolic dysfunction. Hence, once abnormalities in LV systolic
function are noted in MR, systematic RV function assessment
must be done with not only traditional parameters but also
STE, in order to detect subclinical RV dysfunction and reduce
mortality associated with biventricular functional impairment.
5
Severe MR was associated with worse RV function and was
found to be a determinant of RVPSS in a study by Le Torneau
et al
.
5
Volume overload as a result of chronic MR results in LV
remodelling, as noted in our study, and this in turn results in
abnormalities of RV and LV interaction. RV free-wall PSS was
lower in patients with severe MR compared to moderate MR. This
association can be explained by greater chronic volume overload
of the LV and left atrium, accompanied by increased PASP
secondary to backward transmission of increased LV pressure,
as well as remodelling of the pulmonary vasculature in severe
compared to moderate MR.
30
However, a lack of difference in
traditional RV systolic function parameters between the moderate
and severe MR groups was present, and therefore quantitative
RV function assessment in CRMR mandates evaluation by both
conventional indices and RV longitudinal strain.
TR was an independent predictor of RV free-wall PSS.
Significant TR is likely a reflection of deteriorating RV function
secondary to left-sided disease. The increase in RV preload
initially results in increased RV free-wall PSS due to increased
myocardial lengthening in diastole and shortening in systole.
Once RV myocardial contractile dysfunction ensues, however,
RV systolic strain declines, as RV reaches the descending limb of
the Frank–Starling curve.
Finally, the decline in RV free-wall PSS may be partially
attributed to primary RV dysfunction. The intrinsic myocardial
functional abnormalitymay be a result of longstanding activation
of neuro-hormonal pathways and increased afterload secondary
to chronic mitral regurgitation.
8,26
We further speculate that
there may be direct involvement of the RV myocardium by the
rheumatic process.
This study had two limitations: first, lack of reference
standard for RV functional assessment such as additional
imaging in the form of cardiac MRI and three-dimensional
echocardiography, and second, we did not routinely perform
right and left heart catheterisation to assess PASP, pulmonary
vascular resistance and coronary anatomy.
Conclusion
In CRMR patients, RV free-wall PSS was a more sensitive marker
for detecting earlier RV systolic dysfunction than traditional
RV functional parameters. LVGLS and TR were important
determinants of RV free-wall PSS in CRMR.
The first author was the recipient of the Carnegie PhD Fellowship award
(Carnegie Corporation grant no. b8749.r01).
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