Cardiovascular Journal of Africa: Vol 28 No 4 (July/August 2017)

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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 28, No 4, July/August 2017 AFRICA 219
regurgitant lesions. The reason why some patients develop pure
MS is unknown.4 Differences in the interaction of host immunity,
initial or recurrent streptococcal infections and chronic exposure
of the valve leaflets to abnormalities of haemodynamic flow may
account for these difference in morphology and dictate which
lesion may predominate.
The current data confirm that there has been a dramatic
decline in the incidence of rheumatic carditis in the population
of Soweto, although the reasons for this are not entirely clear.
The striking trend toward a substantial decline in ARF has
also been documented in the paediatric section of Baragwanath
Hospital, with a reduction from 64 cases per year in 1993 to three
per year in 2010.16 This decline was attributed to improved socio-
economic status and better access to healthcare.16
Thirty years ago McClaren et al . (by auscultation alone)
reported a RHD incidence of 6.9/1 000 among school children in
Soweto.16 Recently, Engel et al. (by echocardiography) reported
a RHD incidence of 20.2/1 000 cases among scholars in the
Bonteheuwel and Langa communities of Cape Town, with the
prevalence being higher in poorer communities.17 Data from
other areas of the country are scarce; the REMEDY study did
not report on the incidence or prevalence of RHD. However,
25.8% (863/3343) of participants were from upper middle-
income countries (South Africa and Namibia).18
Concomitant with the decline in rheumatic fever, diseases
associated with a Western lifestyle and urbanisation have
emerged. A considerable number of patients with rheumatic MR
currently have co-morbidities of hypertension (52%) and HIV
(26%). These findings differ considerably from previous studies
conducted in our institution. These co-morbidities mandate a
careful assessment of the patient’s clinical presentation, since
symptoms may not be solely attributed to MR; elevated blood
pressure could overestimate the echocardiographic severity of
MR and left ventricular dysfunction may be attributed to
concomitant HIV infection rather than volume overload.
The morphological abnormalities of the mitral apparatus
(thickened and shortened subvalvular apparatus) and the nature
of leaflet dysfunction (Carpentier IIIa) described in the current
population has diagnostic implications. MR jets that are eccentric
may require careful off-axis imaging to accurately delineate
the full extent of the colour jet. Furthermore, an integrated
evaluation of MR severity is mandatory due to the limitations of
quantitative Doppler in some instances of eccentric jets.
Our findings also have important therapeutic implications in
terms of surgery for rheumatic mitral regurgitation. Mitral valve
repair has several advantages compared to replacement, including
lower peri-operative mortality rate, better preservation of post-
operative left ventricular function, no need for anticoagulant
therapy, and a safer pregnancy.19 In younger patients, absence
of advanced subvalvular and valvular thickening, calcification
and restriction of motion make it likely that a variety of repair
techniques would be successful. In the older, contemporary
population that we have described, the need for valve repair is
less pressing compared to younger patients and the probability
of surgical failure higher, given the presence of extensive
subvalvular and valvular disruption.
An important observation was the high frequency of
concurrent TV leaflet abnormality and tricuspid annular
dilatation. These abnormalities were not reported by Marcus
et al.6 and no data on surgical repair were given. Our findings
suggest that once rheumatic MR is identified, careful assessment
of the morphology and function of TV is mandatory when
selecting patients who will undergo mitral valve surgery. This
strategy may reduce the likelihood of the late consequences of
unrepaired TR in rheumatic patients, which has been previously
highlighted.20 Late TR causes increased morbidity and mortality
rates despite the presence of successful mitral valve surgery, and
in addition, a second operation to correct the residual TR carries
increased mortality rates.20
There are several limitations to this study. The initial diagnosis
of HF was made outside of our clinic with no uniform criteria
applied. None of the patients had surgery, so that surgical
confirmation of the echocardiographic abnormality was not
possible. Finally, the population studied may not truly reflect
the nature of the disease in younger rural populations where
a greater prevalence of acute rheumatic carditis may be found.
Conclusion
The modern cohort of patients with rheumaticMRwas older, had
less acute rheumatic fever and greater associated co-morbidities.
Table 4. Clinical and echocardiographic features according to the
presence or absence of hypertension*
Variables
Hyper-
tension
(n = 45)
Normo-
tension
(n = 39) p-value
Clinical parameters
Age (years) 51.7 ± 11.1 35.1 ± 14.2 < 0.0001
Female (%) 86 82 0.62
Systolic blood pressure (mmHg) 127.9 ± 8.4 119.5 ± 12.8 0.0008
Diastolic blood pressure (mmHg) 79.2 ± 8.5 74.2 ± 8.8 0.01
Body mass index (kg/m2 ) 28.6 ± 6.1 25.0 ± 5.8 0.01
Body surface area (m2) 1.7 ± 0.2 1.7 ± 0.2 0.21
NYHA functional class (I/II and III) 29/71 56/44 0.03
Left ventricle
LV end-diastolic diameter (mm) 52.4 ± 8.4 58.3 ± 9.8 0.004
LV end-systolic diameter (mm) 39.7 ± 9.5 43.2 ± 10.9 0.12
Interventricular septal diameter (mm) 9.0 ± 2.3 8.9 ± 4.6 0.97
Posterior wall diameter (mm) 9.1 ± 1.6 8.1 ± 1.3 0.0009
End-diastolic volume indexed (mls/m2)† 87.7 ± 29.9 100.9 ± 32.0 0.05
End-systolic volume indexed (mls/m2)† 35.9 ± 17.7 46.1 ± 27.4 0.046
LV mass indexed (g/m2 )† 100.1 ± 39.4 110.4 ± 40.2 0.24
Relative wall thickness 0.4 ± 0.1 0.3 ± 0.1 0.0001
LV ejection fraction (%) 58.4 ± 12.6 58.1 ± 13.1 0.91
Ejection fraction ≥ 60% 24 24
Ejection fraction < 60% 20 16 0.61
Average E/E′ (cm/s) 19.2 ± 10.9 17.7 ± 8.9
E′ (cm/s) 7.4 ± 2.5 9.9 ± 3.4 0.006
E/A ratio 1.3 ± 0.6 1.6 ± 0.6 0.008
Left atrium
Left atrial volume indexed (ml/m2)† 57.6 ± 24.1 83.37 ± 67.7 0.42
Right ventricle
Right ventricle S′ (cm/s) 14.6 ± 15.6 11.2 ± 2.5 0.18
Pulmonary artery systolic pressure
(mmHg)
33.7 ± 19.2 37.9 ± 16.1 0.28
Tricuspid regurgitation (none/mild/
moderate to severe) (%)
38/36/26 33/31/36 0.46
Mitral regurgitation severity
Moderate mitral regurgitation (%) 82 56
Severe mitral regurgitation (%) 18 44 0.009
*Data are presented as mean ± SD or %. †Values are indexed to body surface
area. LV: left ventricle; NYHA: New York Heart Association.