CARDIOVASCULAR JOURNAL OF AFRICA • Volume 28, No 5, September/October 2017
282
AFRICA
their respective medications are summarised in Table 2. There
was no worsening of left and right ventricular echocardiographic
indices at baseline and at six months of therapy (Table 3).
Based on the integrated assessment (qualitative and
quantitative parameters), MR severity did not change at the
end of six months. No change in quantitative parameters of
MR assessment was noted at the end of six months [(vena cava
width: 6.5
±
1.9 vs 6.0
±
1.6 mm,
p
=
0.2; regurgitant fraction:
31.7 (18.9–57.7) vs 29.2% (15.7–53.5),
p
=
0.2)].
Left atrial peak systolic strain increased at six months (18.7
±
7.7 vs 23.6
±
8.5%,
p
=
0.02). However, no change in right
and left ventricular peak systolic strain was noted at the end of
combination therapy (–15.6
±
5.0 vs –16.4
±
5.9%,
p
=
0.56; –13.9
±
4.3 vs –15
±
4.0%,
p
=
0.28, respectively).
Discussion
The main findings of this study were that patients with rheumatic
MR and HF who were treated with optimal medical therapy had
good short-term clinical outcomes. There was no deterioration in
echocardiographic parameters of cardiac performance, and there
was an improvement in left atrial peak systolic strain.
Some older, pre-echocardiographic studies on rheumatic heart
disease in Western populations demonstrated variable natural
histories, ranging from CRMR being a benign lesion with a
normal life expectancy, to it being a severe, progressive and
ultimately fatal disease.
31-33
Natural history studies in degenerative
MR, with follow up ranging from seven months to 10 years, have
shown increased risk of sudden cardiac death and increased
postoperative morbidity and mortality rates in the presence of
severe MR symptoms, arrhythmias, left ventricular end-systolic
dimensions (LVESD)
≥
45 mm and ejection fraction (EF)
≤
60%.
8,34-39
These studies, primarily pertaining to degenerative,
significant MR, evaluated symptomatic and asymptomatic
patients. Most of them concluded that with conservative
management (medical therapy), outcomes were worse regarding
cardiac death, progression to worsening NYHA functional
class, left ventricular dysfunction, HF, atrial fibrillation and
pulmonary hypertension.
M
ũ
noz
et al
.
40
compared 29 patients with MR on medical
therapy alone to 45 patients who underwent mitral valve
replacement. They found at five-year follow up, a lower
survival rate, faster progression to higher NYHA class, and
more complications such as HF and atrial fibrillation in the
medical therapy group.
40
The main shortcomings of all these
studies are the inclusion of mostly asymptomatic patients with
significant MR, and the medication and dosages used were not
systematically documented.
The subset of patients we followed up had mostly stage D
heart failure due to organic valvular heart disease. They were
on varied combination anti-remodelling therapy as part of their
management. This provided us with the opportunity of observing
this subgroup. The lack of change in left and right ventricular
structural and functional indices may possibly be explained by
the short duration of follow up, the disease-stabilising effect
of anti-remodelling therapy, and/or the relatively younger age
of our patients compared to degenerative MR patients. A lack
of difference in MR severity, even after controlling the systolic
blood pressure in our study, may be explained by the small effect
of change in pressure gradient on regurgitant volume, static left
ventricular volumes, and the rheumatic nature of the disease,
whereby the orifice is fixed and not dynamic, as in degenerative
MR.
5,12,41
There was no change in left and right ventricular longitudinal
strain parameters in our study and this may be attributed to the
short duration of follow up. The reason for marked improvement
in left atrial peak systolic strain may be that the left atrium
remodels and recovers earlier than the ventricles after an injury,
as shown by Therkelsen
et al
.
42
Additionally, left atrial reverse
remodelling has been known to occur independently of left
ventricular reverse remodelling, due to the direct effect of drugs
that inhibit the renin–angiotensin–aldosterone system (RAAS).
4
Also, left atrial strain may be a more sensitive marker for
detecting reverse remodelling than left atrial volumes, as noted
in this study.
Table 2. Comparison between baseline and
maximum medication dose of the study patients
Medication
Number
(%) Baseline dose (mg)
Dose (mg) at
six months
p
-value
Furosemide
30 (97)
75
±
25.9
78.3
±
34.9
0.67
Nifedipine XL
9 (29)
34.4
±
21.8
47.7
±
24.3
0.23
Digoxin
7 (23)
0.125
0.125
1.0
Enalapril
11 (35)
10 (2.5–20)
20 (10–20)
0.17
Perindopril
11 (35)
2.9
±
1
4
±
1.7
0.003
Carvedilol
29 (94)
12.5 (3.125–12.5)
50 (37.5–50)
<
0.001
Spironolactone
28 (90)
25 (12.5–25)
50 (50–75)
0.001
Data are presented as median (interquartile range), mean
±
SD or %. Two patients
were on telmisartan (40 mg at baseline and six months), and one was on atenolol
(12.5 mg up-titrated to 25 mg at six months).
Table 3. Left and right ventricular echocardiographic parameters at
baseline and six months of medical therapy
Variable
Baseline (
n
=
31)
Six months of
therapy (
n
=
31)
p
-value
Left ventricular indices
LVEDD (mm)
55.5
±
8.4
55.1
±
8.0
0.8
LVESD (mm)
42.6
±
9.4
40.7
±
9.5
0.43
EDVi (ml/m
2
)
†
81.8 (68.9–98.1)
79.1 (64.5–99.3)
0.6
ESVi (ml/m
2
)
†
45.4
±
17.8
42.8
±
15.8
0.5
Ejection fraction (%)
46.9
±
8.7
50.4
±
10.1
0.1
E wave (cm/s)
113.2
±
47.2
112.9
±
42.1
0.9
A wave (cm/s)
102.0
±
26.5
99.4
±
28
0.7
E/A wave (ratio)
1.0
±
0.4
1.1
±
0.4
0.3
E´ medial (cm/s)
6.6 (4.5–8.2)
5.9 (4.7–7.8)
0.2
A´ medial (cm/s)
6.7 (5.1–8.2)
7.1 (5.9–8.3)
0.5
Medial E/E´(ratio)
18.5
±
9.5
18.9
±
9.7
0.8
Medial S´(cm/s)
6.1
±
1.4
6.1
±
1.2
1.0
LAVi (ml/m
2
)
†
60.2 (47.1–89.4)
59.5 (44.2–82.4)
0.8
Right ventricular indices
RV base (mm)
38.3
±
6.25
35.8
±
8.8
0.2
TAPSE (mm)
20.5
±
2.9
20.6
±
2.9
0.9
RV S´ (cm/s)
11.1
±
2.7
11.6
±
2.5
0.45
RAVi (ml/m
2
)
†
26.5 (21.7–32)
24.7 (7.4–33.8)
0.6
PASP (mmHg)
33.2
±
12.4
31.4
±
11.5
0.5
Data are presented as median (interquartile range), mean
±
SD or %.
†
Values
are indexed to body surface area. EDVi, end-diastolic volume index; ESVi,
end-systolic volume index; LAVi, left atrial volume index; EDD, end-diastolic
diameter; ESD, end-systolic diameter; LV, left ventricle; PASP, pulmonary artery
systolic pressure; RAVi, right atrial volume index; RV, right ventricle; TAPSE,
tricuspid annular plane systolic excursion.