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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.