Cardiovascular Journal of Africa: Vol 28 No 5 (September/October 2017)

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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 28, No 5, September/October 2017 280 AFRICA
Cardiovascular Topics
Is there a role for combination anti-remodelling therapy
for heart failure secondary to chronic rheumatic mitral
regurgitation?
Ruchika Meel, Ferande Peters, Elena Libhaber, Mohammed R Essop
Abstract
Introduction: The value of combination anti-remodelling
therapy for heart failure (HF) secondary to mitral regurgita-
tion (MR) is unknown. We studied the effect of anti-remod-
elling therapy on clinical and echocardiographic parameters
in patients with severe chronic rheumatic mitral regurgitation
(CRMR) presenting in HF.
Methods: Thirty-one patients (29 females) at Chris Hani
Baragwanath Academic Hospital, treated with combina-
tion therapy for HF due to CRMR and New York Heart
Association functional class II–III symptoms, underwent
prospective six-month follow up.
Results: Mean age was 50.7 ± 8.5 years. No patients died or
were hospitalised for HF during the study period. No wors-
ening of clinical symptoms or functional status, or left and
right ventricular echocardiographic parameters (p > 0.05) was
noted. Peak left atrial systolic strain improved at six months
(18.7 ± 7.7 vs 23.6 ± 8.5%, p = 0.02).
Conclusion: This preliminary analysis suggests that combi-
nation anti-remodelling therapy may be beneficial for HF
secondary to CRMR. We had no HF-related admissions or
deaths, and no deterioration in echocardiographic parameters
of ventricular size and function.
Keywords: heart failure, mitral regurgitation, combination therapy
Submitted 5/6/16, accepted 7/12/16
Cardiovasc J Afr 2017; 28: 280–284
DOI: 10.5830/CVJA-2016-095
For patients with valvular disease, direct pressure or volume
overload results in cardiac remodelling and eventually heart
failure (HF).1-3 Changes in neuro-hormonal signalling and
genotype result in abnormal structure and function of both the
myocyte and interstitial space.2-4 In chronic mitral regurgitation
(MR), the persistent volume overload of the left atrium and
ventricle, after a period of compensation, results in myocardial
dysfunction through these mechanisms.5 This eventually
culminates in atrial fibrillation, HF and death if left untreated.6
At present, surgery is the mainstay of therapy for patients with
symptomatic severe MR and markers of left ventricular (LV)
systolic dysfunction.7 Surgery is associated with non-negligible
morbidity and mortality rates, even in established centres,
especially in patients with LV dysfunction and high New York
Heart Association (NYHA) functional class.8,9
The use of medical therapy for chronic MR has been largely
non-conclusive and controversial.10 Most were small studies
involving angiotensin converting enzyme (ACE) inhibitors and
beta-blockers in degenerative MR.10-12 Guidelines on valvular
heart disease recommend medical therapy for HF (ejection
fraction < 50%) in chronic MR (class IIa, level of evidence B).7
No study has systematically looked at the effects of
combination anti-remodelling therapy (ACE inhibitors, beta-
blockers, aldosterone receptor antagonist) in HF secondary
to MR. There is proven mortality and morbidity benefit of
combination anti-remodelling therapy in systolic HF as a result
of ischaemia and cardiomyopathy.13-15
We hypothesised that a similar benefit may be derived in HF
secondary to CRMR. This could potentially offer an alternative
option to these patients who are at high risk for surgery or are
not inclined to undergo surgical intervention. Furthermore,
the benefit of anti-remodelling therapy may be extended to
asymptomatic patients with significant MR to prevent disease
progression and delay the time to surgery. We therefore aimed
to study the effect of anti-remodelling therapy, including ACE
inhibitors and beta-blockers, in terms of clinical outcome, and
traditional as well as newer echocardiographic parameters, such
as two-dimensional strain in patients with severe CRMR who
presented with HF.
Methods
This prospective, observational sub-study formed part of a larger
study on CRMR at the Chris Hani Baragwanath Academic
Hospital. Patients were enrolled between January and December
2014. The study was approved by the University of the
Witwatersrand ethics committee (M140114). All patients were
screened and those deemed to have severe CRMR and presented
with HF were referred for possible inclusion in the study.
Division of Cardiology, Chris Hani Baragwanath
Academic Hospital and University of the Witwatersrand,
Johannesburg, South Africa
Ruchika Meel, PhD,
Ferande Peters, MD
Elena Libhaber, PhD
Mohammed R Essop, MD