CARDIOVASCULAR JOURNAL OF AFRICA • Vol 23, No 10, November 2012
558
AFRICA
Hb genotype
No association was found between Hb genotype and DCM in
the patients we studied and there are no reports linking different
types of Hb genotypes with DCM.
Summary of studies on DCM in Africa
From all these studies, we can conclude as follows:
•
Hypertension contributes to some of the cases diagnosed
clinically as DCM in Africa. Such patients should be identi-
fied and reclassified as having hypertensive heart failure with
varying degrees of myocardial dysfunction.
•
Chronic alcohol consumption and myocarditis have also been
identified as the causes of myocardial damage in some of the
patients clinically diagnosed as cardiomyopathy in Africa and
even worldwide.
•
Familial cases of DCM have been described in Africa but
limited research has been done on the continent.
•
Lack of facilities and technical know-how have also made the
routine diagnosis of myocarditis in Africa impossible. Many
are therefore missed.
•
Estimation of markers of inflammation such as C-reactive
protein, inflammatory markers such as the tumour necrosis
factor
α
,
and the plasma marker of apoptosis (Fas/Apo-1) may
perhaps help in making a preliminary diagnosis of myocardi-
tis. This needs to be further explored.
•
In patients with PCM, abnormal immune response to preg-
nancy, increased myocyte apoptosis, selenium deficiency,
cultural practices such as those of the Zaria women, and
prolactin excess/cleavage are other causes that have been
advanced by workers in the field. In those with excess prol-
actin production/cleavage, bromocriptine has been found to
improve the cardiac status of these women.
•
Thiamine deficiency is common among Africans with DCM
and it is related to excessive alcohol consumption and/or
malnutrition. By itself, it is not an important cause of DCM.
•
Haemosiderosis has been found in many patients with DCM
and is probably due to excessive consumption of alcohol
stored in iron containers. Haemosiderosis is reversible.
Implication
For a patient’s heart failure to qualify to be labelled as dilated
cardiomyopathy according to the 1980 classification of the
cardiomyopathies,
11
a patient must have been extensively
investigated and no cause for his/her disease found. Under
this classification, diseases whose causes are known should be
named appropriately.
From the above, therefore, we can assert that some of the
patients diagnosed with DCM in Africa have hypertensive heart
disease/failure. Others have alcohol heart disease, viral heart
disease or myocarditis, peripartal heart disease and familial
dilated heart muscle disease. There are other cases of DCMwhose
aetiology does not fall into these categories. The prevalence of
such cases varies among the different communities of Africa.
Restrictive cardiomyopathy
Under the 1980 classification,
11
the term restrictive cardiomyo-
pathy was in our view out of place. While hypertrophic and
dilated cardiomyopathies referred to structural changes within
the heart, restrictive cardiomyopathy referred to haemodynamic
changes. It would have been more consistent if a term such
as fibrotic/obliterative cardiomyopathy was used to describe
endomyocardial fibrosis (EMF) and Löeffler’s endomyocardial
disease, the two diseases the report had in mind. Moreover, with
the advent of echocardiography, it is now known that diastolic
problems of the heart are not limited to endomyocardial fibrosis
and its variants. They occur in several other diseases, including
hypertension and hypertrophic cardiomyopathy, and indeed in
infiltrative disorders such as amyloidosis.
Under the 1980 classification,
11
it was recommended
that Löffler’s cardiomyopathy be relabelled eosinophilic
endomyocardial disease (EED). Both EED and EMF are
characterised by scarring of the endomyocardium of either or
both ventricles, which creates cavity obliteration and restriction
of filling of the ventricles with blood. While the outflow tract
of the affected ventricle is spared, the atrio-ventricular valve
becomes enmeshed with scar tissue, which consequently binds
down the posterior valve leaflet and leaves the valve perpetually
open. Free regurgitation of blood occurs because of this,
resulting in an enormously dilated atrium.
EED was first described in Europe by Löffler
13
in 1936,
while EMF was first described by Bedford and Konstam
12
in
1946
among Nigerian soldiers who served in the second world
war. EMF was similarly reported by Davies
78
in East Africa in
1947,
although observations had been made about the disease
by Arthur Williams
79
as far back as 1938. Despite a myriad
publications on the two diseases in the world literature, there is
still no agreement on their aetiology.
In an excellent review, Bukhman
et al
.
80
summarised the
causes of EMF, which had been proposed by several authors in
the literature as follows:
•
infection – toxoplasmosis, rheumatic fever, malaria, helminth
parasites
•
allergy – eosinophilia, auto-immunity
•
malnutrition – protein deficiency, magnesium deficiency
•
toxic agents – cerium, cassava, thorium, serotonin, plant
toxin, vitamin D.
In addition to these, the following were considered as probable
causes from Ibadan, Nigeria:
•
vitamin E (tocopherol) deficiency
•
obstruction of cardiac lymphatics
•
Schistosoma
infestation:
Schistosoma
ova had been found in
EMF lesions of some Nigerian patients.
Of all these, only the hypereosinophilic syndrome of Löffler
has been shown to be definitely associated with fibrosis and
obliteration of the cardiac apex, similar to tropical EMF. The
cause of tropical EMF still remains largely unknown. However
Löffler’s endomyocardial disease and the tropical forms of
EMF, although similar, do not appear to be the same disease,
as there are important differences between them. These can be
summarised as shown in Table 1.
The questions that arise from all these studies are as follows:
1.
What causes eosinophils to degranulate and attack the
patient’s own tissues? In our view this has not been adequately
addressed. It is known that eosinophils are normally deployed
by the body to fight parasites and are often elevated in those
with allergies, including drug reactions, collagen disorders
such as polyarteritis nodosa and some malignancies. But these
eosinophils do not harm the patient’s tissues. What therefore
