| dc.description.abstract | Heart muscle disease (HMD) is a common cardiovascular disease Nigerians. It presents with cardiomegaly associated with myocardial failure. Some of the patients have mild, transient hypertension when they are in failure but this rapidly improves with treatment of heart failure and without hypotensive drugs. A number of them have incompetence of the mitral valve and sometimes of the tricuspid valve. There is no pathognomonic sign on the electrocardiogram and chest x-ray usually shows cardiomegaly and signs of heart failure. Cardiac angiography shows dilated, poorly contractile left ventricle.
The heart macroscopically is flabby, dilated and hypertrophied with focal areas of fibrosis. Intra-cardiac thromb are common. Histologically, the muscle fibres are hypertrophied; there are areas of myocytolysis and focal scarring with scattered lymphocytes.
A critical review of studies conducted at the University College Hospital, Ibadan, Nigeria and aimed at finding the cause of HMD showed that there was very little evidence to incriminate malnutrition and anaemia as the cause of the disease although they may make the heart more susceptible to other injurious factors. There was strong evidence that hypertension could be an aetiological factor though a number of questions remained unanswered. Thiamine deficiency was present in a significant number of Nigerians with HMD and might produce reversible myocardial damage. It could also act as a catalyst to other factors producing myocardial injury.
These suggested aetiological factors are, however, just a few of the disorders known to cause myocardial damage. Other disorders that have been incriminated in causing myocardial damage were therefore reviewed. A study was then undertaken, using a multifactorial approach, to assess the role of these disorders in the aetiology of HMD.
50 Nigerians with HMD were studied. initial assessment included a comprehensive history and physical examination. A wide range of investigations was also carried out. The patients were treated on admission with digitalis and frusemide and maintained on the same dose of drugs on discharge from hospital. Thiazides, and when necessary, alpha methyldopa were substituted for frusemide if at any stage there was no improvement and if the blood pressure remained elevated. Each patient was followed up for at least 1 year.
Of the 50 patients, 6 were found on left ventricular angiography to have organic mitral incompetence. 18 of the remaining 44 patients presented with a normal blood pressure (diastolic blood pressure below 90 mmHg) and 26 with a diastolic blood pressure of 90 - 1OOmmHg. Of the 18 normotensive patients, 12 remained normotensive throughout the entire observation period. Their heart failure was controlled with digoxin and frusemide both as in-patient and in the subsequent out-patient follow-up. The heart failure of the remaining 6 patients was controlled while in hospital but they developed elevated blood pressures and relapsed into heart failure during out-patient follow-up on digoxin and frusemide. They needed antihypertensive therapy in the form of thiazides or methyldopa with thiazide to keep them out of heart failure. 20 patients with initial raised blood pressures responded to in-patient treatment with a fall in blood pressure and remission of their cardiac failure. During out-patient follow-up the blood pressure became elevated again and cardiac failure reappeared. These patients needed antihypertensive therapy to produce a fall in blood pressure and relief of their heart failure. 6 other patients presented with elevated blood pressures did not respond even as in-patients until antihypertensive therapy had been instituted. Those who needed antihypertensive treatment to improve their heart failure had significantly enlarged aortic shadows on plain chest x-ray and on angiography. Many of them had snail kidneys on intravenous pyelography and one of the patients who died had bilateral contracted kidneys.
20 of the 44 patients with HMD were also alcoholics. All but one of the patients in the high socio-economic group were alcoholics. Many of the patients with HMD had a background of protein malnutrition as reflected in their significantly low serum albumin. They were also significantly thiamine deficient, only 1 patient had a high cardiac output reversed by thiamine administration. There was no significant difference between their serum potassium and controls.
There was also no significant difference in the frequency of toxoplasma infection between patients with HMD and controls. Two female patients with HMD had toxoplasma cardiomyopathy. They became ill in early puerperium and had very high titres against toxoplasma gondii.
Patients with HMD had a significantly higher incidence infection from Coxsackie B viruses than controls. They also had higher levels of antibody titres. Antibodies to Coxsackie viruses B2, B3 and B6 were also more commonly identified in their sera than in controls.
There was no evidence implicating Trypanosoma cruzi as a cause of heart failure in Nigerians. There was also no evidence to incriminate other parasites and eosinophilia as causes of HMD in Nigeria. One patient had hypothyroidism.
83% of the female patients had a high parity although only three were ill during pregnancy or early puerperium.
Two of these had toxoplasma cardiomyopathy; the third had hypertension in addition.
No case of haemochromatosis, amyloidosis or sarcoidosis was identified in the study.
It is concluded that HMD in Nigerians is not caused by a single disease process but is the end-result of myocardial damage produced by a variety of factors. The mild hypertension seem in some of them contributes to their morbidity and is not a result of their heart failure. | en_US |
