Econom ic Development in Developing Oil Rich Countries

* Significant difference

The mean weight observed in the AIDS group was significantly lower than the controls.

This is expected especially in symptomatic HIV infected subjects where the loss of lean body mass especially muscle protein has been well documented.^94-96 In the absence of HIV infection, malnutrition has been known to be associated with decrease in left ventricular mass, left ventricular volume and ventricular function.^94,95 However, the presence of increased left ventricular mass in some patients with HIV infection is an indication that some other factors may have counteracted the usual effects of malnutrition. It remains possible that inadequate nutrition may have contributed to the subnormal hypertrophic responses relative to left ventricular dimension observed in patients with HIV/AIDS. ⁶⁰

There was no significant difference in the mean heart rate, systolic and diastolic blood pressures of the HIV/AIDS and control groups in the present study. Similar findings were reported by Coudray et al⁹⁷ in France. However, the mean heart rate was significantly higher in the AIDS group. This might be as a result of autonomic dysfunction in HIV infected children^68-71.

In the present study, corrected QT interval was found to be prolonged. The implications for affected children are not very clear, but Villa et al⁹⁸ in Italy have suggested that it is a reliable parameter that can be used to indicate the presence of autonomic neuropathy. The T wave amplitude was significantly higher in the control group. While flattened T waves have been reported in HIV infection⁷³, this abnormality was not found in this study except in a single patient who had pericardial effusion. Nevertheless, the T wave

amplitude was indeed significantly smaller in the HIV/AIDS group than the controls.

Currently, there is no hypothesis that can be put forward for this observation. It is conceivable that the difference in the prevalence of the flattening of T-waves is due to some yet unidentified characteristics of study population.

The prevalence rate of pericardial effusion in this study was 12%. The measured values were less than 0.51cm. This corresponds to an estimated volume of less than 100ml. ⁹⁹A comparable prevalence rate of 8.8% to 15% has been reported in the literature^88,100,101 . However, higher rates ranging between 21% and 58%^101,102 have also been documented.

Estok and Wallach¹⁰² in New York reported a rate of 21% in adults while Mast et al¹⁰³ in Brooklyn reported a rate of 58% in children. This figure also included findings at autopsy, which may account for the higher figures stated. Though the volume of effusion found in this study was not significant enough to cause a tamponade, these children will need to be followed up closely.

For this study, a fractional shortening of 25% was taken to be depressed⁸⁸. Many of the children with cardiovascular abnormalities had a significantly depressed FS. They also had a smaller RPA and a heavier LVM. Depressed fractional shortening accounted for 28% of the cardiac impairment observed in this study. This is similar to the 29% rate reported by Lipshultz et al²⁶ in Boston. The increased LVM measurements accounted for 17% of the echocardiographic abnormalities.

It is pertinent to note that the spectrum of cardiovascular abnormalities in children with HIV infection ranges from clinically quiescent to clinically devastating abnormalities.

Thus, the absence of clinical evidence of cardiac involvement in HIV/AIDS does not necessarily exclude its presence in some of these patients. A fuller evaluation of patients with HIV infection should go beyond clinical assessment alone. It should include electrocardiography and echocardiography.

The spectrum of clinical cardiovascular abnormalities found in the subjects in this study included tachypnoea, tachycardia and also clinical evidence of cardiac failure found in 10 (12%) subjects. This

rate is similar to the 10% reported by Starc et al ⁸⁸ in New York. The electrocardiographic abnormalities included prolonged PR and QTc intervals and sinus tachycardia. These abnormalities were seen more in the subjects with AIDS. Depressed fractional shortening, smaller aortic diameter and increased left ventricular mass were the echocardiographic abnormalities found.

The variables investigated for their potential association with cardiovascular abnormalities in HIV infection included age, gender, stage of disease, mean age at diagnosis and the use of ARVs. Gender did not have any significant association with the presence or absence of cardiovascular abnormalities. Also, the prevalence of cardiac involvement was not significantly affected by age. This is not surprising considering the

fact that there is no scientific basis to expect a direct link between age or sex and cardiovascular abnormalities in HIV infection.

Similarly, advanced stage of disease, which is a known risk factor for cardiac involvement in HIV infection,57, 104,105 was not significantly associated with the presence of cardiac abnormality in this study. Most of the subjects with cardiovascular abnormality had clinical category C symptoms. Its effect was not statistically significant. This may not be unconnected with the population studied. Also, the use of Doppler might actually have made it possible to evaluate the valvular functions in these patients and probably improve on the diagnostic yield.

A striking observation in this study was the increased occurrence of cardiovascular abnormalities in subjects on ARV medications when compared to ARV- naive subjects (p=0.009). All the subjects on ARVs were on a combination of Zidovudine, Nevirapine and Lamivudine. The links between HIV infection, ARV treatment and cardiovascular abnormalities have been the subject of commentary in some previous studies. Some authors reported an increase in cardiac dysfunction in HIV-infected patients treated with ARV drugs , especially AZT^46-48. The present study does not support the uniform attribution of cardiovascular abnormalities to HIV infection for a number of reasons.

Firstly, 26 subjects who were not on ARV medications showed evidence of cardiovascular involvement. Secondly, the cross-sectional design of the present study is fundamentally incapable of fully addressing the issue. A longitudinal study of subjects at commencement of ARV treatment and their follow up would be better suited for the purpose. A better alternative might be a randomized control trial comparing various ARV

drugs. A contrary view on the relationships between HIV infection, ARV medications and cardiovascular abnormalities has been expressed by other workers⁶², who reported that AZT had no effect on cardiac changes in HIV infection. This school of thought may be applicable to the 26 subjects who had cardiovascular abnormalities in spite of being ARV-naive. Both schools of thought have merits and neither can be dismissed or wholly accepted based on the findings of this study. It may well be that there are as yet unidentified influences which confound the relationship between HIV-induced cardiovascular abnormalities and the effects of ARV medications. The response of any index patient will then depend on the net effect of these confounding factors.

Apart from representing an advanced stage of disease, the presence of HIV encephalopathy has been shown to be a predictor of cardiovascular involvement in HIV infection ^60,72. However, this could not be demonstrated in this study as none of the patients presented with features suggestive of encephalopathy.