DISCUSSION

HIV/AIDS is a chronic infection associated with chronic weight loss from conditions such as chronic diarrhea, malabsorption and wasting syndrome. The mean body mass index (BMI) in this study was 22.27±4.49 kg/m² in the subjects and 25.13±5.06 in the controls. Although, the majority (53.8%) of the subjects had normal BMI, the mean BMI was significantly lower than that of the controls (p=0.001). Also the percentage of underweight (20%) is higher in the subjects than in the controls (4.6%). This finding can be as a result of the disease process. Significant unexplained weight loss is a cardinal symptom in HIV diagnosis protocol¹. Unlike the study in Congo which showed that BMI

<22kg/m² was predictive of cardiac dysfunctions ¹¹⁷, BMI had no association with pulmonary hypertension in this study.

Progressive dyspnea has been reported by many researchers as the commonest symptom of pulmonary hypertension^20,61 however in this study dyspnea was only present in 16.9% of the subjects and was not associated with pulmonary hypertension. This can be due to the fact that this study was carried out among newly diagnosed HIV treatment nạve subjects who were mainly asymptomatic.

Miller RF et al¹²⁰ found out that more than half of asymptomatic patients in his study had significant echocardiographic abnormalities. The early presentation of some of the patients, the exclusion criteria which exclude patients with hypertension, severe anaemia and history suggestive of pulmonary tuberculosis may also support why dyspnea was not a prominent presentation in the study.

The mean pack cell volume (PCV) was significantly lower in the subjects than the controls and this may be a part of the disease process. HIV/AIDS can lead to low PCV level and several factors have been attributed to cause anaemia in HIV patients some of which are poor appetite, diarrhea and

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malabsorption, low CD4 count, (<200ul/ml), high plasma viral load, women, black race, Zidovudine use etc^123,124.

None of the lipid profile parameters assessed in this study showed significant association with pulmonary hypertension except low density lipoprotein with p value of 0.049. Several studies have reported that HIV patients are prone to cardiovascular risk factors just like the general population¹²⁵. However, some antiretroviral drugs are associated with a an increase in short time risk of CVD that may become greater over a long period of exposure. Patients on protease inhibitors are more proned to develop dyslipidaemia¹²⁶. The association of dyslipidaemia and systemic hypertension has been well studied and the co-existence of the two risk factors has an additive adverse impact on the vascular endothelium, which results in enhanced atherosclerosis, leading to CVD. However, not much has been done to assess the effect of dyslipidaemia and pulmonary hypertension.

Parasitic infections can cause inflammation and eosinophilia due to host response to the parasite antigens. These are likely the critical underlying etiology in many forms of parasites associated pulmonary hypertension (PH) for instance schistosomiasis-associated PH¹²⁷. However, in this study there was no association between parasitic infestation and the development of pulmonary p =0.633.

Twelve (18.5%) of the patients had pericardial effusion and 3 (4.6%) of the controls. This is similar to the finding of 17.4% and 11% found by Ayaskanta Singh et al¹¹¹ and Heidenreich et al¹³⁸ respectively. They found majority of the effusions to be small, and asymptomatic. Other studies have reported higher prevalence of 10-59% of pericardial effusion in HIV/AIDS^38,139. Small pericardial effusion around the heart is usually part of the effusive process that involves the pleura and the peritoneum, it is also known as capillary leak syndrome¹⁴⁰ while large effusions are either due to malignancy or Mycobacterium tuberculosis¹⁴¹.

78 5.3. Prevalence of pulmonary hypertension.

The prevalence of pulmonary hypertension in HIV patients in this study was 9.2%. The finding of 1.5% prevalence in the controls as against the 9.2% in the subjects at ratio 1:6 in this study confirm the reports that HIV infected patients have a greater incidence of PAH compared to general population^19,24. The prevalence of pulmonary hypertension in this study was similar to the work of Pilly Chillo et al¹⁶ that found a prevalence of 12.7% in Tanzania, 11.4% by Ayaskanta Singh et al¹¹¹ in India and 4% by Isiguzo in Jos northern Nigeria¹⁵. The low prevalence in the Jos study compared to this study may be explained by the fact that the subjects in Jos study were already on HAART which some studies have shown to be beneficial^13,18,143. This study is also comparable to studies done by Pellicelli AM et al¹⁹ and Mehta et al²⁰ who also found higher incidence of pulmonary artery hypertension in HIV patients than normal population. Some other studies like those of Onwusu IK et al¹⁷ and Karaye KM et al¹¹² have reported a higher prevalence of 38.5% and 66.25% respectively.

The reason for these high values in these studies may be because of larger population size of 200 in Owusu study and the work of Karaye was done on HIV patients already in heart failure. The prevalence of pulmonary hypertension in HIV in the developed countries has been put at 0.6 -2.0%.¹³ However studies have suggested higher prevalence in Africa as a result of higher prevalence of HIV infection complicated by hyperendemic risk factors, limited access to antiretrovirals, and lack of screening tools^113,114. Also, the studies in the developed countries used right heart catheterization (gold standard and more accurate) for diagnosis whereas most Africa studies including this used echocardiography (alternative method) for diagnosis. The use of echocardiography as in some of these studies reported may lead to overestimation or underestimation of pulmonary pressures in up to 40% of individual patients^115,116.

79 5.4 – Pattern of Left ventricular function.

This study found 13.8% HIV positive treatment nạve subjects with left ventricular systolic dysfunction and 4.6% had dilated cardiomyopathy. None of the controls had these. Diastolic dysfunction was observed in 30.8% of the subjects and 10.8% of the controls. The incidence of left ventricular systolic and diastolic dysfunctions were statistically higher in the subjects than the controls with X² =13.220, p= 0.001 and X² =8.458, p=0.004 for LV systolic and diastolic dysfunctions respectively. These patterns were similar to what was observed by Kelechukwu U et al¹²⁹ in Abia State, Nigeria. He found 13.6% of HIV patients with left ventricular systolic dysfunction and 28.8% with left ventricular diastolic dysfunction. Several authors have reported different percentages of left ventricular systolic dysfunction depending on the characteristics of the studied population and the definition criteria of cardiac abnormality. Danbanchi et al³⁷ found high systolic dysfunction in 19 of 40 patients with stage III/IV HIV/AIDS. He concluded that cardiac involvement was not a prominent feature in the early stages of the HIV. The prevalence of left ventricular systolic dysfunction reported by Cardoso and colleagues ³³ was 6.5% while that to reported by Longo-Mbenza and colleagues¹³⁰ was 85.7%. There were 4.6% of the subjects with dilated cardiomyopathy.

This was similar to the findings of other researchers^38,111. DCM is a well-documented cardiac abnormality in HIV/AIDS, and many Africa researchers have reported prevalence in a range of 7%-57%^33,111.. It is seen in people with severe immunosuppression with low CD4 count less than 100ul which is a marker of bad prognosis in them⁸. The work of Nzuobotane et al.³³ also demonstrated a similar relationship between the degree of immunosuppression and the likelihood of cardiomyopathy.

The cause of dilated cardiomegaly is multifactorial including myocarditis, nutrition, drug and other viral infection. Barbaro et al¹³² reported that asymptomatic HIV patients may have impaired systolic and diastolic functions by echocardiography and Doppler studies and this is usually a pointer to

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involvement of the heart in the disease process. In this study, most patients were asymptomatic yet some had systolic and diastolic dysfunction by echocardiography and Doppler study. Therefore, early recognition of dysfunction and commencement of management may impact on the overall outcome of these patients³³.

Diastolic dysfunction was seen in 30.8 % and is statistically significant. This is similar to the report of Kelechukwu et al¹²⁹ and DA Olusegun-Joseph et al³⁸ who reported prevalence of 28.8% and 32%

respectively. Other studies have found prevalence in the range of 37-50%^131,133. Some of the factors observed to be responsible for diastolic dysfunction include, ventricular filling abnormalities due to a non-compliant ventricle¹³⁴, tachycardia which result in reduced ventricular compliance¹³⁵. Others include hypertension associated with use of ART and treatment with protease inhibitors^136,137. Pericardial effusion (18.5%), tachycardia (higher mean±SD pulse rate in the subjects than controls), are some of the factors in this study that can contribute to the diastolic dysfunction.

5.5 Relationship between pulmonary hypertension and left ventricular systolic and diastolic