Platelet function in adult human immuno-deficiency virus- 1 infected heart naïve patients at Kenyatta National Hospital, Kenya
Awuor, Onjula Rael
MetadataShow full item record
Occurrence of cardiovascular diseases (CVDs) in adult human immuno-deficiency virus-1 (HIV-1) infected patients is associated with 18% of HIV-1 deaths. Availability of highly active antiretroviral therapy (HAART) has prolonged and improved quality of life in HIV patients. However it has led to the appearance of pre-mature cardiovascular events (CVEs) of athero-thrombotic origin with its continued use. It is still unclear whether thrombotic risks associated with increased platelet function are as a consequence of HIV-1 infection alone or of the long-term use of these antiretroviral drugs. This study aimed at determining platelet function in adult HIV-1infected patients not on HAART. In a case-control study design, using convenient and consecutive sampling method a total of 28 participants were recruited. Fourteen adult HIV-1positive HAART naive patients and fourteen HIV negative participants attending Kenyatta National Hospital, comprehensive care clinic (CCC) were enrolled to the study after consenting. Blood samples were collected and platelet concentrates prepared from each sample. Platelet aggregation was determined by measuring time dependent light transmission in response to known agonists (adenosine tri-phosphate (ADP), collagen and arachidonic acid (A.A) on chrono-log 100 aggregometer. Platelet activation was done by measuring P-selectin expression using flow cytometry. In both groups, participants were of similar age and sex. The results show that median Platelet % PSelectin expression levels in HIV positive group was 1.5 times that of the control group (34.5 (IQ) 10.3-63.3 vs 21.1 (IQ) 2.7-46.2),and had a positive correlation with viral load (r=0.634, P= 0.019) but not with CD4 count (r= -0.532, P= 0.7229). Among the three agonists platelet aggregation showed a significant higher response to collagen compared to arachidonic acid and ADP (P=0.00087, P=0.00056 and P=0.019) respectively. Importantly, less percentage maximum platelet aggregation was observed in HIV positive group compared to HIV negative group for all the agonists (Collagen:75±4.8% cases vs 80.4±6.7% controls at 10μg/ml; AA 64±8.1% cases vs 88.4±6.2% controls at 10μg/ml; ADP 60.7±6.7% cases, 71.1±8.1% controls at 5μmol/l). Furthermore, % maximum platelet aggregation correlated inversely with viral load (ADP r=-0.286, P=0.0424; Collagen r=-0.4663, P=0.0177 and A.A r=-0.3, P=0.259) and directly with CD4 counts ADP r= 0.614, P=0.0528; collagen r=0.384, P=0.0273 and A.A r=0.850, P=0.002).This study was able to demonstrate that platelet function in HIV-infected patients is altered. This offered insights into the complex mechanisms underlying occurrences of thrombotic events in HIV positive patients.