Vascular Involvement
Although rare, coronary artery abnormalities have been described in the earliest case reports of cardiac complications in children [35-38]. Joshi et al. found macroscopic lesions in small and medium-sized arteries in six children with AIDS.
The pathologic findings in the coronary artery wall were characterized by intimal fibrosis, fragmentation of the elastic lamellae, and calcification of the media. In one out of six cases, this arterial remodeling involved the coronary arteries and had led to a fatal myocardial infarction by aneurysms and thrombosis of the right coronary artery. The pathophysiology of these arterial anomalies is unknown. It may be related to the viral infection, given the absence of other cardiovascular risk factors. Whether HIV itself is the causal agent or other viruses such as herpes or cytomegalovirus has to be elucidated. The adverse effects of antiretroviral drugs, including dyslipidemia, lipodystrophy, and insulin resistance, are problems in the long-term management of HIV infection. This is of particular importance in children because HIV infection has become a chronic disease in this population. HIV- infected children may live two decades longer than HIV-infected adults. As in the adult population, metabolic toxicity of antiretroviral therapy has been observed in children [39-41], but the long-term cardiovascular consequences in children are unknown. Atherogenic lipoprotein changes in adults treated with protease inhibitors (PIs) have been found and are associated with endothelial dysfunction and increased intima-media thickness [42-44]. However, the relative contributions of antiretroviral therapy, chronic inflammation due to the viral infection, classic cardiovascular risk factors, and their interactions are very difficult to identify. Bozzette et al. showed that the benefit in terms of mortality associated with the extensive use of therapies for HIV was not diminished by any increase in the rate of cardiovascular or cerebrovascular events or related mortality [45]. The pediatric population offers a unique opportunity to study vascular function during HIV infection in the absence of classic cardiovascular risk factors. Symptomatic atherosclerosis is evidently absent at this age, but endothelial function and arterial stiffness can be investigated by noninvasive echo-tracking techniques. We have recently shown that HIV- infected children have a vascular dysfunction that may be an early step in the development of atherosclerosis. We did not find any difference between children receiving antiretroviral therapy and patients who had never been treated [46]. Differences with the control subjects indicate that the HIV infection itself may have a deleterious effect on vascular function. However, others found a contribution of antiretroviral therapy to the vascular impairment in children [47]. This is consistent with autopsy studies during the pre-antiretroviral era, reporting eccentric atherosclerosis lesions in the absence of traditional risk factors [36]. The HIV envelope protein, gp120, activates human arterial smooth muscle cells to express tissue factor, the initiator of the coagulation cascade [48]. In addition, inflammatory cytokines and viral proteins synergistically promote endothelial activation, apoptosis, or cell proliferation [49]. Consequently, the arterial remodeling observed in patients who had never been treated could be a result of direct viral infection, or of the activation of bystander cells (smooth muscle cells and endothelial cells), by HIV viral proteins. Hsue et al. recently proposed that in adults, immunodeficiency and traditional coronary risk factors might contribute to atherosclerosis rather than the deleterious effects of PI treatment [50]. In children, it is possible that antiretroviral therapy counterbalances, at least transiently, HIV-induced injury to the developing vascular bed by reversing or stabilizing the HIV-induced vascular dysfunction.Mild and nonprogressive aortic root dilation was also seen in children with vertically transmitted HIV infection from 2 to 9 years of age. Aortic root size was not significantly associated with markers for stress- modulated growth; however, aortic root dilation was associated with left ventricular dilation, increased viral load, and lower CD4 cell count in HIV-infected children. The aortic root dilation could also be a consequence of increased arterial stiffness affecting the aorta. As prolonged survival of HIV- infected patients becomes more prevalent, some patients may require long-term followup of aortic root size [51-52].
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