This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Abnormalities of LV structure and function are associated with the human immunodeficiency virus (HIV), and possibly nucleoside reverse transcriptase inhibitors (NRTI), non-nucleoside reverse transcriptase inhibitors (NNRTI), and/or protease inhibitors (PI) administered as part of highly active antietroviral therapy (HAART), and result in significant morbidity and mortality to HIV infected children. The abnormalities of LV structure and function associated with HIV cardiomyopathy can be related to depressed contractility from HIV, associated with LV dilation, increased afterload (abnormal LV dimension : wall thickness), and abnormalities of heart rate and blood presure. Similar abnormalities of LV structure and function are observed with components of HAART that may lead to cardiomyopathy in adults or animal models. Because HAART-exposed seroreverters do not have HIV it becomes easier to understand the cardiovascular effects of HAART. We have found the proposed echo parameters of LV structure and function are very sensitive for detecting asymptomatic cardiomyopathies in children with mitochondrial toxicity, the proposed mechanism of HAART-associated cardiotoxicity.
Showing the most recent 10 out of 459 publications
