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May 2, 2002 - 12:00am to May 3, 2002 - 12:00am
Bethesda, Maryland

Etiology of Cardiovascular Complications in HIV Infection
Endothelial Dysfunction in HIV Infection
Cardiovascular Complications from Cocaine Abuse in HIV Infection
Genesis of Cardiomyopathy with HIV Infection and Alcohol Abuse

Sponsored by: National Heart, Lung and Blood Institute and National Institute on Drug Abuse


This meeting was planned, organized and conducted by Lan-Hsiang Wang, Ph.D., of the National Heart, Lung, and Blood Institute and Jag H. Khalsa, Ph.D., of the Center on AIDS and Other Medical Consequences of Drug Abuse (CAMCODA), within the National Institute on Drug Abuse, NIH. A group of nationally and internationally recognized clinicians and scientists, supported by the NHLBI and NIDA presented and discussed;

  • Current data on the etiology and underlying pathophysiology of cardiovascular complications of HIV/AIDS, substance abuse (cocaine, alcohol), and HIV infection,
  • In vitro tests and in vivo models for the study of cardiovascular complications (e.g., cardiomyopathy) of HIV and substance abuse,
  • Endothelial function in HIV infection,
  • The problems of design and conducting such studies in clinical populations.

Recommendations for Future Research:

The role of covariates in HIV-related cardiovascular complications. 

  • Role of other pathogens in HIV-related cardiovascular complications. 
  • Autoimmune mechanisms in HIV-related cardiac conditions, particularly in combination with other pathogens. 
  • Genetic predisposition for transition to dilated cardiomyopathy. 
  • Incidence, prevalence, and pathophysiology of HIV-related cardiovascular disease in other vulnerable populations such as women, infants, and older individuals exposed to HIV and substance abuse. 
  • Influence of other conditions such as diabetes, atherosclerosis, as well as lifestyle and behavior choices such as smoking and recreational drug abuse on HIV-related cardiovascular complications.

Mechanisms of cellular injury in HIV-related cardiovascular complications. 

  • Interactions of viral replication, immune system activation, inflammatory pathways, and reactive oxygen species in HIV-related cardiovascular complications. 
  • Metabolic/energetic mechanisms such as the role of mitochondrial ATP production, cardiac myocyte energetics, increased reactive oxygen species, altered oxygen utilization, and changes in gene expression in HIV-related cardiovascular complications. 
  • Role of highly active antiretroviral therapies (HAART) in HIV-related cardiovascular complications. 
  • Pharmacokinetic drug interactions between HAART and pharmaceuticals use in the treatment of cardiac disease. 
  • Interactions between immune cell (infected and/or uninfected) and cardiac myocytes and their effects on recruitment mechanisms, gene expression alterations, and cell-cell signaling events. 
  • Role of hypothalamic-pituitary-adrenal axis in HIV progression and HIV-related cardiovascular complications.

Pre-clinical investigations for therapies for HIV/AIDS-related cardiovascular complications. 

  • Animal models for studying the effects of antiretroviral and immunorestorative therapies on HIV-related cardiovascular complications. 
  • Animal models for testing optimal therapies for the treatment of HIV-related cardiovascular complications. 

Therapeutics and prevention trials for HIV/AIDS-related cardiovascular complications. 

  • Optimal therapies for treating HIV-related cardiomyopathy considering whether these therapies should be different from other forms of cardiomyopathy. 
  • Possibility and advantage of early intervention for HIV-related cardiovascular complications. 
  • Alternative therapies (e.g., anti-oxidants, immunomodulators, nutritional therapies) for HIV-related cardiovascular complications.