2nd International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV 13-15 September 2000, Toronto, Canada

CARDIOVASCULAR DYSREGULATION IN HIV-INFECTED INDIVIDUALS TREATED WITH HAART

Antiviral Therapy 2000; 5(Suppl. 5):17 (abstract no. O26)

T-J Weber¹, F Bengel², J-R Bogner¹, A Leber³, R Haberl³, M Schwaiger² and F-D Goebel^1
1Medizinische Poliklinik der Universität München, München, Germany; ²Klinikum rechts der Isar, Nuklearmedizinische Klinik und Poliklinik der Technischen Universität München,München, Germany;and ³Medizinische Klinik 1, Klinikum Großhadern d. Universität München, München, Germany

BACKGROUND: HAART induces hypercholesterolemia which is discussed as a risk factor for atherosclerosis and may have an effect on cardiovascular dysregulation.

OBJECTIVES: To investigate cardiovascular dysregulation, atherosclerosis and plaque formation in HIV-infected individuals with HAART-related hypercholesterolemia.

DESIGN: Group A: 11 patients who developed HAART-related hypercholesterolemia (>300 mg/dl) for at least 24 months. Group B: four HIV-infected patients not receiving HAART (cholesterol <200 mg/dl); and Group C: 10 non-HIV-infected individuals (cholesterol <200 mg/dl).

METHODS: (i) Positron emission tomography (PET) (clinical indication to exclude coronary heart disease): measuring heart rate, rate pressure product (RPP), myocardial blood flow (MBF) and coronary vascular resistance (CVR) before and after adenosine induced stress. (ii) Electron beam tomography (EBT): measuring calcium density in coronary arteries and calculation of a calcium score.

RESULTS: Patients in group A (n=ll) had a significantly blunted response regarding heart rate, RPP, MBF after adenosine application and a lower decrease in CVR than group B (n=4) and C (n=10). In group A, 5/8 patients showed normal calcium density and a normal age adjusted calcium score; 3/8 patients showed a moderately increased age adjusted calcium risk score.

CONCLUSIONS: Structural pathology (calcium density) is not increased after two years of severe hypercholesterolemia. Our results strongly suggest that functional myocardial defects result from HAART. Endothelial dysfunction may be discussed as an explanation.

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O26

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