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Coronary vasomotor function is reduced after initiation of antiretroviral therapy in treatment naïve HIV patients: a prospective myocardial perfusion PET study
Presented by Ulrik Sloth Kristoffersen (Denmark).
U.S. Kristoffersen1,2, A.-M. Lebech3, J. Gerstoft4, N. Wiinberg5, H. Gutte1,2, C.L. Petersen5, A. Kjaer1,2
1Copenhagen University Hospital, Rigshospitalet, Department of Clinical Physiology, Nuclear Medicine & PET, Copenhagen, Denmark, 2University of Copenhagen, Cluster for Molecular Imaging, Copenhagen, Denmark, 3Hvidovre University Hospital, Department of Infectious Diseases, Copenhagen, Denmark, 4Copenhagen University Hospital, Rigshospitalet, Department of Infectious Diseases, Copenhagen, Denmark, 5Frederiksberg Hospital, Department of Clinical Physiology and Nuclear Medicine, Copenhagen, Denmark
Background: Recent observational studies have shown antiretroviral therapy (ART) to be associated with increased risk of cardiovascular disease (CVD) in HIV patients. However, a causal connection between ART and CVD remains undiscovered. The aim of the present study was, in a prospective design, to investigate if coronary vasomotor function changed in treatment naïve HIV patients when ART was initiated.
Methods: Myocardial perfusion was assessed by 13N-NH3 positron emission tomography (PET) scans before and one month after initiation of ART in ten treatment naïve HIV patients. At both examinations, the baseline myocardial perfusion, the perfusion during cold pressor testing (left foot in 0°C water), and the maximal hyperaemic perfusion after a pharmalogical stress with dypyridamol (0.56 mg/kg body weight) were determined. A normalized baseline perfusion was obtained by dividing the perfusion at rest with the pulse pressure product and multiplying with 10,000. The myocardial flow reserve (MFR) was calculated by dividing the maximal hyperaemic perfusion with the baseline perfusion and the cold pressor reserve (CPR) was calculated by dividing the perfusion during cold pressor testing with the baseline perfusion. Data from before and after ART initiation were compared with paired t-tests and p< 0.05 was considered significant.
Results: Maximal hyperaemic perfusion decreased from 2.3±0.26 to 1.7±0.16 mL/g/min after initiation of ART (p=0.021). No changes were observed in normalized baseline perfusion (1.2±0.07 to 1.1±0.05 mL/g/min), CPR (1.2±0.08 to 1.2±0.05), or MFR (2.7±0.28 to 2.4±0.23).
Conclusions: Coronary vasomotor function was compromised by a decrease in maximal hyperaemic perfusion one month after initiation of ART in treatment naïve HIV patients. These findings indicate causality between ART initiation and impaired vasomotor function and thus support the findings of increased risk of CVD in recently presented observational studies. Additionally, no change was observed in CPR, suggesting other responsible mechanisms than those typical for endothelial dysfunction.
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