Two studies presented at the Fifth International AIDS Society conference in Cape Town, using new methods to detect vascular changes, help in our understanding of cardiovascular disease and HIV.
Seaberg et al used the sensitive high-resolution B-mode ultrasound of the right common carotid artery to test the hypothesis that duration of HIV infection is associated with carotid artery stiffness. Carotid artery stiffness was quantified using a distensibility index, a ratio of arterial diameter at systole to arterial diameter at diastole.
They found that long-term HIV infection (>15 years) was independently associated with the carotid artery’s stiffness, resulting in higher systolic blood pressures.
Eric Seaberg presented results of 115 HIV-positive men from the Multicenter AIDS Cohort Study (MACS), the world’s longest-running HIV cohort study (launched in 1984), enrolled between 2004 and 2006 into a substudy investigating coronary atherosclerosis. Arterial function in the men was compared with that of 325 HIV-negative men. Nearly half (56) of the HIV-positive men had been diagnosed for more than 15 years, and 91% were taking antiretroviral therapy. The mean age was 52 years, 74% were Caucasian and 19% were classified as obese (having a body mass index (BMI) >30 kg/m2).
They then performed an analysis to see what factors were associated with hardening of the arteries. They took into consideration factors associated with a risk of heart disease (age, race, smoking, family history, diabetes, cholesterol and body mass index) as well as HIV-related factors (duration of HIV infection, CD4 cell count, viral load, use of antiretroviral drugs).
Older age, higher systolic blood pressure and HIV infection for over 15 years were all independently associated with carotid atherosclerosis (p < 0.05).Compared with HIV-negative men, arterial stiffness decreased by 13.4% in men who had lived with HIV for more than 15 years.
Multiple regression analysis revealed that older age, higher systolic blood pressure, and HIV infection for >15 years were independently associated with decreased carotid artery distensibility (p< 0.05). The magnitude of the decrease in carotid distensibility among men infected with HIV for >15 years (-13.4%) was comparable to the effect of aging 10 years (-11.5%) and a 10 mmHg increase in systolic blood pressure (-11.5%). There was a “very, very pronounced threshold effect” after 15 years of HIV infection and there was no association at all between HIV diagnosis and arterial hardening in men who had been diagnosed for less than that time.
In questions following the presentation, Seaberg commented that there appeared to be no association with antiretroviral therapy as the same associations were observed in men not taking therapy, although as this numbered only ten men it was not statistically significant.
He commented that it was impossible to tell whether his findings were directly associated with length of HIV infection or whether some other aspect in the medical history of a fairly select group of long-term HIV survivors from the pre-HAART era had caused the increased rate of arterial stiffness.
In the second study, Ulrik Kristoffersen et al, Copenhagen University, Denmark, monitored coronary artery perfusion in eleven patients starting antiretroviral therapy for the first time. They described an apparent effect on cardiac function in patients who had only been on antiretroviral therapy for a month. Using PET and CT scans to map coronary perfusion, they found a 31% reduction in coronary blood flow in patients taking HIV therapy when subjected to maximum cardiac stress.
The patients, all men, were given coronary perfusion tests before they started antiretroviral therapy, then were started on tenofovir/FTC/efavirenz (N=9), AZT/3TC/efavirenz or AZT/3TC/raltegravir.
Coronary perfusion was then tested again five weeks after the start of therapy. They measured perfusion at rest, with the patient’s foot in a bowl of iced water, which simulates sympathetic nervous system stress, and then after a dose of dipyridamol, a drug that dilates the arteries and mimics intense exercise.
After antiretroviral therapy was started, coronary perfusion was the same in patients at rest, but was decreased by 31%, in patients given a dose of dipyridamol (p = 0.021), representing a decrease from 2.6 to 1.7 ml/g/min.
During questions, Kristofferson commented that it was unusual to see rapid changes in coronary blood flow of this degree a month apart. He commented that this technique could be a useful tool for studies of the pathophysiology of antiretroviral-associated changes in cardiovascular risk. He was unable to speculate whether the changes seen were short-term changes associated with antiretroviral initiation, permanent ones, or would accumulate over time.
References
Seaberg EC et al. Duration of HIV infection is associated with carotid artery stiffness. 5th IAS Conference on HIV Treatment, Pathogenesis and Prevention, abstract MoAb204, 2009.
Kristoffersen US et al. Coronary vasomotor function is reduced after initiation of antiretroviral therapy in treatment naïve patients: a prospective myocardial perfusion PET study. 5th IAS Conference on HIV Treatment, Pathogenesis and Prevention, abstract MoAb205, 2009.
08/04/09
PRN REPORT FROM IAS 2009 CAPE TOWN: HIV and Cardiovascular Disease
Source: Reported from Cape Town for PRN News: Bill Valenti, MD