In this cross-sectional, population-based survey, we determined that Oregon HIV-infected persons had CHD risk factors notable for high rates of smoking and dyslipidemia, findings comparable to reports from HIV cohort studies [5
]. In the DAD study, a multinational collaboration of previously established cohorts, the prevalences of current smoking at baseline was 51.5% and total cholesterol ≥240 mg/dL was 22.2%, compared with 46% and 9%, respectively, in our study [6
]. In DAD, the prevalences of previous cardiovascular disease (1.4%), hypertension (8.5%), and diabetes (2.5%) at baseline were lower than our study, likely because the median age in DAD at baseline was 39 years age, compared with the mean age of 45.5 years age in this study. In contrast, in the HIV Outpatient Study, a cohort study of HIV-infected patients receiving care at 10 U.S. HIV specialty clinics, with median age of 42 years at baseline, 49% had hypertension and 9% had diabetes at baseline; 55% were current or former smokers [5
]. As some CHD risk factors are highly influenced by patient age, ongoing public health surveillance of risk factors in HIV-infected persons, through population-based surveys, can best monitor dynamic patterns of health.
Current smoking was >2.5 times as prevalent among HIV-infected persons in Oregon (46%) compared with adults statewide (18%) [9
]. Especially concerning was the high smoking prevalence among patients with preexisting CHD or diabetes, who are at highest risk for myocardial infarction and CHD death. Similar to other reports, we confirmed that smoking prevalence was inversely associated with education [10
]. Although patients in the older age group were better educated, age differences in smoking prevalence persisted when stratified by education level (data not shown). Survivor bias, however, might have partly explained the lower smoking prevalence among older HIV-infected persons. We did not have information regarding the extent of smoking cessation counseling or treatment to assess to what extent smoking was adequately addressed in clinical settings. Our findings reinforce that intensive strategies to combat smoking and overcome barriers to quitting are needed for HIV-infected persons.
Participants in the Oregon MMP had lipid patterns characterized by low HDL and high triglycerides. We found 55% of Oregon HIV-infected persons had a HDL <40 mg/dL and 42% had triglycerides ≥200 mg/dL, population estimates that were likely overstated because patients with dyslipidemia were more likely to have had lipid panels drawn over a 12 month period in this cross-sectional survey. Other studies in HIV-infected persons have similarly detected high prevalence of dyslipidemia, albeit with lower estimates of low HDL. In the HIV-HEART study, Reinsch et al
. found 27.5% had low HDL and 39% had elevated triglycerides [11
]; in the Swiss HIV cohort study, Glass et al
. found 37.2% had low HDL and 35.7% had elevated triglycerides [12
]. HDL decreases early in HIV infection and typically does not completely return to premorbid levels with viral suppression. Especially concerning was the prevalence of dyslipidemia among HIV-infected persons with preexisting CHD or diabetes. Fewer than one-half of patients with CHD or diabetes had a non-HDL <130 mg/dL, the target goal; one-fifth had a non-HDL >160mg/dL. Although we did not have information about dietary interventions or drug therapy to manage dyslipidemia, our findings reveal that lipid management among the highest-risk group for CHD was suboptimal.
Assisting HIV-infected persons in maintaining a healthy weight is especially relevant for younger persons, who had higher prevalence of obesity (23%). Overall, however, obesity was one-half as prevalent among Oregon HIV-infected persons (17%) compared with NHANES (34%) [13
]. Weight loss from advanced HIV infection did not account for lower obesity; no association existed between obesity and viral load or CD4+
count (data not shown). Finally, we identified prevalences of preexisting heart disease, diabetes, and hypertension that, while divergent from some HIV cohort studies, were comparable to the U.S. adult population with similar age and sex distribution.
This study had certain limitations. First, the sampling frame for the study only included HIV-infected persons who had established care. Thus, the prevalences for diagnoses of CHD, diabetes, and hypertension might have been higher because persons with symptomatic disease might have been more likely to seek care and because persons in care were more likely to have been diagnosed for subclinical conditions. Second, as described previously, a high proportion of the survey group had missing lipid and BMI data. Lipid results were abstracted only during the 12-month surveillance period. If patients without lipid tests recorded were more likely to be judged at low risk for CHD by the clinician or more likely to have had desirable lipid results before the surveillance period, our estimates for the prevalence of dyslipidemia would have been high. Even if all the patients in this survey who had missing lipid data were assumed to have normal lipids, however, 1/4 to 1/3 of Oregon HIV-infected persons would have had dyslipidemia, a higher prevalence than the national adult population in the National Health and Nutrition Examination Survey [14
]. Third, because we did not have blood pressure measurements, we were unable to individually calculate the Framingham risk score, which would have provided a more detailed assessment of CHD risk among this population. Risk prediction models, however, should be validated among HIV-infected persons because the Framingham risk score is considered to underestimate CHD risk among the HIV-infected population [15
]. Finally, our survey was limited to Oregon HIV-infected persons, and findings might not necessarily apply to the national population.