Objectives
The aim of the study was to assess the separate contributions of smoking, diabetes and hypertension to acute coronary syndrome (ACS) in HIV‐infected adults relative to uninfected adults.
Methods
Two parallel case–control studies were carried out. In the first study, HIV‐positive adults diagnosed with ACS between 1997 and 2009 (HIV+/ACS) were matched for age, gender and known duration of HIV infection with HIV‐positive adults without ACS (HIV+/noACS), each individual in the HIV+/ACS group being matched with three individuals in the HIV+/noACS group. In the second study, each individual in the HIV+/ACS group in the first study was matched for age, gender and calendar date of ACS diagnosis with three HIV‐negative individuals diagnosed with ACS between 1997 and 2009 (HIV–/ACS). Each individual in the HIV–/ACS group was then matched for age and gender with an HIV‐negative adult without ACS (HIV–/noACS). After matching, the ratio of numbers of individuals in the HIV+/ACS, HIV+/noACS, HIV–/ACS and HIV–/noACS groups was therefore 1 : 3 : 3 : 3, respectively. We performed logistic regression analyses to identify risk factors for ACS in each case–control study and calculated population attributable risks (PARs) for smoking, diabetes and hypertension in HIV‐positive and HIV‐negative individuals.
Results
There were 57 subjects in the HIV+/ACS group, 173 in the HIV+/noACS group, 168 in the HIV–/ACS group, and 171 in the HIV–/noACS group. Independent risk factors for ACS were smoking [odds ratio (OR) 4.091; 95% confidence interval (CI) 2.086–8.438; P < 0.0001] and a family history of cardiovascular disease (OR 7.676; 95% CI 1.976–32.168; P = 0.0003) in HIV‐positive subjects, and smoking (OR 4.310; 95% CI 2.425–7.853; P < 0.0001), diabetes (OR 5.778; 95% CI 2.393–15.422; P = 0.0002) and hypertension (OR 6.589; 95% CI 3.554–12.700; P < 0.0001) in HIV‐negative subjects. PARs for smoking, diabetes and hypertension were 54.35 and 30.58, 6.57 and 17.24, and 9.07 and 38.81% in HIV‐positive and HIV‐negative individuals, respectively.
Conclusions
The contribution of smoking to ACS in HIV‐positive adults was generally greater than the contributions of diabetes and hypertension, and was almost twice as high as that in HIV‐negative adults. Development of effective smoking cessation strategies should be prioritized to prevent cardiovascular disease in HIV‐positive adults.
Tobacco consumption is the modifiable risk factor contributing most to the development of non-AIDS-defining events among persons living with HIV/AIDS (PLWHA). Clinicians' awareness of this problem is critical and not yet adequate. Practical information issued by public health authorities or contained in experts' clinical guidelines regarding how to address smoking cessation in PLWHA is scarce. The aim of this review is to provide physicians with comprehensive and practical information regarding how to identify HIV-positive patients willing to stop smoking and those more likely to succeed, how to choose the most suitable strategy for an individual patient, and how to help the patient during the process. In the light of current evidence on the efficacy and benefits of stopping smoking in PLWHA, physicians must actively pursue smoking cessation as a major objective in the clinical care of PLWHA.
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