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Factors associated with the development of coronary artery disease in people with HIV
Ari S Mushin1, Janine M Trevillyan2, Sue J Lee3
1Department of Infectious Diseases, Monash University, Melbourne, Vic., Australia.
Insights
People living with HIV (PLHIV) face higher risks of coronary artery disease (CAD). Traditional risk factors like hypertension and smoking, along with abacavir use, are linked to CAD in PLHIV, necessitating aggressive risk management.
Area of Science:
- Cardiology
- Infectious Diseases
- Public Health
Background:
- People living with HIV (PLHIV) exhibit an elevated risk for coronary artery disease (CAD).
- Understanding the specific features associated with CAD in PLHIV is crucial for effective prevention and management strategies.
Purpose of the Study:
- To identify and describe the characteristics and risk factors associated with coronary artery disease (CAD) in people living with HIV (PLHIV).
Main Methods:
- A case-control study was conducted involving PLHIV with CAD (cases) and PLHIV without CAD (controls) at Alfred Hospital, Melbourne.
- Data collected included traditional CAD risk factors, HIV infection details (duration, CD4 counts, viral load), and antiretroviral therapy (ART) exposure.
Main Results:
- Hypertension, current smoking, and lower HDL cholesterol were significant traditional CAD risk factors.
- While HIV-specific factors like CD4 counts were not associated, current and past exposure to abacavir was linked to CAD.
- Conditional logistic regression confirmed hypertension, current smoking, and current abacavir use as significant independent predictors of CAD in PLHIV.
Conclusions:
- Both traditional cardiovascular risk factors and exposure to the antiretroviral drug abacavir are associated with CAD in PLHIV.
- Aggressive management of modifiable cardiovascular risk factors is essential for reducing CAD risk in this population.
Background:
People living with HIV (PLHIV) are at increased risk for coronary artery disease (CAD). This study aimed to describe the features associated with CAD in PLHIV.
Methods:
A case ([n =160] PLHIV with CAD) control ([n =317] PLHIV matched by age and sex without CAD) study was performed at the Alfred Hospital, Melbourne, Australia (January 1996 and December 2018). Data collected included CAD risk factors, duration of HIV infection, nadir and at-event CD4+ T-cell counts, CD4:CD8 ratio, HIV viral load, and antiretroviral therapy exposure.
Results:
Participants were predominantly male (n =465 [97.4%]), with a mean age of 53years. Traditional risk factors associated with CAD in univariate analysis included hypertension (OR 11.4 [95%CI 5.01, 26.33], P <0.001), current cigarette smoking (OR 2.5 [95% CI 1.22, 5.09], P =0.012), and lower high-density lipoprotein cholesterol (OR 0.14 [95%CI 0.05, 0.37], P <0.001). There was no association between duration of HIV infection, nadir or current CD4 cell count. However, current and ever exposure to abacavir (cases: 55 [34.4%]; controls: 79 [24.9%], P =0.023 and cases: 92 [57.5%]; controls: 154 [48.6%], P =0.048, respectively) was associated with CAD. In conditional logistic regression analysis, current abacavir use, current smoking, and hypertension remained significantly associated (aOR=1.87 [CI=1.14, 3.07], aOR=2.31 [1.32, 4.04], and aOR=10.30 [5.25, 20.20] respectively).
Conclusion:
Traditional cardiovascular risk factors and exposure to abacavir were associated with CAD in PLHIV. This study highlights that aggressive management of cardiovascular risk factors remains critical for reducing risk in PLHIV.
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