Abstract and Introduction
Background: Although the HIV can cause myocardial inflammation, the association of HIV infection with subsequent development of heart failure (HF) has not been extensively studied. This nationwide cohort study aimed to determine the risk of incident HF in people living with HIV/AIDS (PLWHA).
Methods: We identified PLWHA using the Taiwan Centers for Disease Control and Prevention HIV Surveillance System. An age- and sex-matched control group without HIV infection was selected from the Taiwan National Health Insurance Research Database for comparison. All patients were followed up until December 2014 and were observed for a new diagnosis of HF. A time-dependent Cox proportional hazards model was used to determine the association of HIV and highly active antiretroviral therapy with incident HF, with death as a competing risk event.
Results: Of the 120,765 patients (24,153 PLWHA and 96,612 matched controls), 641 (0.53%) had incident HF during a mean follow-up period of 5.84 years, including 192 (0.79%) PLWHA and 449 (0.46%) controls. Time to diagnosis of incident HF was significantly shorter in PLWHA than in those without HIV infection (P < 0.001, the log-rank test). After adjusting for age, sex, and comorbidities, HIV infection was found to be an independent risk factor for incident HF (adjusted hazard ratio, 1.52; 95% confidence interval: 1.27 to 1.82). As the duration of highly active antiretroviral therapy increased, the risk of HF decreased (P = 0.014).
Conclusions: HIV infection was an independent risk factor for incident HF. Clinicians need to be aware of the higher risk of HF in PLWHA.
More than 36.7 million people have been infected with HIV worldwide. Moreover, 1.0 million people died of AIDS and other HIV-related illnesses worldwide in 2016. With the success of highly active antiretroviral therapy (HAART), people living with HIV/AIDS (PLWHA) are aging, and more chronic diseases (eg, cardiovascular diseases) are being diagnosed in this population.
Heart failure (HF) in PLWHA can cause significant morbidity and mortality. The pathogenesis of HF is multifactorial, including incident coronary artery disease (CAD), myocarditis, myocardial fibrosis, and cardiac steatosis. Previous studies showed that PLWHA had a higher risk of incident CAD. Cardiac magnetic resonance imaging and spectroscopy revealed that compared with HIV-uninfected individuals, PLWHA had a higher rate of myocardial fibrosis and cardiac steatosis. Despite some evidence suggesting that PLWHA have a higher risk of HF, the association between HIV infection and the development of HF has not been extensively studied. Two previous studies showed that veterans infected with HIV had a 1.2–1.8 fold higher risk of HF than individuals not infected with HIV.[7,8] The higher risk of HF persisted among veterans who did not have a coronary heart disease before the incident HF event. In women with HF, HIV infection increased the risk of HF readmission. However, these previous studies on the association between HIV infection and HF enrolled either only veterans[7,8] or female PLWHA.
HAART plays an important role in improving the survival in PLWHA. Some antiretroviral drugs (eg, zidovudine) can cause mitochondrial damage and focal myocardial necrosis, possibly increasing the risk of HF development.[11,12] However, studies determining the association between HAART and incident HF are limited. Alvi et al followed up 394 antiretroviral therapy–treated PLWHA who were hospitalized with HF and found that PLWHA receiving HAART with protease inhibitors have increased 30-day HF readmission. Therefore, we conducted a nationwide population-based cohort study to examine the association of HIV infection and HAART with the risk of incident HF during 2003–2014 in Taiwan.
J Acquir Immune Defic Syndr. 2019;80(3):255-263. © 2019 Lippincott Williams & Wilkins