Our study showed slightly increased changes in left ventricular internal diameter in ART-naive HIV-infected patients, suggesting that HIV can cause initial changes in the cardiac structure, including an increase in LVM . Increased LVM is associated with increased all-cause mortality in both individuals without HIV infection and children with AIDS [11, 12]. Our findings also suggested that the rate of abnormal left ventricular diastolic function was significantly higher in ART-naive HIV-infected patients than in the general population and that the occurrence of LVDD was independently associated with age, BMI, and CD4 + T lymphocyte count.
HIV infection can lead to dyslipidemia, and our study showed that ART-naïve HIV-infected patients had significantly lower HDL-C and TC and higher TG levels, consistent with the results reported in previous papers [13, 14]. The redistribution of visceral adipose tissue after HIV infection, and the development of dyslipidemia are associated with peripheral fat loss and trunk fat accumulation [15, 16]. HIV infection is associated with lipid metabolism disorders, and patients with HIV show reduced levels of HDL-C before ART. HDL-C transports cholesterol from the vascular wall to the liver for catabolism and exerts an anti-atherosclerotic effect. Decreased HDL-C levels are an independent risk factor for CVD. HDL-C levels in HIV-infected patients increased significantly after ART as HIV viral load decreased and CD4 + T lymphocyte count increased. Since high HDL is a protective factor for CVD, effective ART may reduce the risk of CVD, which suggests the need for early ART.
HIV infection is an independent risk factor for heart failure, and viral replication is associated with a high risk of heart failure. In a cohort study, involving 2,391 and 6,095 patients with and without HIV infection, 97 HIV infected patients (4.1%) developed heart failure during a mean follow-up period of 7.3 years . The most commonly used clinical evaluation markers, LVEF and LVFS, were used to assess cardiac systolic function in our study. The results showed no significant difference between LVEF and LVFS in HIV-infected patients and controls, indicating no significant change in systolic function in HIV-infected patients, consistent with previous studies [18, 19]. Two of the 105 (1.9%) HIV-infected patients in our study had abnormal cardiac systolic function. The low incidence of heart failure in our study may be related to the cross-sectional study design and no long-term follow-up.
The results of our study showed that the E/A ratio, septal e' velocity, and DT were significantly lower in HIV-infected patients than in healthy controls, indicating that left ventricular diastolic function is reduced in ART-naïve HIV-infected patients compared to healthy individuals. The main causes of ventricular dysfunction in HIV-infected patients are: direct myocardial damage by HIV, autoimmune damage, damage to the myocardium by increased bioactive substances, and damage to myocardial function due to opportunistic infections [20, 21]. The prevalence of LVDD in HIV-infected patients in our study was 59.0%, which was significantly higher than the 22.5% in the control group. Previous studies have reported a decrease in left ventricular diastolic function in 85.7% of 49 HIV-infected patients . The prevalence of LVDD in our study was lower than that in previous studies, which may be related to the fact that all patients in our study had new-onset HIV infection, were infected with the virus for a short period of time, and had no serious complications. Both HIV and the related immune activation and inflammatory responses can increase the risk of abnormal cardiac diastolic function in HIV-infected patients [23, 24]. Cardiac steatosis and myocardial fibrosis may be the bases of increased cardiac dysfunction and CVD morbidity and mortality in HIV infected patients [25, 26].
Risk factors for HIV-comorbid CVD include traditional CVD risk factors, ART-related metabolic disorders, and chronic immune activation and inflammation associated with HIV infection [27, 28]. In the multivariate regression analysis, in addition to the traditional factors of increased age and increased BMI, decreased CD4 cell count was an independent risk factor for LVDD in ART-naïve HIV-infected patients. CD4 cells are often destroyed in large numbers as target cells for HIV infection, causing severe defects in human immune function. The main change in AIDS is a progressive decrease in CD4 cell count until failure, which can destroy the immune system of the patient . The results of our study showed that the involvement of cardiac function in ART-naïve HIV-infected patients was positively correlated with the severity of CD4 cell damage, and the more severe the immune system damage, the more severe was the cardiac involvement. The lower the number of CD4 + cells, the greater the risk of developing LVDD, which is a predictor of further increase in the CVD risk as HIV disease progresses. Antiviral therapy is effective in controlling viral replication and reducing HIV-associated inflammation. Although the benefit of ART on cardiac function has not been demonstrated, previous studies have shown no significant deterioration in diastolic function in HIV-infected patients after ART [18, 30]. To effectively reduce cardiac involvement in HIV-infected patients, we recommend regular assessment of cardiac function and reminder to patients to maintain good lifestyle habits for uncontrollable factors, such as age and BMI; and that ART should be initiated as early as possible for controllable factors, such as CD4 cell count, thus reducing the occurrence of cardiovascular events in HIV-infected patients.