Key result
The AIDS stage in HIV-infected patients was significantly associated with a higher risk of myocardial fibrosis compared to asymptomatic HIV infection (OR 6.300).
Why the study?
To investigate subclinical myocardial inflammation and fibrosis by CMR and explore risk factors associated with myocardial fibrosis in a Chinese HIV/AIDS cohort.
Does HIV infection and its severity (AIDS) associate with subclinical myocardial inflammation and fibrosis measured by CMR?
Observational (n=68)
Blinded analysis
No
Does HIV infection and its severity (AIDS) associate with subclinical myocardial inflammation and fibrosis measured by CMR?
Effect estimate: OR 6.300 (95% CI 1.358-29.235)
Absolute Event Rate: 43.8% vs 8%
p-value: p=0.019
HIV infection, particularly at the AIDS stage, is associated with subclinical myocardial inflammation and fibrosis as detected by CMR, suggesting a need for early cardiovascular monitoring.
Objectives: To investigate the subclinical imaging changes in terms of myocardial inflammation and fibrosis and to explore the risk factors associated with myocardial fibrosis by cardiac magnetic resonance (CMR) approach in a Chinese HIV/AIDS cohort. Methods: We evaluated myocardial function (cine), myocardial inflammation (T1, T2), and myocardial fibrosis (through extracellular volume fraction [ECV] and late gadolinium enhancement [LGE]) by a multiparametric CMR scan protocol in a total of 68 participants, including 47 HIV-infected individuals, who were divided into two groups: asymptomatic HIV (HIV+) (n = 30), and acquired immunodeficiency syndrome (AIDS) ( n = 17), and 21 healthy controls. Results: HIV-infected patients had lower left (55.3 ± 6.5 vs. 63.0 ± 7.9%, P < 0.001) and right ventricular systolic function (35.9 ± 15.7 vs. 50.8 ± 9.3%, P < 0.001). Radial systolic strain (30.7 ± 9.3 vs. 39.3 ± 9.4%, P = 0.001), circumferential systolic strain (−17.5 ± 2.6 vs. −19.4 ± 2.7%, P = 0.008), and longitudinal systolic strain (−9.4 ± 5.7 vs. −12.8 ± 3.1%, P = 0.012) were also decreased in HIV. Native T1 relaxation time (1,337.2 ± 70.2 vs. 1,249.5 ± 47.0 ms, P < 0.001), ECV value (33.5 ± 6.2 vs. 28.5 ± 2.9 ms, P = 0.026), and T2 relaxation time (45.2 ± 3.5 vs. 42.0 ± 2.6 ms, P = 0.001) were higher in HIV-infected patients compared with controls. Myocardial fibrosis, predominantly in the mid-inferior wall, was detected in 24.4% of the HIV-infected patients. HIV+ had a significantly lower value of ECV [29.1 (26.1, 31.8) vs. 35.2 (31.8, 41.9) %, P < 0.001] and frequency of LGE [3/25 (8%) vs. 7/16 (43.8%), P = 0.014)] compared with AIDS. AIDS was associated with myocardial fibrosis. Conclusions: HIV-infected patients were associated with changes in myocardial function and higher rates of subclinical myocardial inflammation and fibrosis, which were more abnormal with greater severity of the disease. AIDS was associated with myocardial fibrosis, where the observations supported earlier initiation of antiretroviral therapy in the Chinese HIV/AIDS cohort.
No takes yet. Share an insight, caveat, or question.
Yan et al. (2021) conducted an observational in HIV/AIDS (n=68). Acquired immunodeficiency syndrome (AIDS) stage vs. Asymptomatic HIV (HIV+) was evaluated on Presence of myocardial fibrosis (Late Gadolinium Enhancement) (OR 6.300, 95% CI 1.358-29.235, p=0.019). The AIDS stage in HIV-infected patients was significantly associated with a higher risk of myocardial fibrosis compared to asymptomatic HIV infection (OR 6.300).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: