In the current study, asymptomatic, ART-naïve patients evaluated with echocardiography soon after HIV acquisition were not found to have evidence of systolic dysfunction or reduced global longitudinal strain. Some of the patients were found to have subclinical echocardiographic abnormalities such as RV dilatation and reversible cardiac remodeling however no statistically significant correlation was found with HIV-related risk factors identified. For this reason one may conclude that the uncontrolled viral replication, robust immune activation, and CD4 depletion that occurs shortly after HIV infection do not appear to directly cause asymptomatic pathologic cardiac abnormalities. Prior to ART initiation, HIV-related cardiovascular disease has been attributed to direct myocyte invasion and myocardial toxicity [8]. However there is little known about the pathogenesis of the HIV-induced damage that takes place shortly after infection and before initiation of ART. Most of the studies in the ART era have focused on establishing the association between HIV infection and development of CVD in the aging population. To our knowledge this is the first study to describe subclinical echocardiographic abnormalities found in an actively seroconverting, ART naïve and asymptomatic young group of soldiers living with HIV.
The current evidence supports that PLHIV on ART continue to have generalized immune activation and chronic inflammation which then leads to endothelial dysfunction and earlier development of subclinical cardiovascular disease when compared to the HIV-uninfected population [1, 9, 10]. Within the last decade there has been a focus on elucidating the prevalence of and understanding asymptomatic
CVD among those with HIV infection using advanced noninvasive imaging technology [2-3, 11-12]. A meta-analysis of 9 European studies using echocardiography reports a prevalence of LV dysfunction
(reduced EF) and diastolic dysfunction of 8.3% and 43.4% respectively among asymptomatic patients
[13]. However, patients in these studies typically had a longer duration of HIV infection with the average time from HIV diagnosis to echocardiographic evaluation of 8 years with 98% of the patients on ART for an average of 5 years. There is limited data for echocardiographic evaluation in the ART-naïve population. An observational single-institution study of 41 ART-naïve asymptomatic newly diagnosed
HIV patients in Greece found no echocardiographic evidence of reduced EF, diastolic dysfunction or evidence of elevated pulmonary pressures. However, evidence of GLS abnormalities were observed in all the patients studied and the authors concluded that HIV infection itself has myocardial toxicity and causes subclinical systolic dysfunction. Unfortunately, this study was limited by an unknown duration of HIV infection and heterogeneity of the population studied [14]. In contrast, all the patients in our study were documented HIV seroconverters with an average of 10 months duration of infection prior to echocardiography. It is possible that our patients underwent echocardiography before the development of expected HIV-related GLS abnormalities. However, it must be noted that the prevalence of cardiac remodeling and ventricular dilatation (thought to be secondary to exercise induced adaptation) seen in our study population appears to be slightly higher than what has been previously reported in healthy athletes [15-17]. Despite the minor cardiac abnormalities observed, this study suggests that untreated HIV may have a low impact on the development of echocardiographic abnormalities shortly after seroconversion. Longitudinal studies are warranted to determine the optimal CVD risk assessment strategies for PLHIV.
Limitations:
The main limitation of our study is the lack of an age-matched control group in order to account for the echocardiographic abnormalities observed.