Cardiovascular involvement in patients with human immune deficiency (HIV) has gained significant attention as the improved life expectancy of individuals with HIV has changed the paradigm regarding the long-term impact of the virus on cardiovascular health. We reviewed current literature on the prevalence, diagnosis, and unique characteristics of cardiovascular disease (CVD) in HIV patients, including those treated with protease inhibitors (PIs) and complementary therapies. The incidence of infectious, immunosuppressive, and nutritionally related pathologies in HIV patients has declined, largely due to advancements in highly active antiretroviral therapies (HAART) and supportive care. However, issues related to autoimmunity and chronic inflammation persist. Elevated levels of high-sensitivity C-reactive protein, along with activated cytokines and other pro-inflammatory molecules, are common in HIV patients and contribute significantly to the increased risk for endothelial dysfunction, coagulation disorders, and accelerated atherogenesis. The advent of HAART has significantly improved the prognosis for HIV patients, leading to prolonged life expectancy and a reduction in AIDS-related complications. However, this success has also resulted in a shift in the clinical presentation, with HIV patients showing more chronic and insidious cardiovascular manifestations.

Speckle tracking echocardiography is an advanced imaging technique that allows for a more detailed assessment of cardiac global and regional function. Reference values for segmental longitudinal layered strain (subendocardial, mid-myocardial, and subepicardial) are scarce, limiting the clinical use of these measurements in clinical practice. Two hundred consecutive Caucasian healthy subjects (mean age = 37 ± 11 years) were enrolled in the study. The mean values of global longitudinal strain (GLS) for endocardial (Endo), mid-myocardial (Myo) and epicardial (Epi) layers were −22.9 ± 2.7, −20.0 ± 2.4 and −17.5 ± 2.1, respectively. The GLSEndo/GLSMyo ratio was 1.1 ± 0.05, while the GLSEndo/GLSEpi ratio was 1.3 ± 0.05. The apical strain-sparing ratio was >1 in 10% of the subjects (endocardium) and 7% (mid-myocardium). The lower limits for segmental LS were as follows: for endocardial LS, −10% (basal), −12% (mid), −14% (apical); for mid-myocardial LS, −10% −10% (basal), −10% (mid), −10% (apical); and for epicardial LS, −7% (basal), −8% (mid), −8% (apical). The findings of this study provide data regarding the lower limit of normality of LS for each LV segment and suggest, for practical considerations, that an LS value below 10% should be considered abnormal in any segment. Further larger studies are warranted to confirm these findings.

Adults living with HIV (human immunodeficiency virus) infection (ALHIV) have high rates of cardiovascular events. New approaches are needed to detect subclinical cardiac dysfunction. We used conventional and speckle tracking echocardiography to investigate whether ALHIV display latent cardiac dysfunction. We analyzed 85 young subjects with HIV infection and free from cardiovascular risk factors (31 ± 4 years) and 80 matched healthy volunteers. We measured left ventricular (LV) layered global longitudinal strain, circumferential strain, peak longitudinal strain in the reservoir and contraction phases of the left atrium (LASr respectively LASct). In the HIV group, LV ejection fraction and s’ TDI (tissue doppler imaging) were slightly lower but still in the normal ranges. Layered longitudinal strain showed no significant difference, whereas circumferential global strain was significantly lower in the HIV group (−20.3 ± 3.9 vs. −22.3 ± 3.0, p < 0.001). LASr (34.3% ± 7.3% vs. 38.0% ± 6.9%, p < 0.001) was also lower in ALHIV and multivariate analysis showed that age (β = −0.737, p = 0.01) and infection duration (β = −0.221, p = 0.02) were independently associated with LASr. In the absence of cardiovascular risk factors, adults living with HIV display normal LV systolic function. Left atrial reservoir strain, is, however, decreased and suggests early diastolic dysfunction.