This cross-sectional pilot study included matched people living with and without HIV at the Providence VA Medical Center. There were 85 patients with HIV in total seen at Providence VAMC at the time of the study. Eligible patients (adult males aged 30 to 75 years with a diagnosis of HIV) were identified in Veterans Health Administration electronic health records and matched to controls without HIV by age (±5 years), sex, race, and when possible, smoking status, history of homelessness, and comorbidities such as diabetes, hepatitis C, post traumatic stress disoder (PTSD), and major depression. Potential matching controls were identified using the VA Informatics and Computing Infrastructure before final selection through review of their electronic health records. Individuals with known CVD (myocardial infarction, stroke, heart failure) were excluded. Consent to contact was obtained through mailed letters or their primary care physician, followed by an informational phone call to schedule an enrollment visit. Interested participants signed informed consent at the enrollment visit. The VA Providence Institutional Review Board approved this study (IRB-2019-029).

Participants completed questionnaires, blood tests, a physical exam, treadmill exercise stress test (Bruce protocol), echocardiogram, and coronary CT scan. Twenty-five individuals (15 PLWH and 10 controls) completed an optional cardiac MRI (CMR). Questionnaires assessed demographics (including self-reported ethnicity/race and history of homelessness), physical activity (International Physical Activity Questionnaire), quality of life (EQ-5D Health Questionnaire, Kansas City Cardiomyopathy Questionnaire), and lifestyle habits (eg, smoking, alcohol, and drug use). Medical history and comorbidities were abstracted from electronic health records. A 10-year ASCVD risk scores were calculated using the AHA/ACC ASCVD Risk Estimator Plus, excluding 6 participants <40 years old. For patients with extreme laboratory values, the closest value within the allowed range was imputed. Cardiopulmonary fitness was assessed via peak performance expressed in metabolic equivalents on stress testing. We measured markers of tissue fibrosis, including plasma levels of soluble ST2 (sST2), growth differentiation factor (GDF)-15 and Galectin-3, and CMR values of mean extracellular volume (ECV), and native T1 mapping. Inflammatory markers included plasma levels of IL-6, C-reactive protein (CRP), and CMR-derived T2 mapping. Cardiac structure and function were evaluated using echocardiography and CMR for left ventricular ejection fraction (LVEF), right ventricular ejection fraction (RVEF) and pulmonary artery pressure. CAC was calculated from CT using Agatston scoring, and vascular age was estimated using the Multi-Ethnic Study of Atherosclerosis calculator. Blood samples were preserved for future genetic, epigenetic, and immunologic analyses using appropriate techniques. Descriptive statistics are reported as counts (%) for categorical variables and means (SD) for continuous variables. Skewed variables were log-transformed. Group comparisons used chi-squared tests for categorical variables and t tests for continuous variables. Multivariable linear regression models adjusted for age and smoking status evaluated the associations between outcomes and HIV status. Furhter adjustment for recreational drug use was made in sensitivity analysis. Statistical significance was defined as P <.05; 95% confidence intervals (CI) are reported.Analyses were performed using Stata software (Stata Corp v15, College Station, Texas).

The conceptual framework relating HIV infection, with inflammation, physical fitness, and subclinical cardiac disease, is shown in Figure . We enrolled 21 veterans with HIV (mean age 54 years; 71% White, 29% Black) and 20 controls (mean age 56 years; 70% White, 30% Black) with comparable demographics and comorbidities across groups ( Table 1 ). Participants with HIV had low viral load (mean 31 copies/mL) and normal CD4 counts (mean 615 cells/mm ³). There were no significant differences in circulating fibrosis or inflammatory markers, vascular calcification, vascular age, and exercise tolerance between groups ( Table 2 ). However, CMR revealed several notable findings. Participants with HIV had lower RVEF compared to controls (51.8% vs 57.5%, P =.02), though both values were within the normal range. The LVEF was similar between groups. Native T1 and T2 mapping values (CMR measures of fibrosis and inflammation, respectively) were within normal limits and similar between groups. Mean ECV, another CMR marker of myocardial fibrosis, was higher in the HIV group (although still within normal range) and trended toward significance (21.6% vs 17.9%, P =.071). In a multivariable linear regression model adjusted for age and smoking status, the association between HIV and mean ECV was similarly borderline significant ( β = 3.83, 95% CI [−0.30, 8.0], P =.067). On further multivariable linear regression models adjusted for age and smoking status, HIV status was found to be significantly associated with lower RVEF ( β = −5.78, 95% CI [−10.8, −0.7], P =.027) and increased GDF-15 levels ( β = 109.9, 95% CI [10.6, 209.2], P =.031) but not with T1, Log T1, Log sST2, Galectin-3 (other fibrosis markers), or Log IL-6, CRP, T2, or Log T2 (inflammatory markers) ( Table 2 ). A sensitivity analysis controlling for recreational drug use did not change the results.

Proposed link between HIV infection, inflammation, cardiopulmonary fitness, and subclinical cardiovascular disease.

Table 2

Two-sample t tests and multivariable linear regression models * comparing cardiorespiratory fitness, inflammation, fibrosis, vascular aging, and cardiac dysfunction in PLWH and controls

Variable	HIV+	Control	t Test	Beta	95% confidence	Regression
	Mean (SD)	Mean (SD)	P -value	coefficient	Interval	P -value
Cardiopulmonary fitness
Stress test max time (min)	8.9 (3.0)	8.3 (2.8)	.50	62.1	−31.0, 155.2	.18
METs achieved	11.7 (3.1)	10.4 (3.0)	.22	1.7	0.03, 3.4	.047
Self-reported activity (IPAQ)
Log vigorous activity	3.1 (2.8)	3.9 (2.8)	.38	−0.9	−2.7, 0.9	.33
Log moderate activity	2.9 (2.9)	3.8 (2.6)	.31	−1.0	−2.9, 0.8	.25
Log walking	5.5 (1.7)	5.3 (1.7)	.77	0.1	−1.1, 1.2	.87
Markers of fibrosis
Log sST2	2.5 (0.4)	2.4 (0.6)	.40	0.2	−0.1, 0.5	.23
GDF-15 (pg/mL)	553 (238)	459 (197)	.18	110	11, 209	.031
Galectin-3 (pg/mL)	1,406 (1,007)	1,838 (2,000)	.20	−518	−1,514, 478	.30
Mean ECV (%)	21.6 (4.8)	17.9 (4.2)	.07	3.8	−0.3, 8.0	.067
T1 relaxation time (msec) †	1,093 (299)	1,168 (64)	.44	−56	−258, 146	.57
Markers of inflammation
hs IL-6 (pg/mL) †	2.26 (1.36)	2.47 (2.42)	.73	−0.21	−1.48, 1.06	.74
Log CRP	0.7 (1.0)	0.5 (0.9)	.56	0.1	−0.5, 0.7	.75
T2 relaxation time (msec) †	40 (3.5)	39 (3.5)	.45	1.2	−1.7, 4.0	.41
Cardiac function
LVEF Simpson’s (%)	63.5 (4.7)	65.8 (3.9)	.09	−2.1	−4.9, 0.7	.14
RV TAPSE (cm)	2.2 (0.5)	2.4 (0.4)	.20	−0.2	−0.4, 0.1	.27
PA pressure (mmHg)	26.8 (7.5)	24.5 (4.9)	.36	2.0	−3.2, 7.3	.43
LVEF (%, on CMR)	58.5 (3.9)	60.4 (3.4)	.22	−1.3	−4.3, 1.7	.36
RVEF (%, on CMR)	51.8 (6.1)	57.6 (5.4)	.02	−5.8	−10.8, −0.7	.027
Vascular age
Log Agatston score	2.3 (2.6)	2.0 (2.7)	.73	0.4	−0.8, 1.7	.50
CAC age (y)	55.5 (19.0)	52.6 (19.6)	.71	3.9	−5.3, 13.1	.40

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