Echocardiographic assessment of left cardiac structure and function in ART-naive HIV- infected patients

doi:10.21203/rs.3.rs-1652021/v1

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Echocardiographic assessment of left cardiac structure and function in ART-naive HIV- infected patients

https://doi.org/10.21203/rs.3.rs-1652021/v1

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Background: Patients with human immunodeficiency virus (HIV) are at a significantly higher risk of cardiovascular disease compared to the general population, and cardiovascular disease (CVD) is a significant cause of death in patients with acquired immune deficiency syndrome (AIDS). Accurate assessment of the cardiac function status of HIV-infected patients is important to guide clinical treatment and improve the prognosis. The aim of this study was to investigate structural and functional alterations in the left heart in antiretroviral therapy (ART)-naive HIV infected patients and their associated risk factors for the development of left ventricular diastolic dysfunction (LVDD).

Methods: We retrospectively included 105 ART-naive HIV-infected patients and 40 healthy subjects who underwent physical examination during the same period and performed echocardiography to compare the differences in the left heart structure and function between HIV-infected patients and healthy subjects. Univariate and multifactorial logistic regression were employed to explore the risk factors of the development of LVDD in ART-naive HIV-infected patients.

Results: The left ventricular end-diastolic internal diameter (LVEDD), left ventricular mass index (LVMI), and left atrial volume index (LAVI) were significantly greater in HIV-infected patients than in controls (p＜0.05). Left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were not significantly different between HIV-infected patients and controls (p＞0.05). The ratio of peak early-diastolic flow velocity to peak end-diastolic flow velocity (E/A), early diastolic mitral annular velocity (e'), and deceleration time (DT) of early left ventricular filling were significantly lower in HIV-infected patients than in controls (p＜0.05). Multifactorial logistic regression analysis showed that age, body mass index (BMI), and CD4+count were independent influencing factors for LVDD in ART-naive HIV-infected patients (OR=2.094, 1.229, 0.642, p＜0.05).

Conclusions: Left ventricular systolic function did not differ between HIV-infected patients and controls, and left ventricular diastolic function was lower in HIV-infected patients than in controls. Age, BMI, andCD4+ count were independent factors affecting LVDD in ART-naive HIV-infected patients.

Trial registration: ChiCTR1900021008，2019/01/24

human immunodeficiency virus

Acquired immune deficiency syndrome

Echocardiography

Cardiac function

left ventricular diastolic dysfunction

Acquired immunodeficiency syndrome (AIDS) is a public health issue of global concern. Human immunodeficiency virus (HIV)-specific invasion of CD4 + T lymphocytes leads to severe immune deficiency, which can cause damage to organs and tissues in various systems throughout the body. The risk of cardiovascular disease (CVD) is significantly higher in HIV-infected patients than in the general population and that CVD has become an important cause of death in HIV-infected patients [1, 2]. Damage to the cardiovascular system in HIV-infected patients is often subclinical, and its symptoms are easily masked by other comorbidities. With the prolonged survival of patients with AIDS, the number of patients with cardiac damage has gradually increased, and types of cardiac involvement have diversified, including pericardial effusion, myocarditis, and endocarditis. Left heart dysfunction is the most common cardiac complication in HIV-infected patients, and diastolic dysfunction is an important predictor of cardiovascular events [3, 4]. Timely and accurate assessment of the cardiac function status in HIV-infected patients is important to guide the clinical treatment and improve the management of patients with AIDS.

Previous studies have focused on cardiac involvement in HIV-infected patients after antiretroviral therapy (ART) [4], and one study showed a four-fold increase in the annual incidence of myocardial infarction in HIV-infected patients after the introduction of highly active antiretroviral therapy (HAART) compared to before the introduction of HAART [5]. The high risk of CVD in HIV-infected patients is associated with ART, such as the use of protease inhibitors [6]. A few studies have reported the cardiac structure and function in HIV-infected patients who had not received ART. Simultaneously, the risk factors for cardiac impairment are unclear, and no clear conclusions have been drawn on whether cardiac impairment correlates with the degree of CD4 cell involvement.

The aim of this study was to detect changes in the left cardiac structure and function in ART-naive HIV-infected patients using echocardiography and investigate the risk factors of the development of left ventricular diastolic dysfunction (LVDD) to provide a reference for selecting subsequent antiviral regimens and managing CVD in HIV-infected patients.

Population

This was a case–control study in which we retrospectively included 105 patients with an initial confirmed HIV-positive diagnosis who attended the AIDS Clinic at Beijing Youan Hospital, Capital Medical University, from January 2021 to April 2022. Inclusion criteria were: (1) HIV infection confirmed by both initial screening and confirmatory tests, (2) no initiation of antiretroviral therapy, (3) age of 18–60 years, and (4) available clinical and laboratory data. Exclusion criteria were: (1) comorbid congenital or acquired cardiac disease, (2) comorbid cardiac arrhythmias, (3) comorbid respiratory disease, (4) comorbid chronic kidney disease, (5) comorbid severe HIV-related complications, and (6) breastfeeding or pregnant women. Forty age- and sex-matched HIV-negative healthy subjects who underwent physical examination with complete clinical data in the same time period were included in the control group. This retrospective study was exempted from informed consent and approved by the Research Ethics Committee of Beijing Youan Hospital, Capital Medical University.

Clinical Evaluation

General information, including age, sex, body mass index (BMI), disease history, and HIV exposure, was collected from the subjects by two investigators, and laboratory data, including total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), CD4 + T lymphocyte count, CD4+/CD8 + ratio, HIV RNA copies, within 1 week of echocardiography were retrieved.

Echocardiography

Complete transthoracic echocardiography was performed for all subjects using the ACUSON SC2000 ultrasound scanner (4V1c probe, Siemens, Germany). Image acquisition and measurements were performed by two experienced sonographers in accordance with the latest guidelines recommended by the American Society of Echocardiography [8]. Left atrial diameter (LAD), left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), interventricular septum thickness (IVST), and left ventricular posterior wall thickness (LVPWT) were measured under the parasternal long-axis view. Biplane Simpson’s method was used to measure left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS), a normal LVEF was > 55%. In the apical four-chamber view, the pulsed-wave Doppler technique was used to measure peak early-diastolic flow velocity, peak end-diastolic flow velocity, and E-wave deceleration time (DT) to calculate the E/A ratio of the mitral valve; tissue Doppler imaging was employed to measure early-diastolic mitral annular velocity and calculate the ratio of E to the mean e' (E/e') in early diastole.

At the end of ventricular systole, the endocardium of the left atrial wall was labelled in the apical four- and two-chamber views, respectively, to obtain biplane Simpson's left atrial volume (LAV), and the left atrial volume index (LAVI) was calculated by dividing LAV by body surface area (BSA). Left ventricular mass (LVM) was calculated according to the formula recommended by Devereux et al [8]: LVM (g) = 0.8*[1.04*(IVST + LVPWT + LVEDD) ³-LVEDD³] + 0.6(g), and the left ventricular mass index (LVMI) was obtained by dividing LVM by BSA.

We assessed left ventricular diastolic function according to the 2016 ASE/EACVI guidelines [9]. When sinus rhythm and LVEF were normal, at least three of the following conditions needed to be met to suggest LVDD: (1) mean E/e' ratio > 14 cm/s, (2) septal e' <7 cm/s and/or lateral e' <10 cm/s, (3) Tricuspid regurgitation peak velocity (TR_Peak) > 2.8 m/s, and (4) LAVI > 34 mL/m².

Statistical analysis

Statistical analyses were performed using SPSS 25.0 software. Normality and variance homogeneity tests were carried out for quantitative data and those with normal distribution are expressed as mean ± standard deviation (x¯± s), inter-group comparisons were carried out using independent-samples t-test; and those with non-normal distribution are expressed as median (P25-P75), inter-group comparisons were carried out using the Mann–Whitney U test. Qualitative data are expressed as number (percentage), and the χ² test was used for inter-group comparisons. Risk factors for LVDD in ART-naive HIV-infected patients were analyzed using univariate and multifactorial logistic regression, and variables with p < 0.10 in the univariate analysis were included in the multivariate logistic regression model. A forward stepwise iterative method was used for the multivariate regression analysis. A two-sided test was used, and a difference with p < 0.05 was considered to be statistically significant.

Population

The basic characteristics of the enrolled ART-naive HIV-infected patients and control group are detailed in Table 1. A total of 105 HIV-infected patients were enrolled, with a mean age of 39.1 ± 9.2 years, including 92 men. The control group comprised 40 subjects with a mean age of 37.7 ± 8.8 years, including 32 men. There were no significant differences in age, sex, BMI, hypertension, diabetes, or smoking history between HIV-infected patients and controls (p > 0.05). TC and HDL-C were significantly lower and TG was significantly higher in HIV-infected patients than in controls (p > 0.05).

Table 1

Demographic and clinical characteristiecs of HIV-infected patients and controls
	HIV-infected patients (n = 105)	Controls (n = 40)	t/Z/χ²	P value
Age (years)	39.1 ± 9.2	37.7 ± 8.8	0.854	0.395
Male (n, %)	92 (87.6%)	32 (80.0%)	1.358	0.244
BMI (Kg/m²)	22.8 ± 3.3	23.1 ± 2.9	-0.492	0.624
Hypertension (n, %)	12 (11.4%)	5 (12.5%)	0.032	0.858
Diabetes (n, %)	8 (7.6%)	4 (10.0%)	0.216	0.642
Smoking history (n, %)	33 (31.4%)	15 (37.5%)	0.482	0.487
HIV exposure
Sexual (n, %)	86 (81.9%)	-	-	-
Blood (n, %)	11 (10.5%)	-	-	-
Unknown (n, %)	8 (7.6%)	-	-	-
TC (mmol/L)	4.02 (3.45–4.37)	4.66 (3.81–4.98)	-3.168	0.002
TG (mmol/L)	1.36 (0.98–2.04)	1.14 (0.98–1.46)	-2.418	0.016
LDL-C (mmol/L)	2.45 ± 0.71	2.68 ± 0.62	-1.836	0.068
HDL-C (mmol/L)	1.13 ± 0.35	1.26 ± 0.26	-2.144	0.034
CD4⁺Count (cells/µL)	420 (219–594)	-	-	-
CD4⁺/ CD8⁺Ratio	0.55 (0.34–0.78)	-	-	-
HIV RNA copies (count/µL)	8649 (417-40291)	-	-	-
HIV: human immunodeficiency virus; BMI: body mass index; TC: total cholesterol; TG: triglycerides; LDL-C: low-density lipoprotein cholesterol; HDL-C: high-density lipoprotein cholesterol

Comparison of the left heart structures between HIV-infected patients and controls

The LVEDD, LVMI, and LAVI were significantly greater in HIV-infected patients than in controls (p < 0.05). There were no significant differences in IVST, LVPWT, LAD, and LVESD between HIV-infected patients and controls (p > 0.05) (Table 2).

Table 2

Comparison of left heart structure and function between HIV-infected patients and controls
		HIV patients (n = 105)	Controls (n = 40)	t/Z	P value
Cardiac structure	IVST (mm)	8.72 ± 1.84	8.25 ± 1.53	1.446	0.150
	LVPWT (mm)	8.25 ± 1.30	7.95 ± 1.06	1.293	0.198
	LAD (mm)	35.08 ± 3.62	34.28 ± 3.84	1.171	0.244
	LVEDD (mm)	48.47 ± 4.49	46.75 ± 3.76	2.148	0.033
	LVESD (mm)	29.32 ± 3.68	28.15 ± 3.38	1.754	0.081
	LVMI (g/m²)	81 (74–91)	78 (72–85)	2.102	0.036
	LAVI (mL/m²)	32.49 ± 7.01	29.63 ± 6.42	2.247	0.026
Systolic function	LVEF (%)	67.23 ± 5.69	68.68 ± 5.45	-1.384	0.169
Systolic function	LVFS (%)	37.30 ± 4.80	38.45 ± 4.69	-1.292	0.198
Diastolic function	Mitral E/A ratio	0.99 ± 0.32	1.13 ± 0.30	-2.458	0.015
	Average E/e’ ratio	8.89 ± 2.53	8.07 ± 3.69	1.534	0.127
	Septal e’ velocity (cm/s)	8.52 ± 1.93	9.40 ± 2.14	-2.370	0.019
	Lateral e’ velocity(cm/s)	11.46 ± 1.94	12.06 ± 2.28	-1.587	0.115
	DT (s)	199.57 ± 27.26	211.33 ± 26.17	-2.345	0.020
IVST: interventricular septum thickness; LVPW: left ventricular posterior wall thickness; LAD: left atrium diameter; LVEDD: left ventricular end-diastolic diameter; LVESD: left ventricular end-systolic diameter; LVMI: left ventricular mass index; LAVI: left atrial volume index; LVEF: left ventricular ejection fraction; e': early diastolic mitral annular velocity; E/A: the ratio of peak early-diastolic flow velocity to peak end-diastolic flow velocity; E/e': early-diastolic mitral annular velocity and calculate the ratio of E to e'; DT: deceleration time

Comparison of left heart function between HIV-infected patients and controls

There were no significant differences in LVEF and LVFS between HIV-infected patients and controls (p > 0.05). E/A ratio, septal e' velocity, and DT were significantly lower in HIV-infected patients than in controls (p < 0.05). Average E/e' ratio and lateral e' velocity were not significantly different between HIV-infected patients and controls (p > 0.05) (Table 2).

We assessed the left ventricular diastolic function of subjects according to the 2016 ASE/EACVI guidelines [9]: 62 of the 105 (59.0%) enrolled HIV-infected patients had LVDD, and 9 of the 40 (22.5%) controls had LVDD. The prevalence of LVDD was significantly higher in HIV-infected patients than in controls (p < 0.05).

Logistic regression analysis of risk factors for LVDD in HIV-infected patients

To investigate the factors influencing LVDD in ART-naive HIV-infected patients, we performed a univariate regression analysis with the following factors as independent variables: age (per 10-year increase), BMI, hypertension, diabetes, smoking history, TC, TG, HDL-C, LDL-C, HIV RNA (log-transformed), and CD4 + count (per 200 cells/µL increase) (Table 3). Variables with p < 0.1 in the univariate analysis, including age, BMI, hypertension, TG, HDL-C, LDL-C, and CD4 + count, were included in the multivariate regression analysis, which finally showed that age, BMI, and CD4 + count were independent influencing factors of LVDD in ART-naive HIV-infected patients, see Table 3. The risk of LVDD increased 1.094-fold for every 10-year increase in age of HIV-infected patients, 0.229-fold for every 1 kg/m² increase in BMI, and 0.642 for every 200 cells/µL increase in CD4 cell count. Increased CD4 cell count is a protective factor for left ventricular diastolic function.

Table 3

Logistic regression analysis of risk factors associated with LVDD in HIV-infected patients
Variable	Univariate		Multivariate
Variable	OR (95% CI)	P value	OR (95% CI)	P value
Age (per 10 year increase)	2.059 (1.303 to 3.255)	0.002	2.094 (1.288 to 3.404)	0.003
BMI	1.249 (1.058 to 1.475)	0.009	1.229 (1.028 to 1.469)	0.024
Hypertension	3.537 (0.942 to 13.282)	0.061	-	-
Diabetes	1.697 (0.413 to 6.968)	0.463	-	-
Smoking history	1.323 (0.566 to 3.092)	0.518	-	-
TC (mmol/L)	1.261 (0.846 to 1.879)	0.255	-	-
TG (mmol/L)	1.463 (0.993 to 2.157)	0.055	-	-
LDL (mmol/L)	1.631 (0.915 to 2.907)	0.097	-	-
HDL (mmol/L)	0.203 (0.056 to 0.739)	0.016	-	-
HIV RNA (log-transformed)	1.286 (0.892 to 1.855)	0.178
CD4⁺Count (per 200 cells/µL increase)	0.670 (0.485 to 0.926)	0.015	0.642 (0.449 to 0.918)	0.015

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 [10]. 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 [17]. 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 [22]. 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 [29]. 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.

First, this was a single-center retrospective study with a relatively small sample size that failed to analyze diastolic dysfunction in HIV-infected patients in a graded and detailed manner. Second, this study used conventional echocardiography, which may have limitations in evaluating the sensitivity of changes in cardiac function and cannot accurately reflect the subtle effects of HIV infection on cardiac function, particularly systolic function. Future studies should be performed with expanded sample size and prospective longitudinal design to further evaluate the changes in cardiac structure and function in HIV-infected patients and their relationship with ART. In addition, in the next study, newer cardiac ultrasound techniques, such as speckle tracking imaging, should be used to accurately assess cardiac function.

ART-naive HIV-infected patients have a range of structural and functional cardiac changes, with LVDD being a particularly common presentation. High age, elevated BMI, and decreased CD4 cell counts in ART-naive HIV-infected patients are independent risk factors for LVDD. To further improve the prognosis of HIV-infected patients, regular echocardiography is required, particularly for patients with low CD4 cell counts, for early detecting abnormalities, initiating interventions, controlling risk factors, and reducing the risk of CVD.

HIV: human immunodeficiency virus; AIDS: acquired immune deficiency syndrome; CVD: cardiovascular disease; ART: antiretroviral therapy; HAART: highly active antiretroviral therapy; LVDD: left ventricular diastolic dysfunction; LAD: left atrial diameter; LVEDD: left ventricular end-diastolic internal diameter; LVESD: left ventricular end-systolic diameter; IVST: interventricular septum thickness; LVPWT: left ventricular posterior wall thickness; LVM: left ventricular mass; LVMI: left ventricular mass index; LAV: left atrial volume; LAVI: left atrial volume index; LVEF: left ventricular ejection fraction; LVFS: left ventricular fractional shortening; DT: deceleration time; e': early diastolic mitral annular velocity; E/A: the ratio of peak early-diastolic flow velocity to peak end-diastolic flow velocity; E/e': early-diastolic mitral annular velocity and calculate the ratio of E to e'; BMI: body mass index; BSA: body surface area; TC: total cholesterol; TG: triglycerides; LDL-C: low-density lipoprotein cholesterol ; HDL-C: high-density lipoprotein cholesterol

Ethics approval and consent to participate

This study was approved by the Research Ethics Committee of Beijing Youan Hospital, Capital Medical University (Protocol No.LL-2020-084-K), and the requirement for informed consent was waived.

Consent for publication

Consent for publication was obtained from all the authors.

Availability of data and materials

The datasets generated and analysed during the current study are not publicly available because they contain information that could compromise the privacy of research participants; however, the data are available from the first author ([email protected]) on reasonable request.

Competing interests

The authors declare that they have no competing interests.

Funding

This work was supported by the Natural Science Foundation of Beijing (7212172).

Authors' contributions

Conception and design: Fankun Meng, Xing Hu, Yuan Zhang; data acquisition: Weihua Li, Jing Han; image and statistical analysis: Xing Hu, Yuan Zhang; drafting of the manuscript: Xing Hu; Xuhui Zhang; critical revision of the manuscript: Fankun Meng; Tong Zhang. The authors read and approved the final manuscript.

Acknowledgements

Not applicable

Statement

All methods in our study were performed in accordance with relevant guidelines and regulations. All experimental protocols in this study were approved by the Research Ethics Committee of Beijing Youan Hospital, Capital Medical University (Protocol No.LL-2020-084-K), and the requirement for informed consent was waived.

Feinstein MJ, Hsue PY, Benjamin LA, Bloomfield GS, Currier JS, Freiberg MS, et al. Characteristics, Prevention, and Management of Cardiovascular Disease in People Living With HIV: A Scientific Statement From the American Heart Association. Circulation. 2019; 140(2):e98-e124.
Hemkens LG, Bucher HC. HIV infection and cardiovascular disease. Eur Heart J. 2014; 35(21):1373-1381.
Chen F, Bhardwaj R, Finkel MS. Diastolic dysfunction following HIV infection. AIDS. 2012; 26(7):885-886.
Butler J, Greene SJ, Shah SH, Shah SJ, Anstrom KJ, Kim RJ, et al. Diastolic Dysfunction in Patients With Human Immunodeficiency Virus Receiving Antiretroviral Therapy: Results From the CHART Study. J Card Fail. 2020; 26(5):371-380.
Rickerts V, Brodt H, Staszewski S, Stille W. Incidence of myocardial infarctions in HIV-infected patients between 1983 and 1998: the Frankfurt HIV-cohort study. Eur J Med Res. 2000; 5(8):329-333.
Msoka TF, Van Guilder GP, van Furth M, Smulders Y, Meek SJ, Bartlett JA, et al. The effect of HIV infection, antiretroviral therapy on carotid intima-media thickness: A systematic review and meta-analysis. Life Sci. 2019; 235:116851.
Mitchell C, Rahko PS, Blauwet LA, Canaday B, Finstuen JA, Foster MC, et al. Guidelines for Performing a Comprehensive Transthoracic Echocardiographic Examination in Adults: Recommendations from the American Society of Echocardiography. J Am Soc Echocardiogr. 2019; 32(1):1-64.
Lang RM, Badano LP, Mor-Avi V, Afilalo J, Armstrong A, Ernande L, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. Eur Heart J Cardiovasc Imaging. 2015; 16(3):233-270.
Nagueh SF, Smiseth OA, Appleton CP, Byrd BF, 3rd, Dokainish H, Edvardsen T, et al. Recommendations for the Evaluation of Left Ventricular Diastolic Function by Echocardiography: An Update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr. 2016; 29(4):277-314.
Hsue PY, Hunt PW, Ho JE, Farah HH, Schnell A, Hoh R, et al. Impact of HIV infection on diastolic function and left ventricular mass. Circ Heart Fail. 2010; 3(1):132-139.
Kardys I, Deckers JW, Stricker BH, Vletter WB, Hofman A, Witteman JC. Echocardiographic parameters and all-cause mortality: the Rotterdam Study. Int J Cardiol. 2009; 133(2):198-204.
Fisher SD, Easley KA, Orav EJ, Colan SD, Kaplan S, Starc TJ, et al. Mild dilated cardiomyopathy and increased left ventricular mass predict mortality: the prospective P2C2 HIV Multicenter Study. Am Heart J. 2005; 150(3):439-447.
Riddler SA, Smit E, Cole SR, Li R, Chmiel JS, Dobs A, et al. Impact of HIV infection and HAART on serum lipids in men. JAMA. 2003; 289(22):2978-2982.
Syed SS, Balluz RS, Kabagambe EK, Meyer WA, 3rd, Lukas S, Wilson CM, et al. Assessment of biomarkers of cardiovascular risk among HIV type 1-infected adolescents: role of soluble vascular cell adhesion molecule as an early indicator of endothelial inflammation. AIDS Res Hum Retroviruses. 2013; 29(3):493-500.
Friis-Møller N, Weber R, Reiss P, Thiébaut R, Kirk O, d'Arminio Monforte A, et al. Cardiovascular disease risk factors in HIV patients--association with antiretroviral therapy. Results from the DAD study. AIDS. 2003; 17(8):1179-1193.
Stanley TL, Grinspoon SK. Body composition and metabolic changes in HIV-infected patients. J Infect Dis. 2012; 205 Suppl 3(Suppl 3):S383-390.
Butt AA, Chang CC, Kuller L, Goetz MB, Leaf D, Rimland D, et al. Risk of heart failure with human immunodeficiency virus in the absence of prior diagnosis of coronary heart disease. Arch Intern Med. 2011; 171(8):737-743.
Fontes-Carvalho R, Mancio J, Marcos A, Sampaio F, Mota M, Rocha Gonçalves F, et al. HIV patients have impaired diastolic function that is not aggravated by anti-retroviral treatment. Cardiovasc Drugs Ther. 2015; 29(1):31-39.
Lebech AM, Gerstoft J, Hesse B, Petersen CL, Kjaer A. Right and left ventricular cardiac function in a developed world population with human immunodeficiency virus studied with radionuclide ventriculography. Am Heart J. 2004; 147(3):482-488.
Thienemann F, Sliwa K, Rockstroh JK. HIV and the heart: the impact of antiretroviral therapy: a global perspective. Eur Heart J. 2013; 34(46):3538-3546.
Kelly KM, Tarwater PM, Karper JM, Bedja D, Queen SE, Tunin RS, et al. Diastolic dysfunction is associated with myocardial viral load in simian immunodeficiency virus-infected macaques. AIDS. 2012; 26(7):815-823.
Longo-Mbenza B, Seghers LV, Vita EK, Tonduangu K, Bayekula M. Assessment of ventricular diastolic function in AIDS patients from Congo: a Doppler echocardiographic study. Heart. 1998; 80(2):184-189.
Pozzan G, Pagliari C, Tuon FF, Takakura CF, Kauffman MR, Duarte MI. Diffuse-regressive alterations and apoptosis of myocytes: possible causes of myocardial dysfunction in HIV-related cardiomyopathy. Int J Cardiol. 2009; 132(1):90-95.
Monsuez JJ, Escaut L, Teicher E, Charniot JC, Vittecoq D. Cytokines in HIV-associated cardiomyopathy. Int J Cardiol. 2007; 120(2):150-157.
Holloway CJ, Ntusi N, Suttie J, Mahmod M, Wainwright E, Clutton G, et al. Comprehensive cardiac magnetic resonance imaging and spectroscopy reveal a high burden of myocardial disease in HIV patients. Circulation. 2013; 128(8):814-822.
Ntusi N, O'Dwyer E, Dorrell L, Wainwright E, Piechnik S, Clutton G, et al. HIV-1-Related Cardiovascular Disease Is Associated With Chronic Inflammation, Frequent Pericardial Effusions, and Probable Myocardial Edema. Circ Cardiovasc Imaging. 2016; 9(3):e004430.
Zicari S, Sessa L, Cotugno N, Ruggiero A, Morrocchi E, Concato C, et al. Immune Activation, Inflammation, and Non-AIDS Co-Morbidities in HIV-Infected Patients under Long-Term ART. Viruses. 2019; 11(3).
Vos AG, Dodd CN, Delemarre EM, Nierkens S, Serenata C, Grobbee DE, et al. Patterns of Immune Activation in HIV and Non HIV Subjects and Its Relation to Cardiovascular Disease Risk. Front Immunol. 2021; 12:647805.
El-Sadr WM, Lundgren J, Neaton JD, Gordin F, Abrams D, Arduino RC, et al. CD4+ count-guided interruption of antiretroviral treatment. N Engl J Med. 2006; 355(22):2283-2296.
Luo L, Zeng Y, Li T, Lv W, Wang H, Guo F, et al. Prospective echocardiographic assessment of cardiac structure and function in Chinese persons living with HIV. Clin Infect Dis. 2014; 58(10):1459-1466.

No competing interests reported.

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Echocardiographic assessment of left cardiac structure and function in ART-naive HIV- infected patients

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Abstract

Background

Methods

Population

Clinical Evaluation

Echocardiography

Statistical analysis

Results

Population

Comparison of the left heart structures between HIV-infected patients and controls

Comparison of left heart function between HIV-infected patients and controls

Logistic regression analysis of risk factors for LVDD in HIV-infected patients

Discussion

Limitation

Conclusion

Abbreviations

Declarations

References

Additional Declarations

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