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Cardiac effects in perinatally HIV-infected and HIV-exposed but uninfected children and adolescents: a view from the United States of America.

Lipshultz SE, Miller TL, Wilkinson JD, Scott GB, Somarriba G, Cochran TR, Fisher SD - J Int AIDS Soc (2013)

Bottom Line: Although lymphomas have been found in HIV-infected children, the incidence is low and cardiac malignancy is rare.In non-HIV-infected infants born to HIV-infected mothers, foetal exposure to ART is associated with reduced LV dimension, LV mass, and septal wall thickness and with higher LV fractional shortening and contractility during the first two years of life.Laboratory tests should include a lipid profile, fasting glucose, and HIV viral load.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, Jackson Memorial Medical Center and the Sylvester Comprehensive Cancer Center, Holtz Children's Hospital, University of Miami Miller School of Medicine, Miami, FL, USA. slipshultz@med.miami.edu

ABSTRACT

Introduction: Human immunodeficiency virus (HIV) infection is a primary cause of acquired heart disease, particularly of accelerated atherosclerosis, symptomatic heart failure, and pulmonary arterial hypertension. Cardiac complications often occur in late-stage HIV infections as prolonged viral infection is becoming more relevant as longevity improves. Thus, multi-agent HIV therapies that help sustain life may also increase the risk of cardiovascular events and accelerated atherosclerosis.

Discussion: Before highly active antiretroviral therapy (HAART), the two-to-five-year incidence of symptomatic heart failure ranged from 4 to 28% in HIV patients. Patients both before and after HAART also frequently have asymptomatic abnormalities in cardiovascular structure. Echocardiographic measurements indicate left ventricular (LV) systolic dysfunction in 18%, LV hypertrophy in 6.5%, and left atrial dilation in 40% of patients followed on HAART therapy. Diastolic dysfunction is also common in long-term survivors of HIV infection. Accelerated atherosclerosis has been found in HIV-infected young adults and children without traditional coronary risk factors. Infective endocarditis, although rare in children, has high mortality in late-stage AIDS patients with poor nutritional status and severely compromised immune systems. Although lymphomas have been found in HIV-infected children, the incidence is low and cardiac malignancy is rare. Rates of congenital cardiovascular malformations range from 5.6 to 8.9% in cohorts of HIV-uninfected and HIV-infected children with HIV-infected mothers. In non-HIV-infected infants born to HIV-infected mothers, foetal exposure to ART is associated with reduced LV dimension, LV mass, and septal wall thickness and with higher LV fractional shortening and contractility during the first two years of life.

Conclusions: Routine, systematic, and comprehensive cardiac evaluation, including a thorough history and directed laboratory assays, is essential for the care of HIV-infected adults and children as cardiovascular illness has become a part of care for long-term survivors of HIV infection. The history should include traditional risk factors for atherosclerosis, prior opportunistic infections, environmental exposures, and therapeutic and illicit drug use. Laboratory tests should include a lipid profile, fasting glucose, and HIV viral load. Asymptomatic cardiac disease related to HIV can be fatal, and secondary effects of HIV infection often disguise cardiac symptoms, so systematic echocardiographic monitoring is warranted.

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Risk of myocardial infarction according to exposure to combination antiretroviral therapy. The adjusted relative rate of myocardial infarction according to cumulative exposure to combination antiretroviral therapy was 1.16 per year of exposure (95% CI, 1.09–1.23). The I bars denote the 95% CIs. Reproduced with permission from ref. 57.
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Figure 0001: Risk of myocardial infarction according to exposure to combination antiretroviral therapy. The adjusted relative rate of myocardial infarction according to cumulative exposure to combination antiretroviral therapy was 1.16 per year of exposure (95% CI, 1.09–1.23). The I bars denote the 95% CIs. Reproduced with permission from ref. 57.

Mentions: Atherosclerotic cardiovascular disease (CVD) often results from an environment that is hostile to the endothelium, which may occur from a complex interaction of HIV, the adverse effects of ART, traditional risk factors for CVD, inflammation and co-infections [52]. Autopsies in HIV-infected patients aged 23–32 years who died unexpectedly revealed atherosclerotic plaque with features common to both coronary atherosclerosis and transplant vasculopathy, histologic characteristics more frequently seen with single-vessel disease in which the cause of MI is plaque rupture [53,54]. Imaging data suggest inflammation as the cause of such premature cardiovascular events (Table 2). Endothelial dysfunction is one possible causative link between HIV infection and atherosclerosis. HIV-infected patients have increased expression of vascular adhesion molecules (E-selectin, ICAM, VCAM) and inflammatory cytokines such as interleukin (IL-6) and tumour necrosis factor (TNF)-α [55,56]. The presence of an endothelial response to injury is supported by the correlation of viral load with higher plasma TNF-α, IL-6, and von Willebrand factor concentrations [37,55,57]. The risk of myocardial infarction has been found to increase with the exposure to combination ART (Figure 1) [57].


Cardiac effects in perinatally HIV-infected and HIV-exposed but uninfected children and adolescents: a view from the United States of America.

Lipshultz SE, Miller TL, Wilkinson JD, Scott GB, Somarriba G, Cochran TR, Fisher SD - J Int AIDS Soc (2013)

Risk of myocardial infarction according to exposure to combination antiretroviral therapy. The adjusted relative rate of myocardial infarction according to cumulative exposure to combination antiretroviral therapy was 1.16 per year of exposure (95% CI, 1.09–1.23). The I bars denote the 95% CIs. Reproduced with permission from ref. 57.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3687072&req=5

Figure 0001: Risk of myocardial infarction according to exposure to combination antiretroviral therapy. The adjusted relative rate of myocardial infarction according to cumulative exposure to combination antiretroviral therapy was 1.16 per year of exposure (95% CI, 1.09–1.23). The I bars denote the 95% CIs. Reproduced with permission from ref. 57.
Mentions: Atherosclerotic cardiovascular disease (CVD) often results from an environment that is hostile to the endothelium, which may occur from a complex interaction of HIV, the adverse effects of ART, traditional risk factors for CVD, inflammation and co-infections [52]. Autopsies in HIV-infected patients aged 23–32 years who died unexpectedly revealed atherosclerotic plaque with features common to both coronary atherosclerosis and transplant vasculopathy, histologic characteristics more frequently seen with single-vessel disease in which the cause of MI is plaque rupture [53,54]. Imaging data suggest inflammation as the cause of such premature cardiovascular events (Table 2). Endothelial dysfunction is one possible causative link between HIV infection and atherosclerosis. HIV-infected patients have increased expression of vascular adhesion molecules (E-selectin, ICAM, VCAM) and inflammatory cytokines such as interleukin (IL-6) and tumour necrosis factor (TNF)-α [55,56]. The presence of an endothelial response to injury is supported by the correlation of viral load with higher plasma TNF-α, IL-6, and von Willebrand factor concentrations [37,55,57]. The risk of myocardial infarction has been found to increase with the exposure to combination ART (Figure 1) [57].

Bottom Line: Although lymphomas have been found in HIV-infected children, the incidence is low and cardiac malignancy is rare.In non-HIV-infected infants born to HIV-infected mothers, foetal exposure to ART is associated with reduced LV dimension, LV mass, and septal wall thickness and with higher LV fractional shortening and contractility during the first two years of life.Laboratory tests should include a lipid profile, fasting glucose, and HIV viral load.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, Jackson Memorial Medical Center and the Sylvester Comprehensive Cancer Center, Holtz Children's Hospital, University of Miami Miller School of Medicine, Miami, FL, USA. slipshultz@med.miami.edu

ABSTRACT

Introduction: Human immunodeficiency virus (HIV) infection is a primary cause of acquired heart disease, particularly of accelerated atherosclerosis, symptomatic heart failure, and pulmonary arterial hypertension. Cardiac complications often occur in late-stage HIV infections as prolonged viral infection is becoming more relevant as longevity improves. Thus, multi-agent HIV therapies that help sustain life may also increase the risk of cardiovascular events and accelerated atherosclerosis.

Discussion: Before highly active antiretroviral therapy (HAART), the two-to-five-year incidence of symptomatic heart failure ranged from 4 to 28% in HIV patients. Patients both before and after HAART also frequently have asymptomatic abnormalities in cardiovascular structure. Echocardiographic measurements indicate left ventricular (LV) systolic dysfunction in 18%, LV hypertrophy in 6.5%, and left atrial dilation in 40% of patients followed on HAART therapy. Diastolic dysfunction is also common in long-term survivors of HIV infection. Accelerated atherosclerosis has been found in HIV-infected young adults and children without traditional coronary risk factors. Infective endocarditis, although rare in children, has high mortality in late-stage AIDS patients with poor nutritional status and severely compromised immune systems. Although lymphomas have been found in HIV-infected children, the incidence is low and cardiac malignancy is rare. Rates of congenital cardiovascular malformations range from 5.6 to 8.9% in cohorts of HIV-uninfected and HIV-infected children with HIV-infected mothers. In non-HIV-infected infants born to HIV-infected mothers, foetal exposure to ART is associated with reduced LV dimension, LV mass, and septal wall thickness and with higher LV fractional shortening and contractility during the first two years of life.

Conclusions: Routine, systematic, and comprehensive cardiac evaluation, including a thorough history and directed laboratory assays, is essential for the care of HIV-infected adults and children as cardiovascular illness has become a part of care for long-term survivors of HIV infection. The history should include traditional risk factors for atherosclerosis, prior opportunistic infections, environmental exposures, and therapeutic and illicit drug use. Laboratory tests should include a lipid profile, fasting glucose, and HIV viral load. Asymptomatic cardiac disease related to HIV can be fatal, and secondary effects of HIV infection often disguise cardiac symptoms, so systematic echocardiographic monitoring is warranted.

Show MeSH
Related in: MedlinePlus