Myocardial deformation imaging unmasks subtle left ventricular systolic dysfunction in asymptomatic and treatment-naïve HIV patients
Background Patients infected by the human immunodeficiency virus (HIV) and receiving highly active antiretroviral therapy have a higher incidence of cardiovascular disease than healthy subjects, but little is known about cardiac function in asymptomatic and treatment-naïve patients. We sought to stu...
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Published in | Clinical research in cardiology Vol. 104; no. 11; pp. 975 - 981 |
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Main Authors | , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Berlin/Heidelberg
Springer Berlin Heidelberg
01.11.2015
Springer Nature B.V |
Subjects | |
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Abstract | Background
Patients infected by the human immunodeficiency virus (HIV) and receiving highly active antiretroviral therapy have a higher incidence of cardiovascular disease than healthy subjects, but little is known about cardiac function in asymptomatic and treatment-naïve patients. We sought to study cardiac function in asymptomatic HIV-infected, treatment-naïve patients.
Methods
We studied 41 HIV-infected and treatment-naïve patients and 20 age- and sex-matched healthy controls. Patients with cardiac symptoms, history of cardiac disease or NT-proBNP >100 pg/mL were excluded. We addressed cardiac function using standard echocardiography along with tissue Doppler (TDI) measurements, including strain/strain rate assessment.
Results
Standard echocardiographic parameters did not differ between groups, except for transmitral E wave velocity (64.8 ± 14 cm/s in HIV vs 76.1 ± 10 cm/s in controls,
p
= 0.002). In contrast, TDI mitral and tricuspid annulus s velocity and all strain/strain rate measurements were significantly lower in HIV patients: s lateral, 10.2 ± 2.4/11.3 ± 0.7,
p
= 0.011; s septal, 8.1 ± 1.6/8.7 ± 0.8,
p
= 0.045; s tricuspid, 13.4 ± 2.3/14.9 ± 1.3,
p
= 0.002; strain/strain rate, septal (strain/strain rate, 15.1 ± 5.7/−0.9 ± 0.3, 25.3 ± 1.7/−1.9 ± 0.2,
p
< 0.001), anterior (16.7 ± 3/−1.0 ± 0.1, 26.7 ± 1.7/−1.9 ± 0.2,
p
< 0.001), lateral (16.0 ± 6/−1.0 ± 0.1, 27.5 ± 1.8/−2.2 ± 0.3,
p
< 0.001) and posterior (15.2 ± 5.8/−1.0 ± 0.2, 26.2 ± 1.8/−2.2 ± 0.3,
p
< 0.001) left ventricular wall.
Conclusions
HIV infection itself is accompanied by subclinical systolic dysfunction, not apparent to standard echocardiography that can be unmasked though using sensitive echocardiographic techniques. |
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AbstractList | Patients infected by the human immunodeficiency virus (HIV) and receiving highly active antiretroviral therapy have a higher incidence of cardiovascular disease than healthy subjects, but little is known about cardiac function in asymptomatic and treatment-naive patients. We sought to study cardiac function in asymptomatic HIV-infected, treatment-naive patients. We studied 41 HIV-infected and treatment-naive patients and 20 age- and sex-matched healthy controls. Patients with cardiac symptoms, history of cardiac disease or NT-proBNP >100 pg/mL were excluded. We addressed cardiac function using standard echocardiography along with tissue Doppler (TDI) measurements, including strain/strain rate assessment. Standard echocardiographic parameters did not differ between groups, except for transmitral E wave velocity (64.8 plus or minus 14 cm/s in HIV vs 76.1 plus or minus 10 cm/s in controls, p = 0.002). In contrast, TDI mitral and tricuspid annulus s velocity and all strain/strain rate measurements were significantly lower in HIV patients: s lateral, 10.2 plus or minus 2.4/11.3 plus or minus 0.7, p = 0.011; s septal, 8.1 plus or minus 1.6/8.7 plus or minus 0.8, p = 0.045; s tricuspid, 13.4 plus or minus 2.3/14.9 plus or minus 1.3, p = 0.002; strain/strain rate, septal (strain/strain rate, 15.1 plus or minus 5.7/-0.9 plus or minus 0.3, 25.3 plus or minus 1.7/-1.9 plus or minus 0.2, p < 0.001), anterior (16.7 plus or minus 3/-1.0 plus or minus 0 .1, 26.7 plus or minus 1.7/-1.9 plus or minus 0.2, p < 0.001), lateral (16.0 plus or minus 6/-1.0 plus or minus 0 .1, 27.5 plus or minus 1.8/-2.2 plus or minus 0.3, p < 0.001) and posterior (15.2 plus or minus 5.8/-1.0 plus or minus 0.2, 26.2 plus or minus 1.8/-2.2 plus or minus 0.3, p < 0.001) left ventricular wall. HIV infection itself is accompanied by subclinical systolic dysfunction, not apparent to standard echocardiography that can be unmasked though using sensitive echocardiographic techniques. Background Patients infected by the human immunodeficiency virus (HIV) and receiving highly active antiretroviral therapy have a higher incidence of cardiovascular disease than healthy subjects, but little is known about cardiac function in asymptomatic and treatment-naïve patients. We sought to study cardiac function in asymptomatic HIV-infected, treatment-naïve patients. Methods We studied 41 HIV-infected and treatment-naïve patients and 20 age- and sex-matched healthy controls. Patients with cardiac symptoms, history of cardiac disease or NT-proBNP >100 pg/mL were excluded. We addressed cardiac function using standard echocardiography along with tissue Doppler (TDI) measurements, including strain/strain rate assessment. Results Standard echocardiographic parameters did not differ between groups, except for transmitral E wave velocity (64.8 ± 14 cm/s in HIV vs 76.1 ± 10 cm/s in controls, p = 0.002). In contrast, TDI mitral and tricuspid annulus s velocity and all strain/strain rate measurements were significantly lower in HIV patients: s lateral, 10.2 ± 2.4/11.3 ± 0.7, p = 0.011; s septal, 8.1 ± 1.6/8.7 ± 0.8, p = 0.045; s tricuspid, 13.4 ± 2.3/14.9 ± 1.3, p = 0.002; strain/strain rate, septal (strain/strain rate, 15.1 ± 5.7/-0.9 ± 0.3, 25.3 ± 1.7/-1.9 ± 0.2, p < 0.001), anterior (16.7 ± 3/-1.0 ± 0.1, 26.7 ± 1.7/-1.9 ± 0.2, p < 0.001), lateral (16.0 ± 6/-1.0 ± 0.1, 27.5 ± 1.8/-2.2 ± 0.3, p < 0.001) and posterior (15.2 ± 5.8/-1.0 ± 0.2, 26.2 ± 1.8/-2.2 ± 0.3, p < 0.001) left ventricular wall. Conclusions HIV infection itself is accompanied by subclinical systolic dysfunction, not apparent to standard echocardiography that can be unmasked though using sensitive echocardiographic techniques. Patients infected by the human immunodeficiency virus (HIV) and receiving highly active antiretroviral therapy have a higher incidence of cardiovascular disease than healthy subjects, but little is known about cardiac function in asymptomatic and treatment-naïve patients. We sought to study cardiac function in asymptomatic HIV-infected, treatment-naïve patients. We studied 41 HIV-infected and treatment-naïve patients and 20 age- and sex-matched healthy controls. Patients with cardiac symptoms, history of cardiac disease or NT-proBNP >100 pg/mL were excluded. We addressed cardiac function using standard echocardiography along with tissue Doppler (TDI) measurements, including strain/strain rate assessment. Standard echocardiographic parameters did not differ between groups, except for transmitral E wave velocity (64.8 ± 14 cm/s in HIV vs 76.1 ± 10 cm/s in controls, p = 0.002). In contrast, TDI mitral and tricuspid annulus s velocity and all strain/strain rate measurements were significantly lower in HIV patients: s lateral, 10.2 ± 2.4/11.3 ± 0.7, p = 0.011; s septal, 8.1 ± 1.6/8.7 ± 0.8, p = 0.045; s tricuspid, 13.4 ± 2.3/14.9 ± 1.3, p = 0.002; strain/strain rate, septal (strain/strain rate, 15.1 ± 5.7/-0.9 ± 0.3, 25.3 ± 1.7/-1.9 ± 0.2, p < 0.001), anterior (16.7 ± 3/-1.0 ± 0.1, 26.7 ± 1.7/-1.9 ± 0.2, p < 0.001), lateral (16.0 ± 6/-1.0 ± 0.1, 27.5 ± 1.8/-2.2 ± 0.3, p < 0.001) and posterior (15.2 ± 5.8/-1.0 ± 0.2, 26.2 ± 1.8/-2.2 ± 0.3, p < 0.001) left ventricular wall. HIV infection itself is accompanied by subclinical systolic dysfunction, not apparent to standard echocardiography that can be unmasked though using sensitive echocardiographic techniques. Background Patients infected by the human immunodeficiency virus (HIV) and receiving highly active antiretroviral therapy have a higher incidence of cardiovascular disease than healthy subjects, but little is known about cardiac function in asymptomatic and treatment-naïve patients. We sought to study cardiac function in asymptomatic HIV-infected, treatment-naïve patients. Methods We studied 41 HIV-infected and treatment-naïve patients and 20 age- and sex-matched healthy controls. Patients with cardiac symptoms, history of cardiac disease or NT-proBNP >100 pg/mL were excluded. We addressed cardiac function using standard echocardiography along with tissue Doppler (TDI) measurements, including strain/strain rate assessment. Results Standard echocardiographic parameters did not differ between groups, except for transmitral E wave velocity (64.8 ± 14 cm/s in HIV vs 76.1 ± 10 cm/s in controls, p = 0.002). In contrast, TDI mitral and tricuspid annulus s velocity and all strain/strain rate measurements were significantly lower in HIV patients: s lateral, 10.2 ± 2.4/11.3 ± 0.7, p = 0.011; s septal, 8.1 ± 1.6/8.7 ± 0.8, p = 0.045; s tricuspid, 13.4 ± 2.3/14.9 ± 1.3, p = 0.002; strain/strain rate, septal (strain/strain rate, 15.1 ± 5.7/−0.9 ± 0.3, 25.3 ± 1.7/−1.9 ± 0.2, p < 0.001), anterior (16.7 ± 3/−1.0 ± 0.1, 26.7 ± 1.7/−1.9 ± 0.2, p < 0.001), lateral (16.0 ± 6/−1.0 ± 0.1, 27.5 ± 1.8/−2.2 ± 0.3, p < 0.001) and posterior (15.2 ± 5.8/−1.0 ± 0.2, 26.2 ± 1.8/−2.2 ± 0.3, p < 0.001) left ventricular wall. Conclusions HIV infection itself is accompanied by subclinical systolic dysfunction, not apparent to standard echocardiography that can be unmasked though using sensitive echocardiographic techniques. Patients infected by the human immunodeficiency virus (HIV) and receiving highly active antiretroviral therapy have a higher incidence of cardiovascular disease than healthy subjects, but little is known about cardiac function in asymptomatic and treatment-naïve patients. We sought to study cardiac function in asymptomatic HIV-infected, treatment-naïve patients.BACKGROUNDPatients infected by the human immunodeficiency virus (HIV) and receiving highly active antiretroviral therapy have a higher incidence of cardiovascular disease than healthy subjects, but little is known about cardiac function in asymptomatic and treatment-naïve patients. We sought to study cardiac function in asymptomatic HIV-infected, treatment-naïve patients.We studied 41 HIV-infected and treatment-naïve patients and 20 age- and sex-matched healthy controls. Patients with cardiac symptoms, history of cardiac disease or NT-proBNP >100 pg/mL were excluded. We addressed cardiac function using standard echocardiography along with tissue Doppler (TDI) measurements, including strain/strain rate assessment.METHODSWe studied 41 HIV-infected and treatment-naïve patients and 20 age- and sex-matched healthy controls. Patients with cardiac symptoms, history of cardiac disease or NT-proBNP >100 pg/mL were excluded. We addressed cardiac function using standard echocardiography along with tissue Doppler (TDI) measurements, including strain/strain rate assessment.Standard echocardiographic parameters did not differ between groups, except for transmitral E wave velocity (64.8 ± 14 cm/s in HIV vs 76.1 ± 10 cm/s in controls, p = 0.002). In contrast, TDI mitral and tricuspid annulus s velocity and all strain/strain rate measurements were significantly lower in HIV patients: s lateral, 10.2 ± 2.4/11.3 ± 0.7, p = 0.011; s septal, 8.1 ± 1.6/8.7 ± 0.8, p = 0.045; s tricuspid, 13.4 ± 2.3/14.9 ± 1.3, p = 0.002; strain/strain rate, septal (strain/strain rate, 15.1 ± 5.7/-0.9 ± 0.3, 25.3 ± 1.7/-1.9 ± 0.2, p < 0.001), anterior (16.7 ± 3/-1.0 ± 0.1, 26.7 ± 1.7/-1.9 ± 0.2, p < 0.001), lateral (16.0 ± 6/-1.0 ± 0.1, 27.5 ± 1.8/-2.2 ± 0.3, p < 0.001) and posterior (15.2 ± 5.8/-1.0 ± 0.2, 26.2 ± 1.8/-2.2 ± 0.3, p < 0.001) left ventricular wall.RESULTSStandard echocardiographic parameters did not differ between groups, except for transmitral E wave velocity (64.8 ± 14 cm/s in HIV vs 76.1 ± 10 cm/s in controls, p = 0.002). In contrast, TDI mitral and tricuspid annulus s velocity and all strain/strain rate measurements were significantly lower in HIV patients: s lateral, 10.2 ± 2.4/11.3 ± 0.7, p = 0.011; s septal, 8.1 ± 1.6/8.7 ± 0.8, p = 0.045; s tricuspid, 13.4 ± 2.3/14.9 ± 1.3, p = 0.002; strain/strain rate, septal (strain/strain rate, 15.1 ± 5.7/-0.9 ± 0.3, 25.3 ± 1.7/-1.9 ± 0.2, p < 0.001), anterior (16.7 ± 3/-1.0 ± 0.1, 26.7 ± 1.7/-1.9 ± 0.2, p < 0.001), lateral (16.0 ± 6/-1.0 ± 0.1, 27.5 ± 1.8/-2.2 ± 0.3, p < 0.001) and posterior (15.2 ± 5.8/-1.0 ± 0.2, 26.2 ± 1.8/-2.2 ± 0.3, p < 0.001) left ventricular wall.HIV infection itself is accompanied by subclinical systolic dysfunction, not apparent to standard echocardiography that can be unmasked though using sensitive echocardiographic techniques.CONCLUSIONSHIV infection itself is accompanied by subclinical systolic dysfunction, not apparent to standard echocardiography that can be unmasked though using sensitive echocardiographic techniques. |
Author | Arapi, Sophia Farmakis, Dimitrios Papoutsidakis, Nikolaos Paisios, Nikolaos Lazaros, George Parissis, John Matzaraki, Vassiliki Karavidas, Apostolos Leventopoulos, Georgios Gargalianos, Panagiotis Perpinia, Anastasia Xylomenos, George Pyrgakis, Vlasios |
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Patients infected by the human immunodeficiency virus (HIV) and receiving highly active antiretroviral therapy have a higher incidence of... Patients infected by the human immunodeficiency virus (HIV) and receiving highly active antiretroviral therapy have a higher incidence of cardiovascular... Background Patients infected by the human immunodeficiency virus (HIV) and receiving highly active antiretroviral therapy have a higher incidence of... |
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SubjectTerms | Adult Cardiology Diagnosis, Differential Elastic Modulus Elasticity Imaging Techniques - methods Female HIV Infections - complications HIV Infections - diagnostic imaging HIV Infections - physiopathology Human immunodeficiency virus Humans Image Interpretation, Computer-Assisted - methods Male Medicine Medicine & Public Health Original Paper Reproducibility of Results Sensitivity and Specificity Ventricular Dysfunction, Left - diagnostic imaging Ventricular Dysfunction, Left - etiology Ventricular Dysfunction, Left - physiopathology |
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Title | Myocardial deformation imaging unmasks subtle left ventricular systolic dysfunction in asymptomatic and treatment-naïve HIV patients |
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