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 inClinical research in cardiology Vol. 104; no. 11; pp. 975 - 981
Main Authors Karavidas, Apostolos, Xylomenos, George, Matzaraki, Vassiliki, Papoutsidakis, Nikolaos, Leventopoulos, Georgios, Farmakis, Dimitrios, Lazaros, George, Perpinia, Anastasia, Arapi, Sophia, Paisios, Nikolaos, Parissis, John, Pyrgakis, Vlasios, Gargalianos, Panagiotis
Format Journal Article
LanguageEnglish
Published Berlin/Heidelberg Springer Berlin Heidelberg 01.11.2015
Springer Nature B.V
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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.
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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Issue 11
Keywords Myocardial deformation
HIV
Systolic dysfunction
Strain
Strain rate
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SSID ssj0051034
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Snippet Background 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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springer
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StartPage 975
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
URI https://link.springer.com/article/10.1007/s00392-015-0866-8
https://www.ncbi.nlm.nih.gov/pubmed/25977163
https://www.proquest.com/docview/1727593732
https://www.proquest.com/docview/1728257386
https://www.proquest.com/docview/1746886292
Volume 104
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