Literature DB >> 8911582

Early impairment of systolic and diastolic function in asymptomatic HIV-positive patients: a multicenter echocardiographic and echo-Doppler study. The Gruppo Italiano Per lo Studio Cardiologico dei Pazienti Affetti da AIDS.

G Barbaro1, G Barbarini, G Di Lorenzo.   

Abstract

Human immunodeficiency virus (HIV) possesses an intrinsic cardiopathogenic action that may be detected even in the early stages of HIV disease. To assess an early impairment of systolic and diastolic function in asymptomatic HIV-positive patients (CD4+ > or = 600/mm3), we performed a multicenter echocardiographic and echo-Doppler trial on 1236 asymptomatic NYHA class I HIV-positive patients (885 M and 351 F; mean age 28 years) compared with 1230 healthy subjects (922 M and 308 F; mean age 30 years). The sample size was established considering, as null hypothesis, a difference less than 10% in the values of the principal echocardiographic and echo-Doppler parameters between groups with a 90% statistical power (alpha = 0.01; beta = 0.10). Analysis of echocardiographic and echo-Doppler data revealed a reduction of 19.7% in ejection fraction, an increase of 55.7% in wall motion score, a reduction of 34.6% in the E/A ratio, and an increase of 19.7% in the isovolumetric relaxation time in HIV-positive subjects compared with healthy controls (p < 0.001). Baseline electrocardiographic alterations were observed in 707 (57.2%) HIV-positive subjects and in 169 (13.7%) of the subjects of the control group (p < 0.001). The results of our study have demonstrated that in asymptomatic HIV-positive subjects a significant impairment of systolic and diastolic function may be detected by echocardiographic and echo-Doppler examination, confirming an early involvement of the heart in HIV disease.

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Year:  1996        PMID: 8911582     DOI: 10.1089/aid.1996.12.1559

Source DB:  PubMed          Journal:  AIDS Res Hum Retroviruses        ISSN: 0889-2229            Impact factor:   2.205


  13 in total

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10.  HIV-1-Associated Left Ventricular Cardiac Dysfunction in Humanized Mice.

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