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J Am Soc Echocardiogr. 2005 Aug;18(8):830-8.

Impact of chronic left ventricular preload and afterload on Doppler tissue imaging velocities: a study in congenital heart disease.

Author information

1
Lillie Frank Abercrombie Section of Pediatric Cardiology, Texas Children's Hospital, Baylor College of Medicine, Houston, Texas, USA. beidem@bcm.tmc.edu

Abstract

BACKGROUND:

Doppler tissue imaging (DTI) velocities have been reported to be relatively independent of changes in ventricular loading conditions in adult studies. The clinical impact of altered left ventricular (LV) preload and afterload on DTI velocities in children with congenital heart disease has not been adequately evaluated. The purpose of this study was to evaluate the impact of chronic LV preload and afterload on DTI velocities in children with isolated ventricular septal defect and aortic valve stenosis compared with age-matched normal and abnormal (dilated cardiomyopathy) control groups.

METHODS:

From an apical 4-chamber view, DTI velocities were obtained at the cardiac base at the lateral mitral annulus, lateral tricuspid annulus, and interventricular septum in early diastole, late diastole, and ventricular systole.

RESULTS:

The majority of DTI velocities did not change significantly in patients with increased LV preload. Patients with increased LV afterload had significantly decreased systolic and early diastolic DTI velocities at both the lateral mitral annulus and ventricular septum compared with control subjects. Children with dilated cardiomyopathy had significantly decreased DTI velocities at all myocardial annular locations.

CONCLUSIONS:

We conclude that increases in chronic LV preload do not significantly affect the majority of DTI velocities in children with ventricular septal defects. In addition, significantly increased chronic LV afterload in children with aortic valve stenosis is associated with decreased DTI velocities in the absence of other identifiable abnormalities of LV function. Decreased DTI velocity may be secondary to increased afterload or may alternatively be an early marker of subclinical LV longitudinal dysfunction.

PMID:
16084335
DOI:
10.1016/j.echo.2004.09.011
[Indexed for MEDLINE]
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