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Timing of regional left ventricular lengthening by pulsed tissue Doppler

Journal article
Authors Cecilia Wallentin Guron
Marianne Hartford
Anita Persson
Johan Herlitz
Dag Thelle
Kenneth Caidahl
Published in J Am Soc Echocardiogr
Volume 17
Issue 4
Pages 307-12
ISSN 0894-7317 (Print)
Publication year 2004
Published at Cardiovascular Institute
Institute of Physiology and Pharmacology
Institute of Internal Medicine, Dept of Medicine
Pages 307-12
Language en
Links www.ncbi.nlm.nih.gov/entrez/query.f...
Keywords Acute Disease, Adult, Aged, Blood Flow Velocity/physiology, Coronary Circulation/physiology, Coronary Disease/epidemiology/physiopathology/ultrasonography, *Echocardiography, Doppler, Pulsed, Female, Heart Ventricles/physiopathology/ultrasonography, Humans, Male, Middle Aged, Myocardial Contraction/physiology, Myocardial Infarction/epidemiology/physiopathology/ultrasonography, Observer Variation, Stroke Volume/physiology, Sweden/epidemiology, Syndrome, Time Factors
Subject categories Medical and Health Sciences

Abstract

Pulsed tissue Doppler can measure myocardial velocities with high temporal resolution. Our aim was to determine the onset timing of the regional left ventricular longitudinal early lengthening (e) in relation to the mitral inflow (E) in acute coronary syndromes. We applied pulsed tissue Doppler to the septal, lateral, inferior, and anterior left ventricular basal walls of 160 patients with acute coronary syndromes and 60 control subjects. Maximum systolic and early diastolic velocities were lower for patient than for control walls (6.1 +/- 1.7 vs 7.9 +/- 1.4 cm/s, P <.0001, and 6.9 +/- 2.3 vs 10.0 +/- 2.3 cm/s, P <.0001, respectively) and e started later than E (12 +/- 30 vs 2 +/- 19 milliseconds later, P <.0001). All 3 variables related to the degree of visual left ventricular wall pathology. The intraindividual time range for all 4 e starts was wider for patients (43 +/- 27 vs 30 +/- 18 milliseconds, P <.0001). Our results show that pulsed tissue Doppler can identify a delayed and asynchronous initial wall lengthening in acute coronary syndromes.

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