Vol 39 # 2 June 2007 - Kma.org.kw

June 2007KUWAIT MEDICAL JOURNAL 131equivalent, the amplitude of atrioventricular ringmotion, to be used as an index of ejection fraction.It applies not only to the left ventricle, where it canbe shown to relate to prognosis but also to the rightventricle, where it provides a simple method ofassessing right ventricular function. When overalllong axis amplitude is low, peak shortening andlengthening rates are reduced. In restrictive leftventricular disease, long axis amplitude is low evenwhen cavity size is normal at end diastole,although the effects of this reduction are apparentin a reduced amplitude of wall thickening and thusof shortening fraction [10] .MVA motion, which is recorded by TDI withhigh feasibility and re p roducibility has beenstudied in the evaluation of the left ventricularfunction [5] . It has long been recognized that the leftventricular diastolic function may be abnormal inpatients with left ventricular hypertrophy at a timewhen systolic function is preserved. This has beendocumented by contrast and nuclear angiographyand by M-mode echocard i o g r a p h y. All thesemethods demonstrate that the velocity of earlydiastolic filling is reduced with or withoutsuperimposed asynchro n y. These findings aremirrored in long axis function when both extentand peak velocity of early diastolic lengthening arereduced and that during atrial systole they areincreased [11] . The overall amplitude of motion ishowever, normal. In left ventricular hypertrophy,therefore, long axis function corresponds closely toconventional views of diastolic function and inthese circumstances it may be appropriate tocalculate the ratio of early to late diastoliclengthening. It is also reasonable to suggest thatpeak diastolic lengthening rate determined by TDImay be an index of early diastolic function [ 12 ] .However, these conclusions are limited to caseswithout asynchrony. In addition, the most commoncause of a reduction of early diastolic lengtheningrate is low overall amplitude of ring motion, whichis characteristic of systolic left ventricular disease.Considering peak velocities of long axis motion inisolation, disre g a rding overall amplitude andtiming is thus likely to lead to misleadingconclusions [13] .Our study revealed that both M-modeechocardiogram and TDI of MVA were markers ofleft ventricular longitudinal fibers shortening andlengthening with subsequent effect on the diastolicfilling of LV and revealed that impaired longitudinalfibers function was due to ischemia independent ofthe presence or absence of left ventricularhypertrophy and this in agreement with previousstudies [5,10] . Haluska et al, [1] from the university ofQueensland, Australia, reported that the longitudinalfunction was the only parameter to be significantlyabnormal at rest in patients without contractilereserve and the failure to increase TDI velocitysignificantly with stress corresponded to the EFresponse.Contrary to the frequent appearance of apicalmovement in the apical views, caused by movementof the heart within the scan plane, the apex isnormally in a fixed position. During systole,contraction of subendocardial and subepicardialfibers, which follow a helical course leads tomovement of the base of the heart toward thea p e x [ 14 ] . The contribution of this longitudinalshortening to overall function probably variesaccording to the circumstances and pathology butits role appears to be substantial. This aspect of LVfunction has received limited attention in the past,perhaps reflecting the difficulties experienced in itsmeasurement. However, recent studies have shownthe TDI measurements of the base-apex function tobe a sensitive marker of ischemia [15] and Haluska etal [1] reported that the results of their study suggest itis a sensitive marker of latent LV dysfunction.Henein and Gibson reported that prolonged leftventricular long shortening and delayed onset oflengthening effectively suppress early diastolictransmitral flow even though the minor axisi n c reases and mitral cusps separate appare n t l ynormally and this grossly asynchronous leftventricular relaxation may interfere with filling bydissipating normal ventricular restoring forces [16] .They suggested that delayed and prolonged longaxis shortening is the primary disturbance, but thismay have been the result of activation disturbance,subendocardial ischemia [17,18] or other causes still tobe identified, either alone or in combination. Thisprolonged shortening interacts with rapid thinningof the posterior left ventricular wall, a process thatwe have already suggested to be autonomous and amajor site of restoring forces [19] and the energynormally coupled to filling is thus dissipated as achange in cavity shape.Methodological considerations:1. M-mode echocardiogram of mitral valve is avalid and useful method to evaluate leftventricular function [20] .2. Pulsed wave TDI of MVA is an advancedmethod to study the systolic and diastolic LVfunction [3,5,6] .Limitations of the study:1. Relatively small number of patients.2. Echocardiogram was done by one observer,so intra-observer variability was evaluatedbut it is difficult to evaluate inter-observervariability.3. Study was not completely blind to theobserver.