Br Heart3t 1993;69:501-506

Early changes in left ventricular subendocardialfunction after successful coronary angioplasty

Michael Y Henein, Kim Priestley, Tengis Davarashvili, Nigel Buller, Derek G Gibson

Cardiac Department,Royal BromptonNational Heart andLung Hospital,LondonM Y HeneinK PriestleyT DavarashviliN BullerD G GibsonCorrespondence to:Dr Derek G GibsonCardiac Department, RoyalBrompton National Heartand Lung Hospital, SydneyStreet, London SW3 6NP

Accepted for publication20 January 1993.

AbstractObjective-To study the early effects ofcoronary angioplasty on resting left ven-tricular long axis function, reflecting thatof the subendocardium.Design-Prospective echocardiographicand Doppler examination of patientswith coronary artery disease, before andafter single vessel coronary angioplasty.Setting-A tertiary referral centre forcardiac diseases with facilities for inva-sive and non-invasive investigation.Patients-23 patients with significant leftcoronary disease being considered forcoronary angioplasty.Results-Before angioplasty the mean(SD) isovolumic relaxation time waslonger than normal (75(19) ms v 55 (10),p <0.001) with a significant increase intransverse dimension change beforemitral valve opening, and peak rate ofearly diastolic thinning (8(3) v 10-4 (2.6)cmls (p < 0.001)) was reduced. Longaxis motion was frequently abnormal.The interval from the onset of the Qwave to the onset of shortening was pro-longed (118 (30) ms v 90 (19) at the leftsite and 115 (26) ms v 81 (9) at the septalsite, p < 0.001) and the onset of earlydiastolic rapid lengthening delayed withrespect to the aortic valve closure sound(A2) by 85 (34) ms v 58 (11) at the leftsite and 88 (33) ms v 60 (9) at the septalsite (p < 0.001). Although overall ampli-tude was reduced at the septal site only(1-23 (0.3) cm v 1-5 (0.4), p < 0.05), theextent (0-8 (0.2) cm v 1-04 (0.3) at theleft site and 0-66 (0.2) cm v 0-9 (0.3) atthe septal site, p < 0.001) and peak rate(6.2 (2) cmls v 10 (2 5) at the left site and5.4 (2.3) cmls v 8 5 (2) at the septal site,p < 001) of early diastolic lengtheningwere both much lower than normal. TheE/A ratio on transmitral Doppler wasmodestly reduced (1.0 (0.7) v 1-4 (0.4), p< 0.05). After angioplasty: isovolumicrelaxation time shortened to 64 (18) ms(p < 0.001) and left ventricular incoor-dination regressed. Long axis shorten-ing with respect to Q (98 (32) ms v 118(30) at the left site and 94 (23) ms v 115(26) at the septal site, p < 0.01) and thatof lengthening with respect to A, bothnormalised. Early diastolic peak length-ening rate increased (7 5 (2-1) cm/s v 6-2(2) at the left site, and 6-3 (2.4) cmls v5.4 (2.3) at the septal site, p < 0.001).The early diastolic peak thinning rate ofthe posterior wall significantly increased(10 (3.5) cmls v 8 (3), p < 0.005) as did

mitral E/A ratio 1-2 (0.7) v 1*0 (0.7), p <0.05).Conclusion-Long axis motion, repre-senting the function of longitudinallyarranged subendocardial fibres, is con-sistently abnormal in the resting state incoronary artery disease. These systolicand diastolic abnormalities returntowards normal after successful angio-plasty, suggesting that they are the directeffect of coronary artery stenosis.

(Br HeartJ' 1993;69:501-506)

Changes in the left ventricular minor axis, asrecorded by M mode echocardiography, haveproved useful in documenting abnormal dias-tolic function in left ventricular hypertrophy,ldiabetes,23 and coronary artery disease.4Though the method has been recently sup-planted to a considerable extent by Dopplerechocardiography,5 reservations are nowbeing expressed as to the validity of Dopplerechocardiography in studying diastolic func-tion.6 In left ventricular hypertrophy andcoronary artery disease the two techniques donot give identical information7 8; Doppler esti-mates of filling pattern are very sensitive toevents during isovolumic relaxation contrast-ing strikingly with changes in left ventricularminor axis. In our study, therefore, we aimedto extend earlier work by noting changes inleft ventricular long as well as minor axis inpatients with ischaemic heart disease. Wechose a group of patients with significantcoronary artery disease (>70% stenosis),studying them before and soon after success-ful percutaneous single vessel coronary angio-plasty. Although subject to angina of effortbefore the procedure, patients were studied atrest, and all were symptom free at the timewhen measurements were obtained.

Patients and methodsPATIENTSTwenty three patients with significant coro-nary artery disease and exercise inducedstable angina were studied. All patients sub-sequently underwent successful single vesselcoronary angioplasty defined as a residualstenosis of <50% and no appreciable proce-dural complications. Twelve patients, meanage 63 (SD 9) years (group I, 11 men), hadsingle vessel disease and no history ofmyocardial infarction or cardiac surgery. Tenhad disease of the left anterior descendingartery: eight proximal and two midvessel; onehad disease in the distal circumflex and one

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in the obtuse marginal branch of the circum-flex artery. Of the remaining 11 patients(group II) 10 had multivessel disease (twohad a previous anterior Q wave myocardialinfarction), and five patients had undergonecoronary bypass surgery; all were men ofmean (SD) age 55 (13) years. In all 11patients one culprit vessel was successfullydilated. This was the left anterior descendingartery itself in six patients (proximal in three,midvessel in two, and distal in one), theostium of a left anterior descending vein graftin one patient, and the circumflex in fourpatients (one proximal and three distal).

ITEATMENTAll the patients were subject to exerciselimiting angina incompletely controlled bymedical treatment with individualised com-binations of nitrates and calcium channel and(3 blocking drugs. Apart from minor andinconsistent alteration, medication was thesame after angioplasty. The results from thesepatients were compared with those in 21 nor-mal subjects, mean age 51 (11) years, none ofwhom had any evidence of cardiovascular dis-ease or hypertension. All patients and normalsubjects were in sinus rhythm.

METHODSPatients and controls were studied underresting conditions and had undertaken nounusual physical exertion before the test. Weobtained M mode and cross sectionalechocardiograms with a Hewlett-Packardmodel 77020 A Sonos 1000 echocardiographwith a 2-5 MHz transducer before and within48 hours of angioplasty, with the patient lyingin the left lateral position. The M modeechocardiograms and Doppler mitral velocitytraces were recorded separately on a Honey-well (Ecoline 22) strip chart recorder at apaper speed of 100 mm with simultaneouselectrocardiogram and phonocardiogram.

Standard M mode echocardiograms of theleft ventricular minor axis were recorded atthe tips of mitral valve leaflets. We alsoobtained M mode echocardiograms of the leftventricular long axis represented by atrioven-tricular ring motion that reflects longitudinalventricular function, with the cursor longitu-dinally placed through the left, central fibrousbody (septal) and right sites of the atrioven-tricular ring seen on the apical four chamberview9 (fig 1).

Mitral early and late diastolic flow velocit-ies were measured from the cardiac apex bypulsed Doppler with either the Hewlett-Packard or a Doptek system with a 2 MHztransducer, and were recorded with frequencyshift calibration. Echocardiograms werematched for heart rate; the onset of the Qwave was used to time early systolic eventsand the first high frequency component of theaortic valve closure sound (A2) for earlydiastolic events. The echocardiograms weredigitised'0 to find peak rates of change ofdimension and wall thickness.We took isovolumic relaxation time as the

time interval between aortic valve closure and

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1.5100

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Figure 1 (A) Long axisM mode recordingfrom ahealthy control recorded at left site. Vertical scale in cm.(B) The upperpanel shows the digitised plot of the trace,the lower panel shows its rate ofchange. Vertical linecorresponds to A2. ECG, electrocardiogram; PCG,phonocardiogram; A,, aortic closure; OQ, onset oflong axisshortening; O,, onset oflong axis lengthening; E, earlydiastolic excursion; A, atrial systolic excursion.

the onset of mitral valve cusp separation(ms). End systolic dimension was taken as thetransverse diameter between the left ventricu-lar septum and posterior wall at A2 (cm), enddiastolic dimension as the transverse diameterat the time of the onset of the Q wave of theelectrocardiogram (cm). The peak rate ofposterior wall thinning was measured as theearly diastolic velocity of the posterior wall(cmls).For the left sided, septal, and right sided

long axis traces, we measured the intervalsbetween Q and the onset of shortening and Qand the minimum left ventricular dimension(ms) and thus found the duration of shorten-ing as the difference between the two. Also,we measured the overall amplitude of atrio-ventricular ring motion (cm), early diastolicexcursion (cm); from peak inward motion tothe position at the onset of diastasis, that dur-ing atrial systole was measured as the A wave,occurring after the P wave in the electrocar-diogram. Peak rate of early diastolic lengthen-ing was measured from the digitised tracesand onset of rapid outward motion was theshoulder angling point between shorteningand lengthening. From the Doppler traces wemeasured the peak early E and atrial A wavevelocities, the E/A ratio, and the time intervalfrom A2 to the onset and peak of mitral Ewave (ms).

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Early changes in left ventricular subendocardialfunction after successful coronary angioplasty

STATISTICSValues represent mean (SD). We usedunpaired t tests to compare normal subjectswith patients undergoing percutaneous trans-luminal coronary angioplasty. Patients beforeand after angioplasty were compared bypaired t tests. A 5% probability was taken assignificant. In individual patients, values wereconsidered abnormal when they were morethan two SDs from the corresponding normalmean. Results from the two patient sub-groups were examined separately and sub-sequently pooled in view of their overallsimilarity. Minor but significant differencesbetween the two are presented separately.Differences between the two were subse-quently investigated by unpaired t test both intheir difference from normal and theirresponse to angioplasty.

Table 1 Isovolumic relaxation time and dimension changes

Indices Normal Before PTCA After PTCA(n = 21) (n = 23) (v before PTCA)

RR interval (ms) 940 (240) 950 (230) -15 (87)IVR time (ms) 55 (10) 75 (19)** -12 (9)tIVR dimension changesM (cm) 0-13 (0.07) - 0-23 (0 2)* - 0-05 (0 3)IVR dimension changes L (cm) 0-16 (0-16) - 0-04 (0 2)* - 0-03 (0 2)IVR dimension changes S (cm) 0-1 (0-06) + 0 03 (0 2)** - 0-07 (0-2)

*p < 0-05; **p < 0-01 v normal; tp < 0 05; PTCA, percutaneous transluminary coronaryangioplasty; I, left; S, septal, sites; IVR, isovolumic relaxation; M, minor axis; +, inward move-ment before PTCA; -, outward movement before PTCA; values are mean (SD).

Table 2 M mode echocardiographic data

Indices NorMal Before PICA After PTCA(n = 21) (n = 23) (vs before PTCA)

Total excursionM (cm) 1-7 (0 3) 1-8 (0 4) +0-18 (0 4)Total excursion L (cm) 1-5 (0-3) 1-46 (0-31) +0 04 (0 3)Early diastolic excursion L (cm) 1-04 (0 3) 0 8(0 2)** +0-1 (0-2)Atrial systole L (cm) 0-4 (0-1) 0-62 (0-14)** -0-1 (0-15)tTotal excursion S (cm) 1-5 (0.4) 1-23 (0 3)* + 005 (0 3)Early diastolic excursion S (cm) 0 9 (0 3) 0-66 (0-2)** + 0-06 (0 2)Atrial systole S (cm) 0-5 (0-2) 0-57 (0-11) -0-01 (0-13)Peak rate of thinningM (cm/s) 10-4 (2 6) 8 (3)* + 2 (2 8)tPeak rate of lengthening L (cm/s) 10 (2-5) 6-2 (2)** + 1-3 (1-5)tPeak rate of lengthening S (cm/s) 8-5(2) 5-4 (2.3)** +0-9 (1 3)tA2 to the onset of lengthening L (ms) 58 (11) 85 (34)** -17 (25)4A2 to the onset of lengthening S (ms) 60 (9) 88 (33)** -21 (14)4*p < 0 05; **p < 0-01 v normal; #p < 0-01 v before PTCA; PTCA, percutaneous transluminarycoronary angioplasty; M, minor axis; I, left; S, septal, sites; values are mean (SD).

Table 3 Early systolic changes

Indices Normal Before PTCA After PTCA(n = 21) (n = 23) (v before PTCA)

Q to the onset of shorteningM (ms) 81 (10) 113 (24)** - 17 (27)4Q to the onset of shortening L (ms) 90 (19) 118 (30)** - 19 (27)tOnset to minimum dimension L (ms) 272 (50) 300 (65) -18 (130)Q to the onset of shortening S (ms) 81 (9) 115 (26)** -20 (27)tOnset to minimum dimension S (ms) 300 (48) 350 (75) - 52 (97)

*p < 0 05; **p < 0-01 v normal; #p < 0-01 v before PTCA; PTCA, percutaneous transluminarycoronary angioplasty; M, minor axis; L, left; S, septal sites; values are mean (SD).

Table 4 Dopplerfindings

Indices Normal Before PTCA After PTCA(n = 21) (n = 23) (v before PTCA)

E wave (m/s) 0-7 (0-1) 0-4 (0 2) + 0-1 (0-15)4A wave (m/s) 0-5 (0-1) 0.5 (0-3) - 0-02 (0-17)E/A ratio 1-4 (0-4) 1-0 (0.7)* + 0-26 (0 6)tA2 to the onset ofE (ms) 84 (14) 100 (20) -20 (12)4A2 to the peak ofE (ms) 165 (28) 168 (28) - 16 (19)t

*p < 0 05 v normal; tp < 0-05; tp < 0-01 v before PTCA; PTCA, percutaneous transluminarycoronary angioplasty; E, early diastolic mitral flow velocity; A, late diastolic mitral flow velocity;A2, timing of aortic valve closure; values are mean (SD).

ResultsNORMAL SUBJECTS:Tables 1-4 show that left ventricular cavitysize and wall motion were both by definitionnormal in these subjects. Isovolumic relax-ation time had a mean value of 55 ms, and nosignificant dimension change occurred duringthis period. Long axis shortening began80-90 ms after the onset of the Q wave of theelectrocardiogram, and lengthening started60 ms after A2-that is, at about the sametime as mitral cusp separation and 20 msbefore the first detectable transmitral flow onpulsed Doppler. The greater part of backwarddisplacement of the mitral ring occurred dur-ing early diastole with a peak velocity of8 5-10 cm/s (fig 2).

COMPARISON WMTH PATIENTS WITH CORONARYARTERY DISEASE:Table 1-4 show that the mean values of RRinterval, cavity size, and shortening fractiondid not differ from normal. Isovolumic relax-ation time was, however, significantly pro-longed, with further shortening of the septallong axis consistently occurring during this

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Figure 2 Long axis M mode recordings from a normalsubject taken at left, septal, right, and posterior sites.Traces are recorded with simultaneous ECG and PCGVertical line corresponds to A2. Abbreviations asfig. 1.

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Figure 3 (A) Long axisM mode recordingfrom a patient with severe left anterior descending artery stenosis. Note thedelay in the onset ofshortening with respect to the Q wave on the electrocardiogram, the prolonged inward motion after A,and the decreased early diastolic excursion and lengthening rate. (B) Long axis from the same patient after successftdangioplasty. Note how these disturbances have returned towards normal. Abbreviations as forfig. 1.

period (fig 3A). The onset of shortening atthe start of systole was characteristicallydelayed at the septal and left sites, the intervalfrom Q to the onset of shortening beingdelayed by about 30 ms at both. The onset ofrapid lengthening with respect to A2 was alsodelayed, and again by a very similar amount.During the prolonged period of isovolumicrelaxation, incoordinate wall motion was pre-sent affecting the septum, which showed fur-ther shortening before mitral cusp separation.

Disturbances of filling were also common.

The extent and peak rate of early diastoliclengthening were both reduced at septal andleft sites with a reciprocal increase in theamplitude of ring motion during atrialsystole. Peak E and A wave velocities showedno consistent change although the E/A ratiowas reduced.

EFFECTS OF ANGIOPLASTYAngioplasty did not effect RR interval, butisovolumic relaxation consistently fell by

20 ms. On the transmitral Doppler, E wave

velocity increased, along with E/A ratio, butA wave velocities were unaffected.

Abnormalities of long axis function presentunder control conditions were also consis-tently affected, tending to return towards nor-

mal (fig 3(B)). The time intervals from the Qwave of the electrocardiogram to the onset ofinward motion and from A2 to the onset ofrapid lengthening both fell by 20 ms-that is,by about two thirds of the initial abnormality.Disturbances of early diastole also regressed:the extent and peak rate of early diastoliclengthening both increased and A wave

decreased as the Doppler filling patternreturned towards normal. There was no sig-nificant correlation between peak E wave

velocity and peak rate of early diastoliclengthening.

COMPARISON BETWEEN THE TWO SUBGROUPS

Table 5 shows that when patients with singlevessel coronary artery disease (group I) were

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After PTCA

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Early changes in left ventricular subendocardialffunction after successful coronary angioplasty

Table 5 Differences between two patient subgroups

Variable Single vessel Multivessel pdisease (n = 12) disease (n = 11) Value

Before angioplasty:Fractional shortening 0 35 (0 04) 0-32 (0 05) <0 05Q to the onset shortening S (ms) 103 (21) 129 (27) <0-02Q to the minimum dimension S (ms) 433 (62) 508 (63) <0-02

After angioplasty:IVR dimension change L (cm) -0-23 (0-12) 0-01 (0-13) <0 05A, to the onset lengthening L (ms) 59 (22) 76 (22) <0 05Early diastolic excursion L (cm) 1 0 (0-2) 0-76 (0-2) <0 05

IVR, isovolumic relaxation; L, left long axis site; S, septal long axis site; values are mean (SD).

compared with those with multivessel diseaseand or coronary bypass grafting (group II)their overall behaviour was similar. We didfind, however, that in the control state frac-tional shortening was greater and that thedelay in onset of long axis shortening in earlysystole and of lengthening in early diastolewere both significantly less in group Ipatients. After angioplasty, normalisation ofdimension changes during isovolumic relax-ation and early diastole were all more com-plete in group I patients. Differences betweenthe two groups for all the other measure-ments made were not significant.

RESULTS IN INDIVIDUAL PATIENTSTable 6 gives the numbers of patients inwhom individual values fell outside the 95%confidence intervals (95% CIs) of normal.The disturbances most commonly abnormalwere Q to the onset of shortening, A2 to theonset of rapid lengthening and peak rate ofearly diastolic lengthening, followed by peakE wave velocity, and isovolumic relaxationtime. Either Q to the onset of shortening, A2to the onset of rapid lengthening, or peak rateof lengthening in early diastole were abnor-mal in all but one patient before angioplasty.The variables that became normal most fre-quently were Q to the onset of shortening,peak rate of early diastolic lengthening, andisovolumic relaxation time, each of them over50%. The E wave velocity and A2 to the onsetof rapid outward motion were significantlyless frequently affected. Although change inthe E/A ratio with angioplasty was highly sig-nificant, values remained within normal limitsbefore and after angioplasty. Peak rate ofearly diastolic lengthening increased beforeand after angioplasty.

In individual patients further interrelationsbetween these variables could be defined,when results before and after angioplastywere combined. The delay from Q to theonset of shortening and A2 to the onset ofrapid lengthening was similar both between

Table 6 Distribution of individual abnormalities(number ofpatients with values outside 95% CIs ofnormal)

Before AfterVariables PTCA PTCA

Q to the onset of shortening 13 6Peak rate of lengthening 13 6A, to the onset of lengthening 13 8Peak E wave velocity 10 9Isovolumic relaxation 9 6E/A ratio 2 2

PTCA, percutaneous transluminary coronary angioplasty; E,early diastolic mitral flow velocity; A, late diastolic mitral flowvelocity.

control and coronary artery disease (about 30ms) and between before and after angioplasty(about 20 ms). In patients in whom Q to theonset of inward motion had increased beyondthe 95% CI of normal, the value of A2 to theonset of lengthening was 106 (23) ms, where-as in those with normal Q to the onset ofshortening, lengthening started 85 (19) msafter A2 (p < 0 01). The relation between Qto the onset of shortening and peak E wavewas also striking. When the onset of shorten-ing of both long axes was abnormally delayed(n = 8), peak E wave velocity was alwaysreduced to a mean value of 025 (0d13) ms.When one long axis only was abnormal (n =16), E wave velocity was below the 95% CI ineight (44%), mean value of 0 47 (0.19) ms(p < 0 05). When the movement started nor-mally in both long axes (n = 22), E wavevelocity was reduced in seven (30%) with amean value of 0-56 (0-19) ms. Differencefrom one abnormal axis (p < 0-03), and fromboth axes (p < 0-002).

DiscussionLeft ventricular diastolic function is oftenabnormal in patients with coronary artery dis-ease, even in the absence of acute ischaemia.The rate of decline of left ventricular pressuremay be reduced and isovolumic relaxationtime prolonged. The filling pattern of the leftventricle may be disturbed, so that the pro-portion of the stroke volume entering the ven-tricle during early diastole falls and thatentering during atrial systole increases.Regional wall motion may be incoordinate:with segments of myocardium supplied bystenosed coronary arteries showing prolongedinward moyement and premature outwardmotion elsewhere causing a change in cavityshape."' The myocardial fibres most at riskfrom ischaemia are those situated in thesubendocardial region of the myocardium.'2These are largely longitudinally directed."3 Inour study, therefore, we used echocardio-graphy to investigate the incidence and natureof disturbances of left ventricular long axisfunction in patients undergoing single vesselcoronary artery angioplasty. To ascertain theextent to which the disturbances we foundwere reversible, we studied the patientsbefore and after successful angioplasty.Long axis function was often abnormal

during early diastole in our patients. Themost characteristic disturbances were delay inthe onset of rapid outward motion and areduction in peak rate of lengthening of thelong axis during early diastole. One or otherof these abnormalities was present in all butone of our patients. Less commonly, isovolu-mic relaxation time was prolonged, and thepeak velocity of the E wave was reduced.The extent of these changes was consider-

able: isovolumic relaxation time was pro-longed and the onset of early diastolic rapidlengthening was delayed, each by about 20ms, and peak E wave and peak rate of earlydiastolic lengthening were both reduced toabout 60% of control values. These changes

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had partially resolved within 48 hours of suc-cessful angioplasty strongly suggesting thatthey were related to the presence of coronaryartery stenosis. We conclude, therefore, thatleft ventricular subendocardial function maybe abnormal in patients with coronary arterydisease under resting conditions. Thesedisturbances are partially reversed after revas-cularisation, and so correspond closely to thedefinition of ischaemia as impaired functioncaused by interference with tissue or organperfusion.'4 Such early diastolic abnormalitiesthus extend current ideas of silent ischaemia,as they occurred at rest and in the absence ofchest pain or electrocardiographic abnor-mality.Our results also give some information

about the basic mechanisms involved. It ismost unlikely that all the changes in functionwe found were independent of one another.Prolongation of isovolumic relaxation timefor example, by whatever mechanism, charac-teristically reduces peak E wave velocity."5Any change in the pattern of transmitral flowvelocity is thus likely to give only indirect evi-dence of underlying events. Delay in theonset of rapid lengthening of the long axis atthe start of diastole was one of the common-

est disturbances. Generally, such delay islikely to have occurred either because thetime course of systolic shortening was pro-longed, or because the onset of systolic short-ening was delayed, or from a combination ofthese two mechanisms. We therefore studiedthe early systolic relation between the onset oflong axis shortening and the Q wave of theelectrocardiogram, and found this intervalalso to be consistently prolonged by about 30ms. Not only was this value very similar tothe delay in the onset of rapid lengthening,but also it reverted to normal after angio-plasty. Delay in the start of long axis shorten-ing occurred early in the cardiac cycle andthus seems to be a primary abnormality. Theeventual manifestations are in part diastolic,but the basis is much earlier. It is presumablycaused either by a local disturbance of activa-tion or of electromechanical coupling.Normal values for the extent and duration ofshortening of these segments make impairedsystolic function much less likely. The closerelation in individual patients between a delayin the onset of systolic shortening and peak Ewave velocity raises the possibility that thelow peak rate of early diastolic lengtheningmay be the direct consequence of a low fillingrate. Although we cannot definitely excludethis mechanism, we noted that the timing ofthe E wave usually followed that of peak rateof long axis lengthening, and that the directcorrelation between the two in individualpatients was low. We thus regard delay in theonset of long axis shortening in early systoleand a reduction in its peak rate of lengthening

in early diastole as two primary disturbances.Changes in cavity shape during isovolumicrelaxation and in transmitral flow patternwere secondary to these.

As left ventricular long axis function can soconveniently be studied in humans by com-bined echo and phonocardiography, and we

would stress the necessity of the latter, ourresults may be useful in assessing patientswith coronary artery disease. Values outsidethe 95% CIs of normal were often present,allowing individual patients to be recognised.In this long axis function differs strikinglyfrom Doppler measurements, which havepreviously been reported as changing afterangioplasty, but which in our patientsremained within normal limits throughout.Disturbed long axis function thus seems avery sensitive indicator of ischaemia that canbe identified in individual patients. Thisallows the effects of angioplasty to be seen,and may thus be useful in assessing the effectsof medical or surgical treatment. Clear abnor-malities are present at rest, and do notrequire stress to produce them or specialisedimaging to record and interpret the results.Finally, the possibility of detecting abnormal-ities so intimately related to the presence ofischaemia may well be of potential value inelucidating mechanisms by which myocardialperfusion becomes limited when diastolictime is short. This may lead to a fuller under-standing of the basic pathophysiology ofischaemia due to coronary artery disease orrelated conditions.

Presented at the 65th scientific session of the American HeartAssociation.

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2 Shapiro LM, Leatherdale BA, Mackinnon J, Fletcher RF.Left ventricular function in diabetes mellitus 11: rela-tion between clinical features and left ventricular func-tion. BrHeartJ 1981;45:129-32.

3 Danielsen R, Nordrehaug JE, Lien E, Vik-Mo H.Subclinical left ventricular abnormalities in young sub-jects with long-term type diabetes mellitus detected bydigitized M-mode echocardiography. Am J Cardiol1987;60: 143-6.

4 Upton MT, Gibson DG, Brown DJ. Echocardiographicassessment of abnormal left ventricular relaxation inman. Br HeartJ 1976;38:1001-9.

5 Nishimura RA, Abel MD, Hatle LK, Tajik AJ.Assessment of diastolic function of the heart: back-ground and current applications of Doppler echocardio-graphy. Part 11 clinical studies. Mayo Clin Proc1989;64: 181-204.

6 Choong CY, Herrmann HC, Weyman AE, Fifer MA.Preload dependence of Doppler-derived indexes of leftventricular diastolic function in humans. J Am ColCardiol 1987;10:800-8.

7 Lee CH, Hogan JC, Gibson DG. Diastolic disease in leftventricular hypertrophy: comparison of M mode andDoppler echocardiography for the assessment of rapidventricular filling. Br Heart3' 1991;65:194-200.

8 Spirito P, Maron BJ, Bellotti P, Chiarella F, Vecchio C.Noninvasive assessment of left ventricular diastolicfunction: comparative analysis of pulsed Doppler ultra-sound and digitized M-mode echocardiography. Am JCardiol 1986;58:837-43.

9 Jones CJH, Raposo L, Gibson DG. Functional impor-tance of the long axis dynamics of the human left vent-ricle. BrHeartJ 1990;63:215-20.

10 Gibson DG, Brown D. Measurement of instantaneous leftventricular dimension and filling rate in man, usingechocardiography. Br HeartJY 1973;35:1141-9.

11 Gibson DG, Prewitt TA, Brown DJ. Analysis of the leftventricular wall movement during isovolumic relaxationand its relation to coronary artery disease. Br Heart J1976;38:1010-9.

12 Cobbe SM. Coronary blood flow and myocardialischaemia. In: Julian DG, Camm AJ, Fox KM, et al.Diseases of the heart. 1st ed. London: Bailliere Tindall,1989:1091-2.

13 Williams PI, Warwick R Myocardial architecture. In:Gray's anatomy, 36th ed. Edinburgh: ChurchillLivingstone, 1980:657-9.

14 Woolf N. Ischaemia and infarction; In: McGee JO'D,Isaacson PG, Wright NA, eds. Oxford textbook ofpath-logy. Oxford: Oxford University Press, 1992;1:524-30.

15 Brecker SJD, Lee CH, Gibson DG. Relation of left vent-ricular isovolumic relaxation time and incoordination totransmitral Doppler filling patterns. Br Heart J31992;68:567-73.

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