Diastolic closure rate of normalmitral valve' · Diastolic closure rate ofnormalmitralvalve Io69 formed by physical techniques using a paramagnetic oxygen analyser (Servomex) and

British HeartJournal, I973, 35, I066-i074.

Diastolic closure rate of normal mitral valve'

Clive Layton, Graham Gent,'Ronald Pridie, Alastair McDonald, and Wallace BrigdenFrom the Cardiac Department, The London Hospital, Whitechapel, London

In order to establish the determinants of the diastolic closure rate of the mitral valve measured from echo-cardiographic recordings, 5 normal volunteers have been studied by non-invasive methods and 20 patients inthe course of cardiac catheterization. No correlation was found between the heart rate and the diastolicclosure rate, but a linear relation was established between the left ventricular filling pressure and the diastolicclosure rate. The coefficients of regression of the equations obtainedfrom the individual regression lines were

linearly related to left ventricular diastolic AP/A V and the constants of the equations were related in a linearfashion to the total amplitude of movement of the mitral valve ring.

These findings support the hypothesis that the diastolic closure rate of the structurally normal mitral valvereflects the rate of left ventricularfilling, and also confirm the importance of movement of the valve ring in thecomposite pattern ascribed to the motion of the anterior cusp assessed by echocardiography. Analysis of mitralvalve movement coupled with haemodynamic measurements may provide useful information relating to leftventricular compliance.

Recording of the movement of the anterior cusp ofthe mitral valve using reflected ultrasound has beenincreasingly used in clinical practice. Variations inthe pattern of movement have been described inheart disease, and it has been established thatmeasurement of the. speed with which the mitralvalve closes in early diastole, the diastolic closurerate, is of considerable diagnostic value (Gustafson,I967; Segal, Likoff, and Kingsley, I967). Lowlevels of the diastolic closure rate have been observedin mitral stenosis (Edler, I956) and in hyper-trophic cardiomyopathy (Popp and Harrison, I969;Pridie and Oakley, I970; Shah, Gramiak, andKramer, I969; Moreyra et al., I969) while highlevels are found in mitral or aortic regurgitation(Segal et al., I967; Pridie, I969) and in some casesof myocardial infarction (Tallury, DePasquale, andBurch, I972). On the basis of these observations ithas been suggested that the diastolic closure ratemay reflect the rate of left ventricular filling (Segalet al., I967), but we are unaware of any physio-logical studies to substantiate this hypothesis orto establish the factors which determine the dias-tolic closure rate of the normal mitral valve.

It has also been recognized that movement of themitral valve ring contributes to the apparent move-

Received 7 June I973.1 This study has been supported by grants from theBritish Heart Foundation.

ment of the anterior cusp (Chakorn et al., I972), butno studies have been performed to quantify thisrelation or the factors governing it. Such informa-tion is required if the abnormal findings in myo-cardial or valvular disease are to be interpretedcorrectly, and to explain the changes in be-haviour of the mitral valve in the presence of leftventricular disease without organic valve disease.This study has been designed to assess the impor-tance of the heart rate, the left ventricular fillingpressure, the left ventricular diastolic pressure/volume relation, the stroke volume, and the move-ment of the mitral valve ring as determinants of thediastolic closure rate of the anatomically normalmitral valve.

SubjectsThe investigation was performed in two parts. In the firstsection 5 normal male volunteers, age range 26 tO 47years, were studied using non-invasive recording tech-niques for the assessment of the cardiovascular responseto changes in the heart rate. In the second part 20patients undergoing diagnostic cardiac catheterizationwere studied, including I3 with coronary artery disease,4 with cardiomyopathy, i with hypertension, i withcardiomyopathy with left ventricular inflow tract ob-struction, and i with persistent chest pain in whom nocardiac or coronary abnormality has been shown. Clinicaldetails of these patients are shown in Table I. Informedconsent for the research aspects ofthis study was obtainedfrom all the subjects investigated. Mitral and aortic

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Diastolic closure rate of normal mitral valve 1067

TABLE I Clinical, haemodynamic, and echocardiographic data from 20 patients

Case No. Age Sex Diagnosis Mlean Heart Stroke Diastolic Mean diastolic MeanLVEDP rate/mmn volume AP/AV closure rate amplitude of(mmHg) (ml) (mmHg/ml) (mm/sec) ring movement

(mm)

I 6i M Coronary artery disease II 68 91 0110O 103-2 58 M Coronary artery disease 15 101 30 0'445 38-3 62 M Coronary artery disease 6 65 85 o-ii8 514 52 M Cardiomyopathy 24 104 46 0-34I III-5 58 F Hypertension II 75 54 0-236 37-6 63 M Coronary artery disease I5 77 39 01I78 63-7 61 M LVinflow

obstruction 32 101 29 0o586 29-8 50 M Coronary artery disease 13 75 55 0'355 8o-9 54 M Coronary artery disease 13 73 54 0-326 46 7-0I0 44 M Coronary artery disease i0 55 74 010o6 120 15'7II 56 M Coronary artery disease 13 - - -129 100o12 46 M Coronaryartery disease i0 74 48 0-230 55 111013 6i F Coronaryartery disease 13 65 45 0-320 6i 8-914 48 M Normal 7 80 102 o-o81 82 13'4I5 6o F Coronary artery disease 22

(PADP) - - - xI 12o0i6 43 M Coronary artery disease 13

(PADP) - - -83 101017 39 F Cardiomyopathy i6 72 71 o-io8 73 6-7i8 44 M Amyloid

cardiomyopathy 37 I05 55 O'59 66 7-619 x8 M Cardiomyopathy 21 89 87 0190o 73 8-920 55 M Coronary artery disease i6 67 47 O0220 93 8-7

LVEDP=left ventricular end-diastolic pressure; PADP=pulmonary artery diastolic pressure.

AWE

LV l

~~~~E1iir~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ , .Itr--a-4.IIIIIt- I4 It-

FIG.* i The normal mitral echogram with simultaneous electrocardiogramular pressure.

and left ventric-

4 Al -h A hm 14 10 km . AW iR,.#& kAbi di, II IA i Ai A IN-la II Aii I h Oki6L I Ljjll-i III J Ai AI AWAbil 6 IIII, J.11" ri, -r T'T lqllvllI"T I -r r7wrip 1-1, It, -II lrr

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io68 Layton, Gent, Pridie, McDonald, and Brigden

regurgitation were excluded in all as were the presenceof any intracardiac shunts.

MethodsThe mitral valve echogram was recorded using a Smith-Kline Instruments Ekoline 20 ultrasound recorder pro-viding a repetition rate of iooo pulses a second with afrequency of 2-5 mega Hz. The normal pattern of move-ment of the anterior cusp is shown in Fig. I and con-sists of a rapid early diastolic opening followed immed-iately by closure to a semi-open position. At the onset ofatrial systole the valve opens again, and this movement isfollowed by complete closure as the left ventricularpressure rises at the beginning of systole (Gustafson,I967). The echogram was obtained by placing the trans-ducer in the fourth left intercostal space i to 5 cm fromthe sternal edge and adjusting the angulation until anoptimal trace was obtained. All the recorded beats weresubsequently analysed but only those in which the earlydiastolic opening movement occurred at a rate greaterthan 300 mm a second were accepted as technically satis-factory. Measurement of a valid diastolic closure rate atheart rates above I20 beats a minute was not possible asthe atrial systolic opening movement merged with theearly diastolic movement at these higher rates as a resultof the short diastolic period (Fig. 2). Following therecording of the anterior cusp movement, the movementof the mitral valve ring was also measured in Cases 9 to20 by slightly altering the angulation of the transducersuperiorly and medially but without changing its posi-tion on the chest wall, until the characteristic pattern ofmovement of the valve ring was observed.The 5 normal volunteers were studied not less than 6

hours after the last meal. The output of the ultrasound

ao\

EE 41'

recorder was passed to a Cambridge multichannel photo-graphic recorder using a matching amplifier. Simul-taneous records were made of the electrocardiogram(lead II), phonocardiogram, and mitral echogram. Thephonocardiogram was obtained using a piezoelectriccrystal microphone placed in the second intercostalspace at the left sternal edge. A small cannula was intro-duced into a vein on the dorsum of the hand and controlrecordings performed at a paper speed of I00 mm persecond. An intravenous infusion of atropine sulphate wasthen started at a rate of 0-2 mg every 2 minutes. Furtherrecordings were made at 2-minute intervals until theheart rate reached I20 beats a minute or i 8 mg atropinehad been given.

In the second part ofthe study, 20 patients undergoingroutine diagnostic cardiac catheterization were studied inthe postabsorptive state. Recordings were made in thesupine position before angiography and the patientswere unsedated. Right and left heart catheterization wasperformed using conventional techniques. Pressureswere recorded using either Sanborn type 267 Bc or SEtype 4-82 strain gauges and using the mid-thorax asthe reference level. The left ventricular end-diastolicpressure was measured after the 'a' wave and the leftventricular end-systolic pressure at the lowest point inthe ventricular pressure trace. The natural frequency ofthe catheter-transducer systems used varied from 25to 35 Hz and additional mechanical damping was ob-tained using a modification ofthe method of Sutterer andWood (ig60).

In 17 patients the cardiac output was measured usingthe Fick direct oxygen method. Ventilation was measuredeither by a timed expired gas collection into a Douglas bagor by a pneumotachograph and computing spirometer(Mercury Electronics). Expired gas analysis was per-

1+AS &,01s~~~~

FIG. 2 The mitral echogram with simultaneous electrocardiogram and left ventricular diastolicpressure at higher heart rates. The atrial systolic opening movement is merging with the earlydiastolic movement.

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Diastolic closure rate of normal mitral valve Io69

formed by physical techniques using a paramagneticoxygen analyser (Servomex) and an infrared carbondioxide analyser (Hartmann and Braun) calibrated withknown gas concentrations. The haemoglobin and oxygensaturations of blood samples were measured on a CO-oximeter (IL Laboratories). The stroke volume wasderived from the cardiac output and the heart rate,measured during the period of the collection of theexpired air.The electrocardiogram, intravascular pressures, and

echograms were recorded using either a Hewlett-Packardmultichannel photographic recorder or an SE Labora-tories ultraviolet recorder at a paper speed of ioo mm asecond.

In the first study the diastolic closure rate was com-pared with the heart rate derived from the preceding RRinterval on the electrocardiogram. In the second studythe closure rate was related to the left ventricular fillingpressure as measured by left ventricular end-diastolicpressure in I8 cases and pulmonary arterial diastolicpressure in 2 cases, and a regression equation was calcu-lated. The slope of the regression lines for each subjectwas then plotted against the left ventricular diastolicAP/AV, which was derived from the difference betweenthe end-diastolic and end-systolic pressures and thestroke volume. The constant of each regression equationwas plotted against the total amplitude of movement ofthe mitral valve ring. The statistical significance of theserelations was obtained by the calculation of correlationcoefficients.

ResultsIn the first part of the study a total of i6i beats weretechnically acceptable for analysis. The ranges ofthe diastolic closure rate and the heart rates areshown in Table 2. The heart rates varied between52 and 1I9 beats a minute and the diastolic closurerates from 58 to I39 mm a second. The meandiastolic closure rate for the group was 92 mm asecond (SD I9 mm a second). The differencebetween highest and lowest diastolic closure ratesvaried from 2I to 44 mm/sec. No relation was foundbetween the heart rate and the diastolic closure rateeither for the group (Fig. 3) or for any individualsubject.

140L

100lDIASTOLICCLOSURERATE (mm./sec)

60

20

...-'

o,

40 60 80

HEART RATE

100 120

FIG. 3 The diastolic closure rate at different heartrates derived from the pooled observations in normalsubjects.

In the second part of the study the haemodyn-amic data are shown in Table i. No attempt wasmade to alter the left ventricular filling pressureeither by physical or pharmacological means, butthe variation in pressure found in the subjects atrest ranged from 4.5 to I2 o mmHg. This spon-taneous variation in the pressure, largely related tothe respiratory cycle, permitted the calculation of aregression equation for each subject relating thediastolic closure rate to the left ventricular fillingpressure (Table 3, Fig. 4). In I7 of the 20 patientsstudied the linear relation between these twovariables was highly significant (P <o.ooi) (Fig. 5).The three exceptions were Cases 7, 13, and i8, in

whom changes in the left ventricular end-diastolicpressure produced only very small alteration in thediastolic closure rate resulting in a low coefficientof regression. In order to produce a relation with ahigh level of significance for these patients, a muchlarger range of pressures than were actually ob-served would have been required.The mean left ventricular diastolic AP/AV was

TABLE 2 Diastolic closure rate and heart rate during infusion of atropine

Case No. Heart rate Diastolic closure-rate No. of beats(beats/min) (mmlsec) recordedMinimum Maximum Mimimum Mean Maximum

2I 54 IO9 84 99 II5 3722 52 89 75 84 97 2323 55 II9 65 75 93 2224 54 I06 95 II2 I39 4825 63 88 58 69 79 3I

Total 52 II9 58 92 I39 I6ISD=ig

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1070 Layton, Gent, Pridie, McDonald, and Brigden

TABLE 3 Relation between diastolic closure rate and left ventricular filling pressure in 20 subjects

Case No. Regression equation Correlation P(diastolic closure rate =) coefficient

I 66o x LVFP+ 37 o-889 < O0OOI2 3-4XLVFP-I4 o-834 < OOOI3 5-5 x LVFP+ I9 o-863 <O0OOI4 4-4 x LVFP+4 o8o4 <O0OOI5 3-8 x LVFP-4 o*8i2 < OOOI6 6*oxLVFP-27 0o925 <O0OO07 o-4xLVFP+17 0O316 >O.I8 4-ox LVFP+27 o.854 <00019 3-IX LVFP+4 0848 <OOOlIo 6*9xLVFP+5. o-8o4 <0001I I 7Ox LVFP+ 4I o856 <OOOII2 3-3 x LVFP+ 22 o875 <O0OOI13 2I xLVFP+34 o06i3 <O-II4 5-2 x LVFP+43 0-78i <OOI15 3'4xLVFP+27 0-762 <0001I6 4-5 x LVFP+26 o838 <O-OOII7 5 OxLVFP-7 o853 <O0OOIi8 I-3 XLVFP+ I8 0o455 <01I9 4-ox LVFP-I2 o-886 <o-ooI20 4-8 x LVFP+ I7 o-878 < O-OOI

LVFP=left ventricular filling pressure.

16

DCR-6-Ox LVEDP+37

n. 24

r.+O489120 p.<O001

DCR

[mmnsecJ

LVEDP [mm HglFIG. 4 The relation between the diastolic closure rate and the left ventricular end-diastolicpressure (Case x).

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4 a 12 16 20 24 28 32 36 40 44

LV FILUNG PRESSURE [mm Ho]

FIG. 5 The relation between the diastolic closure rate and the left ventricular filling pressurein 20 patients.

measured in I7 patients using 20 consecutive beatsin the analysis. The slopes of the regression linesobtained from the relation between the diastolicclosure rate and the left ventricular end-diastolicpressure were plotted against the left ventricularAP/AV for the same subjects. Another highlysignificant linear relation (P < o-ooi) was establishedbetween these variables (Fig. 6).

The constants of the regression equations wereplotted against the total amplitude of movement ofthe mitral valve ring in I2 of the subjects and a sig-nificant linear relation (P < o os) was found (Fig. 7).The range of amplitudes of movement of the mitralring was 6-7 to I5 7 mm.

+80-

I-

SLOPE

4.

2-

SLOPE. 9-4xAP/AV

r .- 0-869x p.<O-O01

xx

x x

x x x

x

0-1 0-2 03 0-4 0.5 0-6 0-7

AP/AV [mm HgimlI

FIG. 6 The relation between the slopes of the re-

gression lines and the left ventricular diastolic pres-sure/volume ratio.

+60-

440-

CONSTANT

+20-

0-

xx

x ant.x

xx 5 5 x Ring Amplitude-34

~~~~~~r.0-760p-<005

x

6-0 8-0 10-0 120 14-0 16-0 180RING AMPLITUDE [mmi

FIG. 7 The relation between the constants of theregression equations and amplitude of movement of themitral valve ring.

1801

160

140

120

100DCR

[mmn"cJ80-

60-

40-

20*

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DiscussionThe importance of measurement of the diastolicclosure rate of the mitral valve has been recognizedsince the earliest reports on the use of ultrasoundrecordings of the movement of the anterior cusp.Ranges of normal values for the diastolic closurerate have been previously reported (Edler, I96I;Joyner, Reid, and Bond, I963; Ziady et al., I973).The values for the normal mean closure rate in thisstudy are lower than expected from these earlierreports. However previous studies have used photo-graphic recordings of slow-sweep oscilloscope tracesfor the analysis of the diastolic closure rate. Suchmeasurements are of limited accuracy. This studyhas recognized the need for fast-sweep recordingsin the measurement of time-based cardiovascularvariables, and the differences observed in the meanvalues for the diastolic closure rate obtained for thenormal subjects in this study as compared to pre-vious reports are accounted for by this importantdifference in technique.A reduction in the closure rate is a constant

finding in mitral stenosis (Edler, I967) but this hasalso been reported with hypertrophic cardiomyo-pathy (Popp and Harrison, I969; Pridie and Oakley,I970) and in the elderly without evidence of heartdisease (Derman, 1972). In this study systemichypertension, congestive cardiomyopathy, restric-tive cardiomyopathy, and coronary artery diseasehave also been shown to be associated with anabnormally slow diastolic closure rate. This slowdiastolic closure rate was found even in the presenceof high left ventricular filling pressures and is inobvious contrast to the rapid diastolic closure rateseen in mitral and aortic regurgitation in which thefilling pressure is also raised. This apparent paradoxmay be explained on the basis of the left ventric-ular filling rate as the major determinant of thediastolic closure rate, and, as has been previouslysuggested, with the left ventricular compliance as animportant factor (Shabetai and Davidson, I972).

In order to test the hypothesis of ventricularfilling as the determinant of the diastolic closurerate this study has related the rate to the heart rate,ventricular filling pressure, and an index of ventric-ular diastolic compliance, the diastolic pressure/vol-ume ratio. Only patients with normal valves wereexamined, in order to exclude the possibility ofchanges in the diastolic closure rate arising from ananatomical abnormality of the mitral valve inter-fering with its physical properties, and the presenceof coincident disorders such as valvar regurgitationwhich would prevent the measurement of the leftventricular stroke volume.

Within the range of heart rates observed nochange in the rate of left ventricular filling would be

expected in the normal heart provided that themethod used for the induction of the tachycardiahad no other haemodynamic effects unrelated to thechange in the heart rate (Weissler, Leonard, andWarren, 1957). The response of the cardiac output,stroke volume, and left ventricular filling pressureafter infusion of atropine have been compared tothose occurring during a similar tachycardia in-duced by atrial pacing, and no significant differ-ences found (Kosowsky et al., I966), suggestingthat the use of atropine was valid. After large dosesof atropine and at high heart rates there is a fall inthe stroke volume and cardiac output accompaniedby a fall in the ventricular filling pressure (Berryet al., I959; McMichael and Sharpey-Schafer,I944), but in this study these levels of tachycardiawere not reached, thus validating the conclusionthat the diastolic closure rate did not vary withchanges in the heart rate and duration of diastole innormal subjects during a sinus tachycardia.The relation between the diastolic closure rate

and the left ventricular filling pressure can be ex-pressed in the form of a linear regression equation(Table 3). The linearity of this relation is inde-pendent of the presence or absence of left ventric-ular pathology, and of the nature of that pathology,but there is considerable variation both withrespect to the slope of the lines (representing thechange in the diastolic closure rate for a i mmHgchange in the filling pressure) and the constant ofthe equation even within the group of patientswith the same underlying disorder, namely coronaryartery disease. The relation between the diastolicclosure rate and the filling pressure seems, there-fore, to be determined by a change in left ven-tricular diastolic properties rather than by thenature of the disease causing the change.

In a normal heart only small changes in thefilling pressure are required to produce large varia-tions in the stroke volume and ventricular filling. Ifthe compliance of the left ventricle is impairedlarger changes in the pressure will be required tomaintain a similar change in the stroke volume andrate of filling. The relation between the fillingpressure and the diastolic closure rate follows thesame pattern, with a steep slope to the regressionline in the normal heart and lower levels in thepresence of disease causing impaired ventricularcompliance.

Evidence to suggest that the diastolic closure rateand filling pressure relation is determined in part bythe ventricular compliance is derived from the linearequation found to relate the slopes of the regressionlines with the diastolic AP/AV. Measurements ofthe compliance of the left ventricle are difficult toevaluate because of the non-linearity of the pressure/

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volume relation (Diamond et al., 197I). In anattempt to overcome this problem, measurements ofdiastolic AP/AV have been used as an index of leftventricular wall stiffness (Adolph, I965; Hood et al.,I970). However, it has been shown that AP/AV,which is an approximation for the instantaneousdP/dV, is affected by changes not only in the stiff-ness of the ventricular wall, but also, to a lesserextent, in its volume and contour (Diamond et al.,I971; Diamond and Forrester, I972). Further-more, there is some evidence to suggest that AP/AVmay also be dependent on the absolute level of thefilling pressure (Diamond and Forrester, I972). TheAP/AV is therefore not an acceptable measure-ment of left ventricular wall stiffness but remains auseful index of the mean pressure/volume relationand left ventricular diastolic properties. The linearrelation between the AP/AV and the slopes of thelines relating the diastolic closure rate to the fillingpressure therefore strongly supports the hypothesisthat the ventricular diastolic compliance is an im-portant determinant of the diastolic closure rateas it is also the major factor in determining leftventricular AP/AV.

Since the anterior cusp of the mitral valve arisesdirectly from the valve ring it has been assumed thatthe recorded movement of the cusp represents acomposite of the movement of the two structures(Zaky, Nasser, and Feigenbaum, I968). In systolethe apparent movement of the cusp into the leftventricle can be entirely explained on the basis ofring movement. It is known that movement of thering is in turn related to left ventricular function,and it has been used in the ultrasonic measurementof the stroke volume in conjunction with recordingsof the motion of the interventricular septum andthe left ventricular posterior wall (Feigenbaum,Zaky, and Nasser, I967). Studies have also shownthat the slow diastolic closure rate of the anteriorcusp in mitral stenosis is related to the diminishedamplitude of movement of the ring (Chakorn et al.,I972). The relation between the total amplitude of

movement of the mitral valve ring and the con-stants of the regression equations relating thediastolic closure rate to the filling pressure allowsfor an assessment of the contribution of the ringmovement to the closure rate.The determinants of the diastolic closure rate of

the mitral valve have been shown to include the leftventricular filling pressure and the diastolic pressure/volume relation of the left ventricle and thesefindings strongly support the hypothesis that thediastolic closure rate is a reflection of the rate of leftventricular filling. However, in view of the import-ance of the movement of the mitral valve ring as afurther deterniing factor, the interpretation of thediastolic closure rate as reflecting a particular fillingrate must be made with caution. While, for example,the rapid diastolic closure rate associated with aorticregurgitation may be very largely related to theincreased filling pressure and the absence of a sig-nificant reduction in the left ventricular compliance,the amplitude of the ring movement is also knownto be increased (Chakorn et al., 1972; Zaky, Grab-horn, and Feigenbaum, I967) (Table 4a). Beforethe change in the diastolic closure rate can beinterpreted as reflecting a change in the ventricularfilling rate, the component of the closure rate relatedto the ring movement must be excluded. Similarreservations in analysis apply with mitral regurgita-tion (Chakorn et al., I972; Zaky et al., I967) withthe additional problem relating to a possible ana-tomical abnormality of the valve cusp. Conversely,low levels of the diastolic closure rate may reflect aslow rate of filling due to abnormal ventricularcompliance, but impaired left ventricular systolicperformance causing diminished amplitude of ringmovement is also a factor (Table 4b). The absolutelevel of the diastolic closure rate is therefore not anindication of the state of the left ventricle. A normaldiastolic closure rate may be found even in thepresence of a reduction in compliance if the fillingpressure is sufficiently high or the contribution ofthe ring movement increased (Table 4c). If the

TABLE 4 Interrelation of left ventricular filling pressure, compliance, and amplitude of mitral ring movementin determining diastolic closure rate

Ring Diastolic closureFilling pressure Compliance amplitude rate

aJ High Normal Normal FastNormal Normal High Fast

rNormal Low Normal Slowb High Normal Low Slow

High Low Low Slowc High Low Normal Normal

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diastolic closure rate is to be used as an index ofventricular filling it is important that the level of thefilling pressure and amplitude of the ring movementbe specified. Nevertheless, in many situations raisedfilling pressure may be anticipated from physicalexamination and the chest radiograph (Short, i956).An inappropriately slow diastolic closure rate in thepresence of such signs is evidence of abnormalventricular compliance.

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Requests for reprints to Dr. Clive Layton, CardiacDepartment, The London Hospital, WhitechapelLondon Ei iBB.

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Diastolic closure rate of normalmitral valve' · Diastolic closure rate ofnormalmitralvalve Io69 formed by physical techniques using a paramagnetic oxygen analyser (Servomex) and