~SovQlumet~~ relaxatiQn time( tiontime (I ,2) have shown a ic variables that has been independent of the left ejection fraction and the underlying disease owever, because mitral flow velocity variables are ~~~~~eneed by age (91, loading cand other factrrrs (123,cautian has been urge these results to indivi atrial pressure and the even ; revised mimscript tewivedduly 2, ChristopherP. Appleton, Section of
stration MedicalCenter,Tucson.
Ati-
ventricular diastolic f~r~~ti~~,puimc ity has been analyzed with mitral flow velocity (16-18). In patients undergojug cardiac surgery or catheterization, the systolic fraction of pulmonary venous flow (17,181,or peak
patients l”CfWTd fobs rization who met the inclusion criteria were s, mitral stenosis or more ahmts with arrhyt re excluded because of a mitral regurgitatio possible effect on flow velocities or left atrial size and function that was independent of left ventricular diastolic function. ds. fkQ@nty COiMWtiQe
expirahm apnea. Left
atrial volumes were assessed u!;ing standard orthogonal apical tws- and four-chamber views (18,25). Mitral flow velocity was obtair ed from an apical window with pulsed wave technique 54, pkxing a 3-mm
9. LeR ventricular (EV) pressurerecordingfrom 8 high fidelity micmnanomcter-tipped catheter illustmtingthe MI venttic-
veinat
ular prmun just before mid eontmctior @m-A), left ventricular end-diastolicpmwurt: EXIPI en8 the absolute pressureimwso in tlwlw: wntricl~ that occamd w I muit d Wt atrid ~~nt~~ti~u In
ve~t~~~~~ ~~1~~~ ssure su
ukr pressuresmeasuredin this study.Theseinch&d left ventric-
with no an unpa was ma test. Simple linear md stepwise mu~t~~i~e~r regression was ~~0~~ for the four left ventricular filling pressures to determine the importance of each ec~~ardio~~ph~c variable for each fihing pressure aud to aerate mu~t~v~~ate (29). A p ~~u~t~~~~ to pwdisD theindividual filli pacssures value S: 0.05 was conside~d significant. vatid Miag press
left at&d volumes and CjectiQn fractions
WEI%
calculated in
us ilow in systok was biphosic All patients were men, with an average age years. Sixty-seven patients had coronary artery disease (average number of diseased vessels 1.7 I 1.0). and five patients had aortic stenosis, three of whom did mot have
arplkvu~abk.v. AR phasic prcssu 3 consecutive beats. dewed tolic pressure as well as the left
ues are expressed as mean MDP inc.) for a personal een mean values in each I&
c v~~~~~e~. AL1 patients had normal sinus e average he‘artrate was 69.9 + 10.4 beatslmio. ular ejection fraction was 54.5 9 six patiems left atria1 pressure was measured directly. Right heart pressures were obtained in all patients, but left ventricular pressure was not recorded in five patients either because of dlculty in crossing the aortic valve or for clinical reasons, Table 1 shows hemodynamic and echocardiographic data for each left ventricular filling pressure variable comparing patient subgroups with normal and increased pressures.
us A wave velocity
PWP
cl2mm Hg (I3 = 56)
LV Pre-A Wave
in
LVEDP
A2 mm Hg (a = 14)
EIAratio Mdt (ms) LV IVRT Ims) AFF (%) PVsipVd PVs/PVdVTI PV fx (%) sys
0.83 + 0.22 134* 0.w 228.6 f 36.1 170.9 + 42.P 110.1+ t9.5 41.2 + 7.9 1.46z!E 0.37 1.80+ 0.60 62.5 + 8.4
81.7 f 2O.Y 23.2 r 7.8* 0.81 + 0.4F 0.84 + 0.47* 42.7 f 12.6*
41.7 f 1.9 1.51?z0.35 I.88 2 0.56 64.0 !I 6.9
23.1 + 7.8* 0.79 2 0.4F 0.80 2 0.4@ 41.8 f 12.2*
42.4 f: 8.2 1.55” 0.34 1.91i: 0.57 64.4 1: 6.6
PVa (cm/s) PVa VT1 (cm*) A dur (ms)
30.6 2 6.1 3.1 f 0.9 IX1 + 19.2
3L.3I 1O.F 43.2 * 1.0 1.09f O.&J@ 1.58c 0.38 t.31 f 0.70* 11.93 ‘- o&Q 52.6 + 14.4@ 64.6 + 6.7
33.0 z 10.5 3.7 * 1.9
32.3 %9.9* 8.84r 0.45* 1.399 0.X9* 54.3 * I3.B’
30.4 2 5.6 3.1 + 0.9
30.7 -c 10.3 3.4 t 1.9
30.3 2 5.4 3.t i 1.0
31.0 4 7.9 3.2 + 1.2
381.1z 5.4 3.119 I.0
31.1 * 7-s 3.2 T 1.E
132.2?: 33.6 4.1 z 33.3
111.3” 32.8 180.4” 35.3’ 69.1 Z!C 23.8’
IM.l + 18.8 131.1f 35.2 I.0 f 32.2
110.22 31.1 177.9r 35.4* 67.1 r 24.9*
631.44 18.9 122.6?: 35.5 -8.85 zk35.3
131.39 18.4 114.42 20.3 -16.8 2 21.2
LX! 1 232
Wa dur (ms) PVa-Adur (ms!
,?-ez?-Ys
*p < 0.05 comparedwith the normal (tower)press~ swbgmupfor that left veWicht’ filling p~e%%WevRhble. V&M at% WQanKahn *” 1 SD, A dur e3 Wfbn a ue)to ps? durationof mitral flowat &a9 contraction;AFF = atriaIfillingfraction;EIAratio = ratioofpeakmitralflowv&city at at&d CBnf rl”vcrseplrl flow velocity inearly diastole (E wave); LV IVRT = left ventricular isovolumetricrelaxationtime;Mdt = milti dcc&mtion time;BVam venousHOW velocity at atriai contract.ction; PVadur = durationofreverse flowin the ~II~~NXI~S+Y veh~ at atria!contractioo;PVds Ped ~~~mofl~Y vem.~ d&& flowvelocity; pV5 = peak sy5~0~ puhnonarqrvenous flow velocily; PV sgs fx = fraction of total pulmonary venoM anterogradeflow that occura io sY$tok VT1= velocity time integral. Other abbreviationsas in Table 1.
4
.J---
_..- __-...-_ .I’
‘_,_,b?__
left ventaicula~ pm4 wave, A waveand end-diastolic pres-
In conlrast, hat is&IMS
tieatshowsa pul newsA Ihantk mitralA tin. hn thisgatied,kit ventricular ~ITC-A wavepressuaeisah nod, butleft ventricularen&diastolic pressuwis elevatedbecauseof an abnotmd incnase(9mmHglin leftventhular pressureatatrialcontraction(LV A-wave).Otherabbreviations as in Figure2. ps, althoughthe pulmonary venous A wave dikeace in mitral and pulmonary venous A wave were increased with higher lefi ventricular filling
pressures. Miti and pulmonary venous flow velocities with left ventricular pressure recordings are shown for two of the study patients in Figure 3.
itral valve disease.
8,. This was
assess%
pressure was most strongly related to mitral WA wave vekxity ratio (r = 0.72), left atria1 minimal volume (r = 0.70), left atrial ejection f~ac%~o~ (r = -O.SB), atria! -0.66) and the systolic frackn of pulmonary = -0.64) (Table 3). Left ventricular pre-A to the same variables. Left wave pressure rel olic ssure shovxd a strong relation to the difference in pulmonary venous and mitral A wave duration (r = 0.77), mitral E/A ratio (r = 0.73), the systolic fraction of pulmonary venous flow (r = -0.70) and left atrial ejection fraction (f = -0.70). The left ventricu%arA wave
monary vemms systolic
APPLETON ET AL. DWK’LER VELOCITIES
JACC Vol. 22, No. 7 Idecemhe: ?W: I!47242
AND HEMODYNAMICS
1.A min
(emag)
younger This age subjects who do not have elevated pressures dewndence limits the clioica9usefulness af r&a9 and puC monary venous flow velocity variabks in predicting Ieft ventricular filling pressures in these groups 993,21). ~w9~~~aryvenousand nnltrai A wave durak, which has ou9yrzcentfy been described (221, showed a strong ~~latiura(r = 0.77) with both left ven~~~9ar and-diastolic and 9eFtventricu9arA wave pressures. By multilinearregrersion analysis it was also tbe most rtant determinant of both of these pressures. Previous studies had been unable to identify a Dogpier variable that correlates with an abnormal increase in left ventricular pressure at atria9contraction (2). In patients with impaired left ventricular relaxation and reduced mitra9 E/A wave ratio, separation of ptients with and without elevated pressystolic fractions are expected findings in no
internand systo9iefraction showed some of the strongest pressures (Table 3). these re9ationswould patients with cardiac ntainiw n few normal venous flow velocity ent on qe (9,19,20) and load (IOinfkmccd by hemdynamically sigtation (21,30) or stenosis (39). Increased E/A wave ratios and smaUe: p&mmy venous
I
re 5. A, Scatterplot of the relation between left ventricular
diastoliicpressure (LVEDP) aad the difference in pulmonary venous A wave duration (IV,-A deration), plut of the relation between left ventricular pressure increase at atrial contraction (LV A-wave) and the difference in mitral and pulmonaryvenous A wave duration,
sures may hera!d the early stages of t
ira~§~t~~m to a alore
ow veiocity pattern at is referred to as on” (2,4-6$,21). Conversely, in normal” mitral filling patterns, an mrence in pulmonary crease in left atria1size or wolald increase the venous to mitral A wave certainty that abnormalities of left ventricular diastolic prqerties and filling pressures were present. The hemodynamic correlate for shortening of the mitral A wave duration with increased fillingpressures was shown by
JACC Vol. 22, No. 4 December W93:1972-82
I. The present study did not fi ween left v~nt~~u~~ isovokmetrk relaxation time ad left ventricular filling pressures (r = -0.50~, and this variable was a minor component in muhivtiate equations predicting pressures. The differem~esamong studies are most patient population, with each study group nd disease prevdence. es using both trmsthomic (I&22) and trans9) techniques have studied pulmonary ve~~d~~~rn~~variables in adults with cardiac ts ~~d~rgoi~~cardiac surgery, Kuercherer et alal.(19) found that the systolic fraction of ~~~rno~a~y venous flow was strongly related to mean left atrial pressure (r = -0.88), whereas Mishimura et al. (16) found that ~u~rn~~~ wedge pressure correlated best with peak flow velocity reversal in the puhnonarjl vein at atdd contraction Ir = 0.81). Significant correlations between the systolic &action of pulmonary venous flow and left ventricular pre-A wave (r = -0.70) (22)and pulmonary wedge (r = -0.47) (;8) pressures have also bean wpxted iti @eui.s undergokg
patterms to left ventriwlar diastolic bined hemodynamieand llopplsr e Cardioll9$$;~2:~26-~0.
3, Ratdi
rasek
of
AA Left ventricular diastolic function:~~rnparis~R pulsed
5, Klein AL, Hatle LK, Taliercio CP, et al. Serial hippier cch~ardiographicfdow-up of left ventriculardiastolicfu~~t~~~in cardiacamylaid6. Vanoverschelde
ventricular filling pressures8 studies (16). As previously
wed
in tra~ses~p~agea1
not l$,2~,2~)~ themain ~SAP
nical proMems were limitation ample volume depth and wall motion artifact associated with normal-sized p~~~~~~~ry hnitations, the redies (I]~-43,22)suggcestthat
functio 5.
V~~~~~~~~ and hem-
termination of left veatricular 7. Kuechererw, Ru filling parametersby pulsed Dopplerechocardi phy: a noninvasive methodto predictfiighfilliq pressures in patients with esrOnW WteV disease.Am Heart J 1988;116:11017-21. 8. cular end-diastolicpressurefrom v&city in cardiac patients ~~de~e~d~~t of systolic ColitCardiol MWO: I12--9. 9. Van DamI, Fast J, de Boo‘I’,et al. rmaldiastolic 10,
heart disease, a low mitra1 E/A wave velocity ratio 62,48,17,18), n-&al A wave width that exceeds pulmonary venous A wave width (22), high pulmonary venous systolic fraction (173) and left atrid size and function that are
Cosyns
11,
JLk Pbysicd basis for the mitral flow velocitycurvein assessing
cadM ventricular diastok function.Echocardiography MM,Lab MM.In searchof the holy grail:the
23. MatswlaY,
Qf Jellatrial systohc