Kazuhiro Yamamoto, MD, Rick A. Nishimura, MD, John C. Burnett, Jr., MD, and Margaret M. Redfield, MD, Rochester, Minnesota

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1 Assessment f Left Ventricular nd-diastlic Pressure by Dppler chcardigraphy: Cntributin f Duratin f Pulmnary Venus versus Mitral Flw Velcity Curves at Atrial Cntractin Kazuhir Yamamt, MD, Rick A. Nishimura, MD, Jhn C. Burnett, Jr., MD, and Margaret M. Redfield, MD, Rchester, Minnesta The difference in the duratins f flw with atrial cntractin (A duratin) at the pulmnary veins and mitral valve has been reprted t detect the presence f elevated left ventricular end-diastlic pressure. It is pstulated that with left ventricular filling during atrial cntractin, reduced ventricular cmpliance results in the transmissin f increased pressure int the left atrium, resulting in prlngatin f the pulmnary venus flw with atrial cntractin. Hwever, the relatinship between ventricular cmpliance during atrial cntractin and the pulmnary venus and mitral A duratins and their difference have nt been carefully examined. We perfrmed recrdings f left ventricular pressure and cmplete Dppler analysis f pulmnary venus and transmitral flw in 87 patients" Operant ventricular cmpliance at atrial cntractin was estimated by measuring the increase in ventricular pressure with atrial cntractin (left ventricular a wave) and by using a cmpliance index, which incrprated an estimate f flw int the ventricle with atrial cntractin frm the Dppler transmitral a wave. The difference in pulmnary venus and mitral A duratins crrelated well with left ventricular end-diastlic pressure (r =.73, p <.1) and the pulmnary venus reversal duratin exceeding the duratin f the mitral A velcity curve prvided high sensitivity (82%) and specificity (92%) fr the detectin f an end-diastlic pressure f 2 mm Hg r greater. The pulmnary venus A duratin increased with a mderate decrease in ventricular cmpliance but was nt increased further in patients with a severe decrease in cmpliance. In cntrast, mitral A duratin was nt different in patients with mderate reductin in cmpliance, but was shrter in patients with severe decreases in ventricular cmpliance. Pulmnary venus and mitral A duratins are related t ventricular cmpliance and they change in an ppsite and prgressive manner. Their difference is a sensitive methd fr the detectin f the elevated end-diastlic pressure assciated with reductin in ventricular cmpliance. (J Am Sc chcardigr 1997;1:52-9.) Recent clinical studies ~,2 have shwn that the relative difference in the duratins f flw with atrial cntractin in the pulmnary veins (pulmnary venus A duratin) and acrss the mitral valve (mitral A duratin) as assessed by Dppler echcardigraphy crrelates with left ventricular end-diastlic pressure. This cncept was based n the demnstratin that the left atrial pressure wave with atrial cntractin Frm the Divisin f Cardivascular Diseases and Internal Medicine, May Clinic. Supprted in part by grants frm the Jseph P and Jeanne M Sullivan Fundatin, Chicag, Illinis, and by the May Fundatin, Rchester, Minnesta. Dr. Yamamt was supprted by the Fellwship f the Uehara Memrial Fundatin. Reprint requests: Margaret M. Redfield, MD, The Divisin f Cardivascular Diseases and Internal Medicine, May Clinic, 2 First St., SW, Rchester, MN Cpyright by the American Sciety f chcardigraphy /97 $ /1/ increased in magnitude and duratin as left ventricular diastlic pressures increased? Investigatrs have cncluded that the prlngatin f the left atrial pressure wave at atrial cntractin may be caused by increased wave reflectin frm a nncmpliant left ventricle, causing prlngatin f pulmnary venus A duratin? As perant ventricular cmpliance becmes impaired, a rapid rate f increase f the ventricular pressure ccurs during atrial cntractin (left ventricular a wave) and the left ventricular pressure exceeds the left atrial pressure earlier than nrmal? This may result in a rapid deceleratin and abbreviatin f transmitral flw with atrial cntractin. The relative changes between the pulmnary venus and mitral A duratins with prgressive abnrmalities f ventricular cmpliance have nt been investigated. Therefre, cmplete Dppler echcardigraphic assessment and left ventricular pressure tracings were btained in 87 patients with knwn r

2 Jurnal f the American Sciety f chcardigraphy Vlume 1 Number 1 Yamamt et al. 53 suspected cardiac disease wh were referred fr cardiac catheterizatin. Pulmnary venus and mitral A duratins and their differences were crrelated with left ventricular diastlic pressures and estimates f left ventricular cmpliance. MTHODS This prtcl was apprved by the May Clinic Institutinal Review Bard, and all patients prvided written infrmed cnsent. Study Ppulatin We studied 12 cnsecutive patients referred fr cardiac catheterizatin (64 men and 38 wmen). The age f the patients ranged frm 24 t 84 years (mean age 63 years). All patients had sinus rhythm withut mitral stensis r mre than mild mitral regurgitatin. chcardigraphy Transthracic echcardigraphic examinatins were cnducted with the subjects in the left lateral psitin and during quiet respiratin within 3 hurs befre the cardiac catheterizatin. All patients were in the fasting state, and medicatins were nt withheld befre the study. Bld pressure and heart rate were measured at the time f echcardigraphy. With the use f either a Hewlett-Packard (Andver, MA) r an Acusn (Muntain View, CA) echcardigraphic instrument, pulsed wave Dppler transmitral flw velcity curves were recrded with the sample vlume at the mitral tips. Pulmnary venus flw velcity curves were recrded with the sample vlume t 1 cm int the right superir pulmnary vein using the guidance f clr flw Dppler imaging with the transducer placed at the cardiac apex. 1,4-6 During pulsed wave Dppler examinatin, the filter settings were minimized. Dppler velcity curves were recrded at a hrizntal sweep speed f 1 mm/secnd. Cardiac Catheterizatin Thrugh the femral artery, a 7 F high-fidelity manmetertipped catheter (Millar Instruments; Hustn, TX) r a 6 F pigtail catheter cnnected with fluid-filled transducer was intrduced acrss the artic valve int the left ventricle just after access t the femral artery was gained. The highfidelity left ventricular pressure was zered and calibrated t the fluid-filled left ventricular pressure measured by the fluid-filled lumen f the catheter befre the recrding. 4 Left ventricular pressure was digitized at high speed acquisitin (5 ms intervals) nt an ff-line cmputer. Data Analysis chcardigraphic recrdings were analyzed with the cmmercial analysis sftware supplied with the system. The transmitral flw velcity curve was analyzed fr the mea- surement f the mitral A duratin, the time velcity integral and peak velcity f the mitral A velcity curve, and the peak velcity and the deceleratin time f early transmitral filling (mitral ) velcity curve. 4 The pulmnary venus flw velcity curve was digitized fr the measurement f the duratin f the pulmnary venus A flw. 1,2 When the entire pulmnary A flw velcity curve was nt recrded adequately, the pulmnary venus A duratin was assessed with the time interval between the cessatin f early diastlic flw and the start f frward systlic flw) Frm the left ventricular pressure tracing, we measured the left ventricular end-diastlic pressure, the increase in left ventricular pressure at atrial cntractin (left ventricular a wave), and left ventricular pre-a wave pressure (left ventricular pressure befre atrial cntractin). T further assess perant left ventricular cmpliance at atrial cntractin, a rati f the time-velcity integral fmitral A velcity curve t left ventricular a wave was calculated. 7 Averaged values f ver 3 cnsecutive beats were used fr statistical analysis. Statistical Analysis Values are expressed as mean -+ standard deviatin (SD). The statistical significance f the difference amng the data f grups was tested with an analysis f variance (ANOVA) and Scheffe's F test. Regressin analysis was perfrmed t cmpare tw variables. Results were cnsidered significant at a prbability value f less than.5. All calculatins were perfrmed with the StatView II (Abacus Inc., Berkeley, CA) statistical prgram. ~S~TS Patient Characteristics In 14 f the 12 patients (14%), adequate Dppler recrdings were nt btained, and in 1 patient, the systlic bld pressure had changed significantly (by mre than 5 mm Hg) at cardiac catheterizatin cmpared with the echcardigraphic recrding. Thus the ther 87 patients were included in this study (55 men and 32 wmen, mean age was 63 years). High-fidelity left ventricular pressure was recrded in 9 6 patients, and the fluid-filled left ventricular pressure was recrded in the ther 27 patients. In the 87 patients, the mean differences between systlic arterial pressures, diastlic arterial pressures, r heart rates at echcardigraphy and at catheterizatin were mm Hg, mm Hg, and 1 6 beats per minute, respectively. Of the 87 patients, 55 patients had crnary artery disease (mean number f vessels with mre than 7% stensis = 1.9), 2 had artic stensis, 5 had hypertrphic cardimypathy, 9 had dilated cardimypathy, and 16 had a chest pain syndrme with angigraphically nrmal epicardial crnary arteries.

3 Jurnal f the American Sciety f chcardigraphy 54 Yamamt et al. January-February 1997 A 1-5- ~ r =.73 p<.1 9 I I I ab 2b 3b DP (mmhg) Figure 1 Crrelatin between the difference in pulmnary venus and mitral A duratins (Ad) and left ventricular end-diastlic pressure (DP) in all the subjects. The hrizntal dtted line indicates that the difference in pulmnary venus and mitral A duratins is equal t ms, the vertical dtted line indicates that left ventricular end-diastlic pressure is equal t 2 mm Hg, and the slid line is a regressin line. Relatin f Pulmnary Venus and Mitral A Duratins t Left Ventricular Diastlic Pressures The difference in pulmnary venus and mitral A duratins (pulmnary venus A duratin minus mitral A duratin) crrelated with left ventricular end-diastlic pressure (r =.73, p <.1, Figure l X). The difference in the duratins f ms r greater predicted a left ventricular end-diastlic pressure f 2 mm Hg r greater with a sensitivity f 82%, a specificity f 92%, a psitive predictive value f 82%, and a negative predictive value f 92%. The sensitivity f this index fr predicting a left ventricular end-diastlic pressure f 2 mm Hg r greater exceeded that f traditinal transmitral Dppler parameters such as a shrtened deceleratin time f the mitral velcity curve (sensitivity f deceleratin time 15 ms r less fr detecting left ventricular end-diastlic pressure 2 mm Hg r greater = 33%) and an increased rati f peak mitral velcity t peak mitral A velcity (/A) (sensitivity f an /A rati 2. r greater fr detecting left ventricular end-diastlic pressure 2 mm Hg r greater = 39%). Pulmnary venus A duratin and mitral A duratin als crrelated with left ventricular end-diastlic pressure (r =.58, 9 r = -.32, p <.1, respectively) but the crrelatin was nt as strng. ffects f Operant Ventricular Cmpliance at Atrial Cntractin n Ptdmnary Venus and Mitral A Duratins Pulmnary venus and mitral A duratins and their difference were cmpared with the magnitude f the left ventricular a wave (Figure 2). The patients were assigned t three grups by the magnitude f the left ventricular a wave (grup I = patients with a left ventricular a wave less than 5 mm Hg; grup II = patients with a left ventricular a wave f 5 mm Hg r greater and 1 mm Hg r lwer; grup III = patients with a left ventricular a wave f mre than 1 mm Hg). The pulmnary venus A duratin was lnger in grups II and III than in grup I, but there was n significant difference between grups II and III, which indicated that the pulmnary venus A duratin was prlnged with a mderate increase in the left ventricular a wave but remaincd stable as the left ventricular a wave increased further. In cntrast, mitral A duratin was nt different between grups I and II. Hwever, the mitral A duratin was shrter in grup III, which indicated that mitral A duratin was unchanged with a mderate increase in the left ventricular a wave but was shrtened with marked increases in the left ventricular a wave. As a result, the difference in the duratins was the largest in grup III and the smallest in grup I. xamples f representative patients in each f the three grups are prvided in Figures 3 A t C. T further assess the effects f perant left ventricular cmpliance at atrial cntractin, the relatinships between pulmnary venus A duratin, mitral A duratin, r the difference in the duratins and a rati f the time-velcity integral f mitral A velcity curve t left ventricular a wave were examined at three different levels f cmpliance assessed in this manner (Figure 4). The grup f patients with mderate decreases in cmpliance (with a rati f greater than r equal t 1 but less than 2.6) had prlngatin f the pulmnary venus A duratin but n change in mitral A duratin when cmpared with the grup with the highest ventricular cmpliance (the rati mre than 2.5). Cmpared with the grup with mderate decreases in ventricular cmpliance, pulmnary venus A duratin was nt increased further but mitral A duratin was decreased in the grup with severe reductins in ventricular cmpliance (the rati less than 1.). The difference in pulmnary venus and mitral A duratins increased prgressively, with

4 Jurnal f the American Sciety f chcardigraphy Vlume 1 Number 1 Yamamt et al. 55 decreasing cmpliance being significantly greater in each grup. ffects f Prelad fr Atrial Cntractin n Pulmnary Venus and Mitral A Duratins Pulmnary venus and mitral A duratins and their difference were cmpared with left ventricular pre-a wave pressure (Figure 5). These three indices were nt significantly different between the patients with left ventricular pre-a wave pressure f less than 1 mm Hg and frm 1 t 15 mm Hg. Only in patients with markedly elevated pre-a wave pressure (pre-a wave pressure greater than 15 mm Hg), was the difference in the duratins prlnged, with prlngatin f pulmnary venus A duratin and shrtening f mitral A duratin. The left ventricular a wave was significantly increased nly in the patients with markedly elevated pre-a wave pressure as cmpared with the ther patient grups. DISCUSSION In the current study, the difference in pulmnary venus and mitral A duratins crrelated with left ventricular end-diastlic pressure and the increase in left ventricular pressure at atrial cntractin (left ventricular a wave). This index was sensitive and specific fr the detectin f elevated left ventricular enddiastlic pressure in patients in whm a transthracic apprach (84%) was pssible. The pulmnary venus A duratin was prlnged, with mderate decreases in cmpliance, but did nt increase further in the presence f severe decreases in ventricular cmpliance as estimated by pressure and cmbined pressure and flw measurements. In cntrast, the mitral A duratin was unchanged in the presence f mderate decreases in ventricular cmpliance but decreased in the presence f severely reduced cmpliance. The findings f the current study cnfirm previus studies that examined the accuracy and feasibility f transthracic evaluatin f the transmitral and pulmnary venus flw velcity curves t assess ventricular diastlic pressures. These data extend the previus findings by ffering insight int the mechanisms whereby the degree f difference in pulmnary venus and mitral A duratins crrespnds with increasing left ventricular end-diastlic pressure. Rssvll and Hatle 1 shwed that the mitral A duratin was decreased in patients with the highest left ventricular pre-a wave pressure, but did nt shw prgressive increases in the pulmnary venus A duratin with increasing pre-a wave pressure. When analyzed accrding t different levels f cmpliance as estimated v. "ID W e- C O 1 D. <5 (grup I) e-. "ID m <5 (grup I) 1 I,~f fy'l 5-1 >1 (grup II) (grup III) LVa (mmhg) 5-1 >1 (grup II) (grup III) l.va (mmhg) i <5 (grupl) 5-1 (grupll) >1 (grup III) LVa (mmhg) Figure 2 Bar charts shw the mean (+ SD) f pulmnary venus A duratin, mitral A duratin, r the difference in the duratins (Ad) in patients with an increase in left ventricular pressure at atrial cntractin (left ventricular a wave, LVa) f<5 mm Hg (grup I), frm 5 t 1 mm Hg (grup II) and >1 mm Hg (grup III). **p<.1 versus Lva <5 mm Hg; tp<.5; tl'p <.1 versus LVa frm 5 t 1 mm Hg.

5 Jurnal f the American Sciety f chcardigraphy 56 Yamamt et al. January-February 1997 Lv.\# #. ~..,, ,..... L!+... B Figure 3 Recrdings f left ventricular pressure (left), pulmnary venus flw velcity curve (right upper) and transmitral flw velcity curve (rightlwer) in three patients (panel A = grup I, panel B = grup II, panel C = grup III). In A, left ventricular end-diastlic pressure (DP) is nt elevated with left ventricular a wave (LVa) f<5 mm Hg. In this case, pulmnary venus A duratin was shrter than mitral A duratin. In B, left ventricular end diastlic pressure is elevated with the prlngatin f pulmnary venus A duratin. In C, left ventricular enddiastlic pressure is mre elevated; hwever, pulmnary venus A duratin is nt lnger and mitral A duratin is shrter than in B. The left ventricular a wave was 6 mm Hg in B and 15 mm Hg in C. The left ventricular pressure recrding f panel C shws a simultaneus recrding f high-fidelity and fluid-filled left ventricular pressure tracings and demnstrates that there is n significant difference in determining left ventricular diastlic pressures between these recrdings. (A, mitral A velcity curve; D, diastlic pulmnary venus velcity curve;, mitral velcity curve; CG, electrcardigram; Pre-a, left ventricular pre-a wave pressure; pulmnary venusa, pulmnary venus A velcity curve; S, systlic pulmnary venus velcity curve.) by the left ventricular a wave, the previus study demnstrated that the pulmnary venus A duratin increased prgressively with an increasing left ventricular a wave but did nt bserve a significant decrease in the mitral A duratin in such patients. In the current study with a larger number f patients and mre varied cardiac diseases, changes in determinants f the difference in pulmnary venus and mitral A duratins were examined and insight was gained int the mechanism whereby this index prvides a better crrelatin with left ventricular end- diastlic pressure. As bth cmpnents that determine the difference in the duratins change in an ppsite and prgressive but nnsimultaneus manner, the magnitude f difference is linearly accentuated as ventricular cmpliance decreases and ventricular end-diastlic pressure increases. The nnlinear crrelatin f pulmnary venus and mitral A duratins t indices f ventricular cmpliance and their weaker crrelatin with left ventricular end-diastlic pressure demnstrate that either index alne is a pr substitute fr their difference and that bth shuld be

6 Jurnal f the American Sciety f chcardigraphy Vlume 1 Number 1 Yamamt et al. 57 measured when attempting t assess left ventricular end-diastlic pressure. The current findings are cnsistent with hemdynamic measurements demnstrating prlngatin f the left atrial a wave as the ventricular cmpliance decreases and ventricular diastlic pressures increase. 3 Althugh the previus study did nt measure the perid in which the left atrial pressure exceeded the left ventricular pressure, it appeared that this perid, the determinant fmitral A duratin, was decreased in the presence f marked increases in left ventricular pressure with atrial cntractin. Left ventricular pre-a wave pressure can be used t estimate the prelad fr left atrial cntractin, much as the mean left atrial and pulmnary capillary wedge pressures are used. 8,9 In the current study, a mild r mderate elevatin f the left ventricular pre-a wave pressure was nt assciated with prlngatin f the difference in pulmnary venus and mitral A duratins and the difference in the duratins was prlnged nly in patients with markedly increased pre-a wave pressure. These results are cmpatible with the previusly btained results) The current study further extends these findings by demnstrating that nly the patient grup with markedly increased left ventricular pre-a wave pressure and the prlnged difference in the duratins had a large left ventricular a wave. The left ventricular a wave was nt increased in the ther patient grups, even with mderate elevatin f the pre-a wave pressure (Figure 5). These findings suggest that left ventricular cmpliance r left ventricular late diastlic pressure plays an imprtant rle in determining the difference in the duratins rather than exclusively the level f prelad fr atrial cntractin r mean left atrial pressure. Whereas ventricular cmpliance affects the left atrial pressure wave frm at atrial cntractin, atrial cmpliance and atrial systlic functin als affect the atrial pressure wave frm and the duratin f transmitral and pulmnary venus flw with atrial cntractin. Changes in these factrs may cntribute t the pattern f changes seen with the largest decreases in ventricular cmpliance where pulmnary venus A duratin des nt increase further despite decreases in ventricular cmpliance. Study Limitatins In this study, the left vemadcular vlume was nt measured, and thus left ventricular cmpliance culd nt bc calculated dirccfly. As described abvc, left ventricular a wave is affected by bth lcft ventricular cmpliance and left ventricular filling vlume at atrial cntractin. Thcrcfre, we calculated a rati f the time-velcity ~" 2 t- O m 15- qd loo- e.- Q,) > " 5- C " O,. O.m "ID,< m qd < T > <1. TVI-A/LVa (cm/mmhg) > <1. "FVI-A/LVa (cm/mmhg) > <1. "FVI-A]LVa (cm/mmhg) Figure 4 Bar charts shw that mean (+SD) f pulmnary venus A duratin, mitral A duratin, r the difference in the duratins (Ad) in patients with the rati f the time-velcity integral f mitral A velcity curve t left ventricular a wave (TVI-A/LVa) f>2.5 (with the highest left ventricular cmpliance), frm 1 t 2.5 (with mderately decreased left ventricular cmpliance) and <1. cm/mm Hg (with severely decreased left ventricular cmpliance). *p <.5 and **p <.1 versus TVI-A/LVa >2.5 cm/mm Hg; ttp <.1 versus TVI-A/LVa f cm/mm Hg.

7 I Jurnal f the American Sciety f chcardigraphy 58 Yamamt et al. January February 1997 ""r 2 (-,m 4-1 L_ 15- A 2 15 'ID < (n t- > m t- m a. 1-5-, T < >15 LV pre-a wave pressure (mmhg),m I,. '1 <,m 1 5 < >15 LV pre-a wave pressure (mmhg) lttt tt A --, " -25 A ) "I- "-'5 --I. < >15 LV pre-a wave pressure (mmhg) < >15 LV pre-a wave pressure (mmhg) Figure 5 Bar charts shw that mean (_+SD) f pulmnary venus A duratin, mitral A duratin, the difference in the duratins (Ad), r left ventricular a wave (LVa) in patients with left ventricular (LV) pre-a wave pressure f <1, frm 1 t 15, and >15 mm Hg. **p <.1 versus LV pre-a wave pressure <1 mm Hg; t~fp <.1 versus LV pre-a wave pressure f 1~15 mm Hg. integral f mitral A vclcity curve t left ventricular a wave t minimize the effects f varius filling vlumes amng patients. Because this rati is nt equal t left ventricular cmpliance, we assessed the relatin between Dppler indices and left ventricular cmpliance qualitatively. In additin, the results were similar even if either left ventricular a wave r this rati was used as an index f perant cmpliance. Thus althugh the direct determinatin fventricular vlumes t determine perant cmpliance wuld mre firmly establish ur cn- clusins, the use f the left ventricular a wave and this rati prvides a reasnable estimate f perant cmpliance. Left ventricular pressure was recrded with either high-fidelity manmeter-tipped catheters r fluidfilled catheters. We cnfirmed, hwever, that such a methdlgic difference prduced nly small differences in measured left ventricular diastlic pressure when the left ventricular pressure was measured by a high-fidelity manmeter-tipped catheter as cm-

8 Jurnal f the American Sciety f chcardigraphy Vlume 1 Number 1 Yamamt et al. 59 pared with fluid-filled left ventricular pressure tracings (Figure 3C). Dppler echcardigraphy was nt recrded simultaneusly with left ventricular pressure. Hwever, we cnfirmed that systlic and diastlic arterial pressures and the heart rate did nt significantly change at catheterizatin cmpared with echcardigraphic recrding in the 87 patients whse data were used fr analysis. These patients were underging elective utpatient angigraphy and nne had unstable r rest angina r experienced angina attack befre r during the prcedure n the examinatin day. We cnfirmed that nne had clinically significant arrhythmias, such as frequent atrial r ventricular premature cntractins, at echcardigraphic recrding and catheterizatin. Furthermre, the left ventricular pressure was recrded as the first prcedure befre crnary angigraphy and left ventriculgraphy. In additin, we recrded pulsed wave Dppler transmitral flw velcity curves at catheterizatin in 2 patients. The abslute value f the difference in peak mitral A velcity was 5.7 cm/s (SD = 5.2 cm/s), and the abslute value f the difference in mitral A duratin was 6.3 ms (SD = 4.2 ms). Thus, nnsimultaneus measurement shuld nt significantly affect ur cnclusins. Cnclusins The difference in pulmnary venus and mitral A duratins as assessed by transthracic pulsed wave Dppler echcardigraphy crrelates with left ventricular end-diastlic pressure. The determinants f this new index are clsely related t the perant left ventricular cmpliance at atrial cntractin. A prlngatin f the difference in the duratins with an increase in left ventricular end-diastlic pressure is caused by a prlngatin f pulmnary venus A duratin with mderate decreases in perant left ventricular cmpliance and by a shrtening f mitral A duratin with severe decreases in perant cmpliance. These indices change in an ppsite and prgressive but nnsimultaneus manner as ventricular cmpliance decreases, and their difference crrelates clsely with increases in left ventricular end-diastlic pressure. RFRNCS 1. Rssvll O, Hatle LK. Pulmnary venus flw velcities recrded by transthracic Dppler ultrasund: relatin t left vcntricular diastlic pressures. J Am Cil Cardil 1993;21: Appletn CP, Gallway JM, Gnzalez MS, Gaballa M, Basnight MA. stimatin f left ventricular filling pressures using tw-dimensinal and Dppler echcardigraphy in adult patients with cardiac disease. Additinal value f analyzing left atrial size, left atrial ejectin fractin and the difference in duratin f pulmnary venus and mitral flw velcity at atrial cntractin. J Am Cil Cardil 1993;22: Matsuda Y, Tma Y, Matsuzaki M, et al. Change f left atrial systlic pressure wavefrm in relatin t left ventricular enddiastlic pressure. Circulatin 199;82: Nishimura RA, Schwartz RS, Hlmes DR, Jr, Tajik A]. Failure f calcium channel blckers t imprve ventricular relaxatin in humans. J Am Cil Cardil 1993;21: Masuyama T, Lee JM, Nagan R, et al. Dppler echcardigraphic pulmnary venus flw-velcity pattern fr assessment f the hemdynamic prfile in acute cngestive heart failure. Am Heart J 1995;129: Yamamt K, Masuyama T, Tanuchi J, et al. Intraventricular dispersin f early diastlic filling: a new marker f left ventricular diastlic dysfunctin. Am Heart J 1995;129: Bristw JD, Van Zee B, Judkins MP. Systlic and diastlic abnrmalities f the left ventricle in crnary artery disease: studies in patients with little r n enlargement fventricular vlume. Circulatin 197;42: Braunwald, Brckenbrugh C, Frahm CJ, Rss J. Left atrial and left ventricular pressures in subjects withut cardivascular disease. Circulatin 1961;24: Rahimtla SH, hsani A, Sinn MZ, Leb HS, Rsen KM, Gunnar RM. Left atrial transprt functin in mycardial infarctin: imprtance f its bster pump functin. Am J Med 1975;59: