Transesophageal Pulsed Doppler Echocardiographic

Clin. Cardiol. 20,47-54 (1997)

Transesophageal Pulsed Doppler Echocardiographic Evaluation of Left Atrial Systolic Performance in Hypertrophic Cardiomyopathy: Combined Analysis of Transmitral and Pulmonary Venous Flow Velocities

TAKASHIOM, M.D., ARATAIUCHI, M.D., TOMOTSUGUTABATA, M.D., HIROTSUGUYAMADA, M.D., WUYO MANME, M.D., YOSHIMI KAGEJI, M.D., MLHO hE,M.D., NOBUOFUKUDA, M.D.,* SUSUMU ITO, M.D. The Second Department of Internal Medicine, Tokushima University School of Medicine, Tokushima; *Institute for Clinical Research, Zentsuji National Hospital, Zentsuji, Kagawa, Japan

Summary Results: Left atrial dimension in Group B was significantly greater than that in the other HC groups and the control group. Background: Hypertrophic cardiomyopathy (HC) is char- Furthermore, left atrial volume changes during atrial systole acterized by impaired left ventricular (LV) diastolic function in Group B were significantly smaller than those in the other due to an increase in LV wall thickness. The severity of this HC groups and the control group. Peak atrial systolic PVF ve- disease varies depending on the localization and extent of the locity in Group B was significantlyhigher than that in the con- hypertrophied myocardium and the presence and extent of trol group and in Group C. The duration of the atrial systolic myocardial disarray or fibrosis. waves of the TMF and PVF in Group B was significantly Hypothesis: The purpose of this study was to examine the shorter and longer, respectively, than that in Group A. Left background of hemodynamic abnormalities between the left ventricular end-diastolicpressure (LVEDP) decreased in de- atrium and the left ventricle during atrial systole in patients scendmg order with Group B > Group C > Group A. In all pa- with HC using pulsed Doppler echocardiography. tients there was a significantpositive correlation between the Methods: Hemodynamic abnormalities between the left LVEDP and peak atrial systolic PVF velocity or the difference atrium and left ventricle during atrial systole were evaluated in in duration between the atrial systolic waves of PVF and patients with HC using transmitral flow (TMF) and pulmon- Th4F. Plots of these values shifted toward the left and inferior- ary venous flow (PVF) velocities obtained by transesophageal ly in Group A, and toward the right and superiorly in Group B. pulsed Doppler echocardiography. The study population in- Conclusion: Peak velocity and duration of TMF and PVF cluded 50 patients with HC, including 39 with asymmetric during atrial systole by transesophageal pulsed Doppler echo- septal hypertrophy and 11 with apical hypertrophy, and show- cardiography are useful indices of hemodynamic abnormali- ing fractional shortening of the left ventricle 230%. They ties between the left atrium and the left ventricle during atrial were classified into three groups: (1) Group A (n = 11):the ra- systole, particularly a forceful atrial contraction mismatched tio of the late to early TMF velocity < 1, and peak atrial sys- to the left atrial afterload and seventy of LV diastolic dys- tolic PVF velocity (PVA) c 25 mm/s; (2) Group B (n = 13): function, in HC. their ratio < 1, and PVA 2 25 mm/s; and (3) Group C (n = 26): their ratio 2 1. The mean age of patients in Group A was lower than that in Groups B and C. Key words: left atrial systolic performance, hypertrophic cardiomyopathy, cpansmitral flow, pulmonary venous flow, transesophageal pulsed Doppler echocardiography

Address for reprints: Introduction Takashi Oki, M.D. The Second Department of Internal Medicine Hypertrophiccardiomyopathy (HC) is characterizedby im- Tokushima University School of Medicine paired left ventricular (LV) diastolic function due to an in- 2-50 Kuramoto-cho crease in LV wall The severity of this disease Tokushima 770, Japan varies depending on the localization and extent of the hyper- Received: May 6,1996 trophied myocardium and the presence and extent of myocar- Accepted with revision: August 13, 1996 dial disarray or fibrosis?. 14-17 With the recent development of 48 Clin. Cardiol. Vol. 20, January 1997 transthoracicand transesophagealpulsed Doppler echocardie The transesophageal transducer was manipulated to obtain graphy, transmitral flow (TMF) and pulmonary venous flow a long-axis view of the left ventricle, placing the sample vol- (PVF) velocities now can be clearly recorded, and several ume at the tip of mitral valve leaflets to record the highest ve- studies have been published OII LV diastolic dysfunction using locity of TMF. The probe was then slightly withdrawn and these non- and semi-invasive method^.'^-^^ turned to the left to obtain a clear view of the left upper pul- The purpose of this study was to examine the background monary vein as it emptied into the left atrium. A sample vol- of hemodynamic abnormalities between the left atrium and ume then was placed 1-2 cm into the pulmonary vein. Color the left ventricle during atrial systole, particularly left atrial af- flow imaging was used to obtain a beam direction as parallel terload mismatch and severity of LV diastolic dysfunction, in as possible to venous flow. Flow velocities were recorded on patients with HC using TMF and PVF velocities obtained by a strip-chart recorder at a speed of 50 and/or 100 mdswith transesophageal pulsed Doppler echocardiography. simultaneous electro- and phonocardiogram tracings. The isovolumic relaxation time (IRT) between the aortic component of the second heart sound on the phonocardiogram Methods and the onset of early TMF (TMF-E), the deceleration time (E-DT) from the peak early TMF to the baseline, and the peak Study Patients velocities (TMF-A and PVA, respectively) and durations (TMF-Ad and PVAd, respectively) of both the atrial systolic waves of the TMF and PVF were measured by pulsed Doppler We selected 64 patients (25 women and 39 men, mean age echocardiography (Fig. 1, TMF and PVF). Interatrial septal 48 +. 19 years) with HC in sinus rhythm from 150 consecutive motion was recorded on the horizontal sections, including the patients with cardiovascular disease diagnosed by routine right and left atria, by transesophageal M-mode echocardiog- echocardiography and diagnostic catheterization in our hospi- raphy, and left atrial dimensions immediately before and after tal between July 1993 and February 1996. All patients were atrial systole (LADd and LADS, respectively) were deter- receiving no treatment at the time of the study. Ten patients mined. Volume changes in the left atrium during atrial systole with moderate to severe mitral regurgitation as determined by (LkAV-A) were determined using the equation proposed by left ventriculography and/or color Doppler flow mapping the following formula27(Fig. 1, IAS): were excluded from this study, as mitral regurgitation can significantly affect the pattern of LV filling. The remaining 54 A LAV-A = 0.94 (LADd'.24-LAD~'.24) subjects consisted of 39 patients with asymmetric septal hypertrophy and a fractional shortening of the left ventricle 2 30% by transthoracic M-mode and two-dimensional (2-D) echocardiography, 11 patients with apical hypertrophy of the Japanese type as demonstrated by 2-D echocardiography and TMF PVF IAS left ventric~lography~~and a fractional shortening2 30%,and IRT E-DT TMF-Ad

4 patients with asymmetric septal hypertrophy with fractional S shortening ~30%.~~Eight patients with asymmetric septal hypertrophy had LV outflow obstruction. The control group consisted of 25 subjects (11 women and 14 men, mean age 42 f 8 years) who showed no significant organic cardiovascular disease after echocardiography and cardiac catheterization for chest pain, dyspnea, or heart murmurs on auscultation. ECG d- mi8.-- @- A- Study Design c ?. ' PCG- PCG PCG lla The purpose of the examination was fully expl@nedto all FIG.1 Parameters of transmitral flow (TMF) and pulmonary ve- subjects, and informed consent and approval were obtained. nous flow (PVF) velocities, and interatrial septal (IAS) motion measured by the transesophageal approach. = i~ovolumicrelaxation Left ventricular end-diastolic pressures (LVEDPs) were re- IRT time between the aortic component (IL) of the second heart sound on corded with a #8.3 F fluid-filled pigtail catheter by left heart the phonocardiogram and the onset of early TMF E-DT = decelera- catheterization in all the subjects. Diazepam (5 mg) was rou- tion time from the peak early TMF to the baseline; TMF-E and -A = tinely given as premedication before catheterization.Various early diastolic wave and peak velocity of the atrial systolic wave of types of echocardiographic measurements were performed the TMF, respectively; TMF-Ad and PVAd =durations of both the within 3 h prior to cardiac catheterization.Measurements by atrial systolic waves of the TMF and PVF, respectively; PVSI and transthoracicM-mode echocardiographywere Qbtainedof the PVS:! = first and second systolic waves of the PVF, respectively; PVD =early to mid-diastolic wave of the PVF; PVA = peak velocity LV end-diastolic dimension, percent fractional shortening of of the atrial systolic PVF; LADd and LADS= left atrial dimensions the left ventricle, maximal left atrial dimension at systole, and just prior to and following atrial contraction, respectively; LA = left interventricular septal and LV posterior wall thicknesses at atrium; RA = right atrium; ECG = electrocardiogram; PCG = end-diastole. phonocardiogram. T. Oki et al. : Left atrial systolic performance in HC 49

M-mode and pulsed Doppler echocardiograms were (Fig. 5), and (4) 13 patients (Group B) with a PVA 2 25 mds recorded with commercially available Toshiba SSH-65A (Fig. 6). (Toshiba Corp., Tokyo) and Aloka SSD-870 (Aloka Co., Table I shows the age, atrial systolic parameter of the TMF, Ltd., Tokyo) ultrasound diagnostic systems using a 2.5-MHz PVF and interatrial septal motion, and LVEDP in the control transthoracic probe and a 5-MHz transesophageal probe, re- group and the four groups with HC. The mean patient age in spectively. Each subject was premedicated with 1% lidocaine Group A was significantly lower than that in Groups B, C, and spray applied to the posterior pharynx for the transesophageal D (all p < 0.0o01). There were no significantdifferences in LV echocardiographic examination. Food intake was withheld end-diastolic dimension among Groups A, B and C (Group A: for at least 5 h prior to the procedure. 4.1 & 0.4 cm, Group B: 3.9 & 0.9 cm, Group C:4.3 f 1.3 cm), although that in Group D was significantly larger (5.5 k 1.2 StatisticalAnalysis cm) than that in Groups A and B (both p < 0.0 1). In patients with asymmehic septal hypertrophy, no significantdifferences Values are expressed as mean +. standard deviation. The were noted in the degree of interventricular septal thickness mean of five heart beats with comparatively stable R-R inter- among Group A (22.3 +. 3.9 mm), Group B (25.8 +. 4.6 mm), vals was used for each measurement. Differences between Group C (23.6 t- 8.1 mm), and Group D (22.0 k 4.2 mm). Of groups were assessed using the analysis of variance (ANOVA) 11 patients with apical hypertrophy, 3 were in Group A and 8 and Scheffe’s test. The correlations between two variables were in Group C.Among the 8 patients with LV outflow ob- were determined by linear regression analyses. A p value of struction, 6 were in Group B and 2 were in Group C. 50.05 was considered to be statistically significant. New York Heart Association Functional Class Results All 11 patients in Group A were in New York Heart Asso- Patient Groups ciation functional class I; 10 and 3 patients in Group B were in class 111 and IV,respectively; 11,13,and 2 patients in Group C The relation between late TMF velocity (TMF-A) and peak atrial systolic PVF velocity (PVA) in all patients with HC is shown in Figure 2. The following two groups were formed according to the waveform of the TMF: (1) 28 patients with the ratio of the late to early TMF velocity 4,and (2) 26 patients (Group C) with their ratio 21 (Fig. 3). Furthermore, the former 24 patients, excluding 4 patients (Group D) with a fractional shortening of the left ventricle ~30%(Fig. 4), were classified into the following two subgroups according to the reference value (25 mm/s) relative to the PVA of the control group used in this study: (3) 11 patients (Group A) with a PVA c 25 mm/s

FIG.3 Original recordings of transmitral flow (TMF) and pulmonary venous flow (PVF) velocities (top) and M-mode left ven- FIG.2 Plots of the relation between the peak atrial systolic veloci- tricular echogram (bottom) in a case from Group C WEDP = 15 ties ofpulmonary venous flow (PVA) and trmsmitral flow (TMF- dg).TMF indicates decrease in peak early diastolic velocity (E) A) in 54 patients. Arrows indicate 11 patients with apical hypertro- and compensatory increase in peak atrial systolic velocity (A). The phy, and closed squares (Group D) indicate 4 patients with asym- peak atrial systolic PVF velocity (PVA) is not as high. Left ventricu- metric septal hypertrophy, showing the fractional shortening of the lar wall shows asymmetric septal hypertrophy with normal systolic left ventricle < 30%. 0= Group A, 0= Group B, = Group C, function. Ivs = interventricular septum, Pw = left Ventricular poste- =GroupD. nor wall. Other abbreviations as in Figure I. SO Clin. Cardiol. Vol. 20, January 1997

TMF PVF TMF PVF

u': 'I,

ECG PW PCG

FIG.4 Original recordings of transmitral flow (TMF) and pulmonary venous flow (PVF) velocities (top) and M-mode left ventricular echogram (bottom) in a case from Group D (LVEDP = 20 mmHg). TMF indicates "pseudonormalization" pattern. Both the late TMF (A) and atrial systolic PVF (PVA) are either nearly normal FIG.5 Original recordings of transmitral flow (TMF) and pul- or low in velocity. Left ventricular wall shows asymmetric septal hy- monary venous flow (PVF) velocities (top) and M-mode left ven- pertrophy with impaired systolic function (fractional shortening = tricular echogram (bottom) in a case from Group A (LVEDP = 9 14%).Abbreviations as in Figure 3. mmHg). Both TMF and PVF indicate normal patterns. Left ventricular wall shows asymmetric septal hypertrophy with normal systolic function. Abbreviations as in Figure 3. were in class I, 11, and 111, respectively; and 2 and 2 patients in Group D were in class III and IV, respectively. (p<0.05, p

TABL~I Age, left ventricular end-diastolic pressure, variables of transmitral and pulmonary venous flow, and interatrial septal motion in normal controls and four groups with hypertrophic cardiomyopathy

~~~ No.of Age TMF-A TMF-Ad PVA PVAd LAD ALAV-A LVEDP Group cases (years) (cm/s) (ms) (CW (ms) (cm) (cm') (mmHg) Control 25 42.1 k8.3 S0.4k9.0 128k20 19.3k7.3 98+20 2.8k0.3 12.4k2.1 8.2k 1.4 A I1 23.6k4.8d3k 32.0k4.2" 145_t2lalh 18.9k3.9k 101 -I- 15' 3.3k0.4",' 12.6k2.Sh 9.0k 1.9 B 13 44.Sk12.0 30.1 +6Sd 117+23 37.1 +7.6d 148+27"f 4.2k0.6" 10.8k2.l" 19.5k4.3" C 26 57.7+5.7d3R,i 5S.7+9.5gak 131 k 17h 23.0k6.8a,e2k 140+30dfe 3.7kO.S""' 13.1 k4.3" 11.1 k 4.7",', /, D 4 48+9.6gfm 33.1 k8.8'3" 112+28e 22.0k5.4 146k30'J 4.3k1.2"' 10.023.4 17.6kS.4'"~:' "p<0.05,hp

Group A (p < 0.01, p < 0.05, and p < 0.01, respectively) and in the control group (p

Left Atrial Dimension (LAD)

The maximal left atrial dimension in Groups A, B, C, and D was significantly larger than that in the control group (p < 0.001, p < O.OOO1, p < 0,0001,and p < 0.0001, respectively). The dimension decreased in descending order with Group D > Group B > Group C > Group A.

Left Atrial Volume Change during Atrial Systole (A LAV- A)

The left atrial volume change during atrial systole in Group B was significantly smaller than that in the control group and in Groups A and C (all p < 0.05). No significant differences were observed between Group A apd the control group, and between Groups B and D.

Left VentriculaJ.End-Diastolic Pressure (LVEDP)

FIG.6 Original recordings of transmitral flow (TMF) and pul- The LVEDP in Group B was significantly higher than that monary venous flow (PVF) velocities (top) and M-mode left ven- in Groups A and C (both p < 0.OOOl). This pressure was signif- tricular echogram (bottom) in a case from Group B (LVEDP = 24 mmHg). TMF indicates “pseudonormalization”pattern. The peak icantly higher in Group D than in the control group and in atrial systolic PVF velocity (PVA) is markedly increased. Left ven- Groups A and C (p

Late ’Ikansmitral Flow (TMF-A)

There were no differences in late TMF velocity among the Groups A, B, and D. However, they were all significantly smaller than in Group C (all p < 0.OaOl) and the control group (p <0.0001 and p < 0.001). The duration of late TMF wave in Group B was significantly shorter than that in Groups A and C (both p < 0.05).

Atria! Systolic Pulmonary Venous Flow (PVA)

Peak atrial systolic PVF velocity in Group B was significantly higher than that in the control group and in Group C (both p< 0.0001). This velocity was significantly higher in Group C than in the control group and in Group A (both p < 0.05).However, there were no differences among the control FIG.7 Correlation between the peak atrial systolic velocity of the group and Groups A and D. There were no differences in the pulmonary venous flow (PVA) and left ventricular end-diastolic duration of the atrial systolic wave of PVF among the Groups pressure (LVEDP) in 50 patients of Groups A, B, and C. 0=Group B, C, and D. However, they were all significantlylarger than in A, 0 = Group B, 0 = Group C. 52 Clin. Cardiol. Vol. 20, January 1997

than the magnitude of ventricular hypertrophy in determining 0 0 LV diastolic function. Although there was no difference in the magnitude of inter- 5i 20 * I E ventricular septal hypertrophy between Groups A and B in pa- 5 15. tients with asymmetric septal hypertrophy, the mean age was 8 lower and the LVEDP was nearly normal in Group A. Since !JJ 10‘ 3 late TMF velocity was normal or slightly lower than normal in y = 0.07X + 12.4 both groups, it is inappropriate to discuss differences in dias- 5‘ r = 0.52 tolic function between the two groups solely on the basis of D < 0.0001 ” TMF.On the other hand, a significantly higher peak atrial sys- -100 -io 0 50 100 tolic PVF velocity was observed in group B than in Group A, PVAd-TMF-Ad (ms) and a significantly higher LVEDP was observed in Group B FIG.8 Correlation between left ventricular end-diastolic pressure than in Groups A and C.Although Groups A and B had simi- (LVEDP) and difference between duration of atrial systolic waves of lar ratios of the late to early TMF velocity (< 1) with respect to the pulmonary venous flow and transmitral flow (PVAd-TMF-Ad) TMF, the groups were markedly different from each other in 50 patients of Groups A, B, and C. 0= Group A, 0= Group B, with respect to impairment of LV diastolic function, that is. 0 =Group C. Group A showed no increase in both late TMF and peak atrial systolic PVF velocities.Furthermore, the LVEDP was normal, suggesting that LV end-diastoliccompliance was maintained Discussion reratively well despite significant interventricular septal hypertrophy and prolonged isovolumic relaxation time. In Group Pulsed Doppler echocardiography has made it possible to B, however, blood flow from the left atrium to the left ventricle evaluate impairment of LV diastolic function in various car- during atrial systole was suppressed by significant increases in diac disorders noninvasively using the TME6. 9. 12, 2a32 LVEDP (lower late TMF velocity), suggesting regurgitation For example, abnormalities of LV relaxation are reflected on into the pulmonary vein, a structure that has a higher compli- the TMF as a decrease in the peak early diastolic velocity and ance than the left ventricle (higher peak atrial systolic PVF ve- a prolonged deceleration time, resulting in a compensatory in- l~city).~~In this study, there was a good correlation between crease in peak atrial systolic velocity. However. a significant symptoms and TMF and PVF. This is in contrast to a previous decrease in LV compliance may increase LVEDP, giving rise study.34However, HC is known to cause congestive hem fail- to a “pseudonormalization”pattern of TME resulting in a nor- ure due to LV diastolic dysfunction despite a normal systolic mal or lower late TMF velocity. Therefore, examination of function.35Therefore, pattern analysis of TMF and PVF is TMF is not sufficient to distinguish between patients with useful for evaluation of the severity of LV diastolic dysfunc- “pseudonormalization”caused by impaired LV compliance tion in patients with HC. (Group B in this study) and patients without impairment of LV Assuming that no lesions are present in the left atrial my- diastolic function (Group A in this study). Pulmonary venous ocardium, the left atrium is most likely afterload-mismatched flow patterns can be clearly recorded by transesophageal relative to the left ventricle in Group B.I33 24 Patients with HC pulsed Doppler echocardiography. Several studies have dem- usually have a lower incidence of left atrial myocardial failure onstrated that hemodyndc abnormalities between the left than patients with dilated cardiomyopathy or cardiac amyloi- atrium and LV can be examined in detail by combined analy- do~is.2~9~~However, among the four study patients with HC ses of TMF and PVF.18-24Therefore, we examined LV dias- and LV systolic dysfunction (Group D), occult myocardial tolic function and left atrial systolic performance during end failure of the left atrium should also be taken into considera- diastole in patients with HC using both flow velocities. tion, as in the case illustrated in Figure 4,26 in which no in- Hypertrophic cardiomyopathy is characterized by impair- creases were observed in either late TMF or peak atrial sys- ments of LV relaxation and compliance due to LV hypertro- tolic PVF velocity despite a significant increase in LVEDP (20 7, 8, I. phy. l7 However, the seventy of LV diastolic dys- mrnHg). Most patients in Croup C showed a decrease in early function in this disease varies depending on the localization TMF velocity and a compensatory increase in late TMF ve- and extent of myocardial hypertrophy, and on the presence and locity. In addition, peak atrial systolic PVF velocity was not as degree of myocardial disarray and fibr0~is.l~~~Although LV high as that in Group B. These patients exhibited effective hypertrophy in patients with HC is observed in different re- contraction of the left atrium against a slight to moderate in- gions of the myocardium, it is observed most frequently at the crease in LVEDP. This was indicated by increased inflow from interventricular septum or at the apex. Several reports have the left atrium to the left ventricle (significant increase in late suggested that the severity of LV diastolic dysfunction is influ- TMF velocity) relative to regurgitation from the left atrium to enced by the distribution and severity of LV hypertrophy. the pulmonary vein (slight to moderate increase in peak atrial However, Spirito ef al. and Spirito and Maronl6$l7 have re- systolic PVF velocity).24 ported cases of HC in which LV diastolic function is main- The apical hypertrophic variant of HC generally occurs in tained despite significant LV hypertrophy, arguing that the the elderly. The prognosis of patients with this entity is rela- severity of myocardial disarray or fibrosis is more important tively benign compared with patients with asymmetric septal T. Oki et al.: Left atrial systolic performance in HC 53 hypertr~phy.~'.~~All patients in the apical hypertrophic group 6. Kitabatake A. Inoue M, Asao M. Tanouchi J. Masuyama T, Abe H, in our study belonged to Groups A and C, suggesting that im- Morita H, Senda S, Matsuo H: Transmitral blmd flow reflecting di- pairment of LV diastolic function was not as severe as in pa- astolic behavior of the left ventricle in health and disease: A study by pulsed Doppler technique. Jpn Circ J 1982;46:92- I02 tients in Group B. 7. Bonow RO, FrederickTM, Bacharach SL, Green MV, Goose PW. Recently, the clinical importance of transthoracic record- Maron BJ, Rosing DR: Atrial systole and left ventricular tilling in ing of PVF has been demonstrated in a number of reports. patients with hypertrophic cardiomyopamy: Effect of verapamil. Rossvoll and Hatle22and Appleton et al? have reported that Am JCardiql1983;51:1386-139l as LVEDP increases, the duration of the atrial systolic PVF 8. Qki T, Fukuda N, Iuchi A. Tabata T. Kiyoshige K. Manatw K, Kageji Y, Sasaki M, Hama M, Yamada H. Ito S: Evaluation of left wave increases, and the duration of late TMF wave becomes ventricular diastolic hemodynamics from the left ventricular inflow shorter, demonstrating a significant pssitive correlation be- and pulmonary venous flow velscities in hypertrophic cardiomy- tween the difference of duration between both atrial systolic opathy,Jpn HeartJ 199.5;36:617-627 waves and LVEDP. In our study, significant positive correla- 9. Takenaka K, Dabestani A, Gardin JM. Russell D, Clark S, Allfie A. Henry WL: Left ventricular filling in hypertrophic cardiomyopa- tions also were observed between LVEDP and peak amal sys- thy: A pulsed Doppler echocardiographicstudy. JAni Coll Carrliol tolic PVF velocity or the difference between duration of both l986;7: 1263-127 I atrial systolic waves in all patients with HC. Furthermore, the 10. Iskda Y, Meisner JS, Tsujioka K, Gallo JI. Yoran C. Frater RWM. plots of both correlations shifted toward the left and inferiorly Yellin EL: Left ventricular filling dynamics: Influence of left ven- in Group A and toward the right and superiorly in Group B. tricular relaxation and left atrial pressure. Circularion 1986:74: 187-196 Although PVP aften can be recorded transthoracically, 11. Maron BJ, Spirito P, Green KJ, Wesley YE, Bonow RO. Arce FJ: transesophagealechocardiography provides an alternative for Noninvasive assessment of left ventricular diastolic function by detecting this flow velocity pattern when the transthoracic pulsed Doppler echocadiography in patients with hypertrophic approach is not fea~ible.'~~',~~In particular, when evaluating cardiomyopathy,JArn CONCardiol 1987;I0:733-742 left atrial systolic performance in various myocardial diseases 12. Shaikh MA, Lavine SJ: Effect of mitral regurgitation on diastolic filling with left ventricular hypertrophy. Am J Crrrdiol 1988%I : using the a@al systolic waves of both TMF and PIJF, it is im- 590-594 portant to record PWF using transesophageal pulsed Dqpp!er 13. Sanada H, Shimizu M, Kita Y, Sugihara N. Takeda R: Left atrial af- echocardiography. terload mismatch in hypertrophic cardiomyopathy. Am J Curcliol 1991 ;68: 1049-1054 14. Maron BJ, Gottpdiener JS, Epstein SE: Patterns and significance of distribution of left ventricular hypertrophy in hypertrophic car- Conclusions diomyopathy: A wide angle, two-dimensional echocardiographic study of 125patients.AinJCardiol 1981:48:418428 1.5. Shapiro LM, McKenna WJ: Distribution of left ventricular hyper- Combined analysis of peak velocities and durations of late trophy in hypertrophic cardiomyopathy: A two-dimensional TMF and atrial systolic PVF using transesophageal pulsed echocardiographicstudy. JAni Coll Cam'iol1983:2:437-444 Doppler echocardiographyprovides important information re- 16. Spinto P, Mardn BJ, Chiarella F, Betlotti P. Tramarin R, Pozzoli M. garding the hemodynamic abnormalities between the left atri- Vecchio C: Diastolic abnomalites in patients with hypertrophic um and the left ventricle during atrial systole in patients with cardiomyopathy: Relation to magnitude of left ventricular hypertrophy. Circulation 198.5;72:3 1&3 16 HC. In particular, the technique is useful for diagnosing a 17. Spinto P, Maron BJ: Relation between extent of left ventricular hy- forceful atrial contraction mismatched to the left atrial after- pertrophy and diastolic filling abnormalities in hypertrophic cx- load and severity of LV diastolic dysfunction in this patient diomyopathy. /Am Coll Cam'iol I990 IS:808-8 I3 population. 18. Ogawa S. Oki T, luchi A, Kawano T. Uchida T. Hayashi M. Aoyama Y, Hosoi K, Emi S, Fukuda N. Mori H: Analysis of flow velocity patterns in the superior vena cava and the pulmonary vein in cases of hypertrophic cardiomyopathy.Jprr J Mrd Ultnrsorrics References 1990;17:223-232 19. Nishimura RA, Abel MD, Hatle LK. Tajik AJ: Relation of pulmonary veiu to pitral flow velocities by transesophageal Doppler I, Stewart S, Mpon DT, Braunwald E: Impaired rate of left ventricu- echocardiography:Effect of different loading conditions. Cindtr- lar filling in idiopathic hypertrophic subaortic stenosis and vqlvular !ion 1990;81 : 1488-1497 aortic stenosis. Circulation 1968;37;8-14 20. Kuecherer HF, Muhiudeeo IA, Kusumoto FM. Lee E. Moulinier 2. Gaasch WH, Levine HJ, Quinones MA, Alexander JK: Left vep- LE, Cahalan MK, Schiller NB:Estimation of mean left atrial pres- tricular compliance: Mechanisms and clinical implications. Atn J sure from transesophageal pulsed Doppler echocardiography of Curdiol I976;38:645-6.53 pulmonary venous flow. Circulatiori 1990;82:I 127- I I39 3. Sanderson JE, Gibson DG, Brown DJ, Gopdwin JF: Left ventricu- 21. Kuecherer HF,Kusumoto F, Muhiudeen IA. Caharan MK, Schiller lar filling in hypertrophiccardiomyopathy: An angiographicstudy. NB: Pulmonary venous flow patterns by transesophageal pulsed BrHeon J 1977;39:661-670 Doppler echocardiography: Relation to parameters of left ventricu- 4. Sanderson JE, Trail1 TA, St. John Sutton MG, Brown DJ, Gibson larsystolicanddiastolicfunction.Arn Heart J 1991:122: 1683-1693 DG, Goodwin JF Left ventricular relaxation and filling in hyper- 22. Rossvoll 0, Hatle LK: Pulmonary venous flow velocities recorded trophic cardiomyopathy: An khocgdiographic study. Br Heart J by transthoracic Doppler ultrasound: Relation to left ventriculardi- 1978;40:596-601 astolic pressures. JAtn CON Curdid 1993;21 : 1687-1 696 5. Hanrath P, Mathey JIG,Siegert R, Bleifeld W Left ventricular re- 23. Appleton CP, Galloway JM, Ganzalez MS, Gaballa M, Basnight laxation and filling pattern in different forms of left ventricular hy- MA: Estimation of left ventricular filling pressures using two-di- pertrophy: An echocardiographic study. Am J Cardiol 198045: mensional and Doppler echocardiography in adult patients with 15-23 cardiac disease. Additional value of analyzing left atrial size. left 54 Clin. Cardiol. Vol. 20, January 1997

atrial ejection fraction and the difference in duration of pulmonary pulsed Doppler echocardiographic and hernodynamic indexes in venous and mitral flow velocity at atrial contraction. J Am CoZl subjects with and without coronary artery disease. J Am Coll Curdiol 1993;22:1972- 1982 Cardioll989; 13:327-336 24. Oki T, Fukuda N, Ara N, Iuchi A, Tabata T, Tanirnoto M, Manabe 31. Myreng Y, Smiseth OA, Risoe C: Left ventricular tilling at elevat- K, Kageji Y, Sasaki M, It0 S: Evaluation of left atrial active con- ed diastolic pressures: Relationship between transmitral Doppler traction and relaxation in various myocardial diseases by trans- flow velocities and atrial contribution. Am Heart J 1990;119: esophagealpulsed Doppler echocardiography of left ventricular in- 620-626 flow and pulmonary venous flow. Am J Noninvas Cardiol1994; 32. Thomas JD, Weyman AE: EchocardiographicDoppler evaluation 8: I4@ 145 of left ventricular diastolic function: Physics and physiology. 25. Yamaguchi H, Ishimura T, Nishiyama S, Nagasaki F, Nakanishi S, Circulafion 1991;84:977-990 Takatsu F, Nishijo T, Umeda T, Machii K: Hypertrophic nonob- structive cardiornyopathywith giant negative T waves (apical hy- 33. Goto M, Arakawa M, Suzuki T, Tanaka T, Miyamoto H, pertrophy): Ventriculographicand echocardiographic features in 30 Yamaguchi M, Takaya T, Ito H, Hirakawa S: A quantitative analy- patients. Am J Cardiol1979;44:4OI--4l2 sis of reservoir function of the human pulmonary “venous” system 26. Yutani C, Irnakita M, lshibashi-Ueda H, Hatanaka K, Nagata S, for the left ventricles. Jpn Circ J 1986;50:222-23 1 SakakibaraH, Nimura Y Three autopsy cases of progression to left 34. Nihoyannopoulos P, Karatasakis G, Frenneaux M, McKenna WJ, ventricular dilatation in patients with hypertrophic cardiomyopa- Oakley CM: Diastolic function in hypertrophic cardiomyopathy: thy.Am Heart J 1985;109:545-553 Relation to exercise capacity. JAm Coll Cardioll992; l9:536-S40 27. Toma Y, Matsuda Y, Matsuzaki M, Anno Y, Uchida T, Hiroyama 35. Oki T, Fukuda N, Iuchi A, Tabata T, Kiyoshige K, Fujimoto T, N, Tamitani M, Murata T, Yonezawa F, Moritani K, Katayama K, Manabe K, Yamada H, Ito S: Changes in left ventricular inflow and Ogawa H, Kusukawa R Determination of atrial size by esophageal pulmonary venous flow velocities during preload alteration in hy- echocardiography.Am J Cardiol1983;52:878-880 pertrophic cardiomyopathy.Am J Cam‘iol1996;77:43W35 28. Choong CY, Henmann HC, Weyman AE, Fifer HA: Preload de- 36. Roberts WC, Waller BF: Cardiac amyloidosiscausing cardiac dys- pendence of Doppler-derived indexes of left ventricular diastolic function: Analysis of 54 necropsy patients. Am J Cardiol1983;52: function in humans. JAm Coll Cardiol1987;10:800-808 137-146 29. Appleton CP, Hatle LK, Popp RL: Relation of transmitral flow velocity patterns to left ventricular function: New insights from a 37. Webb JG, Sasson Z, Rakowski H, Liu P, Wigle ED: Apical hyper- combined hernodynamic and Doppler echocardiographic study. J trophic cardiomyopathy:Clinical follow-up and diagnostic corre- Am Coll Cardioll988; 12:426-440 lates. JAm Coll Cardiol1990;15:83-90 30. Stoddard MF, Pearson AC, Kern MJ, Ratcliff J, Mrosek DG, 38. Koga Y, Itaya K, Toshima H: Prognosis in hypertrophiccardiomy- Labovitz AJ: Left ventricular diastolic function: Comparison of opathy. Am Heart .I1984; 108:35 1-359