Hemodynamic Features of Prolapsing and Nonprolapsing Left Atrial Myxoma By RUEY J. SUNG, M.D., ALI R. GHAHRAMANI, M.D., STEPHEN M. MALLON, M.D., STANLEY E. RICHTER, M.D., LEONARD S. SOMMER, M.D., STUART GOTTLIEB, M.D., AND ROBERT J. MYERBURG, M.D. SUMMARY In the course of the evaluation of five patients with left atrial myxoma, it was noted that the movement of the myxoma was related to specific changes in left atrial hemodynamics. Prolapsing tumors, Type I, move from the left ventricle to the left atrium in early systole and from the left atrium to the left ventricle in early diastole, thereby causing prominent c and v waves accompanied by a rapid y descent. Nonprolapsing tumors, Type II, remain in the left atrium during the entire cardiac cycle, impeding flow across the mitral valve. In these latter cases, the y descent is slow and indistinguishable from that caused by mitral valvular stenosis. The cineangiocardiograms and echocardiograms corroborate these two types of hemodynamic observations. The particular value of direct echocardiographic examination of the left atrium prior to cardiac catheterization was evident in two of the three patients with nonprolapsing tumors. Since the hemodynamic pattern of nonprolapsing left atrial myxoma resembles that of mitral valvular stenosis, it is stressed that echocardiography should have an important place in precatheterization assessment of patients with mitral valve disease. If left atrial myxoma is suspected clinically or on the basis of echocardiographic findings, regardless of the pressure curve contours, transseptal cardiac catheterization should be avoided and the left atrium visualized by pulmonary angiography levophase.
Additional Indexing Words: Cardiac catheterization Echocardiography
Cardiac tumors Suprasternal ultrasonography
Cineangiocardiography
NCREASING CLINICAL AWARENESS of intracardiac tumors has been stimulated by the improved diagnostic techniques of cardiac catheterization and the more recent advent of echocardiography. Nevertheless, left atrial myxoma continues to be a diagnostic challenge because of its variable clinical
angiocardiographic and echocardiographic correlation. The purpose of this paper is to define the underlying mechanisms of the hemodynamic alterations and to correlate these physiological changes with the mobility variations found in left atrial myxoma.
presentation.
Materials and Methods Between 1967 and 1973, five patients with left atrial myxoma were encountered at Jackson Memorial Hospital. All were female, four Caucasian and one Negroid (case 4). Their ages ranged from 37 to 66 years. Their clinical profiles are summarized in table 1. One patient (case 1) has been reported fully elsewhere.5 The diagnosis of left atrial myxoma was suspected clinically prior-to cardiac catheterization in two patients (cases 4 and 5). The other three patients were initially suspected to have bacterial endocarditis (case 1) and rheumatic mitral valvular stenosis (cases 2 and 3). In each case, the tumor was surgically removed. At surgery, the mitral valve was found to be normal in all except one (case 3) whose mitral valve was thickened and fibrotic but without microscopic evidence of a rheumatic process. The operative findings are included in table 1. All patients survived surgery except for one (case 3) in whom a fatal cerebral vascular accident occurred in the immediate postoperative period. Right and left heart catheterization was performed in all patients. The left atrium was entered via transseptal technique in one patient (case 2), and inadvertently by a retrograde catheter from the left ventricle in two patients (cases 3 and 5). Simultaneous pressures were recorded using
I
Several excellent reports dealing with the unique hemodynamic events and phonocardiographic features of left atrial myxoma have appeared in the literature. 1-6 A characteristic left atrial and/or pulmonary wedge pressure pulse consisting of prominent c and v waves with a rapid y descent has been considered to be diagnostic of the presence of left atrial myxoma.57 Our experience in five patients with this disease has enabled us to classify two distinct alterations in left atrial hemodynamics with cineFrom the Division of Cardiology, Department of Medicine, and the Division of Nuclear Medicine, Department of Radiology, Jackson Memorial Hospital, University of Miami School of Medicine, Miami, Florida. Address for reprints: Ali R. Ghahramani, M.D., University of Miami School of Medicine, P.O. Box 520875 Biscayne Annex, Miami, Florida 33152. Received September 5, 1974; revision accepted for publication October 14, 1974. 342
Circulation, Volume 51, February 1975
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LEFT ATRIAL MYXOMAS
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SUNG ET AL.
344 a multichannel recorder (Electronics for Medicine, Model DR-I8 or D11-16) with Statham P-23-A strain gauges. Selective cineangiocardiography, with injection of contrast medium irnto the left ventricle, ascending aorta or pulmotnary artery was performed on all patients. Echocardiographic analysis was obtained on two patients (cases 4 arid 5). It was performed by using a Unirad UlItrasonoscope and an unfocused transducer, employing piezoelectric crxstal 9.5 mm in diameter with a primary resonant freqtuerncy of 2.25 MHz. The technique of recording was the same as described by Feigenbaum. 0 Because of the uinust;ual echocardiographic patterns obtained in the conventiornal approach, direct examination of the left atrium was performed uisirng the suprasternial method described by
(;oldberg. Results Two patients (cases 3 and 4) had atrial fibrillation at the time of study, the others were in normal sinus
rhythm. A moderate degree of pulmonary hypertension was noted in two patients (cases 1 and 4). The resting Fick cardiac output and cardiac index were normal in two patients (cases 1 and 2), moderately reduced in two patients (cases 3 and 5), and severely reduced in one patient (case 4). A mitral diastolic gradient was present in all of the patients and a minimal to moderate degree of mitral regurgitation was noted in all but one patient (case 5). Simultaneous recording of the left ventricular pressure and pulmonary wedge or left atrial pressure revealed two distinct hemodynamic features. In Type I (cases 1 and 2) (fig. 1), there are prominent c and v waves accompanied by a rapid y descent in the pulmonary wedge or left atrial pressure pulse, and a notch is present in the ascending limb of the left ventricular pressure
Figure 1 .Sirmultaneous left ventricular (V1') and pulmonary arterial wedge I'AW) pressuires in case 1 (left panel), LV and left atrial (LA) pressures in ease 2 (right panel), illustratinrg a notch on the ascendlitng limb of the IV pressure due to t unmor moveminen t fronm the I,V to LAX and a sharrp y descent indicatirng sudden LA deconmpresslon wvhen the tumor is being propelled irtio the I.
pulse. In Type 1I (cases 3, 4, and 5) (fig. 2), although the v waves may appear prominent, the y descent is slow and there is no notch in the ascending limb of the left ventricular pressure pulse. The hemodynamic data are tabulated in table 2.
R
Figure 2
.Simuitiltaneaous left ventricular (Lv) arid pulmnonary arterial wedge (P XW) pressures. Left and middle panels show cases 3 anid 4 in atrial fibrillation and right patnel (case 5) in sinus rhlythm exhibiting a slow y descent orn the PAW or left atrial (1.1) pressure curves and no notch on the ascending LV pressure curve. Circulation Downloaded from http://circ.ahajournals.org/ by guest on March 18, 2015
Volurnie 51 February 19765
LEFT ATRIAL MYXOMAS
345
Table 2 IIemo(lynarnic Findings of the Five Cases of Left Atrial Myxoma LA-LV
Pressures (mm Hg)
Case
PA (mean)
no.
RA
RV
1 2
10 3 12
66/10 32/3
4 1
9 4
85/7
87/12
8:4/ 1 0
66/24 30/19 35 2/1 85/ 38 32/12
PAW a
e
v
16 28
44
28 20 16
20
30
45 16
LA a
27
c
22
=
Ao
(mean)
CO
CI
PVR
6.3 5).7 :.6
3.8 3.5 2. 0
230 98 222 800 11 5
98/ 50
1l5
1209f)
98/60
20
21 16
13015 112/9
132 88
26
14
168/16
172/80
12 8 24 0-2
25
82 14
IV
109(
Abbrevia,t ions: EA =right at riulm (mean); D V righit vetntric pressuire; LA left atritinm; LV Vleft venlt;ricele; An aort.a M2); PVI pulinonary vascular resistanice (dynes/sec-m).
mea.n
v
diastolic gradient
112/78
pulniona;yart ery; PAW cardiac outpult (L/mil); CI
=
=
2.4
1.4
8.5
2.2
wlmeia y art cry wedge cardiac, izidex (1L/minii
=
The cineangiocardiograms of those patients with Type I left atrial hemodynamics (cases 1 and 2) demonstrated that the tumor moved from the left ventricle to the left atrium in early systole and moved from the left atrium to the left ventricle in early diastole (fig. 3). On the other hand, in those patients with Type I1 left atrial hemodynamics (cases 3, 4, and 5), the tumor remained in the left atrium during the entire cardiac cycle (fig. 4). Echocardiography was available in only two patients (cases 4 and 5) with Type II left atrial hemodynamics. Dense abnormal echoes were demonstrated behind the aortic root within the left atrium in both patients. These echoes remained within the left atrium throughout the cardiac cycle. Direct examination of the left atrium via the suprasternal approach also demonstrated large mass s
- e pr
a-p c
alo
dmostrad
ag
m ss
lesions which remained within the left atrial cavity through systole and diastole (fig. 5). In one patient (case 4) (fig. 6), these abnormal echoes were present beneath the proximal portion of the anterior mitral leaflet during diastole, but they were not seen beneath the more distal portions of the leaflet as the sound beam was directed inferiorly along the major left ventricular axis. This mass, therefore, did not appear to enter the left ventricular cavity. The diastolic slope velocity of the anterior mitral leaflet was reduced in this patient, reflecting the decreased flow across the mitral orifice. Mitral valve movement was normal in the other patient (case 5) (fig. 7). Discussion atrial valvur has been bdescribed to Clinicallv asleftmitr mvxoma ds l enmasquerade as mitral valvular disease, bacterial en-
masque1 rd
Figure 3 Levophase of pulmonary angiograni in right anterior oblique projection. Photographs have been retouched in order to better delineate the tumor in the left atrium during systole (left) and in the left ventricle during diastole (right). Circulation, Volume 51, Febrtuary 1975Downloaded from http://circ.ahajournals.org/ by guest on March 18, 2015
SUNG ET AL.
346
Figure 4 LeVophase of /)ulnronary angiograim delineating the tumor in the left aitriuim during b)0th systole (above) and diastole (right).
(AXgiograrm retouched.)
docarditis, or connective tissue disorders.12"17 Adams et al.P8 reported that over 90% of the cases with this disease were initially diagnosed as having rheumatic mitral valvular stenosis. The clinical distinction of this disease is of considerable importance because it may be lethal if left untreated, but represents a curable form of disease with rare recurrence if treated surgically.1921 Hemodynamically, left atrial myxoma is usually associated with a diastolic pressure gradient across the mitral valve. However, it has been claimed that the contour of the left atrial and/or pulmonary wedge pressure pulse can be used to distinguish left atrial myxoma from mitral valvular stenosis.5 " In the former, prominent c and v waves with a rapid y descent are present. With cineangiocardiograms, we, and others previously,1 2. 5. 6. 22 have demonstrated the mechanisms responsible for these hemodynamic changes referred to herein as Type I left atrial hemodynamics for left atrial myxoma. The tumors move from the left ventricle into the left atrium in early systole, abruptly decreasing the left ventricular volume and causing a notch in the ascending limb of the left ventricular pressure pulse. The concomitant sudden increase in the left atrial volume produces prominent c and subsequently, dominant v waves. In early diastole, the tumors enter the left ventricle,
abruptly decreasing the left atrial volume. Because of this sudden decompression of the left atrium, the y descent is rapid and deep in character. Two of our patients (cases 1 and 2) demonstrated these hemodynamic changes (fig. 1) with cineangiocardiographic correlation (fig. 3). We believe that these features are characteristic of prolapsing left atrial myxomas and it is their movement back and forth across the mitral orifice which results in the observed hemodynamic effects. In contrast, the other three patients (cases 3, 4, and 5) had hemodynamic features indistinguishable from that of mitral valvular stenosis (fig. 2), in which there is no notch present in the ascending limb of the left ventricular pressure pulse and the y descent is relatively slow. In these cases, the cineangiocardiograms revealed that the tumors remained in the left atriuim during the entire cardiac cycle (fig. 4). Accordingly, flow across the mitral valve was impeded throughout diastole, causing a relatively slow y descent. These features are referred to herein as Type 1I left atrial hemodynamics of nonprolapsing left atrial myxomas. At surgery, none of these cases had mitral valvular stenosis, and the mitral valves were normal in all patients except for one (case 3), whose mitral valve was thickened and fibrotic. In this patient, thickening and fibrosis of the mitral valve was felt to have (tirutlatioui, Volumne 51, February 197,5
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347
LEFT ATRIAL MYXOMAS
9
?'
~_0^
1 lvs
Ao
AMV
RPAs
(LA) MYX
PLV Fi
-6
Figure
6
by movitg transducer along the ajor left ventnricular axis frornl the left v ntricle (left) to the level of the aorta (Ao) (rig/it). The diastolic slope of anterior nmitral leaflet (AMVI) closuire is reduiced reflecting decreaised flow across the mitral valve. As the tultrasouind beam is directed superiorly, ablnornmal
Case 4. Echocardiogram obtained rn
e
echoes originatin?g from the miyxonia
Figure 5
resulted from longstanding trauma due to the motion a calcified atrial myxoma, since there was neither commissural fusion nor microscopic evidence of rheumatic process. The echocardiograms of the two patients (cases 4 and 5) with nonprolapsing left atrial myxoma (figs. 5, 6, and 7) were consistent with the observed hemodynamic events. The tumor echoes were identified in the left atrium but not within the left ventricle during diastole in contrast to the usual echocardiographic findings that have been described for left atrial myxoma.23 27 The motion of the anterior mitral leaflet was completely normal in one patient (case 5). Both of these patients also illustrate the particular value of direct echocardiographic examination of the left atrium when a nonprolapsing tumor is present. Such direct examination of the left atrium along the long axis of the left ventricle in the presence of suspected nonprolapsing atrial myxoma was first suggested by Popp and Harrison.28 We found the suprasternal approach proposed by Goldberg" an of
Circulation,
'olumie,i .5
ebruary
atriurm
become apparent.
to
Case 5. Snprazstern7al approac/. The left atriumi (LIA) is almost cotmpletely filled with abnormal echoes which origincate from the inyxonma (MYX). The tunmor remains w;it/lin the left atrium durinrg the eiitire cardiac cycle. CW=-chest wall; ECC = electrocarright pulimonary artery diogram.; IfPA
(MX1tYX) uitliin t/ie left
The echisoes frorm the tumor are seen to fill abouit the level of the descend only the left atrium and atriouenetriciilar cantal imriiediately behind tde proximal attachment of the anterior mitral leaiflet. IVS = interventricular septum,; PLY' = posterior left venttricular wall. (I.A)
effective (fig. 6).
means
to
of examining the left atrium directly
Features similar to our Type II left atrial hemodynamics have been reported in a single patient with left atrial myxoma as an "unusual" finding.29 However, three of our five patients demonstrated these changes. The importance of Type IT left atrial hemodynamics in the presence of left atrial myxoma has not been emphasized previously. Although because of the small number of cases included in this report, statistically one cannot draw a conclusion, we do, however, believe that these changes, related to nonprolapsing tumors, occur more frequently than is generally realized. Failure to recognize this phenomenon may lead to unnecessary and potentially hazardous transseptal left heart catheterization in patients with left atrial myxoma.21 30 In conclusion, two variations in left atrial hemodynamics may occur in left atrial myxoma. In Type I, or prolapsing myxoma, there is a notch in the upstroke of the left ventricular pressure pulse and
1975
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SUNG ET AL.
348
-11
'vs ao
TX
AMV mMYX U-'V
A ~.
I,tS f._t -w r':
| j
J
Figure 7 Case .5. By conventional method, the ultrasound beam is directed from t h e left ventricle (left) a long the nmajo r axis to th2e level of the aortwi root (Ao) and the left atrium (LA). Note the movement of the anterior mitral leaflet (AMV) is nornmal anid is n1ot stuggestive of obstruction to the flow from the left atriun. oNo abnormcal echoes are identified hehinr d thie mnitral leaflet. Abnormally moving echoes originatingfroni the myxomna (MYX) can l)e identified behind the posterior aortic rooi withlinl the left atrium Except for their utnusual motion, they might be confused withi calcificatiorn of the rnitral rirng. (CW= chest wall;, CC = electrocardiogram; RPA = right pulmonary artery. Noise echoes seen in this photograph result from-t tihe high sensitivity settinigs required for recording as well as reverbertation artifacts produced by poor sound trarismiissionr chlar(cteristics associated with mild obstructive pulnionary disease.
prominent c and v waves with a rapid y descent are present in the pulmonary wedge or left atrial pressure pulse. In Type II, nonprolapsing myxoma, there is no notch in the upstroke of the left ventricular pressure pulse and the y descent of the pulmonary wedge or left atrial pressure pulse is slow and indistinguishable from that of mitral valvular stenosis. The important contribution and value of well performed echocardiography in the precatheterization assessment of patients with suspected mitral valve disease is emphasized. It is stressed that irrespective of the left atrial hemodynamic findings, pulmonary angiography with observation of the levophase should be performed in any patient with clinical or echocardiographic evidence suggestive of left atrial myxoma. Acknowledgment W'e are in(lebted tn Dr. Dan Rnehm for referring case 5, to Mr. William Embii anid Mr. Frank Garcia-Moiites for their technical
assistance in preparinig this manuscript, and George Bouchoe for tie art work.
References A, PVii-i- B, SC iA F FE J, C IiEr JM: Mvxoma of the left atriumn. Hemoldynamic and phonocarcliographic consenenices of sudden ttmor movemenit. Circulation 36: 408 1967 PrNN JL Giin (consy JJ, AyMiiis SMSI, GIA\NiNN;I ii S, RoSSI P: Calcified left atrial mvxoma simuilatirng mitral inistifficiencv. Hemodvnamic and phonocardiographic effects of turmor movement. Circulation 36: 417 196'7 ZI TNIK RS, GwLIi si ER, Bs nI IIi HB: Left atrial mvxoma: phonocardiographic ciues to diagniosis. Ami J Cardiol 23: 588# 1969 (CIsGii F. Ai,(_vxny WP: Left atrial myxoma: Diagnosis wsith the help of the phoniocardiogram and apexcardiogramn. Arch Interni Med 29: 470, 1972 GII SHAMANI AR-, ARNOiDo JR HiimE-)\oin FJ, Sosi\vFiin LS, SAxn P: Left atrial inyxoma. Ilemodyllarnic and phonocardiographic featuires. Am J M1ed 52: 525, 1972
1. P1
2.
3. 4. 5.
i-
(Circulation, Volhitme 5t, Febriuaril 197,5 Downloaded from http://circ.ahajournals.org/ by guest on March 18, 2015
LEFT ATRIAL MYXOMAS 6. NASSER WK, DAVIS RH, DILLON JC, TAVEL ME, HELMIEN CH, FEIGENBAuNI H, FISCH C: Atrial myxoma. II. Phonocar-
diographic, echocardiographic, hemodynamic, and angiographic features in nine cases. Am Heart J 83: 810, 1972 7. FiSH RG, TAKARO T, CRYMES T: Left atrial pressure pulses in the presence of myxoma. Circulation 20: 413, 1959 8. WINTERS WL, MARK GE, SOLOFF LA: Left atrial pressure curve in left atrial myxoma. Arch Intern Med 107: 128, 1961 9. OGNIBENE AJ, NELSON WP: Atrial myxoma: Comments on hemodynamic alterations. Report of a case. Dis Chest 52: 699, 1967 10. FEIGENBAIxi H: Echocardiography. Philadelphia, Lea and Febiger, 1973, ch 3, pp 37-41 11. GOLDRBERL BB: Suprasternal ultrasonography. JAMA 215: 245, 1971 12. GooDW,1IN JF: Diagnosis of left atrial myxoma. Lancet 1: 644, 1963 13. GOODWIN JF: Symposium on cardiac tumors. Am J Cardiol 21: 307, 1968 14. H ARXVEY WP: Clinical aspects of cardiac tumors. Am J Cardiol 21: 334, 1968 15. GREENWOOD WF: Profile of atrial myxoma. Am J Cardiol 21: 367, 1968 16. GREENXVOOD WF: Myxoma of the left atrium. Br Heart J 22: 189, 1960 17. NASSER WK, DAXIS RH, DILLON JC, TAVEL ME, HEL.NIEN CH, FEIGENBALUNI H, FISCH C: Atrial myxoma. I. Clinical and pathological features in nine cases. Am Heart J 83: 694, 1972 18. ADAMIS CW, COLLINS HD, DuNINIITI GS, ALLEN JH: Intracardiac myxomas and thrombi: Clinical manifestations,
349 pathology and treatment. Am J Cardiol 8: 176, 1967 19. CASTANEDA AR, VARCo RL: Tumors of the heart: Surgical considerations. Am J Cardiol 21: 357, 1968 20. KABBANI SS, COOLEY DA: Atrial myxoma: Surgical considerations. J Thorac Cardiovasc Surg 65: 731, 1973 21. THoNIAS KE, WINCHELL PC, VARCO RL: Diagnostic and surgical aspects of the left atrial tumors. J Thorac Cardiovasc Surg 53: 535, 1967 22. MOSCOvlITz HL, PANTAZOPOULLOS J, BODENHEINIER M, STEIER M, GELB IJ: Simulated left atrial tumor. A hemodynamic, echocardiographic and cineangiographic study. Am J Cardiol 34: 63, 1974 23. WOLFE SB, Popp RL, FEICENBALNI H: Diagnosis of atrial tumors by ultrasound. Circulation 39: 615, 1969 24. Popp RL, HARlISON DC: Ultrasound for the diagnosis of atrial tumor. Ann Intern Med 71: 785, 1969 25. KoSTIS JB, MACHAD)Am AN: Echocardiographic diagnosis of left atrial myxoma. Chest 58: 550, 1970 26. FiNEGAN RE, HA.RISON DC: Diagnosis of left atrial myxoma by echocardiography. N Engl J Med 282: 1022, 1970 27. SPENCER WH, PETER RH, ORGAIN ES: Detection of a left atrial myxoma by echocardiography. Arch Intern Med 128: 787, 1971 28. Popp RL, HARRIISON DC: Ultrasound for the diagnosis of atrial tumor. Ann Intern Med 71: 785, 1969 29. BOWVER PJ, RITTER DG, CALLAHAN JA, ZITNIK RS: Unusual
hemodynamic findings of diagnostic value in a case of left atrial myxoma. Am J Cardiol 23: 592, 1969 30. MARPOLE DGF, KLOSTER FE, BRISTOW JD, GRISWXoLD HE: Atrial myxoma. A continuing diagnostic challenge. Am J Cardiol 23: 597, 1969
Circulation, Volume 51, February 1975 Downloaded from http://circ.ahajournals.org/ by guest on March 18, 2015
Hemodynamic features of prolapsing and nonprolapsing left atrial myxoma. R J Sung, A R Ghahramani, S M Mallon, S E Richter, L S Sommer, S Gottlieb and R J Myerburg Circulation. 1975;51:342-349 doi: 10.1161/01.CIR.51.2.342 Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 1975 American Heart Association, Inc. All rights reserved. Print ISSN: 0009-7322. Online ISSN: 1524-4539
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Additional Indexing Words: Cardiac catheterization Echocardiography
Cardiac tumors Suprasternal ultrasonography
Cineangiocardiography
NCREASING CLINICAL AWARENESS of intracardiac tumors has been stimulated by the improved diagnostic techniques of cardiac catheterization and the more recent advent of echocardiography. Nevertheless, left atrial myxoma continues to be a diagnostic challenge because of its variable clinical
angiocardiographic and echocardiographic correlation. The purpose of this paper is to define the underlying mechanisms of the hemodynamic alterations and to correlate these physiological changes with the mobility variations found in left atrial myxoma.
presentation.
Materials and Methods Between 1967 and 1973, five patients with left atrial myxoma were encountered at Jackson Memorial Hospital. All were female, four Caucasian and one Negroid (case 4). Their ages ranged from 37 to 66 years. Their clinical profiles are summarized in table 1. One patient (case 1) has been reported fully elsewhere.5 The diagnosis of left atrial myxoma was suspected clinically prior-to cardiac catheterization in two patients (cases 4 and 5). The other three patients were initially suspected to have bacterial endocarditis (case 1) and rheumatic mitral valvular stenosis (cases 2 and 3). In each case, the tumor was surgically removed. At surgery, the mitral valve was found to be normal in all except one (case 3) whose mitral valve was thickened and fibrotic but without microscopic evidence of a rheumatic process. The operative findings are included in table 1. All patients survived surgery except for one (case 3) in whom a fatal cerebral vascular accident occurred in the immediate postoperative period. Right and left heart catheterization was performed in all patients. The left atrium was entered via transseptal technique in one patient (case 2), and inadvertently by a retrograde catheter from the left ventricle in two patients (cases 3 and 5). Simultaneous pressures were recorded using
I
Several excellent reports dealing with the unique hemodynamic events and phonocardiographic features of left atrial myxoma have appeared in the literature. 1-6 A characteristic left atrial and/or pulmonary wedge pressure pulse consisting of prominent c and v waves with a rapid y descent has been considered to be diagnostic of the presence of left atrial myxoma.57 Our experience in five patients with this disease has enabled us to classify two distinct alterations in left atrial hemodynamics with cineFrom the Division of Cardiology, Department of Medicine, and the Division of Nuclear Medicine, Department of Radiology, Jackson Memorial Hospital, University of Miami School of Medicine, Miami, Florida. Address for reprints: Ali R. Ghahramani, M.D., University of Miami School of Medicine, P.O. Box 520875 Biscayne Annex, Miami, Florida 33152. Received September 5, 1974; revision accepted for publication October 14, 1974. 342
Circulation, Volume 51, February 1975
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LEFT ATRIAL MYXOMAS
343 +2+20
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Circulation, Volume 51, February 1975 Downloaded from http://circ.ahajournals.org/ by guest on March 18, 2015
SUNG ET AL.
344 a multichannel recorder (Electronics for Medicine, Model DR-I8 or D11-16) with Statham P-23-A strain gauges. Selective cineangiocardiography, with injection of contrast medium irnto the left ventricle, ascending aorta or pulmotnary artery was performed on all patients. Echocardiographic analysis was obtained on two patients (cases 4 arid 5). It was performed by using a Unirad UlItrasonoscope and an unfocused transducer, employing piezoelectric crxstal 9.5 mm in diameter with a primary resonant freqtuerncy of 2.25 MHz. The technique of recording was the same as described by Feigenbaum. 0 Because of the uinust;ual echocardiographic patterns obtained in the conventiornal approach, direct examination of the left atrium was performed uisirng the suprasternial method described by
(;oldberg. Results Two patients (cases 3 and 4) had atrial fibrillation at the time of study, the others were in normal sinus
rhythm. A moderate degree of pulmonary hypertension was noted in two patients (cases 1 and 4). The resting Fick cardiac output and cardiac index were normal in two patients (cases 1 and 2), moderately reduced in two patients (cases 3 and 5), and severely reduced in one patient (case 4). A mitral diastolic gradient was present in all of the patients and a minimal to moderate degree of mitral regurgitation was noted in all but one patient (case 5). Simultaneous recording of the left ventricular pressure and pulmonary wedge or left atrial pressure revealed two distinct hemodynamic features. In Type I (cases 1 and 2) (fig. 1), there are prominent c and v waves accompanied by a rapid y descent in the pulmonary wedge or left atrial pressure pulse, and a notch is present in the ascending limb of the left ventricular pressure
Figure 1 .Sirmultaneous left ventricular (V1') and pulmonary arterial wedge I'AW) pressuires in case 1 (left panel), LV and left atrial (LA) pressures in ease 2 (right panel), illustratinrg a notch on the ascendlitng limb of the IV pressure due to t unmor moveminen t fronm the I,V to LAX and a sharrp y descent indicatirng sudden LA deconmpresslon wvhen the tumor is being propelled irtio the I.
pulse. In Type 1I (cases 3, 4, and 5) (fig. 2), although the v waves may appear prominent, the y descent is slow and there is no notch in the ascending limb of the left ventricular pressure pulse. The hemodynamic data are tabulated in table 2.
R
Figure 2
.Simuitiltaneaous left ventricular (Lv) arid pulmnonary arterial wedge (P XW) pressures. Left and middle panels show cases 3 anid 4 in atrial fibrillation and right patnel (case 5) in sinus rhlythm exhibiting a slow y descent orn the PAW or left atrial (1.1) pressure curves and no notch on the ascending LV pressure curve. Circulation Downloaded from http://circ.ahajournals.org/ by guest on March 18, 2015
Volurnie 51 February 19765
LEFT ATRIAL MYXOMAS
345
Table 2 IIemo(lynarnic Findings of the Five Cases of Left Atrial Myxoma LA-LV
Pressures (mm Hg)
Case
PA (mean)
no.
RA
RV
1 2
10 3 12
66/10 32/3
4 1
9 4
85/7
87/12
8:4/ 1 0
66/24 30/19 35 2/1 85/ 38 32/12
PAW a
e
v
16 28
44
28 20 16
20
30
45 16
LA a
27
c
22
=
Ao
(mean)
CO
CI
PVR
6.3 5).7 :.6
3.8 3.5 2. 0
230 98 222 800 11 5
98/ 50
1l5
1209f)
98/60
20
21 16
13015 112/9
132 88
26
14
168/16
172/80
12 8 24 0-2
25
82 14
IV
109(
Abbrevia,t ions: EA =right at riulm (mean); D V righit vetntric pressuire; LA left atritinm; LV Vleft venlt;ricele; An aort.a M2); PVI pulinonary vascular resistanice (dynes/sec-m).
mea.n
v
diastolic gradient
112/78
pulniona;yart ery; PAW cardiac outpult (L/mil); CI
=
=
2.4
1.4
8.5
2.2
wlmeia y art cry wedge cardiac, izidex (1L/minii
=
The cineangiocardiograms of those patients with Type I left atrial hemodynamics (cases 1 and 2) demonstrated that the tumor moved from the left ventricle to the left atrium in early systole and moved from the left atrium to the left ventricle in early diastole (fig. 3). On the other hand, in those patients with Type I1 left atrial hemodynamics (cases 3, 4, and 5), the tumor remained in the left atrium during the entire cardiac cycle (fig. 4). Echocardiography was available in only two patients (cases 4 and 5) with Type II left atrial hemodynamics. Dense abnormal echoes were demonstrated behind the aortic root within the left atrium in both patients. These echoes remained within the left atrium throughout the cardiac cycle. Direct examination of the left atrium via the suprasternal approach also demonstrated large mass s
- e pr
a-p c
alo
dmostrad
ag
m ss
lesions which remained within the left atrial cavity through systole and diastole (fig. 5). In one patient (case 4) (fig. 6), these abnormal echoes were present beneath the proximal portion of the anterior mitral leaflet during diastole, but they were not seen beneath the more distal portions of the leaflet as the sound beam was directed inferiorly along the major left ventricular axis. This mass, therefore, did not appear to enter the left ventricular cavity. The diastolic slope velocity of the anterior mitral leaflet was reduced in this patient, reflecting the decreased flow across the mitral orifice. Mitral valve movement was normal in the other patient (case 5) (fig. 7). Discussion atrial valvur has been bdescribed to Clinicallv asleftmitr mvxoma ds l enmasquerade as mitral valvular disease, bacterial en-
masque1 rd
Figure 3 Levophase of pulmonary angiograni in right anterior oblique projection. Photographs have been retouched in order to better delineate the tumor in the left atrium during systole (left) and in the left ventricle during diastole (right). Circulation, Volume 51, Febrtuary 1975Downloaded from http://circ.ahajournals.org/ by guest on March 18, 2015
SUNG ET AL.
346
Figure 4 LeVophase of /)ulnronary angiograim delineating the tumor in the left aitriuim during b)0th systole (above) and diastole (right).
(AXgiograrm retouched.)
docarditis, or connective tissue disorders.12"17 Adams et al.P8 reported that over 90% of the cases with this disease were initially diagnosed as having rheumatic mitral valvular stenosis. The clinical distinction of this disease is of considerable importance because it may be lethal if left untreated, but represents a curable form of disease with rare recurrence if treated surgically.1921 Hemodynamically, left atrial myxoma is usually associated with a diastolic pressure gradient across the mitral valve. However, it has been claimed that the contour of the left atrial and/or pulmonary wedge pressure pulse can be used to distinguish left atrial myxoma from mitral valvular stenosis.5 " In the former, prominent c and v waves with a rapid y descent are present. With cineangiocardiograms, we, and others previously,1 2. 5. 6. 22 have demonstrated the mechanisms responsible for these hemodynamic changes referred to herein as Type I left atrial hemodynamics for left atrial myxoma. The tumors move from the left ventricle into the left atrium in early systole, abruptly decreasing the left ventricular volume and causing a notch in the ascending limb of the left ventricular pressure pulse. The concomitant sudden increase in the left atrial volume produces prominent c and subsequently, dominant v waves. In early diastole, the tumors enter the left ventricle,
abruptly decreasing the left atrial volume. Because of this sudden decompression of the left atrium, the y descent is rapid and deep in character. Two of our patients (cases 1 and 2) demonstrated these hemodynamic changes (fig. 1) with cineangiocardiographic correlation (fig. 3). We believe that these features are characteristic of prolapsing left atrial myxomas and it is their movement back and forth across the mitral orifice which results in the observed hemodynamic effects. In contrast, the other three patients (cases 3, 4, and 5) had hemodynamic features indistinguishable from that of mitral valvular stenosis (fig. 2), in which there is no notch present in the ascending limb of the left ventricular pressure pulse and the y descent is relatively slow. In these cases, the cineangiocardiograms revealed that the tumors remained in the left atriuim during the entire cardiac cycle (fig. 4). Accordingly, flow across the mitral valve was impeded throughout diastole, causing a relatively slow y descent. These features are referred to herein as Type 1I left atrial hemodynamics of nonprolapsing left atrial myxomas. At surgery, none of these cases had mitral valvular stenosis, and the mitral valves were normal in all patients except for one (case 3), whose mitral valve was thickened and fibrotic. In this patient, thickening and fibrosis of the mitral valve was felt to have (tirutlatioui, Volumne 51, February 197,5
Downloaded from http://circ.ahajournals.org/ by guest on March 18, 2015
347
LEFT ATRIAL MYXOMAS
9
?'
~_0^
1 lvs
Ao
AMV
RPAs
(LA) MYX
PLV Fi
-6
Figure
6
by movitg transducer along the ajor left ventnricular axis frornl the left v ntricle (left) to the level of the aorta (Ao) (rig/it). The diastolic slope of anterior nmitral leaflet (AMVI) closuire is reduiced reflecting decreaised flow across the mitral valve. As the tultrasouind beam is directed superiorly, ablnornmal
Case 4. Echocardiogram obtained rn
e
echoes originatin?g from the miyxonia
Figure 5
resulted from longstanding trauma due to the motion a calcified atrial myxoma, since there was neither commissural fusion nor microscopic evidence of rheumatic process. The echocardiograms of the two patients (cases 4 and 5) with nonprolapsing left atrial myxoma (figs. 5, 6, and 7) were consistent with the observed hemodynamic events. The tumor echoes were identified in the left atrium but not within the left ventricle during diastole in contrast to the usual echocardiographic findings that have been described for left atrial myxoma.23 27 The motion of the anterior mitral leaflet was completely normal in one patient (case 5). Both of these patients also illustrate the particular value of direct echocardiographic examination of the left atrium when a nonprolapsing tumor is present. Such direct examination of the left atrium along the long axis of the left ventricle in the presence of suspected nonprolapsing atrial myxoma was first suggested by Popp and Harrison.28 We found the suprasternal approach proposed by Goldberg" an of
Circulation,
'olumie,i .5
ebruary
atriurm
become apparent.
to
Case 5. Snprazstern7al approac/. The left atriumi (LIA) is almost cotmpletely filled with abnormal echoes which origincate from the inyxonma (MYX). The tunmor remains w;it/lin the left atrium durinrg the eiitire cardiac cycle. CW=-chest wall; ECC = electrocarright pulimonary artery diogram.; IfPA
(MX1tYX) uitliin t/ie left
The echisoes frorm the tumor are seen to fill abouit the level of the descend only the left atrium and atriouenetriciilar cantal imriiediately behind tde proximal attachment of the anterior mitral leaiflet. IVS = interventricular septum,; PLY' = posterior left venttricular wall. (I.A)
effective (fig. 6).
means
to
of examining the left atrium directly
Features similar to our Type II left atrial hemodynamics have been reported in a single patient with left atrial myxoma as an "unusual" finding.29 However, three of our five patients demonstrated these changes. The importance of Type IT left atrial hemodynamics in the presence of left atrial myxoma has not been emphasized previously. Although because of the small number of cases included in this report, statistically one cannot draw a conclusion, we do, however, believe that these changes, related to nonprolapsing tumors, occur more frequently than is generally realized. Failure to recognize this phenomenon may lead to unnecessary and potentially hazardous transseptal left heart catheterization in patients with left atrial myxoma.21 30 In conclusion, two variations in left atrial hemodynamics may occur in left atrial myxoma. In Type I, or prolapsing myxoma, there is a notch in the upstroke of the left ventricular pressure pulse and
1975
Downloaded from http://circ.ahajournals.org/ by guest on March 18, 2015
SUNG ET AL.
348
-11
'vs ao
TX
AMV mMYX U-'V
A ~.
I,tS f._t -w r':
| j
J
Figure 7 Case .5. By conventional method, the ultrasound beam is directed from t h e left ventricle (left) a long the nmajo r axis to th2e level of the aortwi root (Ao) and the left atrium (LA). Note the movement of the anterior mitral leaflet (AMV) is nornmal anid is n1ot stuggestive of obstruction to the flow from the left atriun. oNo abnormcal echoes are identified hehinr d thie mnitral leaflet. Abnormally moving echoes originatingfroni the myxomna (MYX) can l)e identified behind the posterior aortic rooi withlinl the left atrium Except for their utnusual motion, they might be confused withi calcificatiorn of the rnitral rirng. (CW= chest wall;, CC = electrocardiogram; RPA = right pulmonary artery. Noise echoes seen in this photograph result from-t tihe high sensitivity settinigs required for recording as well as reverbertation artifacts produced by poor sound trarismiissionr chlar(cteristics associated with mild obstructive pulnionary disease.
prominent c and v waves with a rapid y descent are present in the pulmonary wedge or left atrial pressure pulse. In Type II, nonprolapsing myxoma, there is no notch in the upstroke of the left ventricular pressure pulse and the y descent of the pulmonary wedge or left atrial pressure pulse is slow and indistinguishable from that of mitral valvular stenosis. The important contribution and value of well performed echocardiography in the precatheterization assessment of patients with suspected mitral valve disease is emphasized. It is stressed that irrespective of the left atrial hemodynamic findings, pulmonary angiography with observation of the levophase should be performed in any patient with clinical or echocardiographic evidence suggestive of left atrial myxoma. Acknowledgment W'e are in(lebted tn Dr. Dan Rnehm for referring case 5, to Mr. William Embii anid Mr. Frank Garcia-Moiites for their technical
assistance in preparinig this manuscript, and George Bouchoe for tie art work.
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i-
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diographic, echocardiographic, hemodynamic, and angiographic features in nine cases. Am Heart J 83: 810, 1972 7. FiSH RG, TAKARO T, CRYMES T: Left atrial pressure pulses in the presence of myxoma. Circulation 20: 413, 1959 8. WINTERS WL, MARK GE, SOLOFF LA: Left atrial pressure curve in left atrial myxoma. Arch Intern Med 107: 128, 1961 9. OGNIBENE AJ, NELSON WP: Atrial myxoma: Comments on hemodynamic alterations. Report of a case. Dis Chest 52: 699, 1967 10. FEIGENBAIxi H: Echocardiography. Philadelphia, Lea and Febiger, 1973, ch 3, pp 37-41 11. GOLDRBERL BB: Suprasternal ultrasonography. JAMA 215: 245, 1971 12. GooDW,1IN JF: Diagnosis of left atrial myxoma. Lancet 1: 644, 1963 13. GOODWIN JF: Symposium on cardiac tumors. Am J Cardiol 21: 307, 1968 14. H ARXVEY WP: Clinical aspects of cardiac tumors. Am J Cardiol 21: 334, 1968 15. GREENWOOD WF: Profile of atrial myxoma. Am J Cardiol 21: 367, 1968 16. GREENXVOOD WF: Myxoma of the left atrium. Br Heart J 22: 189, 1960 17. NASSER WK, DAXIS RH, DILLON JC, TAVEL ME, HEL.NIEN CH, FEIGENBALUNI H, FISCH C: Atrial myxoma. I. Clinical and pathological features in nine cases. Am Heart J 83: 694, 1972 18. ADAMIS CW, COLLINS HD, DuNINIITI GS, ALLEN JH: Intracardiac myxomas and thrombi: Clinical manifestations,
349 pathology and treatment. Am J Cardiol 8: 176, 1967 19. CASTANEDA AR, VARCo RL: Tumors of the heart: Surgical considerations. Am J Cardiol 21: 357, 1968 20. KABBANI SS, COOLEY DA: Atrial myxoma: Surgical considerations. J Thorac Cardiovasc Surg 65: 731, 1973 21. THoNIAS KE, WINCHELL PC, VARCO RL: Diagnostic and surgical aspects of the left atrial tumors. J Thorac Cardiovasc Surg 53: 535, 1967 22. MOSCOvlITz HL, PANTAZOPOULLOS J, BODENHEINIER M, STEIER M, GELB IJ: Simulated left atrial tumor. A hemodynamic, echocardiographic and cineangiographic study. Am J Cardiol 34: 63, 1974 23. WOLFE SB, Popp RL, FEICENBALNI H: Diagnosis of atrial tumors by ultrasound. Circulation 39: 615, 1969 24. Popp RL, HARlISON DC: Ultrasound for the diagnosis of atrial tumor. Ann Intern Med 71: 785, 1969 25. KoSTIS JB, MACHAD)Am AN: Echocardiographic diagnosis of left atrial myxoma. Chest 58: 550, 1970 26. FiNEGAN RE, HA.RISON DC: Diagnosis of left atrial myxoma by echocardiography. N Engl J Med 282: 1022, 1970 27. SPENCER WH, PETER RH, ORGAIN ES: Detection of a left atrial myxoma by echocardiography. Arch Intern Med 128: 787, 1971 28. Popp RL, HARRIISON DC: Ultrasound for the diagnosis of atrial tumor. Ann Intern Med 71: 785, 1969 29. BOWVER PJ, RITTER DG, CALLAHAN JA, ZITNIK RS: Unusual
hemodynamic findings of diagnostic value in a case of left atrial myxoma. Am J Cardiol 23: 592, 1969 30. MARPOLE DGF, KLOSTER FE, BRISTOW JD, GRISWXoLD HE: Atrial myxoma. A continuing diagnostic challenge. Am J Cardiol 23: 597, 1969
Circulation, Volume 51, February 1975 Downloaded from http://circ.ahajournals.org/ by guest on March 18, 2015
Hemodynamic features of prolapsing and nonprolapsing left atrial myxoma. R J Sung, A R Ghahramani, S M Mallon, S E Richter, L S Sommer, S Gottlieb and R J Myerburg Circulation. 1975;51:342-349 doi: 10.1161/01.CIR.51.2.342 Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 1975 American Heart Association, Inc. All rights reserved. Print ISSN: 0009-7322. Online ISSN: 1524-4539
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