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The Syndrome of Severe Mitral Regurgitation with Normal Left Atrial Pressure By EUGENE BRAUNWALD, M .D., WILLIAM C. AWE, M.D. Downloaded from http://circ.ahajournals.org/ by guest on April 30, 2017 of them. All ten patients were severely disabled and were considered, on clinical grounds, to be in functional classes III or IV (New York Heart Association). The patient with congenital mitral regurgitation had symptoms for 1 year, whereas the other patients had symptoms for 4 to 19 years (average of 9.3 years). All patients complained of severe fatigability and various degrees of exertional dvspnea. Symptoms or clinical signs of left ventricular failure had been present for 1 to 8 years (average of 3.2 years). All 10 patients were receiving maintenance digitalis therapy at the time of study and had been receiving this medication for 1 to 33 years (average of 7.4 years). Five patients had experienced paroxvsmal nocturnal dyspnea, two of them had had hemoptvses, and five had had ankle edema. Physical Examination All 10 patients had prominent left ventricular lifts and in five of tlhem a strong svstolic thrill was palpable at the apex. A holosystolic murmur, of at least grade III/VI intensity, was heard at the apex and was transmitted into the axilla in all 10 patients, and nine of them also had tie short, low-pitched, mid-diastolic murmur at the apex, which is typically heard in patients Witll severe mitral regurgitation.'6 Hepatomegaly and edema were present in only three instances. None of the patients had clinical or laboratory evidence suggestive of active rheumatic fever at the time of study. Electrocardiograms All 10 patients exhibited atrial fibrillation. Riglit axis deviation was present in one patient, while in the other nine the electrical axis was normal. The voltage criteria for left ventricular hvpertrophyv were satisfied in seven patients. IT HAS BEEN demonstrated repeatedly that when mitral regurgitation is produced in experimental animals, an elevation of left atrial pressure occurs.1-3 Similarly, numerous hemodynamic studies in patients with this valvular lesion have shown that the left atrial413 or pulmonary artery wedge pressures'14 15 generally exceed the values observed in normal individuals, and the V-wave peaks in these pressure pulses are particularly prominent. These pressure elevations have been attributed to the increased volume of blood that enters the left atrium during ventricular systole.1 6 Indeed, elevation of the mean left atrial pressure with particularly tall V waves has become the hemodynamic hallmark of mitral regurgitation, and the diagnosis of this abnormality by cardiac catheterization has been based, in large measure, on these characteristic pressure changes. It is the purpose of this report to focus attention on a group of patients with severe mitral regurgitation in whom these alterations in the left atrial pressure pulse are not evident, and who appear to constitute a distinct segment in the clinical-hemodynamic spectrum of mitral regurgitation. Description of Patients Studies on a total of 10 patients constitute the basis of this report. Congenital mitral regurgitation was present in one patient, an 8-year-old girl. The other nine patients (seven women and two men) have acquired rheumatic mitral valvular regurgitation. These nine patients ranged in age from 27 to 49 years, with an average age of 39 years. History A history of active rheumatic fever was elicited from all nine patients with rheumatic mitral regurgitation, and multiple attacks occurred in seven Roentgenograms Gross cardiac enlargement was evident on the chest roentgenograms of all 10 patients. The left atrium was considered to be nmoderately enlarged in three patients, and markedly enlarged in the remainder (fig. 1). Although it was difficult to define the presence or absence of left ventricular enlargement, this chamber was considered to be enlarged in eight of the 10 patients. Hemodynamic Studies The pulmonary artery or right ventricular svs- From the Cardiology Branch and the Clinic of Surgery, National Heart Institute, Bethesda, Maryland. Circulation, Volume XXVII, January 1963a AND 29 BR3AUNW Alj1). A \V E 30 Downloaded from http://circ.ahajournals.org/ by guest on April 30, 2017 Figure 1 r -dreifpt1qit(oifJo. mrked left atiail enlaJ -.?Rovean tgenoyrams of patient.s with sel itrmitrl mnto t. oad nortttol left atril pXressre.. tolic pressures were witlhin norimial limits for this laboratory (under 30 inni. Hg) in all, except patient R.F. (table 1). The miiean pulmonary artery pressures ranged from-: 13 to 22 mm. Hg. Left atrial pressures. miieasured bv the transseptal17 or transbronchial'8 teehnies, were within the normaal range for this laboratorvI9 (table 1 and figs. 2 and 3). The V-wave peaks were minimally elevated in only three patients, amid were within nonral limits in the other seven patients. The left ventricular end-diastolic pressure ranged froml 2 to 13 mm. Hg. Cardiac output measured by the indicator-dilution technic was abnormallv low in five of seven patients. In eight of the patients indicator-dilution curves recorded from a svstemic artery following injection into the left ventricle or left atrium were eharacteristic of muitral regurgitation (fig. 3). Pathologic Data Nine of the 10 patients included in this report are alive, so that pathologic data are available on one patient (S.H.). In this 8-year-old girl the left ventricle was hypertrophied, and the left atrium was markedly dilated. The anterior mitral leaflet was shortened, and the chordae tendineae to both leaflets were markedlv shortened, preventing valve closure. Discussion The hemodynamie findings ill patients with iititral regurgitation have been well documented.4 15 In patients in whom this is the predominaiit valvular lesion. and who exhibit. congestive heart failure or symniptomxls of di minished cardiac reserve, the cardiac output has frequenitly been noted to be below normal. the mean left atrial pressure elevated, anid the 'V'-wave peaks have been particularly high In a signlificant number of such patients, the pulmonary artery pressure is elevated proportionately inuore than the left atrial pressure due to associated elevations of the pulnmonarv vascular resistance. In this latter group of patients clinical inanifestatioiis of right heart failure are not untusual.5 20 Perusal of the published clinical and hemodynamic data obtainied from patienits with mitral regurgitation has re-vealed an occasional exception to this pattern. In each of several series of patients with this valvular abnormality there have been one or two patients who evidently exhibited clinical maniiCirculation TVofume XXVII Tanutary 196i. 31 SEVERE MITRAL REGURGITATION Downloaded from http://circ.ahajournals.org/ by guest on April 30, 2017 festations of reduced cardiac reserve and who had left atrial enlargement but in whom the left atrial (or pulmonary artery wedge) pressures were within normal limits.8' 10, 13, 20 The data obtained from the patients described in this report focus attention on the syndrome of severe mitral regurgitation with normal left atrial pressure. On clinical grounds, all 10 of these patients had a markedly reduced cardiac reserve, and several were considered to be approaching the termination of their illness. With the exception of the child with congenital mitral regurgitation, the other nine patients had symptoms for many years. The chronicity of the process was also reflected in the atrial fibrillation in all 10 patients. The clinical findings characteristic of mitral regurgitation were unequivocal, and there was no clinical or hemodynamic evidence of any associated cardiovascular abnormality. Whereas other series of patients with rheumatic mitral regurgitation have had a preponderance of male patients,21-23 seven of the nine patients with rheumatic heart disease included in this report were female. Although a history of active rheumatic fever has been reported in 25 to 50 per cent of patients with chronic mitral regurgitation,8 22 it could be elicited in all nine patients with rheumatic mitral regurgitation reported herein. Atrial fibrillation and gross left atrial enlargement were present Figure 2 Left atrial (LA) pressure pulse of patient I.H. in all 10 patients. Although absolute measurements of mitral regurgitant flow in man are not feasible, the contour of the arterial indicator-dilution curves following injection into the left side of the heart were suggestive of massive regurgitation (fig. 3).. If the compliance of the left atrium remained constant, enlargement of this chamber could occur only in association with an increase in the transmural pressure. The association of a normal mean left atrial pressure and a normal left atrial V wave, with a markedly enlarged left atrium indicates that the walls of the left atrium and of the pulmonary venous bed are more compliant than Table 1 Hemodynamic Findings PA Age, yrs., Patient sex S/d, mean mm. Hg LA, mean mm. Hg LA, "V" wave peak mm. Hg LA-LV LVED mm. Hg end-diast. grad. mm. Hg Cardiac index L./min./M.2 1 1.21 6 11 23 27/ 43, F L.P. no. 00-82-40 1.73 5 11 3 0 25/7 (13) P.K. no. 02-68-76 44, F 3 1.07 8 11 3 25/9 (15) H.E. no. 02-55-35 45, F 2 2.68 16 7 10 27/5 (18) 49, F I.R. no. 03-38-41 .. 2.53 14 7 28/10 (20) 40, F A.P. no. 01-25-02 22 0 12 4 32/14 (22) R.F. no. 03-29-28 47, M 22 0 1.40 12 7 28/9 (19) 38, F E.C. no. 03-75-61 2 15 13 9 26/10 (20) R.G. no. 02-96-85 24, F 12 2 3 3.30 9 25/10 (18) B.R. no. 03-88-86 27, M 14 0 8 7 S.H. no. 03-07-20 28/12 (20) 8, F PA, pulmonary artery pressure; S/d, m, systolic/diastolic, mean pressures, LA, left atrial pressure; LVED, left ventricular end-diastolic pressure; LA-LV end-diast. grad., left atrial-left ventricular end-diastolic pressure gradient. Circulation, Volume XXVII, January 1963 32 2BRAITINWALD, AN\V SH #03-07-20 72706 LA !NJ LVI Hg 24 2~ Figure 3 (Ieft) o n t(i0 itin0 s lov<ing ecoi (-id((cthieter le(/ withdr(11v01( from left ventricle (LV) to lett (tl (niu in p ottiet S.1I . Note tli vle ( of left atrial press-ire an1d the absence of a p2iessure gradie-nt across the ioitral l(cclve. Thei ilidici1to1dilation1 0/liC.e on? the right recordedfironm the brachial arlter!y folliorItlfin jectiOnl i) t O the left 111s Downloaded from http://circ.ahajournals.org/ by guest on April 30, 2017 was a t rin (m. usual in the patients described herein. It is s-uggested that long-standing mnitral regurgitation may, in some instances, alter the lengthtension characteristics of the left atrial wall alid therely displace the atrial pressure volnine curve to make it more complianit. so that a niormal pressure exists in a greatli- enilarogd atrium. The possibility that alterations in the pressure-voluimne relationships of the left atriumi m-ay oceur is not a new coneept. It has been postulated by a number of investigators that differenices in atrial comipliance ocecir among dlifferent patients witlh mitral valvex disease0' 13 20, 24-26 Indeed, the difficulties encounitered with analvses of the left atrial pressiure pulse contouir for the separatiomi of patients withl mtitral stenosis froni tihose withi mlitral reg;urgitation ha>ve been attriblnted to variatiomis in the pressure-volume relationships Hin the left atrin-i amid tIme pull-moiary ve-lIus bede6 Although it is possible that chron-iie aetive rheumatic fever played a role in time alterationis of the umechanical properties of tIhe left atriumi. it is evident tliat, since one of the patients( S.H.) haad congenital ratlher thami :rheummatie) disease, the presence of lheumiatic aetiviti is certainl1 not essential to the devel- opmetit of the sv ldromle describedl. Furtfiei milore, none of the nine patienits w:ithi rhen-niatie; umitral regurgitation (cI bIte( anv clinieal or laboratory finidings tlhat sniggeste( the presenee of rheumyiatie aetivity. Sincee all of the patienits had had mlitral regurgoitatio)n for manyr years, it is likely that the chlanges ini atrial distensibility that wvere present lfl thle timne of study had niot beeln present earlier. but had(leveloped duninig the course of the illness. 1 nfortunmately, serial incasuellntents of a tral )pressure lad u-ot been (arr-i 'ed ontt on a,- of thtese latielilts. Studies on a patie-nt n-iot inielucled in this series.2 r ide s(tro::ll suggestive evidenee tfiat tlie inc(-rease in atrial couliplianlee muay Oldr as a late dcvelopmient iii the eourse of elron:ie initral recurgitatiolln Tjiis 9-vear-old boy (levelopedl exertiomal dvspnea at the age of S yeairs and exainina'Itioii at this time revealed that hie had a ret(u-m lar rlythm and the physieal findinigs efiar-ae, teristie of mi-tral recfurgitation. Right heart (athiete rizationi, r --Ivealed elevationi of tile pul 40 monarv arterv pjressure 'S/30, m1-ean ina. Ji r? and transseptal left lheart eatheterizatio0 shiow(-e,d thie left atrial press-ure to be, ed VaI ted C'IsAsTwell I" m-lean- t21 nlm. HI-, V peak: 45) nuns. Ei )Y. The lpatient s syniptomns of eo-ne,stiveiheart failure increased in severity in s];)ite ofr intelisive thelrapv and I vear after thlese,i studies his cardiae rhythmn changed to atrial fibril lation. There was roentgenographie evidence of further increase in the size of tIme left atriui, bhut surprisinclv, the left atria] (gI> eani pressure liad declined cluite strikinigly 15) nim. Hig. V peak - 24 mlm. Ig). Thus, in tfiis patieilt a decline in the imean- left atrial pressu.re an-id tlhe atrial V-wave pealk )resltXle oeciUre(nr in the faee of ani. increase in left atrial size. Since he slhimved striking Tlin ial imnprovemenit a fter operatioin whicel aNl (lts accomipanied b)yr a further decline. of atrial pressure to a mnean of 7 iim. Hg, as xvelI as sponta:neous reversioni to si4nus rhythmi, it would appear that the imierease in atrial eomnplianice is not necessarilv aecoipanied by irreversible depression of left venitricular functioni. The presenee of atrial fibrillation ini thle 10 patients (described herein. as well as I i,J (tv Crculautieon, Volume XX el(try i96A SEVERE MITRAL REGURGITATION Downloaded from http://circ.ahajournals.org/ by guest on April 30, 2017 the transient period of fibrillation in patient A.J. discussed above, suggests the possibility that the process that changed atrial compliance may also have been related in some fashion to the development of this arrhythmia. The compliance of the left atrium and pulmonary venous bed appears to be capable of modifying profoundly the clinical and hemodynamic picture exhibited by patients with mitral regurgitation. On the basis of differences in atrial compliance, three major groups of patients with mitral regurgitation can be identified: 1. A group of patients with mild or moderate enlargement of the left atrium, but with quite striking elevation of the mean left atrial pressure, and particularly of the V wave. In many patieiits in this group, severe mitral regurgitation has developed acutely, as for example those in whom there occurs sudden rupture of chordae tendineae or a tear of a mitral leaflet (fig. 4). Marked elevation of pulmonary vascular resistance occurs with considerable frequency in this group of patients, and therefore right heart failure is not an unusual clinical manifestation.8 2. By far the most common group of patients with mitral regurgitation is represented by those with moderate or massive enlargement of the left atrium, associated with significant elevations of the left atrial pressure. 3. The third group of patients in this spectrum is represented by the patients with the syndrome of severe chronic mitral regurgitation and normal left atrial pressure described in detail in the present report. It seems likely that these three groups form a continuum and that numerous gradations exist between them. Since effective surgical treatment for mitral regurgitation is now becoming a reality,28 29 some comment is warranted on how the variations of left atrial compliance, and the resultant clinical-hemodynamic findings modify the selection of patients. Since, with any given magnitude of regurgitant flow the atrial pressure varies inversely with the compliance of the atrium, the extent to which the atrial pressure can be expected to decline following successful operation will also vary inversely with atrial compliance. Accordinigly, the cliniCirculation, Volume XXVII, January 1965 B. MM. Hg [-0.3 sec.-i Figure 4 Chest roentgenogram (Top) and left atrial (LA) pressure pulse (Bottom) obtained from a 23year-old woman who suddenly developed mitral regurgitation two months before these studies during the course of acute bacterial endocarditis. Although the left atrial enlargement is similar in degree to that exhibited by many of the patients described in this report, note the elevated lef t atrial pressure with particularly tall V waves. cal and hemodynamic benefits of operation may be expected to be greatest in the patients with relatively small left atria and high left atrial pressures. Conversely, the benefit in the patients described in this report would not be expected to be as striking, since their left atrial pressures cannot decline to any significant extent. By diminishing the hemodynamic burden imposed on their left ventricles, however, operation may be expected to elevate the low cardiac outputs in these 34 patients. Indeed, a number of observations suggest that operative intervention should also be considered in patients with the syndrome of severe mitral regurgitation and normal left atrial pressure. Among these are (1) the favorable effects of operation in patient A.J. described above, (2) the fact that patient S.H. succumbed to chronic congestive heart failure in spite of the finding of a normal atrial pressure at catheterization carried out several months earlier, and (3) the faet that these patients, in spite of normal atrial pressures, were all incapacitated. Downloaded from http://circ.ahajournals.org/ by guest on April 30, 2017 Summary It has been generally thought that significant elevations of the left atrial and pulmonary vascular pressures occur in patients with mitral regurgitation of sufficieint severity to produce serious disability and gross enlargement of the left atrium. Ten patienits with severe mitral regurgitation have been encountered in whom gross left atrial enlargement was accompanied by normal left atrial and pulmonary artery pressures. These patients ranged in age from 8 to 49 years, all were in functional classes III or IV, atnd the average duration of symptoms was 7.3 years. Nine patients had rheumatic mitral regurgitation while one had a congenital lesion. Atrial fibrillation and the physical findings of pure mitral regurgitation were presenlt in all patients, as was striking left atrial enlargement on their roentgenograms. Left atrial pressure. determined by left heart catheterization, averaged 9.1 mm. Hg and did niot exceed 12 mmn. Hg in any patienit, and the V wave was not particularly prominent. The eardiae index was markedly depressed aind averaged 2.0 L./min./M.2 B.S.A. The observed discrepancy between left atrial size and pressure must reflect a disturbance in the compliance of the left atrial wall. It is suggested that long-standing mitral regurgitation may modify the meehanieal characteristics of the atrial wall and that the presence of a normal left atrial pressure must not be assumed to exclude the presence of severe mitral regurgitation. The manner in BRAUNWVALD, AWE which variations in left atrial compliance affect the clinical picture of mitral regurgi tation and the selection of patienits for operative intervention are diseussed References 1. WIGGERS, C. J., AND FEIL, H.: The cardio dynamici of mitral insuffieiency. Heart 9: 149, 1922. . HALLER, J. A., AND MORROW, A. G.: Experimental miitra1 insufficiency: AIn operative method witi chronic survival. Anni. Surg. 142: 37, 1955. 3. BRAxNvxxWALD, E., WELCH, G. TH., AND SARNOFi', S. J.: The hemod.ynamic effects of quantittai tively varied experimental mitral regurgitation. Circulation Research 5: 539, 1l937. 4. 1ENT, E. AM., FORD, W. B., FIsHER, 1). L., xi) THERON, C. B.: The estim-ationt of the sexerity of mitIral regurgitationi. An.n, Surg. 141: 47. 1955. 5. MIUSSER, B. G., IOUGAS, J., AND GOLDBERG, H.: Left hieart catheterization: IT. With particular' referenee to mitral and aortic valvular disease. Am. Heart J. 52: 567, 1956. 6. MORROW, A. G., BRAvxwWALD, E., HELLER, J. A., AND SHARP, E. H.: Left atrial pressure pulse in mitral valve disease: A. correlation of pressures obtained by transbronclhial puncture witl the valvular lesion. Cireulationi 16: 399, 1957. R. C., 7. DEXTER, L., NOVA\CK, P., PHINNEY, A. D., .INT_ TixiHNES, F. W.: Mitral insufficelency. Ti. A. . ti. 'P.vsiviciiifs 70: 2f6, 1957. 8. Ross, J., JR., BRATv)vNALD, E., AND MORROW, A. G.: Clinical and hemodvnamie observations in puire mitral iisufficieaicy. Akm. J. Cardiol. 2: 11, 1958. 9. MARSHALL, H. W., WOODWrARD, E., JR., AND WOOD, E. H.: Hemodynamic methods for differentiation of mitral stenosis and regurgitation. Am11. J. Cardiol. 2: 24, 1958. 1.O. DAVILA, "T. C., GLOVER, R. P., VocI, G., JUMBALA, P., TROUT, R. G., AND FRITZ, A. J.: The clinical and physiologic criteria for surgical cor rection of mitral insufficiency. J. Thoracic Surg. 35: 206, 1958. 11. HARVEY, R. M., AND FERRER, M. 1.: A consideration of hemodynamic criteria for operability in mitral steinosis and in mitral insufficiency Circula.tion 20: 442, 1959. 12. DuTREY, D. E., AND DRAKE, E. H.: Pre-operative diagnosis of acquired valvular disease. Am. J. Cardiol. 8: 319, 1961. 13. BENTIVOGLIO, L., URICeHIO, J., AND GOLDBERG, H.: Clinical and hemodynamic features of advanced rheumatic mitral regurgitation. Am. J. Med. 30: 372, 1961. 14. GORLIN, T., TLEWIS, B. M., HAYNES, F. W., AND Circulatio n, Volucme XXVII, January 196S 35 SEVERE MITRAL REGURGITATION 15. 16. 17. Downloaded from http://circ.ahajournals.org/ by guest on April 30, 2017 18. 19. 20. DEXTER, L.: Studies of the circulatory dynamics at rest in mitral valvular regurgitation with and without stenosis. Am. Heart J. 43: 357, 1952. CONNOLLY, D. C., AND WOOD, E. H.: Hemodynamic data during rest and exercise in patients with mitral valve disease in relation to the differentiation of stenosis and insufficiency from the pulmonary artery wedge pressure pulse. J. Lab. & Clin. Med. 49: 526, 1957. NIxON, P. G., WOOLER, C. H., AND RADIGAN, L. R.: The opening snap in mitral incompetence. Brit. Heart J. 22: 395, 1960. BROOKENBROUGH, E. C., BRAUNWALD, E., AND Ross, J., JR.: Transseptal left heart catheterization. A review of 450 studies and a description of an improved technic. Circulation 25: 15, 1962. MORROW, A. G., BRAUNWALD, E., HALLER, J. A., AND SHARP, E. H.: Left heart catheterization by the transbronchial route: Technic and applications in physiologic and diagnostic investigations. Circulation 16: 1033, 1957. BRAUNWALD, E., BROCKENBROUGH, E. C., FRAHM, C. J., AND Ross, J., JR.: Left atrial and left ventricular pressures in subjects without cardiovascular disease. Circulation 24: 267, 1961. BENTIVOGLIO, L., AND UTRioHio, J. F.: The paradox of right ventricular enlargement in mitral insufficiency. Am. J. Med. 24: 193, 1958. 21. CABOT, R. C.: Facts on the Heart Philadelphia, W. B. Saunders Company, 1926, p. 29. 22. BRIDGEN, W., AND LEATHAM, A.: Mitral incompetence. Brit. Heart J. 15: 55, 1953. 23. WOOD, P.: An appreciation of mitral stenosis Parts I and II. Brit. M. J. 1: 1051, and 1113, 1954. 24. DEXTER, L., MCDONALD, L., RABINOWITZ, M., SAXTON, G. A., AND HAYNES, F. W.: Medical aspects of patients undergoing surgery for mitral stenosis. Circulation 9: 758, 1954. 25. HAMER, M. B., SujoY, B. R., AND Dow, J. W.: Determinants of the left atrial pressure pulse in mitral valve disease. Circulation 19: 257, 1959. 26. FAIRLEY, K. F.: The influence of atrial size and elasticity on the left atrial pressure tracings. Brit. Heart J. 23: 512, 1961. 27. CARNEY, E. K., BRAUNWALD, E., ROBERTS, W. C., AYGEN, M. M., AND MORROW, A. G.: Congenital mitral regurgitation. Am. J. Med. 33: 223, 1962. 298. BRAUNWALD, N. S., COOPER, T., AND MORROW, A. G.: Complete replacement of the mitral valve. Successful clinical application of a flexible polyurethane prosthesis. J. Thoracic & Cardiovasc. Surg. 40: 1, 1960. 29. STARR, A., AND EDWARDS, M. L.: Mitral replacement: The shielded ball valve prosthesis. J. Thoracic & Cardiovase. Surg. 42: 673, 1961. Training the Doctor of Tomorrow In matters of health and medical care, the doctor no longer stands alone. He continues to be the leader and captain of the team, or teams, but he is assisted by at least 132 groups who have been specially trained in careers of health service. There are in the United States 2,500,000 people engaged in the so-called health professions. Today, doctors do many things. There are thousands of doctors who are never seen at a patient's bedside. Dr. A travels to the hospital administrator's office or to the Dean's office with a brief case; Dr. B spends his working life amid test tubes; Dr. C. is a detective who can tell whether a woman was hanged or strangled; and Dr. D. tests whether atom scientists have absorbed excessive radiation. Thus, I could go on and on, down the alphabet several times. The doctors who treat patients, however, whether in their offices or at the bedside, are the men responsible for the doctor-patient relationships and are largely responsible for the public attitudes about the profession.-CHESTER S. KEEFER, M.D. Training the Doctor of Tomorrow, Boston, The Boston Medical Quarterly 12: 87, 1961. Circulation, Volume XXVII, January 1963 The Syndrome of Severe Mitral Regurgitation with Normal Left Atrial Pressure EUGENE BRAUNWALD and WILLIAM C. AWE Downloaded from http://circ.ahajournals.org/ by guest on April 30, 2017 Circulation. 1963;27:29-35 doi: 10.1161/01.CIR.27.1.29 Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 1963 American Heart Association, Inc. All rights reserved. Print ISSN: 0009-7322. Online ISSN: 1524-4539 The online version of this article, along with updated information and services, is located on the World Wide Web at: http://circ.ahajournals.org/content/27/1/29 Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published in Circulation can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial Office. Once the online version of the published article for which permission is being requested is located, click Request Permissions in the middle column of the Web page under Services. 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