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EARLY OPERATION FOR PAPILLARY MUSCLE RUPTURE
ing carbon assimilation. nitrogen assimilation, carbohydrate fermentation, starch hydrolysis, and gelatin hydrolysis. I 0- 12 Regarding the morphologic characteristics which were relied upon for identification, it is important to note that Saccharomyces are ascomycetous yeasts. II Budding ceases at a certain stage of growth and the vegetative cells become transformed into ovoid asci, each containing four ascospores. Pairs of germinating ascospores, or the first vegetative cells produced from them, fuse to form diploid vegetative celIs. 12 Diploidy is maintained throughout the entire subsequent period of vegetative development, and meiosis occurs directly prior to formation of ascospores. 11 Other ascomycetous yeasts do not reproduce in exactly this same manner and thus have different characteristic morphologic forms. I " In this case, the characteristic ovoid asci containing four ascospores were demonstrated in all isolates by a modified acid-fast staining technique. ;'\0 attempt was made to identify the organism according to species because there is a difference of opinion concerning criteria for species differentiation among various authors. I :<-1 r, It is unfortunate that identification was not made of the yeasts isolated from the blood and urine during the eighth and twelfth weeks after surgery. These organisms were shown to be true yeasts by morphologic characteristics and carbohydrate fermentation studies. I " The fact that they were true yeasts, and not the more common yeast-like pathogens such as Candida, suggests that they were the same type of fungus, Saccharomyces, that was recovered from subsequent blood samples. Those of us who did not see the patient until three months after surgery (P.S., A.F., and K.H.) wish to thank the physicians responsible for her care prior to that time. ACKNOWLEDG~IE:\"T:
REFERE:-;CES
2 3 4
5 6 7 8
Stein, PO, Harken, DE, Dexter, L: The nature and prevention of prosthetic valve endocarditis, Amer Heart J 71 :391,1966 Andriole, \iT, Kravetz, H~I, Roberts, WC, et al: Candida endocarditis, Amer J ~led, 32:251, 1962 Bessey, EA: ~Iorphology and Taxomony of Fungi, :'>lew York, Hafner Puhlishing Co., 1961 Louria, DB, Blevins, A, AnnstTong, 0, et al: Fungemia caused by "non-pathogenic" yeasts, Arch Intern \Ied 119:247, 1967 Ellis, CA, Spivack, ~IL: The sil':llificance of candidemia. Ann Intern \Ied 67 :.511, 1966 Shelburne. PF, Carey, RJ: Rhodotomla f"ngemia complicating staphylococcal endocarditis, JA\IA, 180: 118, 1962 Climie, ARW, Rachmaninoff, :--;: Fungal (Candida) endocarditis following open-heart surgery, J Thorac Cardiovasc Surg .50:431, 1965 Leffert, RL, Hackett, RL: Aspergillus aortitis following replacement of aortic valve. J Thorac Cardio\'asc Surg 53:866,1967
CHEST, VOL. 58, NO.2, AUGUST 1970
9 :\"ewman, \VH, Cordell, AR: Aspergillus endocarditis after open-heart surgery, J Thome Cardiovasc Surg 48:6,52, 1964 10 Aiello, L, Georg, LK, Kaplan, W, et al: Lah \Ianual for ~le.Jical ~Iycology, Puh. No. 994. 1966, Public Health Sen'ice, U.S. Department Healtb, Education and \\'elfare, 1966 11 Stanier, RY, Doudorff, \1, Adelherg, EA: The ~Iicrobial World (2nd cd), Prentice Hall, Englewood Cliffs, 196.3 12 Henrici, A, Ordahl, E: The Biology of Baeleria (3rd cd) Boston, D. C. Heath and Co., 1948 \.3 Salle, A.J.: Fundamental Principles of Bacteriology (5th ed), '\ew York, ~lcGraw-HiII, 1961 14 Lodder, J, Kreger-Van Rig, i\JY: The Yeasts, Amsterdam, "orth-Holland Puhlishing Co., 1952 \.5 Skinner, CE, Emmons, C\V, Tsuchiya, H~I: Henric;'s ~lolds, Yeasts and Actinomycetes (2nd cd), '\ew York, John Wiley and Sons, 1948
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Reprint requests: Dr. Stein, University of Oklahnma School BOO Xortbeaxt Thirteenth StTeet, Oklahoma City, of ~Iedicine, Oklahoma 73104.
Successful Early Operation for Papillary Muscle Rupture* Robert F. DeBusk, .\I.D., Robert E. Kleiger, M.D., Carl L. Elmo/her, .\I.D., Pat O. Daily, M.D., and Donald C. Harri.son, .\I.D.
This is the earliest reported intervention in a syndrome which clinicians are seeing with increasing frequency. The diagnosis of a ruptured papillary muscle which is one of the disastrous complications of acute myocardial infarction requires early angiocardiography and catheterization when the condition is suspected. When adequate ventricular function is preserved, successful valve replacement is possible. hrnODlTTlO:-;
papillary muscle rupture has been considered a medical curiosity until recently. Recognition of this potentially treatable complication of myocardial infarction has been stimulated by the increasing frequency with which successful surgical treatment has been reported. This is the 22nd reported case of papillary muscle rupture approached surgically, and is to our knowledge the earliest surgical attempt following infarction. CASE REPORT
A .53-year-old electrician wa.' admitted to Stanford Vni\'ersit)' Hospital on Decemb"r II, 1968 hecause of chest pain. In 19.54, he had suffered an uncomplicated acute inferior wall mroeardial infarction. Five days prioT to admission, he had noted transient mild, right upper chest pain radiating to both sides of the neck; electTocardiogram and chest x-ra~ °From the Cardiology Division, Stanford University Sdl<~lJ of ~Iedicine, Palo Alto, California. This work was supported in part by '\IH Grants '\os. HE,5709 and HE-o.5866.
176
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t'xamination _~a\'(' normal rt's,dl<;;; there was no heart mumlUT. Thft,t> days prioT to admission SCOT and LDH were normal. FOUT hours prior to admb... ion the paht'nt e.xperienced st'\'t.'T(' left "nh'rioT du'st pain i.llld diaphoresis. On admission. hlood preSSllTP was 1IOrS(). pulse 60 and regular: the IIlIlJ!S W('f(' dear; a J.!rade 4/6 apical pansystn!ic 1111I TlIIlI T wa" nott'll. Chest pain was initially rdit·\"{·d hy lIleperidille; fOIlT houTs Iatt'r. dlt"st pain and diaphoresis r('('urred, ass(K'iah·d with a fall in hloml pressure to 70/50. The blood pn'SStlTt' \\'as t'lt'vatt:·d to U:=5/iO hy a continuous infusion of IIld;ui.\mlnol. \1odt·ratt·I,.· S('H'f(' dyspnt·a. cyanosi:-o. ami moist hasilar ralt,s appeared five hours after admission, Ch(,~t x-ray film revealed it normal sized Iwart with a right parahilar infiltratt· and slightly promim'nt pulmonary vr ildllli~sioll. In an attt'mpt to illlpron' urine output. IIIdaramillol was di"'l'(mtinued am'! ,~OO ml of 10 pt'r cent dt-'xtro:"e ill walt'r was infus('d over two and a half hours. Three hours after til(' :->tart of tIl(' infusion, ('cntral \'('nolls
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pn'ssure had risen from .1 to 1U elll of water and central \'f.'nOIlS oxygen saturation, with the patit'llt re('ei\'ing oxygen 6 L/min, had fallt-'n from .~() r)(:rt·t'nt to .31) Il(:rt't'nt. Dyspnea. rales, and cyanosis in<:reas(,d; intran'lHllls ftlr()seml output Tt.'lnaim'd scanty and hlood pr(,~~11ft· ,t;~hili7.ed tT oXYCt'li saturation 40 pt.'r<'t'nt. \\'h('n hlood pressure again fell. 23 hours after ;.lthnis~i()n, le\·i.lftt>rt'nol wa" infuwd to maintaill a pn"'llrt' of SO-S5 mill Ug Systolil', Ri\le~ )1t'rsistt'd to J,!ralh· 2'-(j and a third sound was notpd. Chest x-ray ('xamin.ttion [('\'('al('d normal heart size and in<.'Tt';:l<;t,d parahilar pulmonary infiltratt's. Tht' t,It'('trnl'anliocram now shfl\\'t'd de('p Q Wil\'I.'S and loss of H W
CHEST, VOL. 58, NO.2, AUGUST 1970
177
EARLY OPERATION FOR PAPILLARY MUSCLE RUPTURE
FIGt"RE :2. Photomicrograph of mitral vake and papillary Illusclp rt'lllo\'c.. d at surgery. In the top left corneT thl' rupttlred posterollwdial papillary muscle trunk is ShO\\'IL
eathd('rizatioll, pulmonary anl.!i()~raphy. and left ventricular angiography. The f()llowin~ prpSSUTes Wf're Tf?Corded: right atrium: 2 111m Hi! l1lt'an: ril.!ht w-'utride; 4H/O/4: end diastolic, pulmonary artery: .::;1/14/24 mean; pulmonary \'I.'edge
/2-/2-68
papillary llIuscie had mptured, 1..5 em from the lip, and had prolapsed into the left atrium (Fig 2). Utilizing total body h:rpothermia, aortic cross damping, and iced saline cooling of the heart. the mitral valve was excised and replaced with a ,"0... Starr-Edwards prostlwsis. St'\'('ral l'pis(KIt-'s of postopl>rativ(' \'entricular tachycardia were terminated hy intra\,pnous lidocaine. On tlw second post· Opt>rati\'p day. the t"'lectrocardiogram re\'l'alt·d tnl(' posterior and lateral wall infardion ( Fig 1 ), The remaining lXlstopt'rativ£' <"..nurse was unremarkahle, and the patient wa~ dischargt>d Oil the 17th hospital day on warfarin. :; 1llg I>t"r day. At thc timl' of follow-up cathcterization three months later, the patient bad worked at a desk joh for tluPe wet'ks without ,ul.l?;ina or t'xt'rtional dyspnea; exC<'pt for slight fatigu{' he felt t>ntirely well. Physical examination revealed. bl()(x! pressurt.> 120/80, pulse 80, regular. The neck "eins were not distl'Uded, the lungs W{'ft> dear, and. the heart wa.'.; not enlargt'1:L prosthetie \',ll\'l' sounds ''''t're nonnal and. there was no murmur or thrill. Tht' t-ll'ctTllcardiogram showed e"idt'nce (Jf (lid p()Sh'rit)T, inferior and lateral wall infarction; negati\'t' P t<.>rminal fnTt'('s in lead \'1 had inl'ft'ast'd and P wa\'es had hrnadt'lwd in inferior It'ads. Cardiac x-ray films demonstrated a normal sized heart with left \'('ntrkular prominence on the left illlterior ohliqlll' I'rojedion. Com hi ned right and It'ft hl'art ( rdrograde) catlll'krization re\'('aled tht' following pres'o\lIrt's: right atrium .5 mm Hg mean; pulmonary wedge "a" wan' 21. ,\." wan' 2S. mean 1.5 at rest (Fig :»), 2H/4.5/33 mean with eXt'reist,; left ,"('ntride 12-1/0/21 t'nd diastolic at rl'st. 140.-',5/:30 with l'xcrdse. There was a 2-3 mill Hg {'arly diastolic pressure gradient across the mitral "aln' at rest. Cardiac indt \\',l"; :2.3 L/min/\I:? at rest~ 2.H L/min/~I~ with e.xerclst', stroh' index rellla ining appro.\imately 40 ml/min/\I:? L(,ft "l'ntrieular angiogram rl'\'t'alt'd J.?;eneraliZl'd decrease in contractility in comparison to tht' initial shldy; thcre was no paradoxic srstolic expansion and. no leakage of dYl> around the mitral prostlwsis. J
,\
DISCCSSIO:,\
This patient's course illustrates a number of important features in the diagnosis and treatment of papillary muscle infarction. He presented initially the characteristic clinical picture of papillary muscle dysfunction; recent onset of a typical munnur of mitral regurgitation, in the clinical setting of acute
/2-/2-68
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CHEST, VOL. 58, NO.2, AUGUST 1970
'I
DEBUSK ET AL
178 myocardial infarct on. J-:\ Within hours his condition abruptly deteriOl ated. with shock pulmonary edema. and recurrent chest pain occurring. a sequence highly su~ gestive of papillary muscle rupture. 4 - 11 Except during a brief period of right overload, the congestive heart ventricular volum,~ failure which ensu.~d was entirely left sided; the low and falling central venous oxygen saturation provided early eviden ~ of left ventricular failure. 7 This case emph.ISizes the extent to which acute, severe pulmonary :x>ngestion secondary to left ventricular dysfunction may simulate acute pulmonary infarction. The henoptysis observed probably represented "pulmonaT) apaplexy," described by Wood': pulmonary venous hypertension occurring abruptly in the presence of nonnal left atrial compliance, as in acute ventricular dysfunction. may cause rupture of pulmonary-brollchial venous anastomoses, with intrabronchial herr orrhage. Severe mitral regurgitation was present. but the usual corroboratiVl signs in addition to the munnur were lacking; the Leart was normal sized. and there was no thrill or left ventricular heave. The intensity of the munnur 'vas variable, probably due to variations in ventri ~ular contractility; the intensity of this munnur is tho'Jght to reflect the velocity, rather than the volume. o· regurgitation. \I Pulmonary arter, and pulmonary capillary wedge pressure tracings ill this case were distinguished only with difficulty (Fig 3), whereas left ventricular angiography de611itely established the diagnosis This procedure was more of mitral insuffici,~ncy. quickly perfonned than right heart catheterization. and allowed dired observation of the extent of regurgitation. thickness and contractility of the left ventricular wall, size of left ventricular and atrial chambers, and qu.llity of left atrial pulsation. The eccentricity of the regurgitant jet and atrial filling papillary muscle rupture defect strongly su~gested with prolapse as the cause of mitral regurgitation. The vigorous ventricular contraction provided impetus to the decisi"n to perfonn surgery in the face of acute myocardial infarction. \Vben a patient with papillary muscle mpture is deteriorating, diagnostic angiography must be perfonned early, quickly, and with a minimum of contrast agent; our patient suffered marked worsening of pulmonary edema following the combined angiographic procedures, probably owing 10 the increase in intravascular volume produced by the contrast agent. Jo· 11 Rupture of the entire papillary muscle trunk, rather than of a single bead,· has been considered incompatible with life. ~ Our patient demonstrates that it is more likely the degree of ventricular compensation thall the extent of papillary muscle damage which do~tennines the outcome: if the
ventricle is basically sound, even rupture of an entire trunk may be tolerated long enough for surgery to be perfonned, whereas post-infarction papillary muscle dysfunction without rupture in the diffusely diseased ventricle may quickly lead to fatal pulmonary edema. 2 The electrocardiogram initially simulated the pattern of anterior papillary muscle infarction (Type 1) of Phillips J 2; ST depression in the inferior leads was an important clue that the damage lay elsewhere. Only after surgery was there evidence of lateral and posterior infarction, and it would appear that the initial infarction extended into these areas during and! or follOWing operation. The diminished ventricular contractility seen on the follow-up angiogram, without clinical evidence of further cardiac necrosis after hospital discharge, supports this thesis. Objective evidence of cardiac dysfunction remains, despite the lack of clinical s}wptoms, and the prognosis is uncertain. The apparent extension of the infarction associated with surgery is unfortunate, but there is little doubt that early surgery was lifesaving. REFERE~CES
Bashour FA: ~litral regurgitation following myocardial infarction: the syndrome of papillary mitral regurgitation, Dis Chest 48: 113, 1965 2 Heikkila J: \titral incompetence as a complication of acute myocardial infarction, Acta Med Scan Suppl 475: 1967 3 Burch GE, DePa.,quale NP and Phillips JH: The syndrome of papillary muscle dysfunction, Amer Heart J 7.5:399, 1968 4 Sanders RJ, Neubuerger KT and Ravin A: Rupture of papillary muscles: occurrence of mpture uf the posterior muscle in posterior myocardial infarction, Dis Chest,
41 :316. 19.57 .5 \Iorrow AG, Cohen LS, Roberts WC, Braunwald NS and Braunwald E: Severe mitral regurgitation following acute myo(,'ardial infarction and mptured papillary muscle, Circulation 37: (Supp\. II): 124, 1968 6 Austen WG, Sokol D~I, DeSancti., RW and Sanders CA: Surgical treabnent of papillary muscle mpture complicating myocardial infarction, New Eng J ~Ied 278: 1137, 196B 7 Goldman RH, Braniff B, Harri.,on DC and Spivack AP:
The use of central venous oxy~en saturation measure68: 1.280, ments in a coronary care unit. Ann Int ~fed
1968 8 W,xxI P: Diseases of the Heart and Circulation, Philadelphia, J B Lippincott Co, 1956 9 BnlIl$, DL: A general theory of the causes of murmurs in the cardiovascular system, Amer J \Ied 27:360,1959 10 Brown R, Rahimtoola SH, Davis GD and Swan HJC: The effect of angiocardiographic contrast medium on circulatory dynamics in man, Circulation 31 :234, 1965 II Bristow JD, Porter GA, Kloster FE and Griswold HE: Hemodynamic (·hanl'les attending angiocardiography, Radiology 88:939, 1967 12 Phillips JH, DePasquale NP and Burch GE: The electrocardiogram in infarction of the anterolateral papillary muscle, Amer Heart J 66:338, 1963
CHEST, VOL. 58, NO.2, AUGUST 1970