JACC Vol. 9. No. IJanuary j9X7215-20

CASE REPORTS

215

Acute Rupture of Myxomatous Mitral Valve Presenting as RefractoryCardiopulmonary Arrest

DAVID W. FERGUSON, MD, FACC, ROBERT W. KIEFABER, MD, DAVID S. ZIEGELMAN, MD,

RUTH E. UPHOLD, MD, RICHARD S. JACKSON, MD, BURTON S. TABAKIN, MD, FACC

Burlington, Vermont

A 59 year old white woman had an out of hospital suddencardiac arrest. Resuscitation at the scene restored spon­taneous pulse, blood pressure and respiration but car­diovascular collapse recurred within 30 minutes of hos­pital arrival. Medically refractory cardiogenic shock ofunclear origin prompted the placement of an intraaorticballoon pump, and hemodynamic stabilization wasachieved over several hours. Acute rupture of the chor­dae tendineae of a myxomatous mitral valve was diag­nosed as the cause of the cardiac arrest. Mitral valve

Myxomatous mitral valve prolapse has been increasinglyrecognized as a common cardiac anomaly since its initial

description by Barlow et al. (1,2) in 1963. Although it is

usually a benign condition, some patients with this disorder

develop major complications including chest pain, heart

failure secondary to mitral insufficiency, cerebral ischemic

events and sudden death (3). The mechanism of sudden

death in the few reported cases is not certain, but is usually

attributed to malignant ventricular arrhythmias.

This report presents a case of acute rupture of the chordaetendineae in a patient with myxomatous mitral valve pro­lapse resulting in acute, fulminant pulmonary edema andcardiopulmonary arrest. To our knowledge, this is the firstreport of sudden death in this syndrome due to mechanicalrupture of the mitral valve. The differential diagnosis ofsudden death in this syndrome is reviewed and several in­teresting management topics related to this patient's difficultresuscitation are discussed.

From the Departments of Medicine and Surgery. University of VermontCollege of Medicine. Medical Center Hospital of Vermont. Burlington.Vermont.

Manuscript received February 10, 1986: revised manuscript receivedApril 16. 19X6. accepted May 14. 19X6.

Address for reprints: David W. Ferguson. MD, Cardiovascular Divi­sion, Department of Internal Medicine. University of Iowa Hospitals. IowaCity, Iowa 52240.

«'J 1987by the American Collegeof Cardiology

replacement was performed and the patient made anuneventful recovery.

This report describes the first known case of ruptureof a myxomatous mitral valve presenting as sudden car­diac death. The differential diagnosis of sudden deathin this disorder is reviewed, the role of mechanical cir­culatory assistance in refractory cardiac arrest is dis­cussed and several interesting hemodynamic aspects ofthe case are considered.

(J Am Coil Cardiol 1987;9:215-20)

Case ReportA 59 year old woman with a history of hypertension

presented to the emergency department at this hospital on

November 25, 1985 after sudden collapse. Witnesses re­

ported that the patient complained of not feeling well and

collapsed minutes later. When the Fire Department RescueSquad arrived on the scene at II: 15 AM, the patient was

unresponsive, without palpable pulse or spontaneous res­

pirations. Cardiopulmonary resuscitation with closed chestcardiac massage and artificial ventilation were instituted andwithin 2 minutes spontaneous pulse and labored respirationsresumed.

Emergency management. On arrival in the emergencydepartment at II :30 AM, the patient had fulminant pulmo­nary edema with severe ventilatory insufficiency. Initial vi­tal signs were blood pressure (by sphygmomanometry)224/1 10 mm Hg and pulse !30/min with sinus rhythm.Physical examination revealed cold mottled extremities,

marked respiratory distress, bilateral diffuse rales and rhon­chi and no apparent cardiac murmur. The patient demon­strated purposeful movements and had no focal neurologicabnormalities. Initial arterial blood gases with the patient

using a 1.00 FlO:, rebreathing face mask revealed a pH of

6.81, partial pressure of carbon dioxide (Pco:,) of 109 torrand partial pressure of oxygen (Po:,) of 157 torr. The patient

was intubated and large amounts of pink frothy pulmonaryedema fluid were suctioned from the trachea. Short-term

0735-I0971X7/$3.50

21 6 FERGUSON ET AL.ACUTE MITRAL VALV E RUPTURE

JACe Vol. Y. No, IJanuary IYS7:215- 20

therapy included intravenous furosemide and morphine sul­fate. topical application of nitropaste, mechanical ventila­tion and placement of a central venous line.

During the first 30 minutes after hospital arrival. thepatient became profoundly hypotensive and unresponsive,with systolic blood pressure falling to 50 min Hg by Dop­pler-assisted auscultation. The cardiac rhythm was sinustachycardia at a rate of 100 beats/min. The nitropaste wasremoved and the patient was given naloxone hydrochlorideand sodium bicarbonate intravenously. Despite these effortsshe remained profoundly hypotensive and unresponsive andan intravenous infusion of dopamine was initiated.

The electrocardiograms obtained on arrival at the emer­gency department and repeated sequentially showed non­specific ST segment and T wave changes without evidenceof acute myocardial ischemia or injury. Admission labo­ratory data were remarkable for a serum potassium of 6.8rn fiq/liter (at which time the blood pH was 6.81) . Serumcreatine kinase. obtained on arrival immediately after re­suscitation. was 633 ll.l/Iiter (normal = I to 67); subsequentvalues were all less than 40 [U/iiter with negative MB frac­tions. The admission chest X-ray film showed perihilar pul­monary edema.

Hospital course. After transfer to the cardiac intensivecare unit at 12:31 PM . the patient' s true intraarterial (fem­oral) systemic pressure was noted to be 78/43 mm Hg ona dopamine infusion at 23 jLg/kg per min. A thermodilutionSwan-Ganz catheter was inserted and the patient' s initialhemodynamics were as follows: mean right atrial pressure24 mm Hg. right ventricular pressure 5011 8 mm Hg. pul­monary arterial pressure 40/30 mm Hg, mean puimonarycapillary wedge pressure 36 mm Hg, cardiac index 1.36Iiters/min per Iil2 and heart rate 130 beats/min. There wasno evidence of abnormal Vwaves on the pulmonarycapillarywedge tracing (Fig. I).

Because of medically refractory cardiogenic shock ofunclear origin , a 1O.5F percutaneous intraaortic balloonpump was inserted at I:30 PM for mechanical circulatoryassistance during continued resuscitation efforts. Over the

next several hours the patient' s hemodynamic status mark­edly improved and by 6:00 PM she was successfully weanedoff all vasopressors. Repeat hemodynamic assessment atthat tirrie revealed her systemic arterial pressure to be 103/58rnm Hg, heart rate 82 beats/min. mean right atrial pressure13 rnm Hg, right ventricular pressure 45/24 mm Hg, cardiacindex 1.9 liters/min per m' and mean pulmonary capillarywedge pressure 15 rnrn Hg with no abnormal V waves. By10:00 PM . the pulmonary capillary wedge pressure had sta­bilized at 20 mm Hg after volume loading and the cardiacindex was 2.6 liters/min per rrr' .

All echocardiogram performed at 3:45 PM revealed markedsymmetric hypertrophy of a hyperdynamic left ventricle witha myxomatous appearing mitral valve. The anterior leafletof the mitral valve showed prolapse and there was a sig­nificantly flail posterior leaflet (Fig. 2) with mitral regur­gitation detected by Doppler ultrasound. A radionuclideventriculogram performed at 4:30 PM revealed an ejectionfraction of 75% for the left ventricle and 54% for the rightventricle. Six sets of blood cultures drawn over the first 24hours were negative for bacterial or fungal growth.

Hemodynamic data obtained at the bedside the followingmorning, 19.5 hours after placement 01" the Swan-Ganz cath­eter. revealed significant abnormal V waves in the pulmo­nary capillary wedge pressure tracing. At the same time,the appearance of a blowing systolic murmur at the cardiacapex became evident.

Cardiac catheterization the same day revealed the fol­lowing hemodynamic data on intraaortic balloon counter­pulsation support at 1:4 augmentation: mean right atrialpressure J3 mm Hg, right ventricular pressure 5311 6 mrnHg, pulmonary artery pressure 42/26 mm Hg, mean pul­monary capillary wedge pressure 22 rnm Hg, cardiac index2.37 liters/min per m' . systemic arterial pressure 100/60rnm Hg and heart rate 90 beats/min. Simultaneous hemo­dynamic tracings (Fig. 3) revealed an end-diastolic pressureof 16 mm Hg in the right ventricle and 32 rnm Hg in theleft ventricle with a mean pulmonary capillary wedge pres­sure of 22 mm Hg and V waves of 36 to 44 mm Hg. Biplane

60

4O ...l~

20

o

Figure I. In itial hemodynamic tracings obtained at12:31 PM in the cardiac intensive care unit. Hemo­dynamics were consistent with severe biventricularheart failure. Wave form analysis revealed no evi­dence of abnormal V waves in the pulmonary cap­illary wedge tracing. ECG = electrocardiogram.

FEMORALARTERY

RIGHTATRIUM

RIGHT PULMONARYVENTRICLE ARTERY

PULMONARYCAPILLARY

WEDGE

JACC Vol. 9, No.1January 1987:215-20

FERGUSON ET AL.ACUTE MITRAL VALVE RUPTURE

217

Figure2. Bedside echocardiogram obtained 4.5 hoursaftercardiac arrest. Modified apical four chamber viewdemonstrates a flail posterior mitral valve leaflet (PMVLj.AMVL = anterior mitral valve leaflet; LV = leftventricle; RV = right ventricle.

left ventricular cineangiography showed a hyperkinetic leftventricle without wall motion abnormalities and with anejection fraction of 83% by the area-length method. Severemitral insufficiency was present with a visible flail posteriormitral valve leaflet (Fig. 4). The coronary arteries werenormal.

Surgical exploration the following day revealed a myxo­matous appearing mitral valve with two ruptured major chor­dae tendineae to the posterior leaflet. The mitral leafletswere excised and a 31 mm Medtronic mechanical prosthesiswas inserted. Pathologic examination of the excised valverevealed no mass lesions or vegetations. The patient wassuccessfully weanedfrom intraaortic balloon assistance within24 hours postoperativelyand was extubated within48 hours.She made an uneventful recovery and was discharged 13days after admission.

Discussion

To our knowledge, this case represents the first report ofan out of hospital cardiac arrest due to acute rupture of a

myxomatous mitral valve and of the use of mechanical cir­culatory assistance with the intraaortic balloon pump forreversal of medically refractory cardiovascular collapse inthis condition.

Complications of mitral valve prolapse. Since the firstcomplete characterization of the prolapsing mitralvalve (c1ick­murmur) syndrome by Barlow et al. (l,2) in 1963, therehas been increasing recognition of this disorder. Althoughusually thought to be a relatively benign condition (3-6),reported complications include chest pain (2,3,7,8), infec­tive endocarditis (2-5,9,10), ventricular arrhythmias (11-16),severe mitral insufficiency (5,17-21) and sudden death(2,3,5,8, 11,12-14,20-28).

Although myxomatousmitral valve prolapse is a commoncardiac abnormality, occurring in up to 17% of variouspatient groups studied by echocardiography (29), suddendeath is an uncommon complication (30); it has been re­ported to occur in only small numbers of patients with mitralvalve prolapse since the initial review of 12 such cases byJeresaty (23). The most common explanation offered forthis complication is that of malignant ventricular arrhyth-

Lead nFigure3. Hemodynamic recordings obtained atcar- 4O--+-+--+----+-+----l.......-----+---~--_+-_4_+_-_+

diac catheterization with simultaneously recordedpressures revealing moderate elevation of both right(RV) and left ventricular (LV) end-diastolic pres-sures. Large prominent V waves are apparent in the f 201~-..d-+~+-11--~1---i:..-..l,d-+-~'<f--f-¥-+-+*-~--1f-7"t"F:::..,pulmonary capillary wedge tracing (peW).

0-----------------1-...:..::=::...--1----

218 FERGUSON ET AL.ACUTE MITRAL VALVE RUPTURE

JACC Vol. 9, No. IJanuary 1987:215-20

Figure 4. Left ventricular cineangiogram obtained inthe 30° right anterior oblique projection. The end-sys­tolic frame is shown demonstrating severe mitral re­gurgitation and a flail posterior mitral valve leaflet(arrowhead).

mias (3,13 ,16,23), but their significance remains unclear(15) . Serious arrhythmias or sudden death in these patient shas been associated with cardiomyopathic changes in theventricle (31,32), prolongation of the QT interval (33-35),thrombosis of the sinoatrial artery (27), premature aging andscleros is of the cardiac skeleton with involvement of theatr ioventricular node and trifascicular conduction system(36) . coronary artery disease (37), myocardial infarctionpresumably due to spasm of anatomically normal coronaryarteries (38) and endocardial friction lesions secondary tofriction between the chordae tendineae and the left ventric­ular mural endocardium (39).

Acute rupture of mitral chordae tendineae. This com­plication was first described by Corvi sart (40) in 1806 andin the absence of Marfan's syndrome or endocarditis it wasrecogn ized 40 to 50 years ago (41.42). Spontaneous chordalrupture has now been identified at surgery or by serial echo­cardiography in 7 to 38% of patients with mitral valve pro­lapse (43- 46). Such rupture is often associated with thedevelopment of significant mitral insufficiency and heartfailure (47- 49). However, it is now clear that chordal rup­ture in this condition may occasionally be a clinically silentphen omenon detected only throu gh incidental echocardio­graphic examination (45) revealing the classic feature ofcon sistent loss of systolic mitral valve leaflet coaptation(50.5 1). The basic abnormality appears to be a dissolutionof co llagen in the support structures of the valves (25,52).

Mechanism of cardiac arrest and resuscitation. Be­cause our patient was not being mon itored at the time ofcardi ac arrest, a primary cardiac arrhythmia such as ven­tricul ar fibrillation cannot be absolutely excluded as theinitiating event. Nevertheless, she was rapidly resuscitatedwith external cardiac massage and artificial ventilation alone,without the administration of antiarrhythmic agents or elec­trical countershock. Successful recovery from ventricular

fibrillation under these circum stances would be most unu­sual. On hospital arrival, the patient had fulminant pul­mona ry edema by both clini cal and hemodynamic criteria.Her subsequent diagnostic evaluation excluded myocardialinfarction or endocarditis as the cause of her ruptured mitralvalve and severe mitral insufficiency. The rapid arterialimpedance reduction afforded by the intraaortic balloon pump(53.54) probabl y played the key role in her resuscitation byacutely reducing the degree of regurgitation and facilitatingadequate forward cardiac output.

Mechanical circulatory assistance during resuscita­tion. The use of mechanical circulatory support durin g car­diopulmonary resuscitation was described as early as 1957by Clowes and Neville (55), who utilized temporary place­ment of a membrane oxygenator for resuscitation of twopatients after open chest cardi ac massage was unsuccessful.The use of the intraaortic balloon pump for assistance inongoing cardiopulmonary resuscitati on has been previouslydescribed (56) but primarily in the setting of refractory ven­tricul ar arrhythmias (57), card iac arrest complicating cardiaccatheterization (58) or acute rupture of the left ventriclecomplicating acute myocardial infarction (59,60) . Thi s tech­nique was applied for resuscitation of our patient with med­ical1y refractory cardiovascular col1apse after rupture of amyxomatous mitral valve . Presumabl y. the efficacy of theintraaortic balloon pump in this setting is similar to thatconfirmed for its use in the setting of acute mitral insuffi ­ciency complicating myocardial infarction (61).

Hemodynamic observations. Our patient did not dem­onstrate auscultatory or classic hemod ynamic evidence ofsevere mitral regurgitation for the first 20 hours after cardiacarrest. Fuchs et al. (62) documented that up to one third ofpatients with severe mitral regurg itation have minimal Vwaves in the pulmonary capillary wedge pressure tracing ,However, their patients had chronic, not acute, mitral in-

JACC Vol. 9, NO.1January 1987:215-20

FERGUSONET AL.ACUTE MITRAL VALVE RUPTURE

219

sufficiency. Anecdotal reports (63,64) have suggested thatpatients with acute mitral regurgitation due to acute chordalor papillary muscle rupture, for example, usually have largeV waves. Patients with ruptured chordae tendineae usuallyhave larger V waves in left atrial tracings, a smaller maximalleft atrial volume and a less compliant left atrium than dopatients with chronic mitral insufficiency due to rheumaticheart disease (48). The less compliant "stiff" left atriumin such cases leads to increased pulmonary congestion dueto higher pulmonary capillary pressure for any given mitralregurgitant volume (48).

In our patient, we can only conjecture regarding the de­layed appearance of significant V waves and murmur ofmitral regurgitation. It is possible that the initial severelydepressed left ventricular systolic function due to severemetabolic and respiratory acidosis, followed by the rela­tively acute preload reduction and increased forward flowafforded by placement of the intraaortic balloon pump pre­vented the early appearance of the' 'classic" giant V wavescharacteristic of acute mitral insufficiency. It was only whenthe acidosis had resolved, the cardiac filling status optimizedand vasopressor support withdrawn that large V waves anda murmur consistent with mitral insufficiency were simul­taneously detected.

We gratefully acknowledge Dennis A. Plante, MD for thoughtful reviewof this manuscript, and Deborah Senesac, RN and Patricia Matthews, RNfor invaluable assistance in the care of this patient.

ReferencesI. Barlow IB, Pocock WA, Marchand P, Denny M. The significance of

late systolic murmurs. Am Heart 1 1963;66:443-52.

2. Barlow IB, Bosman CK, Pocock WA, Marchand P. Late systolicmurmurs and non-ejection ("mid-late") systolic clicks. An analysisof 90 patients. Br Heart 1 1968;30:203-18.

3. Jeresaty RM. Mitral valve prolapse-click syndrome. Prog CardiovascDis 1973;15:623-52.

4. Allen H, Harris A, Leatham A. Significance and prognosis of anisolated late systolic murmur: a 9- to 22-year follow-up. Br Heart 11974;36:525-32.

5. Mills P, Rose 1, Hollingsworth 1, Amara I, Craige E. Long-termprognosis of mitral-valve prolapse. N Engl 1 Med 1977;297:13-8.

6. Leatham A, Brigden W. Mild mitral regurgitation and the mitral pro­lapse fiasco. Am Heart 1 1980;99:659-64.

7. Criley 1M, Lewis KB, Humphries 10, Ross RS. Prolapse of the mitralvalve: clinical and cine-angiographic findings. Br Heart 1 1966;28:488-96.

8. Hancock EW, Cohn K. The syndrome associated with midsystolicclick and late systolic murmur. Am 1 Med 1966;41: 183-96.

9. Corrigall D, Bolen 1, Hancock EW, Popp RL. Mitral valve prolapseand infective endocarditis. Am 1 Med 1977;63:215-22.

10. Lachman AS, Bramwell-lones DM, Lakier JB, Pocock WA, BarlowJB. Infective endocarditis in the billowing mitral leaflet syndrome. BrHeart 1 1975;37:326-30.

II. Shappell SD, Marshall CE, Brown RE, Bruce TA. Sudden death andthe familial occurence of mid-systolic click, late systolic murmursyndrome. Circulation 1973;48:1128-34.

12. Campbell RWF, Godman MG, Fiddler GI, Marquis RM, lulian DG.Ventricular arrhythmias in syndrome of balloon deformity of mitralvalve. Definition of possible high risk group. Br Heart 1 1976;38:1053-7.

13. Ritchie Jl., Hammermeister KE, Kennedy lW. Refractory ventriculartachycardia and fibrillation in a patient with the prolapsing mitral leafletsyndrome: successful control with overdrive pacing. Am 1 Cardiol1976;37:314-6.

14. Winkle RA, Lopes MG, Popp RL, Hancock EW. Life-threateningarrhythmias in the mitral valve prolapse syndrome. Am 1 Med1976;60:961-7.

15. Savage DD, Levy D, Garrison Rl, et al. Mitral valve prolapse in thegeneral population. 3. Dysrrhythmias: the Framingham study. AmHeart 1 1983;106:582-6.

16. Pocock WA, Bosman CK, Chesler E, Barlow IB, Edwards lE. Suddendeath in primary mitral valve prolapse. Am Heart 11984;107:378-82.

17. Davis RH, Schuster B, Knoebel SB, Fisch C. Myxomatous degen­eration of the mitral valve. Am 1 Cardiol 1971;28:449-55.

18. Ranganathan N, Silver MD, Robinson TI, et al. Angiographic-mor­phologic correlation in patients with severe mitral regurgitation dueto prolapse of the posterior mitral valve leaflet. Circulation1973;48:514-8.

19. Salomon NW, Stinson EB, Griepp RB, Shumway NE. Surgical treat­ment of degenerative mitral regurgitation. Am 1 Cardiol 1976;38:463-8.

20. Rose 10, Mills P, Hollingsworth 1, Craige E. Long term prognosisof mitral valve prolapse-53 patients followed for 10-22 years (mean14 years) (abstr). Am 1 Cardiol 1977;39:272.

21. Kolibash Al, Bush CA, Fontana MB, Ryan 1M, Kilman 1, WooleyCF. Mitral valve prolapse syndrome: analysis of 62 patients aged 60years and older. Am 1 Cardiol 1983;52:534-9.

22. Marshall CE, Shappell SD. Sudden death and the ballooning posteriorleaflet syndrome. Detailed anatomic and histochemical investigation.Arch Patho! 1974;98: 134-8.

23. leresaty RM. Sudden death in the mitral valve prolapse-click syn­drome. Am 1 Cardiol 1976;37:317-8.

24. Koch FH, Hancock EW. Ten year follow-up of forty patients withthe mid-systolic click/late systolic murmur syndrome (abstr). Am 1CardioI1976;37:149.

25. Davies Ml, Moore BP, Braimbridge MV. The floppy mitral valve.Study of incidence, pathology, and complications in surgical, nec­ropsy, and forensic material. Br Heart 1 1978;40:468-81.

26. Mair Wl. Sudden death in young females with floppy mitral valvesyndrome. Aust NZ 1 Med 1980;10:221-3.

27. Bharati S, Rosen KM, Miller LB, Strasberg B, Lev M. Sudden deathin three teenagers (abstr). Circulation 1981;64(suppl IV):IV-72.

28. Chesler E, King RA, Edwards lE. The myxomatous mitral valve andsudden death. Circulation 1983;67:632-9.

29. Savage DD, Garrison Rl, Devereux RB, et al. Mitral valve prolapsein the general population. I. Epidemiologic features: the FraminghamStudy. Am Heart 1 1983;106:571-6.

30. Barlow JB, Pocock WA. The problem of nonejection systolic clicksand associated mitral systolic murmurs: emphasis on the billowingmitral leaflet syndrome. Am Heart 1 1975;90:636-55.

31. Gulotta Sl, Gulco L, Padmanabhan V, Miller S. The syndrome ofsystolic click, murmur, and mitral valve prolapse-cardiomyopathy?Circulation 1974;49:717-28.

32. Mason lW, Koch FH, Billingham ME, Winkle RA. Cardiac biopsyevidence for a cardiomyopathy associated with symptomatic mitralvalve prolapse. Am 1 Cardiol 1978;42:557-62.

33. Swartz MH, Teichholz LE, Donoso E. Mitral valve prolapse. A reviewof associated arrhythmias. Am 1 Med 1977;62:377-89.

34. Criley 1M. Heger 1. Prolapsed mitral leaflet syndrome. CardiovascClin 1979;10:213-20.

35. Forbes RB, Morton GH. Ventricular fibrillation in a patient with

220 FERGUSON ET AL.ACUTE MITRAL VALVE RUPTURE

JACC Vol. 9, No. 1January 1987:215-20

unsuspected mitral valve prolapse and a prolonged Q-T interval. CanAnaesth Soc 1 1979;26:424-7.

36. Bharati S, Granston AS, Liebson PR, Loeb HS, Rosen KM, Lev M. 51.The conduction system in mitral valve prolapse syndrome with suddendeath. Am Heart 1 1981;101:667-70.

37. Aranda 1M, Befeler B, Lazzara R, Embi A, Machado H. Mitral valve 52.prolapse and coronary artery disease. Clinical, hemodynamic, andangiographic correlations. Circulation 1975;52:245-53.

38. Chesler E, Matisonn RE, Lakier lB, Pocock WA, ObeIIWP, Barlow 53.lB. Acute myocardial infarction with normal coronary arteries. Apossible manifestation of the billowing mitral leaflet syndrome. Cir-culation 1976;54:203-9. 54.

39. Chesler E, King RA, Edwards JE. The myxomatous mitral valve andsudden death. Circulation 1983;67:632-9.

40. Corvisart IN. Essai sur les maladies et les lesions organiques du coeur 55.

et des gros vaisseau. Paris: Imprimerie de Migneret, 1806:222.

41. Frothingham C, Hass GM. Rupture of normal chordae tendineae ofthe mitral valve. Am Heart 1 1934;9:492-9. 56.

42. Bailey O'T, Hickam lB. Rupture of mitral chordae tendineae. Clinicaland pathologic observations on seven cases in which there was nobacterial endocarditis. Am Heart 1 1944;28:578-600. 57.

43. Cooley DA, Gerami S, Hallman GL, Wukasch DC, Hall Rl. Mitralinsufficiency due to myxomatous transformation: "floppy valve syn-

58.drome ". 1 Cardiovasc Surg 1972;13:346-9.

44. Chandraratna PAN, Aronow WS. Incidence of ruptured chordae ten-dineae in the mitral valvular prolapse syndrome. An echocardiographic

59.study. Chest 1979;75:334-9.

45. Grenadier E, Alpan G, Keidar S, Palant A. The prevalence of rupturedchordae tendineae in the mitral valve prolapse syndrome. Am Heart

60.1 1983;105:603-10.

46. Alpan G, Grenadier E, Palant A. Chordal rupture: aetiology and nat-ural history. Br Heart 1 1984;52:595-6.

61.47. Roberts WC, Braunwald E, Morrow AG. Acute severe mitral regur-

gitation secondary to ruptured chordae tendineae. Clinical, hemody-namic, and pathologic considerations. Circulation 1966;33:58-70.

62.48. Baxley WA, Kennedy lW, Feild B, Dodge HT. Hemodynamics in

ruptured chordae tendineae and chronic rheumatic mitral regurgitation.Circulation 1973;48: 1288-94. 63.

49. Sanders CA, Austen WG, Harthome lW, Dinsmore RE, Scannell IG.Diagnosis and surgical treatment of mitral regurgitation secondary to 64.ruptured chordae tendineae. N Engl 1 Med 1976;276:943-9.

50. Mintz GS, Kotler MN, Parry WR, Segal BL. Statistical comparison

of M mode and two dimensional echocardiographic diagnosis of flailmitral leaflets, Am 1 Cardiol 1980;45:253-9,

DePace NL, Mintz GS, Ren 1-F, et al. Natural history of the flailmitral leaflet syndrome: a serial 2-dimensional echocardiographic study.Am 1 Cardiol 1983;52:789-95.

King BD, Clark MA, Baba N, Kilman lW, Wooley CF. "Myxo­matous" mitral valves: collagen dissolution as the primary defect.Circulation 1982;66:288-96.

Scheidt S, Collins M, Goldstein 1, Fisher 1, Mechanical circulatoryassistance with the intraaortic balloon pump and other counterpulsationdevices. Prog Cardiovasc Dis 1982;25:55-76.

Weber KT, lanicki IS, Intraaortic balloon counterpulsation. A reviewof physiological principles, clinical results, and device safety. AnnThorac Surg 1974;17:602-36.

Clowes GHA Jr, Neville WE. Membrane oxygenator. In: Allen JG,ed. Extracorporeal Circulation. Springfield, IL: Charles C Thomas,1958.

Vignola PA, Swaye PS, Gosselin Al. Guidelines for effective andsafe percutaneous intraaortic balloon pump insertion and removal. Am1 Cardiol 1981;48:660-4.

Culliford AT, Madden MR, Isom OW, Glassman E, Intra-aortic bal­loon counterpulsation. Refractory ventricular tachycardia. lAMA1978;239:431-2.

Leinbach RC, Goldstein 1, Gold HK, Moses lW, Collins MB, Sub­ramanian V. Percutaneous wire-guided balloon pumping. Am 1 Car­dioI1982;49:1707-10.

Hochreiter C, Goldstein 1, Borer IS, et al. Myocardial free-wall rup­ture after acute infarction: survival aided by percutaneous intraaorticballoon counterpulsation. Circulation 1982;65: 1279-82.

Pifarre R, Sullivan Hl, Grieco 1, et al. Management of left ventricularrupture complicating myocardial infarction. j Thorac Cardiovasc Surg1983;86:441-3.

McEnany MT, Kay HR, Buckley Ml, et al. Clinical experience withintraaortic balloon pump support in 728 patients. Circulation1977;58(suppl 1):1-124-32.

Fuchs RM, Heuser RR, Yin FCP, Brinker lA. Limitations of pul­monary wedge V waves in diagnosing mitral regurgitation. Am 1Cardiol 1982;49;849-54.

Braunwald E, Awe We. The syndrome of severe mitral regurgitationwith normal left atrial pressure. Circulation 1963;27:29-35.

Grunberg BH, Massie BM, Brundage BH, Botvinick EH, ParmleyWW, Chatterjee K. Beneficial effects of hydralazine in severe mitralregurgitation. Circulation 1978;58:273-9.