Apex cardiogram in patients with prolapsing mitral valve

Apex Cardiogram in Patients with Prolapsing Mitral Valve

WILLIAM H. SPENCER, III, MD, FACC VICTOR S. BEHAR, MD EDWARD S. ORGAIN, MD, FACC Durham, North Carofina

From the Cardiovascular Division, Department of Medicine, Duke University Medical Center, Durham, N.C. This study was supported in part by Public Health Service Training Grant HL-5736. Manuscript accepted March 7, 1973. Address for reprints: Edward S. Orgain, MD, Box 3085, Duke University Medical Center, Durham, N.C. 27710.

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The characteristics of the apex cardiogram in patients with a prolapsing mitral valve were investigated. Twenty-four patients having typical echocardiographic evidence of prolapsing mitral leaflets and midsystolic clicks (with or without apical systolic murmurs) were studied. Of the 24 patients, 16 (67 percent) had a sharp systolic retraction on the apex cardiogram occurring simultaneously with the systolic click. Sharp systolic retractions were not observed on the apex cardiogram of normal subjects or patients with rheumatic mitral insufficiency. Eight of the 16 patients had either no or a small systolic retraction at rest, but the systolic retraction was elicited or accentuated by standing or inhalation of amyl nitrite. In patients with the sharp systolic retraction at rest, the click and the systolic retraclion occurred earlier in systole during standing or inhalation of amyl nitrite. In 12 patients prolapsing mitral valves were confirmed by left ventricular cineangiograms. Sharp systolic retractions were present in the apex cardiograms in eight of these patients; seven of the eight had moderate lo severe prolapse of both milral leaflets. In the four remaining patients who underwent catheterization no sharp systolic retraction was seen on the apex cardiogram, and there was only mild prolapse of one or both leaflets. Sharp systolic retractions occur on the apex cardiogram in the majority of patients with prolapsing mitral valves, and their presence suggests an abnormal contraction due to the systolic decompression of the left ventricle by the prolapsing mitral leaflets.

In recent years the syndrome of the midsystolic click and late systolic murmur has been clearly related to a systolic prolapse of one or both leaflets of the mitral valve. 1-1~ Intracardiac phonocardiography has localized the clicks and systolic murmurs to the mitral valve apparatus. 13-1~ The findings of Kesteloot and Van Houte s and Willems et al., 6 who demonstrated an abnormal systolic retraction of the apex impulse on the apex cardiogram, suggest the use of an additional noninvasive technique for identifying this abnormality. Although this syndrome was originally described as benign, 16,17 more recent observations have demonstrated that the patients are subject to sudden death, 12.1s postexercise arrhythmias, 19,20 bacterial endocarditis or hemodynamically significant mitral regurgitation. 21 It is therefore important to identify such patients so that appropriate antibiotic prophylaxis and antiarrhythmic therapy may be instituted. This report describes the echocardiographic findings in this syndrome and the prevalence and dynamic characteristics of the apex cardiogram alluded to by previous investigators. Methods

Twenty-four patients with nonejection clicks or systolic murmurs, or both, were evaluated by echocardiography and phonocardiography. In addi-

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PROLAPSING MITRAL VALVE--SPENCER ET AL.

NORMAL

TABLE I

Diastole

Selected Clinical Features in ;)4 Cases of Prolapsing Mitral Valve no. of Patients

Sex Age History

Symptoms

Physical findings

18 F, 6 M 14-66 years Suspected rheumatic heart disease Coronary artery disease Cardiomyopathy Nonanginal chest pain Palpitations Dyspnea on exertion Apical systolic murmur and/or midsystolic click

ANTERIOR

7 2 1 10 7 7

Anterior Leaflet Mitral Valve

24

EKG tion, 12 of the patients underwent complete right and left heart catheterization including left ventriculography at a filming speed of 60 frames/sec. The clinical characteristics of the patients (Table I) are similar to those reported by previous investigators. 9,z°,z2`18 Eighteen of the 24 patients were female, and 6 were male. Their ages ranged from 14 to 66 years. The echocardiograms were performed with an Ekoline 20 Ultrasonoscope employing a 2.25 mHz, 1/2 inch diameter transducer with a repetition rate of 1,000 impulses/ sec. Patients were examined in the supine position, as described by previous investigators. '-'2.'~ The transducer was directed more inferiorly and laterally than usual for anterior leaflet echograms in an attempt to record the movement of both the anterior and posterior leaflets of the mitral valve. The echograms were displayed on an oscilloscope and photographed by a Polaroid camera. The apex cardiograms were obtained employing a Sanborn no. 374 pulse wave adapter connected by means of polyethylene tubing to the side outlet of a Sanborn microphone bell (no. 62-1500-C13) which recorded the heart sounds. The patients were placed in a 30* to 40* left lateral decubitus position, as described by Benchimol and Dimond, 24 and special care was taken to localize the apex impulse. The apex cardiogram and phonocardiogram were simultaneously recorded on an Electronics for Medicine, DR-8, multichannel recorder. The effect of changes in body position or the inhalation of amyl nitrite, or both, was evaluated in all patients. When amyl nitrite was used, the filter and sensitivity settings were not changed from those of the control tracing before inhalation so that meaningful comparisons could be made.

POSTERIOR Systole FIGURE 1. Normal echogram of anterior leaflet of the mitral valve.

mitral valve which was confirmed angiographically in the 12 patients undergoing cardiac catheterization. Figure 1 illustrates a normal echocardiogram-of the anterior leaflet of the mitral valve. The gentle anterior unbroken m o v e m e n t of the echo during systole is i m p o r t a n t a n d represents the motion of the entire mitral a p p a r a t u s coincident with the systolic ejection of blood and shortening of the left ventricular long axis. In the presence of systolic prolapse of one or both mitral leaflets, the anterior motion of the

Prolapsing Anterior Leaflet ANTERIOR

Results The 24 patients included in this s t u d y were selected on the basis of the classic a u s c u l t a t o r y findings of the midsystolic click or systolic m u r m u r of mitral regurgitation, or both, d e m o n s t r a t e d on phonocardiograms. T w e n t y of the patients had a midsystolic click, and 23 had an apical systolic m u r m u r , which was pansystolic in 2. Nineteen patients had both a midsystolic click and a late systolic m u r m u r . The intensity of the click did not seem to correlate with the presence or absence of the systolic retraction on the apex cardiogram (see later). Eehoeardiogram: All patients had the characteristic echocardiographic a p p e a r a n c e of a prolapsing

POSTERIOR Systole FIGURE 2. Echogram of prolapsing anterior mitral leaflet. Midsystolic posterior movement of leaflet echo (arrow) represents valvular prolapse.

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Prolapsing Leaflets

NORNAL APEXCARDIOGRAM

Anterior and Posterior

E Point

ANTERIOR

~ EndSystolic

EKG

I A Wo~e J

I ~

Shoulder ~/ Slow filling

\/

W°ve

Si

J,. IlF--

PHONOCAROIOGRAN

POSTERIOR

S2"%~'0 Point

_L_ T

I

Systole FIGURE 3. Echogram of prolapse of both mitral leaflets. Posterior systolic movement (arrow) with late systolic separation of the echoes denotes prolapse of anterior and posterior mitral leaflets.

mitral leaflet echo is interrupted, and an abrupt, mid or late systolic, posterior displacement of the leaflet into the left atrium is detected. The echocardiographic patterns of this posterior displacement may be detected as a backward movement of the anterior leaflet only (Fig. 2), or backward displacement of both anterior and posterior leaflets (Fig. 3). Both leaflets could be identified on the echocardiogram in 23 of the 24 patients studied. Twenty of the 23 pa-

I

.5 Sec. FIGURE 4. Apex cardiogram and simultaneous apical phonocardiagram from a normal subject showing A wave, E point, endsystolic shoulder, O point, and diastolic waves in normal relation. $1 = first heart sound; $2 = second heart sound.

tients had prolapse of both leaflets, whereas 3 demonstrated prolapse of only the posterior leaflet, and 1 of only the anterior leaflet. In the latter patient the posterior leaflet was not identified on the echocardiogram but was seen to prolapse on the left ventriculogram. The left ventricular cineangiograms were evaluated independently for mitral leaflet prolapse and the presence of mitral regurgitation. Prolapse of both leaflets was observed in the 12 patients under-

E P~oi n t

E A

~

Slow ~fillinw~

[,. Slli I PHONOCARDIOGRAM= _ . . , A I , *

L

Rapid filling ~ - - Wave

Sharp

Systolic--,. Retraction

I

CLICK ~

--

0 Point

J ~1~, j,= . . . . .

W

SI\ • I

;

!

)

.s2_

.5 Sec. FIGURE 5. Apex cardiogram demonstrating sharp systolic retraction occurring simultaneously with a loud midsystolic click. A late systolic murmur is also present. The aortic component of the second heart sound was identified from carotid pulse tracings (not shown).

FIGURE 6. Apex cardiogram showing a prominent sharp systolic retraction (SSR) with a faint midsystolic click and a late systolic murmur.

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v

-

-

.PROLAPSING MITRAL VALVE--SPENCER ET AL.

E

E

E

E

J

,L c c;/o/ S2

I

RESTING

.ssec.

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t

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!

AFTERAMYL NITRITE INHALATION

FIGURE 7. Apex cardiogram showing the effects of administration of amyl nitrite. The systolic retraction (SSR) and the midsystolic click are both accentuated after inhalation of the drug.

going catheterization. A comparison of the echocardiogram and ventriculogram in these 12 patients showed excellent correlation. In 10 of' the patients, prolapse of both leaflets was demonstrated by the two methods; in 1 patient, the echocardiogram disclosed prolapse of only the posterior leaflet whereas the ventriculogram disclosed prolapse of both leaflets. In the 12th patient, mentioned earlier, the echocardiogram demonstrated prolapse of the anterior mitral leaflet only. Apex c a r d i o g r a m : In the normal apex cardiogram (Fig. 4), the a wave, representing atrial contraction, is followed by the systolic components of the apex impulse. During the preejection period and early ventricular ejection the apex cardiogram records a rapidly rising deflection which peaks at the E point when ventricular ejection begins. As ejection continues, the systolic wave of the apex cardiogram shows a rapid descent with a plateau in midsystole. Frequently, an end-systolic shoulder is recorded at or about the time the aortic component of the second heart sound is recorded, as reported by Tafur et al. 2a It has been observed 26 that the shoulder may be accentuated during hyperkinetic cardiovascular states. At the end of systole, the apex recording rapidly descends to the O point at the time o~' mitral valve opening. Rapid and slow diastolic filling waves are followed by the next cardiac cycle. A sharp systolic retraction on the apex cardiogram was demonstrated in 16 of the 24 patients with a prolapsing mitral valve (Fig. 5 and 6). The retraction occurred almost simultaneously with the midsystolic click when both were present. In 7 of these 16 patients either a small or no sharp systolic retraction

~

SUPINE

.5 Sec.

I

STANDING

FIGURE 8. Supine and standing apex cardiograms demonstrating movement of midsystolic click and simultaneous sharp systolic retraction to earlier systole on standing. A pansystolic murmur is present.

was present at rest, but a retraction developed or was accentuated during standing or after the inhalation of amyl nitrite (Fig. 7). The temporal relation of the midsystolic click and the sharp systolic retraction was maintained with both interventions (Fig. 8). The patient whose apex cardiogram is illustrated had a prominent systolic retraction on the apex cardiogram and a loud midsystolic click as well as a pansystolic murmur on the phonocardiogram. When the patient was standing, the click and the systolic retraction both occurred in early systole. A technically Satisfactory standing apex cardiogram was obtained in only 11 patients; a systolic retraction developed or was accentuated in 4 of these 11. Eight of the 24 patients with documented prolapsing mitral leaflets showed no sharp systolic retractions on the apex cardiogram at rest, and in 5 no retraction could be induced with changes in posture or after the inhalation of amyl nitrite. Sharp systolic retractions have not been recorded in normal subjects or in patients with forms of mitral insufficiency other than idiopathic hypertrophic subaortic stenosis in which a second systolic wave is commonly found. 28 Care was taken to avoid mistaking the exaggeration of a normal end-systolic shoulder for a sharp systolic retraction. Correlation with catheterization data: Table II illustrates the relation between the degree of mitral leaflet prolapse demonstrated by left ventricular cineangiograms and the presence or absence of a sharp systolic retraction on the apex cardiogram. Seven patients with a systolic retraction on the apex cardiogram were found to have severe prolapse of one or

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TABLE II

Midsystolic clicks and late systolic murmurs were believed for many years to be due to pleuropericardial adhesions. 27 The presence of ischemic T wave changes on the electrocardiogram in these patients led to the name of the electrocardiographic-auscultatory syndrome.12,16 This syndrome was believed to be extracardiac in origin until the reports of Barlow et al. 2 and Barlow and Bosman 3 describing mitral regurgitation (1963) and prolapse of the mitral leaflets into the left atrium during ventricular systole (1966) in these patients. Similar angiographic findings have been reported by other investigators, 4 and the similarity of these patients to those with the systolic "whoop" or precordial "honk" has been described by Behar et al. s Intracardiac pl~onocardiography has localized these sounds to the region of the mitral apparatusJ 3-15 The nonejection clicks have been ascribed to a sudden tensing of abnormallY elongated, redundant chordae tendineae, for which Reid 2s coined the term "chordal snap." Several investigators9,29, 3o demonstrated myxomatous degeneration of the mitral leaflets resulting in their redundancy and prolapse, and others have postulated that abnormal dilatation of the mitral annulus or an abnormal left ventricular myocardium in the mitral

region may be responsible for the prolapsing mitral leaflets.11,31 Although this syndrome has been described as a specific electrocardiographic-auscultatory syndrome, there are probably multiple causes for nonejection clicks, 1s,2°,32 prolapsing mitral valve leaflets, s and late systolic murmurs. 33-35 The clinical presentation of these patients frequently includes anxiety, palpitations, dyspnea, chest pain and a strong familial incidence of similar electrocardiographic and auscultatory findings. 7,1°,1s,2° In recent years it has become clear that the prognosis in these patients is not as benign as once thought. Linhart and Taylor 21 described four patients who had progressive mitral regurgitation and symptoms of congestive heart failure and a fifth patient who had bacterial endocarditis in the same clinical setting. In addition, such patients have been demonstrated to have multifocal ventricular extrasystoles after the cessation of exercise, 19,2° unexplained sudden death (two cases) 12,1s and an increased incidence of sudden death in relatives of those whose syndrome was recognized.3 This report describes a unique apex cardiographic abnormality present in 67 percent of our patients with a prolapsing mitral valve studied in this laboratory. Kestleloot and Van Houte 5 and Willems et al. 6 have described similar findings, and illustrations of an apex cardiogram in a patient with a systolic "whoop" described by Benchimol and Dimond 24 (Fig. 7) showed a marked systolic retraction. The significance of this abnormality in the latter patient was apparently not appreciated by the authors. The instrument employed in our study and by Benchimol and Dimond 24 tends to exaggerate peaks and troughs on the apex cardiographic tracing, perhaps augmenting the sharp systolic retractions described herein. However, this phenomenon was not observed in normal subjects, indicating that it is a real event and useful in identifying patients with prolapsing mitral valve leaflets. Significance and mechanism of sharp systolic retraction: The near simultaneous occurrence of the midsystolic click and the sharp Systolic retraction indicates that both are temporally related to maximal leaflet prolapse, as described by Criley et al. 4 A comparison of the left ventriculograms and the apex cardiograms in our patients demonstrated that all patients with severe prolapse of the mitral leaflets had sharp systolic retractions. Although the pathophysiology of the mitral apparatus dysfunction in these patients is not known, it seems likely that the sharp systolic retraction on the apex cardiogram represents a "checking" phenomenon associated with the abrupt halt of blood flow beneath the billowing mitral leaflets. One may postulate that this phenomenon represents an abrupt change in the systolic impedance to left ventricular ejection as the suddenly taut mitral leaflets halt the transfer of blood beneath them directing the ejection of the remaining stroke volume exclusively into the aorta against a higher impedance. Alternatively, significant mitral regnrgi-

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Correlation of Apex Cardiograms and Left Ve'ntricular'Cineangioorams Systolic Retraction on Apex Cardiogram

Degree of Mitral Leaflet Prolapseon Cineangiogram Mild

Present Absent

Severe

1 4

7 0

Total 8 4

both mitral leaflets, whereas one patient had only mild prolapse. Four patients had no systolic retraction on the apex cardiogram, and all four had only m i l d prolapse of one or both leaflets. All eight patients with systolic retraction and severe prolapse had mild to severe mitral regurgitation, whereas only two of the four patients without retraction and with mild prolapse had mitral regurgitation. Because of the history of chest pain and the findings of mitral insufficiency, coronary arteriograms were obtained in six patients; two of the six were thought to have significant coronary artery disease, but neither had angiographic or electrocardiographic evidence of a previous myocardial infarction to suggest papillary muscle dysfunction as a cause of the mitral regurgitation. None of the 12 patients who underwent catheterization had resting gradients or abnormalities of anterior mitral leaflet motion on angiograms to suggest idiopathic hypertrophic subaortic stenosis. Results of provocative testing with inhalation of amyl nitrite and infusion of Isuprel ® in six patients were negative. Discussion

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tation would be expected to have the opposite effect by reducing late systolic impedance to left ventricular ejection. In contrast to the consistent relation between the severity of leaflet prolapse and systolic retraction, ventriculography revealed a wide range of degrees of mitral regurgitation in patients with systolic retractions, and no consistent relation was noted between the severity of mitral regurgitation and the presence or absence of systolic retractions. We therefore suggest that maximal mitral leaflet prolapse with its coincident midsystolic click and the sharp systolic retraction results in a sudden tensing of the mitral apparatus followed by an alteration in the pattern of left ventricular systolic decompression. The reduction in left ventricular size associated with standing or inhalation of amyl nitrite should result in greater redundancy of the mitral apparatus and more severe leaflet prolapse. Since the presence of systolic retraction on the apex cardiogram is related to the severity of leaflet prolapse, the appearance or accentuation of retraction with these interventions is compatible with this hypothesis. Differential diagnosis: The relation between the hemodynamic events in the left heart chambers and the apex cardiogram has been previously report-

ed. 25,a6 Normally the only palpable systolic motion ends before the last third of systoleY, ss The sharp systolic retraction on the apex cardiogram described in our study represents an additional example of a bifld apical impulse. Such an impulse may be the result of either diastolic events secondary to atrial contraction or ventricular filling waves, or systolic events occurring in idiopathic hypertrophic subaortic stenosis 26 and ischemic heart disease. 24,a9 Although there may be difficulty in differentiating between these abnormalities clinically, the echocardiographic movement of the anterior mitral leaflet satisfactorily differentiates idiopathic hypertrophic subaortic stenosis from chronic rheumatic mitral regurgitation and prolapsing mitral valve. In our study of patients with prolapsing mitral valves there was excellent correlation between cineangiographic and echocardiographic data with respect to the leaflet or leaflets involved. The need to identify the origin of the mitral regurgitation in such patients has become increasingly more important with the relatively recent appreciation of the complications that may occur, such as arrhythmias and endocarditis. The apex cardiogram represents an important adjunct to the diagnosis of the origin of mitral insufficiency.

References 1. Segal BL, Likoff W: Late systolic murmur of mitral regurgitation. Amer Heart J 67:757-763, 1964 2. Barlow JB, Pocock WA, Marchand P, et al: The significance of late systolic murmurs. Amer Heart J 66:443-452, 1963 3. Barlow JB, Bosman CK: Aneurysmal protrusion of the posterior leaflet of the mitral valve. An auscultatory-electrocardiographic syndrome. Amer Heart J 71:166-178, 1966 4. Criley JM, Lewis KB, Humphries JO,et al: Prolapse of the mitral valve: clinical and cine-angiocardiographic findings. Brit Heart J 28;488-496, 1966 5. Kesteloot I-I, Van Houte O: On the origin of the telesystolic murmur preceded by a click. Acta Cardiol (Brux) 20:197209, 1965 6. Willems J, Raelandt J, DeGeest H, et al: Late systolic murmurs an'd systolic non-ejection clicks. Acta Cardiol (Brux) 24:456-481, 1969 7. Stannard M, Sloman JG, Hare WSC, et al: Prolapse of the posterior leaflet of the mitral valve: a clinical, familial and cineangiographic study. Brit Med J 3:71-74, 1967 8. Behar VS, Whalen RE, Mclntosh liD: The ballooning mitral valve in patients with the "precordial honk" and "whoop." Amer J Cardiol 20:789-795, 1967 9. Bittar N, Sosa JA: The billowing mitral valve leaflet. Report on fourteen patients. Circulation 38:763-770, 1968 10. Fontana ME, Pence I-IL, Leighton RF, et al: The varying clinical spectrum of the systolic click-late systolic murmur syndrome. A postural auscultatory phenomenon. Circulation 41:807-816, 1970 11. Ehlers KH, Engle MA, Levin AR, et al: Left ventricular abnormality with late mitral insufficiency and abnormal electrocardiogram. Amer J Cardiol 26:333-340, 1970 12. Barlow JB, Bosman CK, Pococ WA: Late systolic murmurs and non-ejection ("mid-late") systolic clicks. An analysis of 90 patients. Brit Heart J 30:203-218, 1968 13. Ronan JA, Perloff JK, Harvey WP: Systolic clicks and the late systolic murmur. Intracardiac phonocardiographic evidence of their mitral valve origin. Amer Heart J 70:319-325, 1965 14. Leighton RF, Page WL, Goodwin RS, et al: Mild mitral regurgitation. Its characterization by intracardiac phonocardi-

15.

16. 17. 18. 19. 20.

21. 22. 23. 24. 25. 26.

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ography and pharmacologic responses. Amer J Med 41:168-182, 1966 Leon DR, Leonard JJ, Kroetz FW, et al: Late systolic murmurs, clicks, and whoops from the mitral valve. A transseptal intracardiac phonocardiographic analysis. Artier Heart J 72:325-336, 1966 Humphries JO, McKusick VA: The differentiation of organic and "innocent" systolic murmurs. Progr Cardiovasc Dis 35:152-171,1962 Levine SA, Harvey WP: Clinical Auscultation of the Heart, Second edition. Philadelphia, WB Saunders, 1959, p 555 Hancock EW, Cohn K: The syndrome associated with midsystolic click and late systolic murmur. Amer J Med 41:183-196, 1966 Pocock WA, Barlow JB: Postexercise arrhythmias in the billowing posterior mitral leaflet syndrome. Amer Heart J 80:740-745, 1970 Pocock WA, Barlow JB: Etiology and electrocardiographic features of the billowing posterior mitral leaflet syndrome. Analysis of a further 130 patients with a late systolic murmur or nonejection systolic click. Amer J Med 51:731-739, 1971 Unhart JW, Taylor WS: The late apical systolic murmur. Clinical, hemodynamic and angiographic observations. Amer J Cardiol 18:164-168, 1966 Kerber RE, Isaeff DM, Hancock EW: Echocardiographic patterns in patients with the syndrome of systolic click and late systolic murmur. New Eng J Med 284:691-693, 1971 Dillon JC, Haine CL, Chang S, et al: Use of echocardiography in patients with prolapsed mitral valve. Circulation 43:503-507, 1971 Benchimol A, Dimond EG: The normal and abnormal apexcardiogram. Its physiologic variation and its relation to intracardiac events. Amer J Cardio112:368-363, 1963 Tafur E, Cohen LS, Levine HD: The normal apexcardiogram. Its temporal relationship to electrical, acoustic, and mechanical cardiac events. Circulation 30:381-391, 1964 Tafur E, Cohen LS, Levine HD: The apexcardiogram in left ventricular outflow tract obstruction. Circulation 30:392399, 1964

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27. Gallavardin L: Pseudo dedoublement deuxieme bruit de coeur simuiant le dedoublement mitral por bruit extra-cardiaque" telesystolique surjouite. Lyon Med 121:409-477, 1913 28. Reid JVO: Mid-systolic clicks. S Afr Med J 35:353-355, 1961 29. Read RC, Thai AP, Wendt VE: Systomatic valvular myxomatous transformation (the floppy valve syndrome). A possible forme fruste of the Marfan syndrome. Circulation 42:897910, 1965 30. Pomerance A: Ballooning deformity (mucoid degeneration) of atrio-ventricular valves. Brit Heart J 31:343-351, 1969 31. Leachman RD, Lufschanowski R, Cokkinos DV: The midsystolic click and late systolic murmur. Clinical, electrocardiographic and hemodynamic characteristics (abstr) Ann Intern Med 74:820, 1971. 32. Steelman RB, White RS, Hill JC, et ah Midsystolic clicks in arteriosclerotic heart disease; a new facet in the clinical syndrome of papillary muscle dysfunction. Circulation 44:503-515, 1971

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33. Braunwald E, Morrow AG, Cornell WP, et al: idiopathic hypertrophic subaortic stenosis. Clinical, hemodynamic and angiographic manifestations. Amer J Med 29:924-945, 1960 34. Phillips JH, Burch GE, De Pasquale NP: The syndrome of papillary muscle dysfunction. Its clinical recognition. Ann intern Med 59:508-520, 1963 35. Wells BG, Rappaport EE, Sprague HB: The sounds and murmurs in coarctation of the aorta. A study by auscultation and phonocardiography. Amer Heart J 38:69-79, 1949 36. Tavel ME, Campbell RW, Feigenbaum H, et ah The apex cardiogram and its relationship to hemodynamic events within the left heart. Brit Heart J 27:829-839, 1965 37. Beilin L, Mounsey P: The left ventricular impulse in hypertensive heart disease. Brit Heart J 24:409-421, 1962 38. Deliyannis AA, Gillam PMS, Mounsey JPD, et ah The cardiac impulse and the motion of the heart. Brit Heart J 26:396-411, 1964 39. Ahuja SP, Gutierrez MR: Apexcardiography in the elucidation of a double or multiple impulse apex beat. Amer J Cardio119:468-473, 1967

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