The echocardiogram in papillary muscle dysfunction

The echocardiqgram

in pupikwy

muscle

dysfuncfion

V. K. Tallury, M.D. N. P. DePasquale, M.D. G. E. Burch, M.D. New York, N. Y., and New Orleans, La.

M

itral valve competence depends upon the structural and functional integrity of the atrioventricular ring, the mitral valve leaflets, the chordae tendineae, and the papillary muscles. Mitral regurgitation secondary to papillary muscle dysfunction has been described previously.1-4 Although a number of diseases may produce papillary muscle dysfunction, ischemia and infarction are probably the most frequent causes of the dysfunction. The degree of impairment of papillary muscle function in patients with ischemic heart disease may not be fixed but may vary with the state of the circulation. For example, the murmur associated with papillary muscle dysfunction may be audible only during an episode of angina pectoris. Experience has indicated that the murmur of papillary muscle dysfunction is particularly variable during the first one or two weeks following acute myocardial infarction. Since the echocardiogram displays mitral valve motion, it was considered of interest to record serial echocardiograms of patients with acute myocardial infarction. Materials

and

methods

Echocardiograms were recorded from 25 patients, selected at random, who were

admitted to the coronary care unit with definite electrocardiographic (ECG) evidence of acute myocardial infarction. The patients varied in age from 31 to 87 years (mean, 61 years). Twenty-one patients were male and four were female. The localization of the acute myocardial infarct as determined by ECG’s was as follows: inferior wall, 8 patients; anteroseptal, 9 patients; anterolateral, 3 patients; anterior, 2 patients; subendocardial, 2 patients; apical, 1 patient. Echocardiograms were recorded as soon as possible after admission of the patient to the coronary care unit. However, admission to the coronary care unit did not always coincide with the first day of myocardial infarction. Echocardiograms were recorded at one- or two-day intervals in the coronary care unit and at weekly intervals after discharge from the unit. Echocardiograms of mitral valve motion were recorded by means of a Physionic Portascan* apparatus. Movement of the anterior leaflet of the mitral valve was searched for in the “A” presentation and the image was photographed in the “B” presentation with a Polaroid camera from a calibrated, storage oscilloscope screen. The Portascan apparatus has a frequency

From

the Cardiovascular Service, Lenox Hill Hospital, New York, N. Y., and the Department University School of Medicine, New Orleans. La. Received for publication April 2, 1971. Reprint requests to: George E. Burch. M.D., 1430 Tulane Ave., New Orleans. La. 70112. *Model TMA-2 ultrasonic echograph. Physionic Engineering, Inc.

12

American Heart Journal

January, 1972

of Medicine,

Tulane

Vol. 83, No. 1, pp. 12-18

Volume Number

83 1

Echocardiogram

in papillary

muscle dysfiknction

13

Electrocardiogram

Phonocordioqram

A-C C-D

interval -complete closing of mitral valve ofter atrial systole interval-anterior dispbcement of entire mitral valve opporotus during wdriculor ejection D-E interval-Opening of mitral vdve to nwximum E-F interval - portiol closure of mitral valve duriq diostole F-A interval-reopeni of mitral valve during otriol systde C-E:vwticol distonco 7 rom C lo E reflects the intensity of mitral valve echo E-F:a diastolic sbpe

Fig. 1. Relationship of the normal echocardiogram to the ECG and phonocardiogram. The upward deflections D-E and F-A represent motion of the anterior leaflet of the mitral valve anteriorly toward the transducer, whereas the downward deflections A-C and E-F represent motion of the valve leaflet posteriorly away from the transducer. Point D occurs about 0.10 sec. after the aortic component of the second heart sound and represents the beginning of diastole. Point E represents the maximum anterior excursion of the leaflet of the open mitral valve into the cavity of the left ventricle. Thereafter, the mitral valve leaflet moves posteriorly (E-E) to close the valve but reopens with atria1 contraction, represented by point A which occurs after the P wave. Point C occurs within 0.02 sec. of the first heart sound and represents maximum posterior excursion of the mitral valve leaflet during isovolumetric contraction.

of 2.0 megacycles per second, with pulse duration of 2.5 psec. and a pulse rate of 500 per second. During registration of the echocardiogram, the transducer was placed at the fourth left intercostal space, 1 to 4 cm. from the midsternal line with the patient in the supine position. With care it was possible to keep the transducer position constant for each patient. Echocardiograms were analyzed for the diastolic slope (Fig. 1, interval E to F)* and for amplitude (Fig. 1, intervals C to E). The diastolic slope represents the rate of posterior movement of the anterior leaflet of the mitral valve after the anterior movement associated with opening of the valve.5 The velocity represented by the diastolic *The

degree of slope re0ects the velocity ment of the mitral valve leaflet.

of the posterior

move-

slope is expressed in millimeters per second. The amplitude of the mitral valve echo represents the entire anteroposterior excursion of the anterior leaflet of the mitral valve. The upper limits of normal for the diastolic slope have not been definitely established. Nevertheless, most observers agree that a slope greater than 200 mm. per second is definitely abnormal. In addition to the echocardiogram, indirect graphic studies including apexcardiogram, phonocardiogram, and carotid pulse tracing were obtained at the time of registration of the echocardiogram. Results The echocardiogram displayed significant variation in the diastolic slope in 6 of the 2.5 patients (24 per cent) studied. The location of the myocardial infarction was apical in one patient, inferior in one, anterior in one,

14

Tallury,

DePasquale,

Am. Heart J. January. 1972

and Burch

” J.G.

A .T.

L. F !

WA

L.G.

>

345

DAYS

AFTER

MYOCARDIAL

Fig. 2. Variations in the diastolic slope of serial echocardiograms top) with acute myocardial infarction.

a 10

INFARCTION from six patients(indicated by initials across

Fig. 4. Serial echocardiograms of a patient with acute anteroseptal myocardial infarction. The increase in the diastolic slope which occurred between Jan. 17 and Jan. 26 was associated with the development of an apical systolic murmur recorded in the phonocardiogram on the right.

Fig. 3. Serial echocardiograms of a patient with acute myocardial infarction showing variations in the diastolic slope attributed to changes in papillary muscle function.

and anteroseptal in three patients. The variations in the diastolic slope of these 6 patients are shown in Fig. 2. In two patients the diastolic slope increased on the second or third day following myocardial

infarction and then decreased to normal levels (Figs. 2, 3, and 4). In three patients the degree of the diastolic slope was abnormally large at the time of the initial study but then decreased to normal levels (Figs. 2, 5, 6, and 7). In one patient the diastolic slope increased between the third and fourth days following myocardial infarction, decreased between the fourth and fifth days, and increased again between the fifth and eighth days (Figs. 2 and 8). The amplitude (Fig. 1, intervals C to E)

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83 1

Echocardiogram

Fig. 5. Serial echocardiograms myocardial infarction.

of a patient with acute

Fig. 7. Serial echocardiograms acute myocardial infarction.

of a third patient with

in papillary

muscle dysfunction

15

Fig. 6. Serial echocardiograms of a second patient with acute myocardial infarction.

Fig. 8. Serial echocardiograms apical myocardial infarction,

of a patient with acute

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Tallury,

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Am. Heart 1. January, 1972

and Burch

Fig. 9. ECG of the same patient whose echocardiogram myocardial infarction and a convex upward deformity dysfunction.

of the mitral valve echo varied consonantly with the diastolic slope, so that amplitude increased or decreased as the diastolic slope increased or decreased. An apical systolic murmur was heard in all patients. In each patient the murmur varied in intensity and quality from day to day (Fig. 4). It was not unusual for the murmur to disappear on one day and reappear on the next. The following case history illustrates the variation in the apical systolic murmur. Case report W. A., a 63-year-old man, came to the emergency room because of severe substernal pain of several hours duration. An episode of ventricular fibrillation, which was successfully terminated with D.C. countershock, occurred ten minutes after his arrival in the emergency room. He was admitted to the coronary care unit in a semicomatose condition. The arterial blood pressure was 120/75 mm. Hg, and the pulse rate was 90 beats per minute and regular. No murmurs were audible. The ECG displayed an acute apical myocardial infarction with frequent multifocal ventricular premature beats. The serum glutamic oxaloacetic transaminase (SGOT) concentration was 60 units on admission and increased to 495 units and 950 units on the second and third days, respectively, following admission to the coronary care unit. Two days after admission to the coronary care unit the patient developed a sinus tachycardia associated with a diastolic gallop sound, and &les were audible over both lower lung fields posteriorly. An apical systolic murmur was heard for the first time on the fifth hospital day. The murmur was no longer audible on the seventh hospital day, but reappeared on the ninth hospital day and persisted until the patient was discharged from the hospital.

is shown in Fig. 4. The ECG of the S-T segments indicative

displays anteroseptal of papillary muscle

Discussion

The increase in the intensity of the apical systolic murmur noted on auscultation coincided with the increase in magnitude of the diastolic slope of the mitral valve echo. The same phenomenon is shown for patient L. G. in Fig. 4. On the day of admission to the hospital for an acute anteroseptal myocardial infarction, the diastolic slope was 93 mm. per second and a faint systolic murmur was barely audible at the apex (Fig. 4). Besides anteroseptal myocardial infarction, the ECG displayed a convex upward deformity of the S-T segment and an inversion of the T waves in the left precordial leads (Fig. 9). These changes were consistent with ischemia of the anterolateral papillary muscle.2 Echocardiograms showed a progressive increase in the diastolic slope associated with an increase in the intensity of the apical systolic murmur (Figs. 2 and 4). The fast component (Fig. 1, interval E to F) of the diastolic slope of the echocardiogram of mitral valve motion is considered to represent the initial movement of the anterior leaflet of the mitral valve toward the atrioventricular ring after opening of the valve.5 The amplitude of the mitral valve echo (Fig. 1, intervals C to E) represents the entire range of excursion of the anterior leaflet. The amplitude of both the mitral valve echo and the diastolic slope has been found to be increased in patients with rheumatic valvulitis and mitral in-

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sufficiency.6B7 An example of the mitral valve echo in a 52-year-old patient with chronic rheumatic valvulitis and angiocardiographic evidence of severe mitral regurgitation confirmed at surgery is illustrated in Fig. 10. In this study, 6 of 2.5 patients (24 per cent) with acute myocardial infarction had significant variations in the diastolic slope of the echocardiogram. In all of these patients the diastolic slope exceeded 200 mm. per second at least once during the first week following acute myocardial infarction. More important than the absolute magnitude of the diastolic slope was the fact that the slope varied from one day to the next and that the variations in slope were associated with alterations in the intensity of the murmur of mitral regurgitation. It should be pointed out that changes in the transducer position may produce a variation in the diastolic slope from one examination to the next, but such variation does not exceed 15 mm. per second. The magnitude of the changes in diastolic slope observed in the six patients reported in this paper far exceeded 15 mm. per second. As indicated in previous reports, the papillary muscles may be rendered partially or completely incapable of contraction as a result of infarction or ischemia.r+* Failure of a papillary muscle to shorten during ventricular ejection allows a portion of each mitral valve leaflet to evert into the left atrium as the apex moves toward the base; this occurs because the slack in the chordae tendineae is not taken up by papillary muscle shortening. Eversion of the mitral valve leaflets is associated with mitral regurgitation. The papillary muscles may be considered as akinetic or dyskinetic areas of the myocardium. The dynamic state of the papillary muscles may vary during the early days of myocardial infarction. We have postulated previously that the myocardium surrounding an area of myocardial infarction may become electrically and/or mechanically silent but not necessarily biologically dead (myocardial concussion syndrome) .8 Angiocardiograms have confirmed a high incidence of akinetic and dyskinetic areas of the myocardium in patients with ischemic heart disease.g The

in papillary

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17

Fig. 10. Echocardiogram of a patient with rheumatic heart disease who had severe mitral insufficiency demonstrated by cardiac catheterization and later confirmed at surgery. Note the steep diastolic slope from E and the increased amplitude of the mitral valve echo. Diastolic slope = 260 mm./sec. Amplitude = 30 mm.

papillary muscles, being subendocardial structures, are particularly susceptible to ischemia and/or infarction when coronary blood flow is reduced. It is well known that the intensity of the first heart sound may vary during the early days of myocardial infarction independently of changes in the P-R interval. Similarly, an apical systolic murmur may wax and wane during the early stages of myocardial infarction. We have attributed variations in the intensity of an apical systolic murmur to alterations in papillary muscle function. It has been postulated that ischemia or infarction renders a papillary muscle mechanically silent but not necessarily biologically dead-i.e., the muscle may regain the ability to contract. Partial or complete recovery of papillary muscle contraction would then result in variations in the intensity of the murmur of papillary muscle dysfunction. The echocardiograph provides a method for studying such variations in papillary muscle function. Summary Serial echocardiograms were recorded in 2.5 patients with acute myocardial infarction. Significant variations in the diastolic

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Tallury,

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and Burch

slope as well as in the amplitude of the mitral valve echocardiogram were found in six patients (24 per cent). An apical systolic murmur was audible in each of the six patients. Day-to-day variations in the degree of the diastolic slope as well as in the intensity of the apical systolic murmur were attributed to alterations in the dynamic (contractile) state of the papillary muscles. Thus, during the early stages of acute myocardial infarction, ischemia and/or infarction of a papillary muscle render the muscle partially or totally incapable of shortening. Failure of the muscle to shorten results in mitral regurgitation. The echocardiogram offers a safe and convenient method for studying the day-to-day variations in papillary muscle function. REFERENCES 1.

Burch, G. E., DePasquale, N. P., and Phillips, J, H.: Clinical manifestations of papillary muscle dysfunction, Arch. Intern. Med. 112:112, 1963.

Am. Heart 1. January, 1972

2. Phillips, J. H., DePasquale, N. P., and Burch, G. E.: The electrocardiogram in infarction of the anterolateral papillary muscle, AM. HEART J. 66:338, 1963. 3. DePasquale, N. P., and Burch, G. E.: The necropsy incidence of gross scars of acute infarction of the uaoillarv muscles of the left ventricle. Am. J. Carhiol. 17i169, 1966. 4. Burch, G. E., DePasquale, N. P., and Phillips, J. H.: The syndrome- of papillary muscle dysfunction. An%. HEART I. 75:399. 1968. 5. Edler, I:: The diagnostic use of ultrasound in heart disease, Acta Med. Stand. (Suppl. 308):32, 1955. 6. Segal, B. L., Likoff, W., and Kingsley, B.: Echocardiography. Clinical application in combined mitral stenosis and mitral regurgitation, Am. J. Cardiol. 19:42, 1967. 7. Segal, B. L., Likoff, W., and Kingsley, B.: Echocardiography. Clinical application in mitral regurgitation, Am. J. Cardiol. 19:50, 1967. 8. DePasquale, N. P., Burch, G. E., and Phillips, J. H.: Electrocardiographic alterations associated with electrically “silent” areas of the myocardium, AM. HEART J. 68:697, 1964. 9. Herman, M. V., and Gorlin, R.: Implications of left ventricular asynergy, Am. J. Cardiol. 123538, 1969.