Experimental evidence in man of the electrocardiographic manifestations of papillary muscle dysfunction

Experimental evidence in man of the electrocardiographic manifestations of papillary muscle dysfunction T. D. Giles, M.D. G. E. Burch, M.D. New Orleans, La.

T

he electrocardiographic changes associated with papillary muscle dysfunction due to fibrosis, myopathy, and/or infarction of the left ventricle have been described previously. 1-4 Electrocardiographic changes associated with acute diseases of the papillary muscles consist of marked depression of Junction J usually associated with a slight convexity-upward deformity of the S-T interval (Fig. 1, A). The changes ordinarily seen in subacute disease of the papillary muscle consist of slight to moderate depression of Junction J usually associated with a slight convexity-upward deformity of the S-T interval and terminal inversion of the T wave. The electrocardiographic changes associated with chronic, fibrotic disease of the papillary muscle usually consist of moderate depression of Junction J and the S-T segment with a concavity-upward deformity of the S-T segment. The concavity-upward deformity of the S-T segment varies in extent from slight to marked (Fig. 1, B). U-wave inversion and/or depression of the T-U segment are found in the electrocardiogram (ECG) of most patients with papillary From

muscle disease. Characteristically, the Q-T or Q-U interval is markedly prolonged. It should be emphasized that the abovedescribed ECG changes of papillary muscle disease are part of a spectrum of change and may thus exhibit a great deal of overlapping. Involvement of the left ventricular anterolateral papillary muscle by disease is suggested when the above changes are observed in Leads I, aVL, Vr,, and VS, whereas changes in Leads II, III, aVF, and Vr through V4 suggest involvement of the posteromedial papillary muscle. Excellent correlation has been found between these electrocardiographic changes and papillary muscle disease in postmortem specimens.l-* Experimental evidence for the papillary muscle origin of the observed ECG changes in man has not been reported previously. However, a “ready-made” experiment, namely mitral valve surgery, affords an opportunity to observe in man the ECG changes due to papillary muscle injury. This is so because replacement of the mitral valve in man with a prosthetic device requires excision of the papillary

the Department of Medicine of the Tulane University New Orleans, La. Supported by grants HE06769 from the National Heart Rudolph Matas Memorial Fund for the Kate Prewitt search in Heart Disease. Received for publication Oct. 21. 1970.

Vol. 82, No. 2, pp. 193-198

August, 1971

School

of Medicine

and the Charity

Hospital

Institute of the United States Public Health Hess Laboratory, and the Rowe11 A. Billups

of Louisiana, Service. the Fund for Re-

American Heart Journal

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A. Acute disease of papillary

B. Chronic

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I;ig. I. ;I, ECG recorded from a M-year-old WOIII~II just prior to death, showing changes acute papillary muscle disease. Examination of the heart at necropsy showed acute infarction tricular anterolateral papillary muscle. B, ECG recorded from a 70.year-old woman showing teristic of chronic papillary muscle disease. ,It necrol)sy the left ventricular anterolateral showed dlffLlse scarring and fihros15.

Fig. 2. K-e- and muscles excised. disease.

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characteri>tic of of the left venchanges characpapillary muscle

postoperative ECG’s of a S-year-old woman who had the mitral valve replaced and papillary The postoperative tracing shows changes characteristically found in acute papillary muscle

muscles at their bases, leaving a ralv, injured endocardial surface in these areas. Thus, the ECG changes of “papillary muscle injury” would be expected if the previously presented hypotl~esisr-4 concerning their origin is correct. Therefore, we reviewed clinical records of patients before and after replacement of the mitral valve to learn whether or not ECG changes characteristic of papillary muscle disease followed. The ECG’s of patients who had an “open” mitral commissurotomy while on cardiopulmonary bypass were examined since in those patients the 21s “controls”

papillary muscles were not excised or damaged, except possibly for minor damage secondary to manipulations. Clinical

material

The clinical records of adult patients hospitalized at Charity Hospital of Louisiana at New Orleans on the Tulane University Medical Service who underwent mitral valve replacement or mitral commissurotomy, with the use of total cardiopulmonary bypass in both, were randomly examined for pre- and postoperative configurations of the ECG’s. Since the ECG changes indic-

ECG man+/+estation.s of papillary

muscle dysfunction.

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Fig. 3. Pre- and postoperative ECG’s recorded from a 12-year-old girl who had the mitral valve and papillary muscles excised and a prosthetic valve inserted. The early postoperative tracings (April 8, 1968 and April 15, 1968) show changes characteristic of those found in acute disease of the papillary muscles. A later tracing (April 10, 1969) shows a return to the preoperative configuration, apparently representative of healing of the injured myocardial area.

ative of papillary muscIe disease are reflected best in the precordial leads, a large number of early postoperative ECG’s were not available for study because the surgical dressings on the chest in most instances permitted only Leads I, II, III, aVR, aVL, and aVF to be recorded immediately postoperatively. Thus, no effort was made to determine the incidence of ECG changes of papillary muscle injury. Most patients were receiving digitalis preparations and a diuretic prior to operation, but drugs were usually discontinued one or two days preoperatively. Operations for both mitral valve replacement and mitral commissurotomy were performed

with the use of total cardiopulmonary bypass without coronary artery perfusion. “Pump times” for mitral valve replacement (3.5 to 45 minutes) were slightly longer than for commissurotomy (20 to 35 minutes). Results

Mitral valve replacement. Six patients whose ECG series were suitable for study had ECG’s with patterns typical of papilIary muscle injury following excision and replacement of the mitral valve. Fig. 2 shows an ECG of a patient who developed classical changes of acute papillary muscle injury following operation. Fig. 3 illustrates

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Fig. 4. Pre- and postoperative ECG’s recorded fr-om a 19.year-old man who had mitral valve replacement with excision of the papillary muscles. The early postoper,rtive tracings (Sept. 8, 1965 and Sept. 21, 1965) show changes previously attributed to CNS damage as well as changes characteristically fouud in acute papillary muscle disease, Later tracings (March 21, 1966 and Sept. 1.5, 1969) show a return of the ECG to a preoperative configuration, compatible with healing.

tracings from another patient with ECG changes of acute papillary muscle injury following operation and also changes associated with healing. The ECG of another patient (Fig. 4) illustrates not only papillary muscle injury but also changes described previously for injury to the central nervous system (CNS).5 CNS disturbances are well known to occur during open-heart surgery in which total cardiopulmonary bypass is used.‘j*’ The ECG’s which showed changes postoperatively always suggested

involvement of the left ventricular anterolateral papillary muscles, whereas changes associated with posteromedial papillary infarction were rarely seen. “Open” mitral commissurotomy. No ECG’s showed typical changes of papillary muscle infarction in patients who merely had open mitral commissurotomy. Six patients had ECG’s suitable for study recorded early in the postoperative period. Only minor changes in an occasional ECG occurred (Fig. 5), which apparently re-

Volztme Number

82 2

ECG manifestations

of papillary

muscle dysfunction

36

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Fig. 5. Pre- and postoperative ECG’s recorded from a 36-year-old woman who had an “open” mitral surotomy. The T waves are inverted in the early postoperative ECG (May 29, 1961), but the changes tion J and S-T segment are minor and not characteristic of acute papillary muscle disease. These show the greatest changes encountered in the six patients who had “open” mitral commissurotomy.

sulted from manipulations of the papillary muscles during the operation. The muscles were not excised. Discussion

ECG’s following mitral valve replacement at which time the papillary muscles were excised, leaving a raw, injured endocardial surface, showed changes typical of those described previously for acute papillary muscle injury. 1-4These characteristic patterns were not present in any of the preoperative tracings. ECG’s recorded from patients after “open” mitral commissurotomy in which the papillary muscles were not excised did not show such changes. These findings support the concept that injured papillary muscles produce typical ECG changes previously described for papillary muscle disease.‘-4The mechanism responsible for the S-T segment shift is essentially as described for currents of injury.8 The role of electrolyte shifts during cardiopulmonary bypass, from drug therapy or anesthetic agents, and the like that might be considered to produce these ECG changes was excluded since these factors were essentially the same for both types of open mitral valve surgery.

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commisin Junctracings

The patients with papillary muscle excision whose early postoperative ECG’s included the precordial leads always had changes of papillary muscle injury. Since it is likely that some papillary muscle damage occurs even during commissurotomy, occasional slight ECG changes of papillary muscle injury should be expected after such procedures. In fact, this may explain some of the minor changes observed in such patients during this study (Fig. 5). These tracings also reveal the extreme sensitivity of the ECG in detecting even slight injury to the papillary muscles. The papillary muscles are subendocardial structures which may be subjected to large amounts of stress9 In addition, the arterial blood supply is tenuous.1° Thus, it is not surprising that the papillary muscles are often the site of myocardial damage, especially with cardiomyopathy, myocarditis, and coronary artery disease. The precise mechanism by which papillary muscle injury produces ECG changes is not completely known. However, the changes observed in this study can be readily explained with the use of present concepts of currents of injury.* The downward shift of Junction J is likely due to a

“current of injury” effect. located at the raw surface where the papillar>* muscle \vas excised thus leaving an injured surface underlying the exploring electrode. This resting “current of injury” resulting from the raw injured surfaces left at the area of the basal attachments of the papillary muscles to the left ventricular endocardial surface would tend to shift the ECC; base line upward. However, because of compensating balancing forces in the EU;, a downward shift of Junction J results.” Since both the medial and lateral papillary muscles are injured during replacement of the mitral valve with an artificial prosthesis, one might have expected to see ECG changes of papillary muscle injury in all precordial leads. Yet, the changes recorded were of ant-erolateral papillary muscle injury alone. One possible explanation for this observation is that the manifested electrical forces originating from the anterolateral papillary muscle group are relatively stronger than and thereby negate the electrical forces originating from the posteromedial group. Also, since the exploring electrodes (V, and LTe) are much closer and perpendicularly oriented to the anterolateral papillary muscle than those overlying the posteromedial muscles (VI through \iq), the manifested injury current forces are more effectively oriented for recording by IT: and V6 than by \ll leads are through VA. The precordial semidirect and would, therefore, reflect larger deflections than the standard leads. Finally, thoracotomy and cardiac manipulations alter the spatial anatomic orientation of the heart within the thorax \vith respect to electrode placements OII the anterior chest \vall. This could explain why changes produced by injury to the posteromedial papillary muscles were less evident in the postoperative recordings than in patients who have nonsurgical injury to these muscles such as with ni>‘ocardial infarction.

Summary

ECG changes previously ascribed to disease of the anterolateral papillary muscles were seen in the six patients who had excision of the papillary muscle with replacement of the mitral valve, whereas no patients who had “open” commissurotomy without injury to or removal of the papillary muscles had such changes. These findings support the concept that electric forces originating in the injured papillary muscle cause ECG changes previously described for papillary muscle disease and dysfunction. REFERENCES 1. Burch, G. E., DePasquale, N. P., and Phillips, J. H.: Clinical manifestations of papillary muscle dysfunction, Arch. Intern. Med. (Chicago) 112:112, 1963. 2. Phillips, J. H., DePasquale, N. I’., and Burch, G. E.: The electrocardiogram in infarction of the anterolateral papillary muscle, AMER. HEART J. 66:338, 1963. G. E., DePasquale, N. P., and Phillips, 3. Burch, J. H.: The syndrome of papillary muscle dysfunction, AMER. HEART J. 75:399, 1968. 4. Burch, G. E., Sun, S. C., Chu, K. C., Colcolough, H. I,., and Sohal, Ii. S.: Relationships between pathologic findings of left ventricular papillary muscle and the electrocardiogram, Acta Cardiol. (Brux.) 24:285, 1969. 5. Burch, G. E., Meyers, R., and Abildskov, J. A.: A new electrocardiographic pattern observed in cerebrovascular accidents, Circulation 9:719, 1954. 6. Gilman, S.: Cerebral disorders after open-heart operations. New Enc. I. Med. 272:489. 1965. 7. T’ufo, H. i%, Ostfeld: A. M., and Shekeile, R.: Central nervous system dysfunction following open-heart surgery, J.A.M.A. 212:1333, 1970. T.: A primer of elec8. Burch, G. E., and Winsor, trocardiography, ed. 5, Philadelphia, 1966, Lea & Febiger, Publishers, pp. 42, li3. 9. Burch. G. E.. and DePasauale. N. P.: Time course of tension in papillary muscles of heart, J.A.M.A. 192:701, 1965. 10. Ranganathan, N., and Burch, G. E.: Gross morphology and arterial supply of the papillary muscles of the left ventricle of man, 4~~1~. HEART J. 77:506, 1969. I

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