Letters to the Editor
Complication of right ventricular myxoma To the Editor: I enjoyed reading the article "Diagnostic features of right ventricular myxoma," by Snyder and associates in the February, 1976, issue of the AMERICAN HEART JOURNAL (91:240, 1976). One notes that no gradient was present across the tricuspid valve in their patient. We reported a case of right ventricular myxoma causing obstruction across both the tricuspid and pulmonary valve in the July, 1973, issue of the American Journal of Cardiology. ~ The bibliography in the Snyder article reviewed the hterature up to the year 1971 which failed to emphasize obstruction to right ventricular inflow as well as outflow. Our patient's symptoms of edema extending to the waist, accompanied by fatigue and dyspnea, had been a tell-tale symptom. James R. S. Zager, M. D., F.A.C.P., F.A.C.C. 3621 East Century Blvd. Lynwood, Calif. 90262
REFERENCE 1.
Zager, J., Smith, J. O., Goldstein, S., and Franch, R. H.: Tricuspid and pulmonary valve obstruction relieved by removal of a myxoma of the right ventricle, Am. J. Cardiol. 32:101, 1973.
Reply To the Editor: I wish to thank Dr. Zager for his comments on our article. We are aware of the inflow tract obstruction which may be produced by right ventricular myxoma but since our patient did not have a gradient across the tricuspid valve, we did not comment on this complication. We certainly appreciate Dr. Zager's interest and hope that his letter will remind your readers of this potential complication of right ventricular myxomas. Stanley N. Snyder, M. D. 9209 Colima Rd. Whittier, Calif. 90605
The phonocardiogram in right ventricular myxoma To the Editor: Snyder and associates report an interesting case of right ventricular myxoma (AM. HEART J. 91:240-248, 1976). These authors make an issue of the finding of wide splitting of the second heart sound due to a delayed pulmonic closure. But, is that early diastolic sound the pulmonic closure sound? The simultaneous jugular pulse tracing shows that the sound labeled P occurs more than 50 msec. after the opening of the tricuspid valve as determined by the peak of the "V" wave. If the authors postulate that the pulmonic valve remains open in
American Heart Journal
early diastole because of the tumor, what produces its ultimate closure? The authors refer to a previous report of a right ventricular tumor that was also associated with an early diastolic sound? The authors of that report were not certain about the origin of the sound nor did they show data to suggest its connection to the pulmonic closure.' Since the early diastolic sound coincides with the rapid filling phase of the right ventricle, and there is also a late diastolic sound following atrial systole, it is reasonable to assume that they are indeed related to ventricular filling and most likely produced either by the tumor hitting the ventricular wall or by abnormal intraventricular flow patterns induced by the tumor. The prominent "a" wave on the phlebogram suggests the latter. Jorge A. Levisman, M.D. Assistant Professor UCLA School of Medicine Center for the Health Sciences Los Angeles, Calif. 90024
REFERENCE 1. Sakakibara, S., Osawa, M., Konno, S., et al.: Myxoma of the right ventricle of the heart: Report of a case with successful removal and review of the literature, AM. HEART J. 69:382, 1965.
Reply To the Editor: Dr. Levisman's comment on the etiology of the prominent early diastolic sound are appropriate. We felt that the sound represented a combination of events of which closure of the pulmonic valve could not be excluded. Certainly the protrusion of the tumor mass through the pulmonic valve contributed to the events during late systole and early diastole. Whether it was the tumor mass, the closure of the pulmonic valve, or the presence of pulmonary emboli, or some combination thereof that caused this sound is difficult to ascertain and we recognize the difference of opinion. It was conceivable to us that a ball valve-like effect of the tumor protruding into the pulmonary artery could maintain the pulmonic valve in the open position during right ventricular filling. Then,~ as' the right ventricular cavity enlarged, the tumor mass, as the separation between the free right ventricular wall and intraventricular septum increased, could retreat from its position in the pulmonary artery and return to within the right ventricular cavity. If this process occurred abruptly during right ventricular dilatation, the valve, with sudden relief of pressure, could conceivably suddenly snap shut producing a delayed and accentuated P_~. We also felt that atrial systole certainly could disturb the tranquility of the tumor mass in the right ventricle and set up a vibration but we concluded, since there was such a prominent A-wave in the jugular venous pulse, that the "S~," was produced by the same mechanism as the $4 in other disease
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Complication of right ventricular myxoma To the Editor: I enjoyed reading the article "Diagnostic features of right ventricular myxoma," by Snyder and associates in the February, 1976, issue of the AMERICAN HEART JOURNAL (91:240, 1976). One notes that no gradient was present across the tricuspid valve in their patient. We reported a case of right ventricular myxoma causing obstruction across both the tricuspid and pulmonary valve in the July, 1973, issue of the American Journal of Cardiology. ~ The bibliography in the Snyder article reviewed the hterature up to the year 1971 which failed to emphasize obstruction to right ventricular inflow as well as outflow. Our patient's symptoms of edema extending to the waist, accompanied by fatigue and dyspnea, had been a tell-tale symptom. James R. S. Zager, M. D., F.A.C.P., F.A.C.C. 3621 East Century Blvd. Lynwood, Calif. 90262
REFERENCE 1.
Zager, J., Smith, J. O., Goldstein, S., and Franch, R. H.: Tricuspid and pulmonary valve obstruction relieved by removal of a myxoma of the right ventricle, Am. J. Cardiol. 32:101, 1973.
Reply To the Editor: I wish to thank Dr. Zager for his comments on our article. We are aware of the inflow tract obstruction which may be produced by right ventricular myxoma but since our patient did not have a gradient across the tricuspid valve, we did not comment on this complication. We certainly appreciate Dr. Zager's interest and hope that his letter will remind your readers of this potential complication of right ventricular myxomas. Stanley N. Snyder, M. D. 9209 Colima Rd. Whittier, Calif. 90605
The phonocardiogram in right ventricular myxoma To the Editor: Snyder and associates report an interesting case of right ventricular myxoma (AM. HEART J. 91:240-248, 1976). These authors make an issue of the finding of wide splitting of the second heart sound due to a delayed pulmonic closure. But, is that early diastolic sound the pulmonic closure sound? The simultaneous jugular pulse tracing shows that the sound labeled P occurs more than 50 msec. after the opening of the tricuspid valve as determined by the peak of the "V" wave. If the authors postulate that the pulmonic valve remains open in
American Heart Journal
early diastole because of the tumor, what produces its ultimate closure? The authors refer to a previous report of a right ventricular tumor that was also associated with an early diastolic sound? The authors of that report were not certain about the origin of the sound nor did they show data to suggest its connection to the pulmonic closure.' Since the early diastolic sound coincides with the rapid filling phase of the right ventricle, and there is also a late diastolic sound following atrial systole, it is reasonable to assume that they are indeed related to ventricular filling and most likely produced either by the tumor hitting the ventricular wall or by abnormal intraventricular flow patterns induced by the tumor. The prominent "a" wave on the phlebogram suggests the latter. Jorge A. Levisman, M.D. Assistant Professor UCLA School of Medicine Center for the Health Sciences Los Angeles, Calif. 90024
REFERENCE 1. Sakakibara, S., Osawa, M., Konno, S., et al.: Myxoma of the right ventricle of the heart: Report of a case with successful removal and review of the literature, AM. HEART J. 69:382, 1965.
Reply To the Editor: Dr. Levisman's comment on the etiology of the prominent early diastolic sound are appropriate. We felt that the sound represented a combination of events of which closure of the pulmonic valve could not be excluded. Certainly the protrusion of the tumor mass through the pulmonic valve contributed to the events during late systole and early diastole. Whether it was the tumor mass, the closure of the pulmonic valve, or the presence of pulmonary emboli, or some combination thereof that caused this sound is difficult to ascertain and we recognize the difference of opinion. It was conceivable to us that a ball valve-like effect of the tumor protruding into the pulmonary artery could maintain the pulmonic valve in the open position during right ventricular filling. Then,~ as' the right ventricular cavity enlarged, the tumor mass, as the separation between the free right ventricular wall and intraventricular septum increased, could retreat from its position in the pulmonary artery and return to within the right ventricular cavity. If this process occurred abruptly during right ventricular dilatation, the valve, with sudden relief of pressure, could conceivably suddenly snap shut producing a delayed and accentuated P_~. We also felt that atrial systole certainly could disturb the tranquility of the tumor mass in the right ventricle and set up a vibration but we concluded, since there was such a prominent A-wave in the jugular venous pulse, that the "S~," was produced by the same mechanism as the $4 in other disease
6 73
