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SUBAORTIC STENOSIS DUE TO ACCESSORY TISSUE ON THE MITRAL VALVE
SUBAORTIC STENOSIS D U E T O ACCESSORY TISSUE O N THE MITRAL VALVE Lloyd D. MacLean, M.D.*
John A. Culligan, M.D.,
Dennis J. Kane, M.D., St. Paul and Minneapolis,
and Minn.
S
stenosis was clearly described by Arthur Keith in 1909.1 The heart, from a male patient 20 years of age, showed a fibrous (membranous) collar immediately below the aortic annulus together with endocarditis of the noncoronary cusp of the otherwise normal aortic valve. Since that time, membranous subaortic stenosis has been repeatedly recognized at autopsy, 2 ' 3 diagnosed during life,4 and successfully treated by surgery. This anomaly is believed to arise from incomplete atrophy of the bulbus cordis 1 ' 4 which was phylogenetically important as a "depulsator" between the gills and the ventricular pump, thereby maintaining a steady flow of blood through the gills. 1 ' 5 Muscular stenosis, also referred to as functional, 6 diffuse,7 or acquired 6 subaortic stenosis, was described by Brock in 1957.6 This variety of obstruction may be primary, as reported by Brachfeld and Gorlin 5 and by Morrow and Braunwald, 8 or secondary to systemic arterial hypertension 6 or valvular and supravalvular aortic stenosis.9 A third type of subaortic stenosis has been described by Lauer, DuShane, and Edwards 10 and by Bjork, Hultquist, and Lodin. 11 In this anomaly there is abnormal attachment of the anterior leaflet of the mitral valve, either directly to the interventricular septum 11 or via abnormal chordae tendineae to the septum, 10 producing thereby an obstruction to the left ventricular outflow tract. It is the purpose of this communication to describe a fourth type of subaortic stenosis which is uniquely suited to surgical correction. UBAORTIC
CASE REPORT Mr. J. 8. (A-260030), 29 years of age, was admitted to the Ancker Hospital on J a n . .15, 1962, with the major complaint of progressive exercise intolerance. The patient had had a known heart murmur since childhood and was rejected from military service for this reason. I n addition to exercise intolerance, t h e p a t i e n t had noticed increased fatigability, orthopnea, palpitations, and occasional choking sensations for 2 or 3 months prior to admission. The patient had not experienced loss of consciousness or angina. From Ancker Hospital, St. Paul, Minn., and the Departments of Surgery and Medicine, University of Minnesota, Minneapolis, Minn. Received for publication May 21, 1962. •Present address: Royal Victoria Hospital, Montreal, Quebec, Canada. 382
Vol. 45, No. 3 March, 1963
SUBAOETIC S T E N O S I S
383
Physical examination revealed a strong, well-nourished man. Blood pressure was 100/80 mm. H g ; pulse was 84 and regular. Abnormal physical findings included: situs inversus, a Grade 3/4 systolic ejection murmur, heard best over the base of the heart and at the left sternal border. There was also a Grade 1/4 diastolie murmur at the base. A thrill was palpable to the left of the superior aspect of the sternum. Laboratory findings were within normal limits. An electrocardiogram was interpreted as showing "dextrocardia w i t h considerable left ventricular strain." Cardiac fluoroscopy showed dextrocardia w i t h dilatation of the ascending aorta (Fig. 1). No calcifications were evident. Retrograde angiogram with injection immediately distal to t h e aortic valve demonstrated a normal valve with three leaflets and without evidence of insufficiency, a dilated ascending aorta, a single innominate a r t e r y passing t o t h e left, right aortic arch and right descending aorta (Fig. 1). Right heart catheterization revealed no shunt and normal pressures.
Fig. 1.—Posteroanterlor chest roentgenogram and lateral arch aortogram reveal dextrocardia with mild dilatation of the ascending aorta. The aortic valve appears normal without evidence of regurgitation.
Simultaneous pressure recordings from the left ventricle and brachial artery showed a peak systolic gradient of 70 mm. H g (Fig. 2 ) . A diagnosis of congenital aortic stenosis was made and operation was performed on March 21, 1962. Through a midline sternotomy incision, t h e typical anatomy of dextrocardia was found, w i t h the addition of a large persistent right superior vena cava which communicated with the coronary sinus. F o r this reason a single large (40 Fr.) catheter was placed in the right atrium for venous return to the pump oxygenator. Under moderate total body hypothermia (28° C.) and with i n t e r m i t t e n t coronary perfusion with blood a t 10° C , the aortic valve and subaortic area were explored. The heart was packed in saline slush. The aortic valve was tricuspid and normal. A laryngoscope was passed through the valve into the left ventricle and two "parachute-like" structures with attachment to the aortic cusp of the mitral valve were immediately seen (Fig. 3). I t was possible to remove these from t h e ventricular aspect of the mitral valve without injury to this structure.
384
MAC LEAN, CULLIGAN, K A N E
J. Thoracic and
Cardiovas. Surg.
200 100
o 200 100
I L. VENTRICLE
MS?-*4
. o L P*U ." BRACHIAL ART. PRE-OP.
BRACHJAU ART* POST-OB'^i.*
Fig. 2.—Pressure tracings from left ventricle ana brachial artery. The preoperative peak systolic gradient is 70 mm. Hg. Postoperatively, using the same technique and calibration, the peak systolic gradient is lowered to 5 mm. Hg. (Mr J. S.)
Aorta
Fig. 3.—Illustration of findings at operation. o, Dextrocardia (complete situs inversus) with a large persistent right superior vena cava which communicated with the coronary sinus. A single large (40 Fr.) catheter was placed in the right atrium for venous drainage to the pump oxygenator. b, Sterile laryngoscope was passed into the aorta via an aortotomy above the noncoronary sinus of Valsalva. c, Parachute-like structures attached to ventricular surface of anterior leaflet of the mitral valve. d, View of diverticula from above. There was one chorda tendinea to the larger of the accessory structures, which had no other attachment to the mitral valve. No other evidence of obstruction, either membranous or muscular, was visualized or palpated. After re-establishment of normal circulation the thrill which had been prominent in the ascending aorta disappeared. The cup-shaped structures were endothelized on both surfaces and were composed of edematous appearing connective tissue. There was no evidence of inflammation on gross or microscopic examination (Fig. 4 ) . On April 17, 1962, 3 weeks after operation, the patient was readmitted to hospital and simultaneous blood pressures were recorded from the left ventricle (transthoracic) and
Vol. 45, No. 3 March, 1963
•SUBAORTIC STENOSIS
385
right brachial artery, with the use of the same technique and calibration as had been utilized preoperatively. The peak systolic gradient was lowered from 70 mm. Hg to 5 mm. Hg (see Fig. 2). The patient is subjectively improved and has been able to return to his occupation which he had been forced to leave prior to operation because of exercise intolerance. There is no clinical evidence of mitral insufficiency. DISCUSSION
It is believed that the accessory tissue arising as two diverticula from the ventricular surface of the anterior leaflet of the mitral valve produced a ballvalve obstruction to the outflow tract of the left ventricle. The cup-shaped structures were so oriented as to fill with blood and to obstruct flow during systole (Fig. 3, c). Excision of the accessory tissue alone reduced the peak systolic pressure gradient across the aortic valve from 70 to 5 mm. Hg.
Fig. 4.—Diverticula removed at operation. Cup-shaped appearance of one of these is clearly demonstrated. The gross and microscopic appearance suggested accessory valvular tissue.
The use of a laryngoscope to visualize the left ventricular cavity, as recommended by Gordon,9 was very helpful in the present case. It was possible to define precisely the limits of the accessory tissue and to remove these structures without injuring the mitral valve. In the arrested heart, accessory tissue may be difficult to recognize unless carefully searched for. This cause of aortic stenosis should be considered in patients in whom no apparent causa for a significant pressure gradient is found at operation. It is possible that left ventricular angiography 15 would have established the diagnosis preoperatively. Similar lesions have been recognized at postmortem. Edwards 12 noted a saclike formation on the ventricular aspect of the common atrioventricular valve in a 3-day-old infant with single atrium and atrioventricularis communis. A similar saclike structure, measuring 3 by 2.5 em., hanging down from the ventricular aspect of the anterior leaflet of the mitral valve was found at postmortem in a child of 11 years by C. P. Deal, Jr. 1 3 A Grade 4/6 systolic murmur, loudest in the aortic area, and systolic thrill had been noted. Electrocardiogram showed left ventricular hypertrophy and strain. Left ventricular enlargement was pres-
386
MAC LEAN, CULLIGAN, KANE
Fig. 5.—A, Membranous subaortic stenosis.
J. Thoracic and Cardiovas. SurR.
B, Muscular subaortic stenosis.
Fig:. 6.—Abnormal attachment of anterior leaflet of mitral valve creating- subaortic stenosis. Abnormality may be chordal fixation to the septum or direct attachment as illustrated. Division of the apparent membrane from above will produce mitral insufficiency.»
ent on roentgenogram. A pressure gradient of 70 mm. Hg (peak systolic) was measured across the aortic valve. The lesion in the collapsed state was not seen at operation. Subpulmonary stenosis due to accessory valvular tissue has been found at autopsy in corrected transposition of the great vessels on three occasions by Edwards. 12 Figs. 5 and 6 illustrate the three other types of subaortic stenosis with differences in appearance of each type as viewed from above the aortic valve. The lesion herein described is quite distinct from the semilunar pockets which form on the lower border of the endocardial ring of membranous subaortic stenosis.14 The major complications associated with subaortic stenosis are: (1) subacute bacterial endocarditis which was reported in most of the early cases, (2)
Vol. 45, No. 3 Mirch, 1963
SUBAOETIC STENOSIS
387
congestive heart failure, and (3) gradual muscular hypertrophy which accentuates the outflow tract obstruction which in turn increases myocardial demand with further hypertrophy. Since muscular obstruction is the least remediable to surgical therapy of the various forms of subaortic stenosis, surgical repair should be considered early. Some pessimism has existed in the past concerning the treatment of muscular subaortic stenosis unassociated with either valvular or membranous subvalvular stenosis.8'1Ci However, Kirklin and Ellis 7 have used both aortotomy and left ventriculotomy in the treatment of this type of stenosis with initial success. Unusual forms of muscular obstruction have been described in which asymmetrical hypertrophy or hamartoma of the interventricular septum causes an obstruction to outflow of both the left and right ventricles. In these patients a pressure gradient may be noted in the right ventricle as well as in the left.10 With increased use of left heart catheterization, other causes of subaortic obstruction will undoubtedly be discovered and the natural history of existing types further clarified. SUMMARY AND CONCLUSIONS
The successful surgical treatment of a new form of subaortic stenosis has been described. In this type of stenosis, cup-shaped structures attached to the ventricular aspect of the anterior leaflet of the mitral valve produce a ball-valve obstruction to the outflow tract of the left ventricle. Removal of this accessory tissue without damage to the mitral valve was possible and reduced the left ventrieulo-brachial artery systolic pressure gradient from 70 mm. Hg before operation to 5 mm. Hg after operation. Similar lesions have been recognized at postmortem previously. Recognition and removal at operation is assisted by the visualization of the left ventricular cavity offered by passing a laryngoscope through the aortic valve. A short review is made of the four types of subaortic stenosis with emphasis on recognition at the time of operation. REFERENCES 1. Keith, A.: Malformations of the Heart, Lancet 2: 350-363, 1909. 2. Abbott, M. E.: Congenital Cardiac Disease, Osier's Modern Medicine, ed. 3, Philadelphia, 1927, Lea & Febiger, pp. 743-746. 3. Wiglesworth, F . W.: A Case of Subaortic Stenosis With Acute Aortic Endocarditis, .T. Tech. Methods 17: 102-105, 1937. 4. Mason, D. G., and Hunter, W. C : Subaortic Stenosis, Am. J . P a t h . 18: 343-348, 1942. 5. Brachfeld, N., and Gorlin, R.: Subaortic Stenosis: A Revised Concept of the Disease, Medicine 38: 415-433, 1959. 6. Brock, R.: Functional Obstruction of the Left Ventricle, Guy's Hosp. Rep. 106: 221238, 1957. 7. Kirklin, J . W., and Ellis, F . H.: Surgical Relief of Diffuse Subvalvular Aortic Stenosis, Circulation 24: 739-742, 1961. 8. Morrow, A. G., and Braunwald, E.: Functional Aortic Stenosis: A Malformation Characterized by Resistance to Left Ventricular Outflow Without Anatomic Obstruction, Circulation 20: 181, 1959. 9. Gordon, A. S.: The Surgical Management of Congenital Supravalvular, Valvular, and Subvalvular Aortic Stenosis Using Deep Hypothermia, J . THORACIC SUBG. 43: 141153, 1962.
388
MAC L E A N , C U L L I G A N , K A N E
J. Thoracic and Cardiovas. Surg.
10. Lauer, R. M., DuShane, J. W., and Edwards, J. E.: Obstruction of Left Ventricular Outlet in Association With Ventricular Septal Defect, Circulation 22: 110-125, 1960. 11. Bjbrk, V. O., Hultquist, G., and Lodin, H.: Subaortic Stenosis Produced by an Abnormally Placed Anterior Mitral Leaflet, J . THORACIC SURG. 4 1 : 659-669, 1961. 12. Edwards, Jesse: Personal communication. 13. Deal, C. P., J r . : Personal communication. 14. Christian, H. A.: Congenital and Acquired Aortic Stenosis in Adults, M. Clin. North America 16: 773-780, 1933. 15. Bjbrk, V. O., Jonsson, B., and Nordenstrom, B.: Subaortic Stenosis, Thorax 13: 201203, 1958. 16. Goodwin, J. P., Hollman, A., Cleland, W. P., and Teare, D.: Obstructive Cardiomyopathy Simulating Aortic Stenosis, Brit. H e a r t J. 22: 403-414, 1960.
John A. Culligan, M.D.,
Dennis J. Kane, M.D., St. Paul and Minneapolis,
and Minn.
S
stenosis was clearly described by Arthur Keith in 1909.1 The heart, from a male patient 20 years of age, showed a fibrous (membranous) collar immediately below the aortic annulus together with endocarditis of the noncoronary cusp of the otherwise normal aortic valve. Since that time, membranous subaortic stenosis has been repeatedly recognized at autopsy, 2 ' 3 diagnosed during life,4 and successfully treated by surgery. This anomaly is believed to arise from incomplete atrophy of the bulbus cordis 1 ' 4 which was phylogenetically important as a "depulsator" between the gills and the ventricular pump, thereby maintaining a steady flow of blood through the gills. 1 ' 5 Muscular stenosis, also referred to as functional, 6 diffuse,7 or acquired 6 subaortic stenosis, was described by Brock in 1957.6 This variety of obstruction may be primary, as reported by Brachfeld and Gorlin 5 and by Morrow and Braunwald, 8 or secondary to systemic arterial hypertension 6 or valvular and supravalvular aortic stenosis.9 A third type of subaortic stenosis has been described by Lauer, DuShane, and Edwards 10 and by Bjork, Hultquist, and Lodin. 11 In this anomaly there is abnormal attachment of the anterior leaflet of the mitral valve, either directly to the interventricular septum 11 or via abnormal chordae tendineae to the septum, 10 producing thereby an obstruction to the left ventricular outflow tract. It is the purpose of this communication to describe a fourth type of subaortic stenosis which is uniquely suited to surgical correction. UBAORTIC
CASE REPORT Mr. J. 8. (A-260030), 29 years of age, was admitted to the Ancker Hospital on J a n . .15, 1962, with the major complaint of progressive exercise intolerance. The patient had had a known heart murmur since childhood and was rejected from military service for this reason. I n addition to exercise intolerance, t h e p a t i e n t had noticed increased fatigability, orthopnea, palpitations, and occasional choking sensations for 2 or 3 months prior to admission. The patient had not experienced loss of consciousness or angina. From Ancker Hospital, St. Paul, Minn., and the Departments of Surgery and Medicine, University of Minnesota, Minneapolis, Minn. Received for publication May 21, 1962. •Present address: Royal Victoria Hospital, Montreal, Quebec, Canada. 382
Vol. 45, No. 3 March, 1963
SUBAOETIC S T E N O S I S
383
Physical examination revealed a strong, well-nourished man. Blood pressure was 100/80 mm. H g ; pulse was 84 and regular. Abnormal physical findings included: situs inversus, a Grade 3/4 systolic ejection murmur, heard best over the base of the heart and at the left sternal border. There was also a Grade 1/4 diastolie murmur at the base. A thrill was palpable to the left of the superior aspect of the sternum. Laboratory findings were within normal limits. An electrocardiogram was interpreted as showing "dextrocardia w i t h considerable left ventricular strain." Cardiac fluoroscopy showed dextrocardia w i t h dilatation of the ascending aorta (Fig. 1). No calcifications were evident. Retrograde angiogram with injection immediately distal to t h e aortic valve demonstrated a normal valve with three leaflets and without evidence of insufficiency, a dilated ascending aorta, a single innominate a r t e r y passing t o t h e left, right aortic arch and right descending aorta (Fig. 1). Right heart catheterization revealed no shunt and normal pressures.
Fig. 1.—Posteroanterlor chest roentgenogram and lateral arch aortogram reveal dextrocardia with mild dilatation of the ascending aorta. The aortic valve appears normal without evidence of regurgitation.
Simultaneous pressure recordings from the left ventricle and brachial artery showed a peak systolic gradient of 70 mm. H g (Fig. 2 ) . A diagnosis of congenital aortic stenosis was made and operation was performed on March 21, 1962. Through a midline sternotomy incision, t h e typical anatomy of dextrocardia was found, w i t h the addition of a large persistent right superior vena cava which communicated with the coronary sinus. F o r this reason a single large (40 Fr.) catheter was placed in the right atrium for venous return to the pump oxygenator. Under moderate total body hypothermia (28° C.) and with i n t e r m i t t e n t coronary perfusion with blood a t 10° C , the aortic valve and subaortic area were explored. The heart was packed in saline slush. The aortic valve was tricuspid and normal. A laryngoscope was passed through the valve into the left ventricle and two "parachute-like" structures with attachment to the aortic cusp of the mitral valve were immediately seen (Fig. 3). I t was possible to remove these from t h e ventricular aspect of the mitral valve without injury to this structure.
384
MAC LEAN, CULLIGAN, K A N E
J. Thoracic and
Cardiovas. Surg.
200 100
o 200 100
I L. VENTRICLE
MS?-*4
. o L P*U ." BRACHIAL ART. PRE-OP.
BRACHJAU ART* POST-OB'^i.*
Fig. 2.—Pressure tracings from left ventricle ana brachial artery. The preoperative peak systolic gradient is 70 mm. Hg. Postoperatively, using the same technique and calibration, the peak systolic gradient is lowered to 5 mm. Hg. (Mr J. S.)
Aorta
Fig. 3.—Illustration of findings at operation. o, Dextrocardia (complete situs inversus) with a large persistent right superior vena cava which communicated with the coronary sinus. A single large (40 Fr.) catheter was placed in the right atrium for venous drainage to the pump oxygenator. b, Sterile laryngoscope was passed into the aorta via an aortotomy above the noncoronary sinus of Valsalva. c, Parachute-like structures attached to ventricular surface of anterior leaflet of the mitral valve. d, View of diverticula from above. There was one chorda tendinea to the larger of the accessory structures, which had no other attachment to the mitral valve. No other evidence of obstruction, either membranous or muscular, was visualized or palpated. After re-establishment of normal circulation the thrill which had been prominent in the ascending aorta disappeared. The cup-shaped structures were endothelized on both surfaces and were composed of edematous appearing connective tissue. There was no evidence of inflammation on gross or microscopic examination (Fig. 4 ) . On April 17, 1962, 3 weeks after operation, the patient was readmitted to hospital and simultaneous blood pressures were recorded from the left ventricle (transthoracic) and
Vol. 45, No. 3 March, 1963
•SUBAORTIC STENOSIS
385
right brachial artery, with the use of the same technique and calibration as had been utilized preoperatively. The peak systolic gradient was lowered from 70 mm. Hg to 5 mm. Hg (see Fig. 2). The patient is subjectively improved and has been able to return to his occupation which he had been forced to leave prior to operation because of exercise intolerance. There is no clinical evidence of mitral insufficiency. DISCUSSION
It is believed that the accessory tissue arising as two diverticula from the ventricular surface of the anterior leaflet of the mitral valve produced a ballvalve obstruction to the outflow tract of the left ventricle. The cup-shaped structures were so oriented as to fill with blood and to obstruct flow during systole (Fig. 3, c). Excision of the accessory tissue alone reduced the peak systolic pressure gradient across the aortic valve from 70 to 5 mm. Hg.
Fig. 4.—Diverticula removed at operation. Cup-shaped appearance of one of these is clearly demonstrated. The gross and microscopic appearance suggested accessory valvular tissue.
The use of a laryngoscope to visualize the left ventricular cavity, as recommended by Gordon,9 was very helpful in the present case. It was possible to define precisely the limits of the accessory tissue and to remove these structures without injuring the mitral valve. In the arrested heart, accessory tissue may be difficult to recognize unless carefully searched for. This cause of aortic stenosis should be considered in patients in whom no apparent causa for a significant pressure gradient is found at operation. It is possible that left ventricular angiography 15 would have established the diagnosis preoperatively. Similar lesions have been recognized at postmortem. Edwards 12 noted a saclike formation on the ventricular aspect of the common atrioventricular valve in a 3-day-old infant with single atrium and atrioventricularis communis. A similar saclike structure, measuring 3 by 2.5 em., hanging down from the ventricular aspect of the anterior leaflet of the mitral valve was found at postmortem in a child of 11 years by C. P. Deal, Jr. 1 3 A Grade 4/6 systolic murmur, loudest in the aortic area, and systolic thrill had been noted. Electrocardiogram showed left ventricular hypertrophy and strain. Left ventricular enlargement was pres-
386
MAC LEAN, CULLIGAN, KANE
Fig. 5.—A, Membranous subaortic stenosis.
J. Thoracic and Cardiovas. SurR.
B, Muscular subaortic stenosis.
Fig:. 6.—Abnormal attachment of anterior leaflet of mitral valve creating- subaortic stenosis. Abnormality may be chordal fixation to the septum or direct attachment as illustrated. Division of the apparent membrane from above will produce mitral insufficiency.»
ent on roentgenogram. A pressure gradient of 70 mm. Hg (peak systolic) was measured across the aortic valve. The lesion in the collapsed state was not seen at operation. Subpulmonary stenosis due to accessory valvular tissue has been found at autopsy in corrected transposition of the great vessels on three occasions by Edwards. 12 Figs. 5 and 6 illustrate the three other types of subaortic stenosis with differences in appearance of each type as viewed from above the aortic valve. The lesion herein described is quite distinct from the semilunar pockets which form on the lower border of the endocardial ring of membranous subaortic stenosis.14 The major complications associated with subaortic stenosis are: (1) subacute bacterial endocarditis which was reported in most of the early cases, (2)
Vol. 45, No. 3 Mirch, 1963
SUBAOETIC STENOSIS
387
congestive heart failure, and (3) gradual muscular hypertrophy which accentuates the outflow tract obstruction which in turn increases myocardial demand with further hypertrophy. Since muscular obstruction is the least remediable to surgical therapy of the various forms of subaortic stenosis, surgical repair should be considered early. Some pessimism has existed in the past concerning the treatment of muscular subaortic stenosis unassociated with either valvular or membranous subvalvular stenosis.8'1Ci However, Kirklin and Ellis 7 have used both aortotomy and left ventriculotomy in the treatment of this type of stenosis with initial success. Unusual forms of muscular obstruction have been described in which asymmetrical hypertrophy or hamartoma of the interventricular septum causes an obstruction to outflow of both the left and right ventricles. In these patients a pressure gradient may be noted in the right ventricle as well as in the left.10 With increased use of left heart catheterization, other causes of subaortic obstruction will undoubtedly be discovered and the natural history of existing types further clarified. SUMMARY AND CONCLUSIONS
The successful surgical treatment of a new form of subaortic stenosis has been described. In this type of stenosis, cup-shaped structures attached to the ventricular aspect of the anterior leaflet of the mitral valve produce a ball-valve obstruction to the outflow tract of the left ventricle. Removal of this accessory tissue without damage to the mitral valve was possible and reduced the left ventrieulo-brachial artery systolic pressure gradient from 70 mm. Hg before operation to 5 mm. Hg after operation. Similar lesions have been recognized at postmortem previously. Recognition and removal at operation is assisted by the visualization of the left ventricular cavity offered by passing a laryngoscope through the aortic valve. A short review is made of the four types of subaortic stenosis with emphasis on recognition at the time of operation. REFERENCES 1. Keith, A.: Malformations of the Heart, Lancet 2: 350-363, 1909. 2. Abbott, M. E.: Congenital Cardiac Disease, Osier's Modern Medicine, ed. 3, Philadelphia, 1927, Lea & Febiger, pp. 743-746. 3. Wiglesworth, F . W.: A Case of Subaortic Stenosis With Acute Aortic Endocarditis, .T. Tech. Methods 17: 102-105, 1937. 4. Mason, D. G., and Hunter, W. C : Subaortic Stenosis, Am. J . P a t h . 18: 343-348, 1942. 5. Brachfeld, N., and Gorlin, R.: Subaortic Stenosis: A Revised Concept of the Disease, Medicine 38: 415-433, 1959. 6. Brock, R.: Functional Obstruction of the Left Ventricle, Guy's Hosp. Rep. 106: 221238, 1957. 7. Kirklin, J . W., and Ellis, F . H.: Surgical Relief of Diffuse Subvalvular Aortic Stenosis, Circulation 24: 739-742, 1961. 8. Morrow, A. G., and Braunwald, E.: Functional Aortic Stenosis: A Malformation Characterized by Resistance to Left Ventricular Outflow Without Anatomic Obstruction, Circulation 20: 181, 1959. 9. Gordon, A. S.: The Surgical Management of Congenital Supravalvular, Valvular, and Subvalvular Aortic Stenosis Using Deep Hypothermia, J . THORACIC SUBG. 43: 141153, 1962.
388
MAC L E A N , C U L L I G A N , K A N E
J. Thoracic and Cardiovas. Surg.
10. Lauer, R. M., DuShane, J. W., and Edwards, J. E.: Obstruction of Left Ventricular Outlet in Association With Ventricular Septal Defect, Circulation 22: 110-125, 1960. 11. Bjbrk, V. O., Hultquist, G., and Lodin, H.: Subaortic Stenosis Produced by an Abnormally Placed Anterior Mitral Leaflet, J . THORACIC SURG. 4 1 : 659-669, 1961. 12. Edwards, Jesse: Personal communication. 13. Deal, C. P., J r . : Personal communication. 14. Christian, H. A.: Congenital and Acquired Aortic Stenosis in Adults, M. Clin. North America 16: 773-780, 1933. 15. Bjbrk, V. O., Jonsson, B., and Nordenstrom, B.: Subaortic Stenosis, Thorax 13: 201203, 1958. 16. Goodwin, J. P., Hollman, A., Cleland, W. P., and Teare, D.: Obstructive Cardiomyopathy Simulating Aortic Stenosis, Brit. H e a r t J. 22: 403-414, 1960.