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Fat infiltration of myocardium as a cause of cardiac conduction defect∗
Case Reports Fat Infiltration
of Myocardium
of Cardiac Asuox
Conduction
as a Cause Defect*
M. BAISAVER, M.B., AZORIDES R. MORALES, M.D. and FRED W. WHITEHOUSE, M.D Detroit,
Michigan
T
HE human cardiac conduction system has been studied extensively, and numerous anatomic lesions associated with conduction defects have been described.1-3 However, fatty infiltration has only rarely been mentioned as a cause of conduction defect. This paper reports a study of the conduction system in an unusual case of fatty infiltration of the myocardium associated with sinus bradycardia and chronic atria1 fibrillation.
for many years, and at admission her weight was 190 pounds, her height 60 inches. On admission, her temperature was 98.4’ F. and pulse rate 45/min. t The ocular fundi showed grade 1 hypertensive changes. Blood pressure was 240/120 mm. Hg. The lungs were free of rales, but cardiomegaly, hepatomegaly and bilateral varicosities of the legs with pretibial edema were present. The initial chest roentgenogram (Fig. 1A) confirmed cardiomegaly with striking right-sided enlargement. The electrocardiogram (Fig. 2) indicated a sinus bradycardia with episodes of sinus arrest and nodal escape beats. No evidence of ventricular hypertrophy was present.
CASE REPORT A 49 year old housewife
was first admitted to the Henry Ford Hospital in 1958 with complaints of shortness of breath and ankle swelling. Hypertension had been known for five years. She had been obese
t It is noteworthy that the bradycardia use of digitalis in this patient.
FIG. 1. Chest roentpenopzms. A, December 1958, demonstrating marked cardiac enlargement mainly right-sided. B, 5 years later (Dec. 1963), showing no change in the cardiac silhouette.
* From the Departments VOLUME
19,
FEBRUARY
1967
which appears to be
of Pathology and Medicine, Henry Ford Hospital, Detroit, Mich. 261
pwceded the
Kalsaver,
262
Morales
and Whitehouse
Summary
of Cardiac
Catheterization
Oxygen Content Sat. (x-01. “;,) (!F)
Pressures (mm. Hg)
Superior vena Right atrium Right ventricle
Mean
SjU
;; 23
17;;o 50/‘4-12
10.5 10.1 9 9
65 62 61
26
46/18
10.4
64
13 15
22/8 17jl4
cava
Pulmonary artery I eft pul rnonary artery wedge Left hepatic vein wedge Sat.
FIG. 2.
Elec~rocardG~~ramtaken in 1958 (standard
leads) demonstrates sinus and nodal escape brats.
FIG.
3.
bradycardia
Electrocardiogram taken
with
in 1963
sinus
limb arrest
(limb
leads)
Findinqs
= saturation.
The patient was treated with bed rest, digitalis and diuretics. At rest, her blood pressure averaged 160/90 and her weight at discharge from the hospital She was given a leotard for treatwas 169 pounds. ment of the venous stasis. Cardiac catheterization was performed three months later. Table I summarizes the data. There was evidence of moderate elevation of right atrial, right ventricular and pulmonary artery wedge pressures. of undetermined A diagnosis of “myocardiopathy No change in her program was nature” was made. advised. For the next 5 years the patient was normally active and was seen regularly; there was no significant change in physical findings. Bradycardia persisted, Digithe apical rate averaging 40 to 60 per minute. toxin,
0.1 mg. daily, was continued throughout this Arterial blood pressure was usually elevated, period. and antihypertensive treatment with hydralazine and
shows
atria1
fibrillation THE
with
very
AMERICAN
slow
ventricular
JOURNAL
rate.
OF CARDIOLOC
:Y
Fat Infiltration
of Myocardiurn
36.1
chlorothiazide was instituted. In December 1963 readmission was necessary because of chest pain. Atria1 fibrillation with slow ventricular rate was now noted (Fig. 3). A roentgenogram of chest (Fig. 1B) was unchanged when compared to that of 1958. Digitoxin was continued as before. She was discharged symptomatically improved on the eighth hospital day. ~~I?FIP~ iast admission occurred in January 1965 following a cerebral vascular accident. Atria1 fibrillation was still present. She died 36 hours after admission. Her lveight two weeks before death was 175 pounds. Autopsy: The body was 150 cm. long and weighed 172 pounds. The heart weighed 550 gm.? and the epicardial surface revealed a large amount of fat. This fatty tissue was more prominent on the anterior surface of the right ventricle where it measured 2 cm. in thickness (Fig. 4). There was extensive infiltration of this epicardial fat into the underlying myocardium. ‘I‘his \vas more severe on the right side, and, in places, the adipose tissue extended through the entire thickThe right ness of the right ventricular myocardium. ventricular myocardium measured 1 cm. in thickness and the left ventricle measured 2 cm. The myocardium showed no fibrosis or infarction, and there were no mural thrombi in any of the cardiac chambers. The valve rings and the valve cusps were unremarkable? and the openings of the coronary arteries were large and patent. Examination of the coronary arteries and their branches showed moderate to severe atherosclerotic narrowing of the lumen without occlusion. The arteries to the sinoatrial and A-V nodes arose from the right coronary artery, and sections through them did not reveal any narrowing or occlusion. However, the artery to the sinoatrial
FIG. 5. Grossfihotograjh of the right atria1 wall in the region of the sinus nods. Arrow points to the superficial-appearing sinus node artery. SVC = superior vena cava.
VOLUME
19,
FEBRUARY
1967
shows the prominent cardiurn with streaks cardium.
accumulation of fat in the epiof fatty infiltration of thr myo-
264
Balsaver,
Morales
and Whitehouse node, normally embedded within the substance of the node, was situated quite superficially at the sinoatrial junction (Fig. 5). A large amount of adipose tissue \Gas present in this region and about the atriovcntricular node. Serial secticns throqhout the conduction system murculature revealed extensive fatty replacement of the sinus node musculature (Fig. 6) where only occasional nodal fibers could be recognized. ‘The atrioventricular node appeared infiltrated by fat to a lesser degree. Fatty infiltration was also demonstrated in the bundle of His (Fig. 6), while serial sections of the bundle branches showed a focus of fatty tissue only about the right branch. Moderate fatty infiltration was noted in the pancreas and the adrenals. The lungs showed moderate edema, and a recent thromboembolus was noted in one of the smaller arterial branches. Healed infarcts, probably related to previous embolism, were seen in both the kidneys. The brain weighed 1,300 gm. It was edematous and asymmetrical, the left hemisphere showing extensive softening of the frontotemporal parietal regions. The left middle cerebral artery contained an occluding thrombus which appeared to be embolic in nature.
COMMENT
FIG. 6. Photomicrographs of the conduction system. A, sinus node shows prominence of fat and atrophy of the substance of the nodal tissue around the artery. Section was taken through the thickest portion of the sinus node. (Masson’s trichrome; X 35 reduced by 157&) B, sinus node. Higher power view of the same section. Arrows point to isolated nodal fibers. ART (upper left) = wall of the sinus node artery. (Masson’s trichrome ; X 150 reduced by 1570.) C, bundle of His (penetrating po&n), showing fat vacuoles in the substance of the bundle. (Hematoxylin and eosin; X 90 reduced by 1 57r.)
The pertinent histologic finding was the abundant fat within the right ventricular myocardium and in the conduction system. It is readily conceivable that such adipose tissue within the sinus node could, by mechanical interference, produce conduction defects. For several years, this patient gave evidence of interference with normal conduction from the sinus node. This was manifested by bradycardia Later, with sinus arrest and nodal escape. chronic atria1 fibrillation occurred, with slow ventricular response. While systemic hypertension associated with left ventricular hypertrophy was present, the intense degree of fatty infiltration into the myocardium, particularly involving the right ventricle and the conduction system, separates this case from the common findings of the hypertensive heart. The observation of replacement by adipose tissue of the conduction system musculature has been given little attention in the literature. One of the earliest reports was that of Nuzum4 in 1914, who reviewed 27 cases of Adams-Stokes syndrome and found 2 with “lipomatosis.” He also mentions previous reports of fatty change in the bundle of His associated with heart block and sudden death. In 1924 MGnckeber$ reviewed the literature on fatty infiltration of the myocardium and referred to involvement of the conduction sys THE
AMERICAN
JOURNAL
OF
CARDIOLOGY
Fat
Infiltration
te111. In their review of 58 cases of myocardial fat infiltrat’on, Saphir and Corriganfi found 2 casts in \t:hich this change was the only obvious callse of death. The series also included 1 case of an ilrtra\-c‘lltriclllar bundle branch block xvhich showed fat infiltration of the bllndle of His with atrophy of the fibers. Spain and Cathcart’ reported a case of right-sided heart failllre M.ith heart block in which fatty infiltration of the right ventricular rnyocardium and the inter\.entricular septum was noted. M’e collld find only one report of a detailed study of the conduction system in fatty infiltration of the nlyccardilml. Bronzini and Novi* studied the atrioventricular conduction system in 11 fatty hearts and 15 nonfatty hearts. Infiltration of the fatty tissue into the A-V bundle and the atrio\xxtricular node was noted only in the fatty hearts. The nonfatty hearts showed fatty tissue around the bundles without infiltration into, or replacement of, muscle fibers. Their report, howe\:er, does not make any reference to conduction defects in the hearts with fatty infiltration of the conduction system. In a study of 64 adult hearts, Hudson2 reported a number of lesions in the cardiac pacemaker, one of the cases being described as showing ‘
\‘OLUME 19. FEBRUARY 1967
of Myocardium
265
this problem and may prove frrlitful.
its association
\vith obesit)
SUMMARY
Fatty- infiltration has only rarclv bcsen reported as a callse of a cardiac conduc;iorr defect. A case of chronic sinoatrial block and atria1 fibrillation \\ith severe fatty infiltration of the myocardium and the conduction system is reported. The literature on conduction defects due to fatty infiltration is reviewed. REFERENCES 1. IJJMB, G. and SI~ACKLETT, K. S. Human cardiac conduction tissue lesions. Am. ./. Path., 36: 411, 1960. 2. IJUOSON, R. E. R. The human pacrlnaker and its pathology. &it. Hmrt J., 22: 153, 1960. The normal anatomy of the conduction 3. LEV, M. system in man and its pathology in atrioventricular block. Ann. il;pw J’crh Acad. SC.. 111: 817, 1964. 4. NUZUM, F. Fatty infiltration (lipomatosis) of the auriculoventricular bundle of His, with sudden unexpected death. A M.A. Arch. Znt. Mpd., 13: 640, 1914. Herz und Gefaesse. 5. MZ~NCKEBERC, .J. G. In: Handbuch der Speziellen Pathologischen Anatomic und Histologie, Vol. 2, p. 345. Edited by HENKE, F. und LUBARSCH, 0. Berlin, 1924. Julius Springer. 6. SAPHIR, 0. and CORRIGAN, M. Fatty infiltration of the myocardium. A.M.il. Arch. Int. .\f~d., 52: 410, 1933. 7. SPAIN, D. M. and CATHCART, R. T. Heart block caused by fat infiltration of the intcrventricular septum (“car adiFosum”). Am. Hmr-t J., 32: 659, 1946. 8. BRONZINI,E. and NOVI, A. M. II systema di conduzione atrioventricolare nell. “Adipositas cordis.” Pathologica, 53: 231, 1961. 9. Lev, M. Anatomic basis for atrioventricular block. z4m. J. Med., 37: 742, 1964. 10. LEV, M. The pathology of complete atrioventricular block. Prq. Cardiovas. Dis., 6: 317, 1964. 11. LEV, M. Aging changes in the human sinoatrial node. J. Cerontol.,9: 1, 1954. 12. ERICKSON, E. E. and LEV, M. .4ging changes in the human atrioventricular node, bundle and bundle branches. J. Gem&l., 7: 1, 1952.
of Myocardium
of Cardiac Asuox
Conduction
as a Cause Defect*
M. BAISAVER, M.B., AZORIDES R. MORALES, M.D. and FRED W. WHITEHOUSE, M.D Detroit,
Michigan
T
HE human cardiac conduction system has been studied extensively, and numerous anatomic lesions associated with conduction defects have been described.1-3 However, fatty infiltration has only rarely been mentioned as a cause of conduction defect. This paper reports a study of the conduction system in an unusual case of fatty infiltration of the myocardium associated with sinus bradycardia and chronic atria1 fibrillation.
for many years, and at admission her weight was 190 pounds, her height 60 inches. On admission, her temperature was 98.4’ F. and pulse rate 45/min. t The ocular fundi showed grade 1 hypertensive changes. Blood pressure was 240/120 mm. Hg. The lungs were free of rales, but cardiomegaly, hepatomegaly and bilateral varicosities of the legs with pretibial edema were present. The initial chest roentgenogram (Fig. 1A) confirmed cardiomegaly with striking right-sided enlargement. The electrocardiogram (Fig. 2) indicated a sinus bradycardia with episodes of sinus arrest and nodal escape beats. No evidence of ventricular hypertrophy was present.
CASE REPORT A 49 year old housewife
was first admitted to the Henry Ford Hospital in 1958 with complaints of shortness of breath and ankle swelling. Hypertension had been known for five years. She had been obese
t It is noteworthy that the bradycardia use of digitalis in this patient.
FIG. 1. Chest roentpenopzms. A, December 1958, demonstrating marked cardiac enlargement mainly right-sided. B, 5 years later (Dec. 1963), showing no change in the cardiac silhouette.
* From the Departments VOLUME
19,
FEBRUARY
1967
which appears to be
of Pathology and Medicine, Henry Ford Hospital, Detroit, Mich. 261
pwceded the
Kalsaver,
262
Morales
and Whitehouse
Summary
of Cardiac
Catheterization
Oxygen Content Sat. (x-01. “;,) (!F)
Pressures (mm. Hg)
Superior vena Right atrium Right ventricle
Mean
SjU
;; 23
17;;o 50/‘4-12
10.5 10.1 9 9
65 62 61
26
46/18
10.4
64
13 15
22/8 17jl4
cava
Pulmonary artery I eft pul rnonary artery wedge Left hepatic vein wedge Sat.
FIG. 2.
Elec~rocardG~~ramtaken in 1958 (standard
leads) demonstrates sinus and nodal escape brats.
FIG.
3.
bradycardia
Electrocardiogram taken
with
in 1963
sinus
limb arrest
(limb
leads)
Findinqs
= saturation.
The patient was treated with bed rest, digitalis and diuretics. At rest, her blood pressure averaged 160/90 and her weight at discharge from the hospital She was given a leotard for treatwas 169 pounds. ment of the venous stasis. Cardiac catheterization was performed three months later. Table I summarizes the data. There was evidence of moderate elevation of right atrial, right ventricular and pulmonary artery wedge pressures. of undetermined A diagnosis of “myocardiopathy No change in her program was nature” was made. advised. For the next 5 years the patient was normally active and was seen regularly; there was no significant change in physical findings. Bradycardia persisted, Digithe apical rate averaging 40 to 60 per minute. toxin,
0.1 mg. daily, was continued throughout this Arterial blood pressure was usually elevated, period. and antihypertensive treatment with hydralazine and
shows
atria1
fibrillation THE
with
very
AMERICAN
slow
ventricular
JOURNAL
rate.
OF CARDIOLOC
:Y
Fat Infiltration
of Myocardiurn
36.1
chlorothiazide was instituted. In December 1963 readmission was necessary because of chest pain. Atria1 fibrillation with slow ventricular rate was now noted (Fig. 3). A roentgenogram of chest (Fig. 1B) was unchanged when compared to that of 1958. Digitoxin was continued as before. She was discharged symptomatically improved on the eighth hospital day. ~~I?FIP~ iast admission occurred in January 1965 following a cerebral vascular accident. Atria1 fibrillation was still present. She died 36 hours after admission. Her lveight two weeks before death was 175 pounds. Autopsy: The body was 150 cm. long and weighed 172 pounds. The heart weighed 550 gm.? and the epicardial surface revealed a large amount of fat. This fatty tissue was more prominent on the anterior surface of the right ventricle where it measured 2 cm. in thickness (Fig. 4). There was extensive infiltration of this epicardial fat into the underlying myocardium. ‘I‘his \vas more severe on the right side, and, in places, the adipose tissue extended through the entire thickThe right ness of the right ventricular myocardium. ventricular myocardium measured 1 cm. in thickness and the left ventricle measured 2 cm. The myocardium showed no fibrosis or infarction, and there were no mural thrombi in any of the cardiac chambers. The valve rings and the valve cusps were unremarkable? and the openings of the coronary arteries were large and patent. Examination of the coronary arteries and their branches showed moderate to severe atherosclerotic narrowing of the lumen without occlusion. The arteries to the sinoatrial and A-V nodes arose from the right coronary artery, and sections through them did not reveal any narrowing or occlusion. However, the artery to the sinoatrial
FIG. 5. Grossfihotograjh of the right atria1 wall in the region of the sinus nods. Arrow points to the superficial-appearing sinus node artery. SVC = superior vena cava.
VOLUME
19,
FEBRUARY
1967
shows the prominent cardiurn with streaks cardium.
accumulation of fat in the epiof fatty infiltration of thr myo-
264
Balsaver,
Morales
and Whitehouse node, normally embedded within the substance of the node, was situated quite superficially at the sinoatrial junction (Fig. 5). A large amount of adipose tissue \Gas present in this region and about the atriovcntricular node. Serial secticns throqhout the conduction system murculature revealed extensive fatty replacement of the sinus node musculature (Fig. 6) where only occasional nodal fibers could be recognized. ‘The atrioventricular node appeared infiltrated by fat to a lesser degree. Fatty infiltration was also demonstrated in the bundle of His (Fig. 6), while serial sections of the bundle branches showed a focus of fatty tissue only about the right branch. Moderate fatty infiltration was noted in the pancreas and the adrenals. The lungs showed moderate edema, and a recent thromboembolus was noted in one of the smaller arterial branches. Healed infarcts, probably related to previous embolism, were seen in both the kidneys. The brain weighed 1,300 gm. It was edematous and asymmetrical, the left hemisphere showing extensive softening of the frontotemporal parietal regions. The left middle cerebral artery contained an occluding thrombus which appeared to be embolic in nature.
COMMENT
FIG. 6. Photomicrographs of the conduction system. A, sinus node shows prominence of fat and atrophy of the substance of the nodal tissue around the artery. Section was taken through the thickest portion of the sinus node. (Masson’s trichrome; X 35 reduced by 157&) B, sinus node. Higher power view of the same section. Arrows point to isolated nodal fibers. ART (upper left) = wall of the sinus node artery. (Masson’s trichrome ; X 150 reduced by 1570.) C, bundle of His (penetrating po&n), showing fat vacuoles in the substance of the bundle. (Hematoxylin and eosin; X 90 reduced by 1 57r.)
The pertinent histologic finding was the abundant fat within the right ventricular myocardium and in the conduction system. It is readily conceivable that such adipose tissue within the sinus node could, by mechanical interference, produce conduction defects. For several years, this patient gave evidence of interference with normal conduction from the sinus node. This was manifested by bradycardia Later, with sinus arrest and nodal escape. chronic atria1 fibrillation occurred, with slow ventricular response. While systemic hypertension associated with left ventricular hypertrophy was present, the intense degree of fatty infiltration into the myocardium, particularly involving the right ventricle and the conduction system, separates this case from the common findings of the hypertensive heart. The observation of replacement by adipose tissue of the conduction system musculature has been given little attention in the literature. One of the earliest reports was that of Nuzum4 in 1914, who reviewed 27 cases of Adams-Stokes syndrome and found 2 with “lipomatosis.” He also mentions previous reports of fatty change in the bundle of His associated with heart block and sudden death. In 1924 MGnckeber$ reviewed the literature on fatty infiltration of the myocardium and referred to involvement of the conduction sys THE
AMERICAN
JOURNAL
OF
CARDIOLOGY
Fat
Infiltration
te111. In their review of 58 cases of myocardial fat infiltrat’on, Saphir and Corriganfi found 2 casts in \t:hich this change was the only obvious callse of death. The series also included 1 case of an ilrtra\-c‘lltriclllar bundle branch block xvhich showed fat infiltration of the bllndle of His with atrophy of the fibers. Spain and Cathcart’ reported a case of right-sided heart failllre M.ith heart block in which fatty infiltration of the right ventricular rnyocardium and the inter\.entricular septum was noted. M’e collld find only one report of a detailed study of the conduction system in fatty infiltration of the nlyccardilml. Bronzini and Novi* studied the atrioventricular conduction system in 11 fatty hearts and 15 nonfatty hearts. Infiltration of the fatty tissue into the A-V bundle and the atrio\xxtricular node was noted only in the fatty hearts. The nonfatty hearts showed fatty tissue around the bundles without infiltration into, or replacement of, muscle fibers. Their report, howe\:er, does not make any reference to conduction defects in the hearts with fatty infiltration of the conduction system. In a study of 64 adult hearts, Hudson2 reported a number of lesions in the cardiac pacemaker, one of the cases being described as showing ‘
\‘OLUME 19. FEBRUARY 1967
of Myocardium
265
this problem and may prove frrlitful.
its association
\vith obesit)
SUMMARY
Fatty- infiltration has only rarclv bcsen reported as a callse of a cardiac conduc;iorr defect. A case of chronic sinoatrial block and atria1 fibrillation \\ith severe fatty infiltration of the myocardium and the conduction system is reported. The literature on conduction defects due to fatty infiltration is reviewed. REFERENCES 1. IJJMB, G. and SI~ACKLETT, K. S. Human cardiac conduction tissue lesions. Am. ./. Path., 36: 411, 1960. 2. IJUOSON, R. E. R. The human pacrlnaker and its pathology. &it. Hmrt J., 22: 153, 1960. The normal anatomy of the conduction 3. LEV, M. system in man and its pathology in atrioventricular block. Ann. il;pw J’crh Acad. SC.. 111: 817, 1964. 4. NUZUM, F. Fatty infiltration (lipomatosis) of the auriculoventricular bundle of His, with sudden unexpected death. A M.A. Arch. Znt. Mpd., 13: 640, 1914. Herz und Gefaesse. 5. MZ~NCKEBERC, .J. G. In: Handbuch der Speziellen Pathologischen Anatomic und Histologie, Vol. 2, p. 345. Edited by HENKE, F. und LUBARSCH, 0. Berlin, 1924. Julius Springer. 6. SAPHIR, 0. and CORRIGAN, M. Fatty infiltration of the myocardium. A.M.il. Arch. Int. .\f~d., 52: 410, 1933. 7. SPAIN, D. M. and CATHCART, R. T. Heart block caused by fat infiltration of the intcrventricular septum (“car adiFosum”). Am. Hmr-t J., 32: 659, 1946. 8. BRONZINI,E. and NOVI, A. M. II systema di conduzione atrioventricolare nell. “Adipositas cordis.” Pathologica, 53: 231, 1961. 9. Lev, M. Anatomic basis for atrioventricular block. z4m. J. Med., 37: 742, 1964. 10. LEV, M. The pathology of complete atrioventricular block. Prq. Cardiovas. Dis., 6: 317, 1964. 11. LEV, M. Aging changes in the human sinoatrial node. J. Cerontol.,9: 1, 1954. 12. ERICKSON, E. E. and LEV, M. .4ging changes in the human atrioventricular node, bundle and bundle branches. J. Gem&l., 7: 1, 1952.