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Heart failure and hyperthyroidism
t I E A R T F A I L U R E AND H Y P E R T H Y R O I D I S 3 I ~:~ W I T H SPECIAL REFERENCE TO ETIOLOGY L . M . HI21~X'rltAL, M . D .
BOST0?¢, ~IAss. F 1 V E h u n d r e d cases of h y p e r t h y r o i d i s m persona lv examined (luring the past fifteen months at the L a h e y Clinic have"been reviewed.for the purpose of answering tile following questions which pertain to the etiology of heart failure in thyrotoxicosis. F i r s t - - D o e s thyrotoxicosis injure the healthy normal heart muscle or is a previously damaged heart necessary for the p r o d u c t i o n of congestive heart failure in h y p e r t h y r o i d i s m ? S e c o n d - - D o e s thyrotoxicosis haYe a specific stimulating effect on the heart aside from the over-activity of increased work'? T h i r d - - D o e s h y p e r t h y r o i d i s m cause h y p e r t r o p h y and dilatation of the normal heart from increased work. or from a specific stimulating effect, or both~? In consideration of the first question, if it can be demonstrated that myocardial i n j u r y results from thyrotoxieosis, it can be safely assmned that congestive heart failure will eventually result front prolonged intoxication. Wilson ~ has examined the hearts of 21 patients with hyperthyroidism, ]8 of which showed m a r k e d lipoid changes. These patients fall in the age group where degeneratiYe changes are frequently seen, so that, unless some specific pathological change due to thyroid toxicity is demonstrated, we must rely more on clinical observation to arrive at the probable answer to this question. Itami[tmff has stated that, in his opinion, thyroid toxicity has a selective action on certain individual hearts. Since he floes not specify what is characteristic of these individual hearts, this conclusion cannot be accepted until more definite clinical data have been presented. As to previous cardiac i n j u r y precipitating heart failure, we would expect in a comm u n i t y where rheumatic t~eart disease is prevalent many eases of failure in h y p e r t h y r o i d i s m assoeiated with mitral stenosis. F u r t h e r more, as the age advanees in which we find congestive heart f a i h r e , we should expeet t.o find a considerable number with associated arteriosclerotic and hypertensive changes. Coneerning the second question, that of a specific stimulating effect of thyrotoxieosis on the heart aside from the increased work present, clinical observation supports this supposition. In m a n y patients who have lost most signs of toxieity, and whose pulse and basal metabolie rates have r e t u r n e d to normal as the result of iodine administration *From the Zahe¥ Clinic, Boston, 154rass. Read before the American Heart Assoeiation at Minneapolis, June 12, 1928. 103
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and rest, the characteristic thyroid thrust of the heart is often present far out of proportion to the then present demands of the eircu!ation. The t h y r o i d gland has undergone involution, tile bruit disappears, the low diastolic pressure returns to normal limits, and still the thrust remains. As Willius and B o o t h b y have pointed out I in other conditions where the basal metabolic rate is increased as in leucemia, or in moderate exercise, such as walking, the heart impulse is barely if at all palpable. This specific stimulation of the heart is, we believe, an imp o r t a n t secondary f a c t o r in the p r o d u c t i o n of cardiac failure. I n r e g a r d to the third question, Boas ~ believes that cardiac hypert r o p h y in h y p e r t h y r o i d i s m is the result of increased o x y g e n demands and the increased flow t h r o u g h the t h y r o i d gland. The latter he compares to an arterio-venous a n e u r y s m or shunt. Igead ~ believes that increased metabolic rate adds to the w o r k of the h e a r t and, if long contfimed, will result in m y o c a r d i a l failure. I t is our impression, based on repeated t e l e r o e n t g e n o g r a m s - - a n d others, I believe, are of the same opinion ~, 5 - - t h a t cardiac h y p e r t r o p h y is rare in h y p e r t h y roidism, except in a certain group of eases and in these it can usually be explained by coexistent cardiovascular disease. Our experience has been that the heart is too often considered enlarged because of the characteristic t h r u s t and the movement of the thoracic cage. As a rule, the t h y r o i d heart f o u n d in the patient dying" of h y p e r t h y r o i d i s m is flabby, ~, 6 and this impression is also gained by fluoroscopy. Such a condition would be consistent with some dilatation and we feel that the functional systolic m u r m u r s so f r e q u e n t in h y p e r t h y r o i d hearts cannot adequately be explained on any other basis. Such dilatation and flabbiness are not characteristic of work hypertrophy, but is more consistent with the general nmseular weakness which is so characteristic of t h y r o i d over-activity. CL~WaL DATA Of the 500 eases of hyperthyroidism, 479 were of the exophthaimic type and 21 were of the toxic adenomatous type. The usual criteria were used in establishing the clinical diagnosis of hyperthyroidism and all eases studied showed confirmatory pathological changes in the gland removed at operation. The criteria for diagnosis of cardiac changes were as follows: 1. Nheumatie heart disease with mitral stenosis was diagnosed only when a well-deflned mitral diastolie murmur was e%-ident. 2. Questionable rheumatic heart disease was diagnosed when there was a harsh apieai systolic murmur, often a rhemnatie history and usua]ly some degree of enlargement. 3. ttyperte~sion was diagnosed in the presence of a blood pressure of 190/90 ram. or more, or with a dhastoiie pressure of 100 ram. or more, regardless of the systolic pressure.
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4. Arteriosclerosis was considered p r e s e n t when there was w e l l - m a r k e d hypertrophy, t o r t u o s i t y , a n d h a r d e n i n g of t h e p e r i p h e r a l vessels. 5. L u e t i e a o r t i t i s was d i a g n o s e d when a n aortic r e g u r g i t a n t m u r n m r was p r e s e n t along with a positive W a s s e r m a n n . ( T h e two eases included both h a d dilated aortic arches.) 6. E s t a b l i s h e d a u r i c u l a r fibrillation was d i a g n o s e d when this i r r e g u l a r i t y m a i n e d p r e s e n t f r o m the time of a d m i s s i o n to the hospital u n t i l operation.
re-
7. P a r o x y s m a l a u r i c u l a r fibrillation occurred in m o s t cases postoperatively, a n d was d i a g n o s e d only when p e r s o n a l l y observed. 8. T r a n s i e n t congestive h e a r t failure. All p a t i e n t s h a v i n g a clear-cut h i s t o r y of p a s t f a i l u r e relieved by rest a n d iodine before coating u n d e r our observation were placed in this group. 9. P a r o x y s m a l t a e h y c a r d i a a n d a u r i c u l a r flutter were identified by the electrocardiogram. 10. True congestive h e a r t failure. All of these p a t i e n t s h a d p i t t i n g e d e m a o ' t h e legs, t h e neck veins were always d i s t e n d e d in t h e u p r i g h t positiou a n d t h e liver edge was down. O r t h o p n e a of v a r y i n g degrees was present. The degree of f a i l u r e varied, of course, some clearing with rest a n d iodine, while others required the use of d i g i t a l i s a n d diuretics.
TABLE I CLASSIFICATION O]~ I~EAETS IN 500 CASES OP I-[YPERTHYROIDIS~[
TYPE
I. No c h a n g e I I . P a r o x y s m a l auric. £ b r i l l a t i o n With heart changes III. Probable rheumatic heart W i t h f a i l u r e a n d aurie, fibrillation IV. ]~heumatie h e a r t W i t h f a i l u r e a n d aurle, fibrillation V. E s t a b l i s h e d a u r i c u l a r fibrillation (3 h y p e r t e n s i v e ) (all t y p e s )
NUMBE,R
AVEI~AG E
DURATION OF
OF
AGE IN
HYPEI~THYR,OIDI SM I N 5{,ONTHS
CASES
YEARS
339 20 20 14 2 21 2 36 56
35 49
17 mo. 12 mo.
27 42 35 50 49 53
13 too. (7 mo.-8 yr.) 11 mo. 11 too. 14 too. 16 mo.
42 57 54
7 mo. 8 too. 18 too.
60
10 too.
50 62 54
11 me. (7 too.-8 yr.) 28 too.
51
38 mo.*
VI. Transient congestive failure
VII. VIII. IX. X. XI. XII.
N o r m a l r h y t h m (4 h y p e r t . ) W i t h est. aur. fib. (1 h y p e r t . ) Hypertensive heart W i t h luetic aortitis Cardiac h y p e r t r o p h y ? of c a u s e - - n o f a i l u r e A n g i n a pectoris (1 h y p e r t . ) Paroxysmal tachycardia A u r i c u l a r flutter Congestive h e a r t f a i l u r e (a) R h e u m a t i c (b) .~ R h e u m a t i c (e) Arteriosclerotic a n d h y p e r t e n s i v e ( d ) L a c t i c (included in above) (e) ? Cause
13 3 24 1 4 2 2 2 26 2 2 13 1 9
Total C. H . F .
26
49
*Th~ duration in this group showed a m e a n of a b o u t 18 m o n t h s ; two patients dated their onset 8 and 12 y e a r s but in each case it w a s questionable.
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JOURNAL
DISCUSSION
There are certain v e r y obvious facts to be noted f r o m this tabulation. In the first place, the duration of the h y p e r t h y r o i d i s m does not seem t.o play a consistent p a r t in the p r o d u c t i o n of auricular fibrillation, or of eongestive h e a r t failure. The basal metabolic rate varied considerably and showed no relation to the degree of e,ongestive h e a r t failure. No a t t e m p t was made to correlate the basal metabolic rates because of the f r e q u e n t iodinization before coming u n d e r our observation. Of i m p o r t a n c e we feel is the f r e e d o m fr.om Congestive h e a r t failure in the group with m i t r a l stenosis. On the assmnption that previous m y o c a r d i a l d a m a g e is necessary to p r e c i p i t a t e failm'e in h y p e r t h y roidism, this finding is r a t h e r surprising. On the other hand, the a v e r a g e age of this group is the same as those eases which we considered as h a v i n g no h e a r t changes. This brings up the i m p o r t a n t point of age, which we will a g a i n emphasize as being a p a r a m o u n t f a c t o r in the p r o d u c t i o n of congestive failure in h y p e r t h y r o i d i s m . The low a v e r a g e age of the questionable r h e u m a t i c h e a r t group serves to confirm the clinical diagnosis which was made in these eases. H e r e again those showing failure were f a r above the a v e r a g e age of all the r h e u m a t i c eases. I t is interestino' to note in r e g a r d to age t h a t we find more h e a r t distm'banees ( p a r t i c u l a r l y established or p a r o x y s m a l fibrillation) as we a p p r o a c h fifty years. The a v e r a g e age of the established a u r i c u l a r fibrillation g r o u p was forty-nine, while in those showing congestive h e a r t failure with this i r r e g u l a r i t y it was above fifty years. Onethird of the total of 36 eases with h y p e r t e n s i o n showed f r a n k congestive h e a r t failure. H e r e again we note the f a c t o r of age, for the average of this group is fifty-four years. Those patients showing wellm a r k e d arteriosclerosis h a d an a v e r a g e age of fifty-six y e a r s ; of these patients four were males. I f arteriosclerosis were more common in females, we feel t h a t we would see a g r e a t e r n u m b e r of eases showing ~ongestive h e a r t failure. Ill the 26 eases of congestive h e a r t failure 17 showed definite h y p e r t e n s i v e or arteriosclerotic changes. The ~:emaining 9 eases in the eong'estive failure group, in so far as could be determined, showed lie evidence or gave no history of coincident cardiovascular disease. These patients showed m a n y f e a t u r e s in common. Cardiac e n l a r g e m e n t was p r e s e n t in most instances and by x - r a y the e n l a r g e m e n t was often shown to be both to left and right. E l e c t r o c a r d i o g r a m s showed no p r e p o n d e r a n c e of either ventricle; low voltage was seen in half the eases and auricular fibrillation was present in the m a j o r i t y . Congestive failure was not of the extreme type, having been i m p r o v e d in all eases by rest, iodine, and (occasionally) digitalis. Sufficient time to f o r m a final opinion as to the end-results in all the congestive failure cases hl this group has not elapsed, but previ-
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ous experience gives us the impression t h a t the prognosis in each ease depends on the amount of coexisting' eardiovascular disease present. Three of the failure group herein r e p o r t e d are dead. One died o f pneumonia before operation, another died of congestive heart failure five months after operation, having had hypertensive and rheumatic heart disease, and a third died suddenly after four months of eomparat i r e freedom from cardiac disability. CONCLUSIONS
F r o m the data presented what conclusions call we draw in r e g a r d to the etiology of congestive heart failure in h y p e r t h y r o i d i s m ? First, if thyrotoxieosis injures the normal healthy heart we believe there should be more evidence of i n j u r y below the age of forty. The average age of the congestive heart failure group being above fifty years, with a large percentage showing coexisting cardiovascular disease, leads us to conclude, on a clinical basis at least, t h a t if there is a selective action of h y p e r t h y r o i d i s m it chooses the heart in patients who are over f o r t y years old. If auricular fibrillation is to be considered evidence of myocardial damage from thyrotoxieosis, it certainly should be present more often in the y o u n g e r patient and particularly should it have a more definite relationship to duration aml degree of toxicity. The nine eases showing ~o clinical evidence of coexisting cardiovascular disease, present an i m p o r t a n t group in r e g a r d to the question of myocardial i n j u r y as the result of thyrotoxieosis. Because of the small n u m b e r of patients and their advanced age we feel we cannot attribute their heart failure to thyrotoxieosis directly, but believe that these patients have some unrecognized myocardial weakness either from previous u n k n o w n i n j u r y or because they belong to that group of individuals who inherit a predisposition to cardiovascular degeneration. The drive of hyperthyroidism serves to bring out this inherited weakness, and although the average duration of the disease is somewhat longer in this grollp, this seems a natural explanation in view of the lack of gross clinical evidence of' more advanced cardiovascular disease. Second, we believe that thyrotoxieosis has a specific excitatory effect on the heart and that this, more than the inereased work fronl circulatory demands, produces failure in a heart weakened by the degenerative processes of age. Third, our elinieal observation leads us to believe that h y p e r t r o p h y of the h e a r t does not take place in a normal healthy h e a r t as the result of hyperthyroidism, but that dilatation is probably frequent. Duration, we feel, plays a v e r y little part in a general way. 1% is obvious, however, f r o m f r e q u e n t examinations of thyroid patients t h a t duration as well as degree of toxicity plays an i m p o r t a n t r61e in individual
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cases. Immediate removM of thyroid toxicity by surgical procedure is undoubtedly the quickest and surest method of averting the onset of congestive heart failure. Therefore, in conclusion, we consider the most significant causes of congestive heart failure in hyperthyroidism: (1) age and the eoexistil~g cardiovascular changes associated with it; (2) the specific heart drive incited by thyrotoxicosis; (3) auricular fibrillation; (4) duration and intensity of thyroid overaetivity. REFERENCES 1Willius, F. l-I., Boothby, W. -~L, and Wilsm b L. B.: The tteart in Exophthahnie Goiter and Adenoma With Hyperthyroidisn b Meal. Ciin. No. Am., 1923, vii, 189. eHamiiton, B . E . : Heat Failure of the Congestive Type Caused by Hyperthyroidism, Jour. Am. 5'Ied. Assn', 1924, lxxxii% 405. uBoas~ E. P.: Cardise Disorders Accompanying Exophthalmie Goiter, Jour. Am. Ned. Assn., 1923, lxxx, 1638. ~Read, J. Marion: Treatment of Cardiac Disturbances Due to Thyroid Disease, Jour. Am. Med. Assn., 1927, lxxxix, 493. aFoster~ N . B . : Goiter HHHeart, Am. Jour. Med. Se., 1925, elxix: 662. 6Smith, L . W . : Personal communication. (For discussion, see page 116.)
BOST0?¢, ~IAss. F 1 V E h u n d r e d cases of h y p e r t h y r o i d i s m persona lv examined (luring the past fifteen months at the L a h e y Clinic have"been reviewed.for the purpose of answering tile following questions which pertain to the etiology of heart failure in thyrotoxicosis. F i r s t - - D o e s thyrotoxicosis injure the healthy normal heart muscle or is a previously damaged heart necessary for the p r o d u c t i o n of congestive heart failure in h y p e r t h y r o i d i s m ? S e c o n d - - D o e s thyrotoxicosis haYe a specific stimulating effect on the heart aside from the over-activity of increased work'? T h i r d - - D o e s h y p e r t h y r o i d i s m cause h y p e r t r o p h y and dilatation of the normal heart from increased work. or from a specific stimulating effect, or both~? In consideration of the first question, if it can be demonstrated that myocardial i n j u r y results from thyrotoxieosis, it can be safely assmned that congestive heart failure will eventually result front prolonged intoxication. Wilson ~ has examined the hearts of 21 patients with hyperthyroidism, ]8 of which showed m a r k e d lipoid changes. These patients fall in the age group where degeneratiYe changes are frequently seen, so that, unless some specific pathological change due to thyroid toxicity is demonstrated, we must rely more on clinical observation to arrive at the probable answer to this question. Itami[tmff has stated that, in his opinion, thyroid toxicity has a selective action on certain individual hearts. Since he floes not specify what is characteristic of these individual hearts, this conclusion cannot be accepted until more definite clinical data have been presented. As to previous cardiac i n j u r y precipitating heart failure, we would expect in a comm u n i t y where rheumatic t~eart disease is prevalent many eases of failure in h y p e r t h y r o i d i s m assoeiated with mitral stenosis. F u r t h e r more, as the age advanees in which we find congestive heart f a i h r e , we should expeet t.o find a considerable number with associated arteriosclerotic and hypertensive changes. Coneerning the second question, that of a specific stimulating effect of thyrotoxieosis on the heart aside from the increased work present, clinical observation supports this supposition. In m a n y patients who have lost most signs of toxieity, and whose pulse and basal metabolie rates have r e t u r n e d to normal as the result of iodine administration *From the Zahe¥ Clinic, Boston, 154rass. Read before the American Heart Assoeiation at Minneapolis, June 12, 1928. 103
104
THE
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and rest, the characteristic thyroid thrust of the heart is often present far out of proportion to the then present demands of the eircu!ation. The t h y r o i d gland has undergone involution, tile bruit disappears, the low diastolic pressure returns to normal limits, and still the thrust remains. As Willius and B o o t h b y have pointed out I in other conditions where the basal metabolic rate is increased as in leucemia, or in moderate exercise, such as walking, the heart impulse is barely if at all palpable. This specific stimulation of the heart is, we believe, an imp o r t a n t secondary f a c t o r in the p r o d u c t i o n of cardiac failure. I n r e g a r d to the third question, Boas ~ believes that cardiac hypert r o p h y in h y p e r t h y r o i d i s m is the result of increased o x y g e n demands and the increased flow t h r o u g h the t h y r o i d gland. The latter he compares to an arterio-venous a n e u r y s m or shunt. Igead ~ believes that increased metabolic rate adds to the w o r k of the h e a r t and, if long contfimed, will result in m y o c a r d i a l failure. I t is our impression, based on repeated t e l e r o e n t g e n o g r a m s - - a n d others, I believe, are of the same opinion ~, 5 - - t h a t cardiac h y p e r t r o p h y is rare in h y p e r t h y roidism, except in a certain group of eases and in these it can usually be explained by coexistent cardiovascular disease. Our experience has been that the heart is too often considered enlarged because of the characteristic t h r u s t and the movement of the thoracic cage. As a rule, the t h y r o i d heart f o u n d in the patient dying" of h y p e r t h y r o i d i s m is flabby, ~, 6 and this impression is also gained by fluoroscopy. Such a condition would be consistent with some dilatation and we feel that the functional systolic m u r m u r s so f r e q u e n t in h y p e r t h y r o i d hearts cannot adequately be explained on any other basis. Such dilatation and flabbiness are not characteristic of work hypertrophy, but is more consistent with the general nmseular weakness which is so characteristic of t h y r o i d over-activity. CL~WaL DATA Of the 500 eases of hyperthyroidism, 479 were of the exophthaimic type and 21 were of the toxic adenomatous type. The usual criteria were used in establishing the clinical diagnosis of hyperthyroidism and all eases studied showed confirmatory pathological changes in the gland removed at operation. The criteria for diagnosis of cardiac changes were as follows: 1. Nheumatie heart disease with mitral stenosis was diagnosed only when a well-deflned mitral diastolie murmur was e%-ident. 2. Questionable rheumatic heart disease was diagnosed when there was a harsh apieai systolic murmur, often a rhemnatie history and usua]ly some degree of enlargement. 3. ttyperte~sion was diagnosed in the presence of a blood pressure of 190/90 ram. or more, or with a dhastoiie pressure of 100 ram. or more, regardless of the systolic pressure.
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HEART FAILURE AND HYPERTi(4YROIDISM
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4. Arteriosclerosis was considered p r e s e n t when there was w e l l - m a r k e d hypertrophy, t o r t u o s i t y , a n d h a r d e n i n g of t h e p e r i p h e r a l vessels. 5. L u e t i e a o r t i t i s was d i a g n o s e d when a n aortic r e g u r g i t a n t m u r n m r was p r e s e n t along with a positive W a s s e r m a n n . ( T h e two eases included both h a d dilated aortic arches.) 6. E s t a b l i s h e d a u r i c u l a r fibrillation was d i a g n o s e d when this i r r e g u l a r i t y m a i n e d p r e s e n t f r o m the time of a d m i s s i o n to the hospital u n t i l operation.
re-
7. P a r o x y s m a l a u r i c u l a r fibrillation occurred in m o s t cases postoperatively, a n d was d i a g n o s e d only when p e r s o n a l l y observed. 8. T r a n s i e n t congestive h e a r t failure. All p a t i e n t s h a v i n g a clear-cut h i s t o r y of p a s t f a i l u r e relieved by rest a n d iodine before coating u n d e r our observation were placed in this group. 9. P a r o x y s m a l t a e h y c a r d i a a n d a u r i c u l a r flutter were identified by the electrocardiogram. 10. True congestive h e a r t failure. All of these p a t i e n t s h a d p i t t i n g e d e m a o ' t h e legs, t h e neck veins were always d i s t e n d e d in t h e u p r i g h t positiou a n d t h e liver edge was down. O r t h o p n e a of v a r y i n g degrees was present. The degree of f a i l u r e varied, of course, some clearing with rest a n d iodine, while others required the use of d i g i t a l i s a n d diuretics.
TABLE I CLASSIFICATION O]~ I~EAETS IN 500 CASES OP I-[YPERTHYROIDIS~[
TYPE
I. No c h a n g e I I . P a r o x y s m a l auric. £ b r i l l a t i o n With heart changes III. Probable rheumatic heart W i t h f a i l u r e a n d aurie, fibrillation IV. ]~heumatie h e a r t W i t h f a i l u r e a n d aurle, fibrillation V. E s t a b l i s h e d a u r i c u l a r fibrillation (3 h y p e r t e n s i v e ) (all t y p e s )
NUMBE,R
AVEI~AG E
DURATION OF
OF
AGE IN
HYPEI~THYR,OIDI SM I N 5{,ONTHS
CASES
YEARS
339 20 20 14 2 21 2 36 56
35 49
17 mo. 12 mo.
27 42 35 50 49 53
13 too. (7 mo.-8 yr.) 11 mo. 11 too. 14 too. 16 mo.
42 57 54
7 mo. 8 too. 18 too.
60
10 too.
50 62 54
11 me. (7 too.-8 yr.) 28 too.
51
38 mo.*
VI. Transient congestive failure
VII. VIII. IX. X. XI. XII.
N o r m a l r h y t h m (4 h y p e r t . ) W i t h est. aur. fib. (1 h y p e r t . ) Hypertensive heart W i t h luetic aortitis Cardiac h y p e r t r o p h y ? of c a u s e - - n o f a i l u r e A n g i n a pectoris (1 h y p e r t . ) Paroxysmal tachycardia A u r i c u l a r flutter Congestive h e a r t f a i l u r e (a) R h e u m a t i c (b) .~ R h e u m a t i c (e) Arteriosclerotic a n d h y p e r t e n s i v e ( d ) L a c t i c (included in above) (e) ? Cause
13 3 24 1 4 2 2 2 26 2 2 13 1 9
Total C. H . F .
26
49
*Th~ duration in this group showed a m e a n of a b o u t 18 m o n t h s ; two patients dated their onset 8 and 12 y e a r s but in each case it w a s questionable.
106
TtIE
AMERICAN
HEART
JOURNAL
DISCUSSION
There are certain v e r y obvious facts to be noted f r o m this tabulation. In the first place, the duration of the h y p e r t h y r o i d i s m does not seem t.o play a consistent p a r t in the p r o d u c t i o n of auricular fibrillation, or of eongestive h e a r t failure. The basal metabolic rate varied considerably and showed no relation to the degree of e,ongestive h e a r t failure. No a t t e m p t was made to correlate the basal metabolic rates because of the f r e q u e n t iodinization before coming u n d e r our observation. Of i m p o r t a n c e we feel is the f r e e d o m fr.om Congestive h e a r t failure in the group with m i t r a l stenosis. On the assmnption that previous m y o c a r d i a l d a m a g e is necessary to p r e c i p i t a t e failm'e in h y p e r t h y roidism, this finding is r a t h e r surprising. On the other hand, the a v e r a g e age of this group is the same as those eases which we considered as h a v i n g no h e a r t changes. This brings up the i m p o r t a n t point of age, which we will a g a i n emphasize as being a p a r a m o u n t f a c t o r in the p r o d u c t i o n of congestive failure in h y p e r t h y r o i d i s m . The low a v e r a g e age of the questionable r h e u m a t i c h e a r t group serves to confirm the clinical diagnosis which was made in these eases. H e r e again those showing failure were f a r above the a v e r a g e age of all the r h e u m a t i c eases. I t is interestino' to note in r e g a r d to age t h a t we find more h e a r t distm'banees ( p a r t i c u l a r l y established or p a r o x y s m a l fibrillation) as we a p p r o a c h fifty years. The a v e r a g e age of the established a u r i c u l a r fibrillation g r o u p was forty-nine, while in those showing congestive h e a r t failure with this i r r e g u l a r i t y it was above fifty years. Onethird of the total of 36 eases with h y p e r t e n s i o n showed f r a n k congestive h e a r t failure. H e r e again we note the f a c t o r of age, for the average of this group is fifty-four years. Those patients showing wellm a r k e d arteriosclerosis h a d an a v e r a g e age of fifty-six y e a r s ; of these patients four were males. I f arteriosclerosis were more common in females, we feel t h a t we would see a g r e a t e r n u m b e r of eases showing ~ongestive h e a r t failure. Ill the 26 eases of congestive h e a r t failure 17 showed definite h y p e r t e n s i v e or arteriosclerotic changes. The ~:emaining 9 eases in the eong'estive failure group, in so far as could be determined, showed lie evidence or gave no history of coincident cardiovascular disease. These patients showed m a n y f e a t u r e s in common. Cardiac e n l a r g e m e n t was p r e s e n t in most instances and by x - r a y the e n l a r g e m e n t was often shown to be both to left and right. E l e c t r o c a r d i o g r a m s showed no p r e p o n d e r a n c e of either ventricle; low voltage was seen in half the eases and auricular fibrillation was present in the m a j o r i t y . Congestive failure was not of the extreme type, having been i m p r o v e d in all eases by rest, iodine, and (occasionally) digitalis. Sufficient time to f o r m a final opinion as to the end-results in all the congestive failure cases hl this group has not elapsed, but previ-
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ous experience gives us the impression t h a t the prognosis in each ease depends on the amount of coexisting' eardiovascular disease present. Three of the failure group herein r e p o r t e d are dead. One died o f pneumonia before operation, another died of congestive heart failure five months after operation, having had hypertensive and rheumatic heart disease, and a third died suddenly after four months of eomparat i r e freedom from cardiac disability. CONCLUSIONS
F r o m the data presented what conclusions call we draw in r e g a r d to the etiology of congestive heart failure in h y p e r t h y r o i d i s m ? First, if thyrotoxieosis injures the normal healthy heart we believe there should be more evidence of i n j u r y below the age of forty. The average age of the congestive heart failure group being above fifty years, with a large percentage showing coexisting cardiovascular disease, leads us to conclude, on a clinical basis at least, t h a t if there is a selective action of h y p e r t h y r o i d i s m it chooses the heart in patients who are over f o r t y years old. If auricular fibrillation is to be considered evidence of myocardial damage from thyrotoxieosis, it certainly should be present more often in the y o u n g e r patient and particularly should it have a more definite relationship to duration aml degree of toxicity. The nine eases showing ~o clinical evidence of coexisting cardiovascular disease, present an i m p o r t a n t group in r e g a r d to the question of myocardial i n j u r y as the result of thyrotoxieosis. Because of the small n u m b e r of patients and their advanced age we feel we cannot attribute their heart failure to thyrotoxieosis directly, but believe that these patients have some unrecognized myocardial weakness either from previous u n k n o w n i n j u r y or because they belong to that group of individuals who inherit a predisposition to cardiovascular degeneration. The drive of hyperthyroidism serves to bring out this inherited weakness, and although the average duration of the disease is somewhat longer in this grollp, this seems a natural explanation in view of the lack of gross clinical evidence of' more advanced cardiovascular disease. Second, we believe that thyrotoxieosis has a specific excitatory effect on the heart and that this, more than the inereased work fronl circulatory demands, produces failure in a heart weakened by the degenerative processes of age. Third, our elinieal observation leads us to believe that h y p e r t r o p h y of the h e a r t does not take place in a normal healthy h e a r t as the result of hyperthyroidism, but that dilatation is probably frequent. Duration, we feel, plays a v e r y little part in a general way. 1% is obvious, however, f r o m f r e q u e n t examinations of thyroid patients t h a t duration as well as degree of toxicity plays an i m p o r t a n t r61e in individual
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cases. Immediate removM of thyroid toxicity by surgical procedure is undoubtedly the quickest and surest method of averting the onset of congestive heart failure. Therefore, in conclusion, we consider the most significant causes of congestive heart failure in hyperthyroidism: (1) age and the eoexistil~g cardiovascular changes associated with it; (2) the specific heart drive incited by thyrotoxicosis; (3) auricular fibrillation; (4) duration and intensity of thyroid overaetivity. REFERENCES 1Willius, F. l-I., Boothby, W. -~L, and Wilsm b L. B.: The tteart in Exophthahnie Goiter and Adenoma With Hyperthyroidisn b Meal. Ciin. No. Am., 1923, vii, 189. eHamiiton, B . E . : Heat Failure of the Congestive Type Caused by Hyperthyroidism, Jour. Am. 5'Ied. Assn', 1924, lxxxii% 405. uBoas~ E. P.: Cardise Disorders Accompanying Exophthalmie Goiter, Jour. Am. Ned. Assn., 1923, lxxx, 1638. ~Read, J. Marion: Treatment of Cardiac Disturbances Due to Thyroid Disease, Jour. Am. Med. Assn., 1927, lxxxix, 493. aFoster~ N . B . : Goiter HHHeart, Am. Jour. Med. Se., 1925, elxix: 662. 6Smith, L . W . : Personal communication. (For discussion, see page 116.)