Cardiac irregularities associated with diseases of the thyroid gland

CARDIAC IRREGULARITIES ASSOCIATED WITH DISEASES OF THE THYROID GLAlND* SHELBY W.

WISHART,

EVANSVILLE,

T

HIS discussion wGl1 be confined to those irregularities or disturbances in the mechanism of the heart beat so frequentIv found associated with thyrotoxicosis. The irregularities found in that group of young adults living in the region of the &eat Lakes who show simpIe ~olloicl enkgement of the thyroid gIand arc probably due to some other cause and ho‘11t’ no connection lvith the gIanduIar enlargement. A number of excellent papers have recently been published on the changes in the heart associated with hypothyroidism an d myxedema. H!:pertensron, nephritis a n d :lrterioscIerosis are so frequently associated with this disease, that it would be diflicult or impossibIe to determine lvhich factor was directIN responsibIe for an?- disturbances in the mechanism of the heart beat which might be present. Patients with toxic goiter, whether of the csophthalmic type or those showing adenomntous degenerative changes with h>-perth?;roidism,. usuaI1~ have a definite increase in the resting heart rate. This hinus tachycardia practically eliminates from our discussion t\vo of the most frequently encountered cardiac, irregularitic5 : sinus arrh>-thmia and premature contractions. Sinus arrhythmia is almost :~I~va~-s found when the heart is beating slo\vl\. and tends to disappear as the heart rate increases. Premature contractions, or the so-called extras;\-stolic type of nrrh!-thmias, usuaI1~ disappear promptly with :III increase in the heart rate. Premature c.ontrac.tions are unusual with :I ventricular rate :lbo\,e 120. \C’e I-~ax~c seen but one case of p;~rox~smaI aur_icuIar tachycnrdia associated w+th toxic Igoiter. This occurred in n voung woman aged twenty-two \vho gave a history of

M.D.

INDIANA

having had similar attacks since early childhood. They had their onset follobving a se\-ere attack of scarIet fever when she was eleven years old. She had numerous attacks while being prepared for operation and t.he>- continued to occur postoperatively, but at less frequent intervals, and the attacks w-ere of shorter duration. While the condition may have been aggravated by the presence of the thyrotoxicosis we were of the opinion that the two were not directIy related. UndoubtedIy the most frequently encountered disturbance in the mechanism of the heart beat in th;c-rotoxicosis is auricular fibrillation. It was present at some time in the course of the disease in 23 per cent of our cases. Auricular flutter was much less frequent but since both are due to a circus rhythm and since the changes in the myocardium which permit their presence are probabIy identical, we h ave grouped them together and they byill be discussed as possessing similar si\yere evident. III. Those shokving permanently estaljlished fibriIIation or flutter and in tvhich toxic symptoms were easily distinguishnblc. 1~. Those in kvhich fibriIIntion or flutter did not appear until after operation and then as a part of the so-caIled thyroid shock or crisis with a \.er>’ rapid \;entric.-

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uIar rate and other signs of profound intoxication. This discussion will be restricted to those cases which faII into group I. To date we have studied 6 patients who showed auricuIar fibriIIation or flutter so earIy in the course of the disease that carefu1 repeated physica and Iaboratory examinations faiIed to show any of the other signs of thyrotoxicosis for weeks or months foIIowing the first paroxysm. The histoq and course of the individua1 cases are so simiIar that we have chosen one case for discussion which is typica of the group. Miss L. K., a twenty-eight-year-OH accountant, was referred to us with a tentative diagnosis of paroxysma auricuIar tachycardia. The patient stated that with the exception of measIes and whooping cough at five years of age she couId not remember of having hacl a day’s illness in her lifetime. Three weeks before she came to us, whiIe exerting herseIf rather violently in a gymnasium, the heart rate suddenly became very rapid, she became markedIy dyspneic, her face and body were covered with a cold perspiration, and sfle felt very weak, exhausted and nauseated. She was assisted to the dressing room and her famiIy physician was caIIed. It was about twenqminutes before he couid reach her and in the interim the attack ceased as suddenly as it began, following which the patient felt perfectIy weI1. Her physician made a diagnosis of “nervous heart” and suggested that she stop her gymnasium work for a time. GoIf was suhstituted for exercise in the gymnasium ant1 for the next three weeks she enjoyed her usua1 good heaIth. At the end of the third week while waIking rapidly up a hi11 she had another attack. She said that her heart rate seemed much faster than during the first seizure, and in addition to her previous symptoms she vomited. She was immediately taken home where she was met by her family physician, who had an opportunity to observe the character of the attack. He made a diagnosis of paroxysma tachycardia and referred the patient to me for further study. PhysicaI examination showed a welldeveloped, weII-nourished young woman with excellent coIor and apparentIy in the best of health. The tonsiIs were moderateIy enIarged and some pus could be expressed from the

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crypts. Roentgen-ray examination of the teeth shelved an apical abscess of the first molar in the right Io\vcr jaw. Examination of the eyes sIlowet no exophthalmos or lid-lag. The lobes of the thyroid were palpable with cIiff~cuIt~-, but swaIIowing revealed some slight enlargement in the region of the isthmus. Lt’ith the arms estended and the fingers wideI>- spread there \vas no tract of fine tremor. She was very caIm during the examination and while the skin over the hod>was soft and moist there was no abnormal perspiration. When questioned about nervousness the patient said that the examination did not clisturb her at a11 and that she had never been nervous in her life. She said that she perspired only on strenuous exertion. Examination of the heart showed little of significance. The rate at the apex was 80 per minute; the rhythm was reguIar, with no evidence of overactivity. The heart was not cnIargec1, the left border being in the fifth intercosta1 space we11 within the mid-clavicuIar line. AuscuItation at the apex reveaIed a very soft, distant, bIowing systoIic murmur but no ciiastolic murmurs were audibIe either at the apex or at the base. The examination of the

lungs was negative. The remainder of her physica examination showed nothing signiticant. The bIood pressure was 120/70. The urine was normaI. A teIeoroentgenogran1 showed the heart to be smal1, norma in shape, with no change in the vessels at the base. The Danzer ratio was 0.43. The lung fieIds were negative. An eIectrocardiographic tracing showed a ventricuIar rate of 80 per minute, there was no sign of fine muscIe tremor in the tracing and no preponderance of either side of the heart. The conduction time was norma!. The bIood Wassermann and Kahn reactions were negative. Examination of the bIood showed nothing abnorma1. A basal metabolic rate was not done at this time. Since the patient reveaIed no abnormaIities except infected tonsiIs and one denta abscess, and not having seen her in an attack, I made a provisional diagnosis of paroxysma auricuIar tachycardia. The patient was told to have her tonsiIs and the abscessed tooth removed at once and if she had any more attacks to come in for an eIectrocardiographic tracing. There was no change in her condition for nine weeks after the remova of the tonsiIs and tooth. One evening after hurriedly going up stairs she was seized with another severe

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paroxysm of tachycardia. She was brought to the hospital at once in an ambulance. An eIectrocardiographic tracing was taken, nhich showed auricuIar fibriIIation with a very rapid ventricular response of I80 per minute. She was very uncomfortabIe and was given morphine suIphate grains >i and IO C.C. of a proprictary digitalis preparation intravenousIy which had an approximate cat unit strength of one cat unit per cubic centimeter. Two hours later the ventricujsr rate had faIIen to I IO per minute. The attack persisted, however, until four o’clock the following afternoon. At this time the patient was again carefuIIy questioned regarding any previous manifestations of rheumatic infection and the heart was re-examined for mitra1 or aortic disease. Our findings did not justify such a diagnosis. For three successive days foIIowing cessation of the attack basa1 metaboiic determinations were made. She cooperated we11 and the tests were considered entirely satisfactory. The rates were plus 12, pIus 11 and pIus 16, an average of plus 14. The patient was again re-examined in the hope of finding some evidencc of thyrotosicosis. Our fincIings were practically icIentica1 with those found on previous examination and whiIe we were very suspicious of this condition, we did not fee1 just,ifiecl in making such a diagnosis. She was discharged with instructions to keep us informed as to subsequent attacks and to keep careful watch for nervousness, tachycardia, sweating, etc. She had four more attacks of fibriIIation during the next seven months. Electrocardiographic tracings were obtained during a11 of these attacks which Iasted from one hour to two cfags. BasaI metabolic rates were taken following each attack and the highest reading obtained was pIus 20 just after the last attack. The patient was aIso re-examined foIIowing each paroxysm. Nothing was found on clinica examination to justify a diagnosis of either rheumatic heart disease or thyrotosicosis. Three weeks after the Iast attack she came to my o&e compIaining of increasing nervousness with a desire to be constantIy on the move. She also complained of moderate tachycardia, profuse sweating, particuIarIy at night, insomnia and some sIight dyspnea on exertion. Her physica examination at this time showed a sinus tachycardia of I IO; the heart was definitely overactive; there was now a distinct fine tremor of the fingers; the bIood pressure

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13jj 90 and the skin \yas coverod with perspiration. The basal metabolic rate w;as plus 40. The eIectrocardiogram now’ showed a sinus tachycardia with fine muscJe tremor quite marked in al1 three leads. As >-et there \vas no change in the e!-es. A diagnosis of Graves’ disease was made anti the patient admittec1 to the hospital. She \vas given the usua1 preoperative treatment incIuding Lugol’s iodine minims 5, three times daiI\-. By the end of the second week her J>asaI metabolic rate had faIIen to pIus 20, and most of the nervousness, sweating and tachycarclia had disappeared. A thyroidcctom\\vas done on the fifteenth day. Her progress following operation was uneventful and she was allowed to go home at the end of the third week. ILiicroscopic examination of the tissue removed showecl the typical epithelial hypertrophy and h)-perpIasra and Iymphoid hyperplasia of Graves’ disease. This patient has been observer1 for over a year foIlowing operation. Her genera1 health has been esceIIent and there has hccn no return of the fibriIIation.

fine

DISCUSSION

Cases of this type raise two questions in my mind. First, shouId auricular fibriIIation or flutter be considered one of the earliest manifestations of thyrotoxicosis in certain cases; second, are the changes in the myocardium in this disease which permit the onset of circus rhythm always indicative of widespread and permanent structura1 changes in the heart muscle. To answer question one in the a&mative without expIanation or reservation wouId undoubtedly Iead to misunderstanding and criticism. We know that to find auricuIar fibriIIation in thyrotoxicosis Iong before there is a detectabIe change in the basa1 metaboIic rate or other clinical manifestations of the disease is the exception rather than the rule. However, the case we have discussed is only one of 6 which we have coIIected and serves to emphasize that in certain cases GbriIIation may be the earIiest manifestation of the disease. If we keep this point constantIy in mind a great many more such cases wouId undoubtedIy be found. Question two is very diffIcuIt to answer,

and we are doubtful if an accurate opinion couId be rendered. We know IittIe of the nature of the myocardial changes produced by thyroid intoxication. Whether the changes in the myocardium which permit the onset of the circus rhythm are structura1, physicochemica1, or a combination of both IS not cIear. We fee1 that permanentIy estabIished auricuIar fibriIIation is probabIy associated with more or less permanent damage to the heart muscle, since fibriIIation usuaIIy recurs in this type of case after being abolished by quinidine. PaIe muscle fibers with indistinct striations, IipoidaI changes, and IocaIized necroses have been described as changes in the heart muscIe secondarv to toxic thyroid disease. Whether these changes are specific for this disease has certainIy not been established. The mechanism of the production of transient or paroxysma fibrillation in the type of cases described above is probabIy due to temporary changes in the myo-

cardium. The fact that the paroxyms of fibriIIation cease following operation indicates that the myocardium probably recovers more or Iess compIeteI\- from whatever injury maJ- ha\-e occurred. This viewpoint is also supported by the absence of subsequent cardiac enIargement, changes in the T-wave in the eIectrocardiogram or the development of signs of cardiac weakness or failure. CONCLUSIONS I. AuricuIar fibriIIation or flutter are the most frequentIy encountered irreguIarities or disturbances in the mechanism in the heart beat associated with thyrotoxicosis. 2. Auricular fibriIIation or flutter may be the earIiest detectable sign of thyrotoxicosis. 3. The nature of the changes in the myocardium which accompany the deveIopment of earIy paroxysma fibriIIation has not been established, but the]- are apparentI? transient.