Forfar JC, Miller HC, Toft ADOccult thyrotoxicosis: a correctable cause of "idiopathic" atrial fibrillation.Am J Cardiol 1979AMERICAN JOURNAL OF CARDIOLOGY4419-12Serum total thyroxine, triiodothyronine and thyrotropin response to thyrotropin-releasing hormone were measured in 75 consecutive patients presenting to a cardiology clinic with atrial fibrillation with no obvious cardiovascular cause. A lack of response of serum thyrotropin to thyrotropin-releasing hormone, indicative of thyrotoxicosis, was found in 10 patients (13 percent), not all whom had raised serum thyroid hormone levels. These 10 patients were predominantly male, had no clinical signs of thyrotoxicosis and a relative excess of nonpalpable autonomous thyroid nodules demonstrated with scintigraphy. Eight of the 10 patients had reversion to stable sinus rhythm after treatment with iodine-131 or carbimazole, either spontaneously or after direct current cardioversion. It would appear that clinically occult thyrotoxicosis can be identified consistently only with the thyrotropin-releasing hormone test and is the cause of "idiopathic" atrial fibrillation in a significant proportion of patients.Cobler JL, Williams ME, Greenland PThyrotoxicosis in institutionalized elderly patients with atrial fibrillation.Arch Intern Med 1984ARCHIVES OF INTERNAL MEDICINE14491758-60We hypothesized that hyperthyroidism would be an infrequent cause of atrial fibrillation in older persons because atherosclerotic, hypertensive, and degenerative heart disorders are more prevalent with aging. We determined the cardiac rhythm and thyroid status of 316 patients older than 65 years of age residing in a nursing home. One (11%) of the nine elderly men and five (31%) of the 16 women with atrial fibrillation had laboratory evidence or a history of hyperthyroidism. The elderly patients with cardiac rhythms other than atrial fibrillation (n = 291) had only a 1.7% prevalence of hyperthyroidism. The analysis for elderly women demonstrated a statistically significant association between atrial fibrillation and hyperthyroidism, but the association was not statistically significant for men. These findings indicate that hyperthyroidism is common in institutionalized elderly women with atrial fibrillation.s the cause of "idiopathic" atrial fibrillation in a significant proportion of patients.Bar-Sela S, Ehrenfeld M, Eliakim MArterial embolism in thyrotoxicosis with atrial fibrillation.al fibrillation.Arch Intern Med 1981ARCHIVES OF INTERNAL MEDICINE14191191-2The incidence of atrial fibrillation (AF) in 142 patients with thryotoxicosis was 21% and that of thromboembolic disease was 8.5%. Male sex, increasing age, and associated rheumatic or hypertensive heart disease were significantly associated with the presence of AF. Thromboembolic episodes occurred in 12 (40%) of the patients with AF and in none of the 112 patients without AF. Cerebral emboli accounted for 53% of the episodes. In view of the grave prognosis of the embolic episodes, patients with thyrotoxicosis should be treated with heparin during attacks of AF and with oral anticoagulants when they have chronic fibrillation.women demonstrated a statistically significant association between atrial fibrillation and hyperthyroidism, but the association was not statistically significant for men. These findings indicate that hyperthyroidism is common in institutionalized elderly women with atrial fibrillation.s the cause of "idiopathic" atrial fibrillation in a significant proportion of patients.Staffurth JS, Gibberd MC, S Ng Tang FuiArterial embolism in thyrotoxicosis with atrial fibrillation.al fibrillation.Br Med J n Med 1977BRITISH MEDICAL JOURNALICINE216088688-90In 262 patients with thyrotoxicosis and atrial fibrillation there were 26 episodes of arterial embolism (17 cerebral and nine elsewhere) in 21 patients. Twelve incidents occurred with active thyrotoxicosis, three on reversion to sinus rhythm, and 11 after the patients were euthyroid. This important complication is more common than is realised, and most patients should be put on prophylactic anticoagulants when first seen with atrial fibrillation. prognosis of the embolic episodes, patients with thyrotoxicosis should be treated with heparin during attacks of AF and with oral anticoagulants when they have chronic fibrillation.women demonstrated a statistically significant association between atrial fibrillation and hyperthyroidism, but the association was not statistically significant for men. These findings indicate that hyperthyroidism is common in institutionalized elderly women with atrial fibrillation.s the cause of "idiopathic" atrial fibrillation in a significant proportion of patients.Scott GR, Forfar JC, Toft ADg Tang FuiGraves' disease and atrial fibrillation: the case for even higher doses of therapeutic iodine-131.Br Med J [Clin Res] 1984BRITISH MEDICAL JOURNAL [CLINICAL RESEARC289.6442399-400Seventy five consecutive patients with Graves' disease complicated by atrial fibrillation were given a large single therapeutic dose of 600 MBq (16.2 mCi) iodine-131 in an effort to control their hyperthyroidism rapidly and thus restore sinus rhythm. Patients were initially followed up every three months after treatment and then at yearly intervals. The mean period of follow up was 3.1 years. A total of 44 of the patients became hypothyroid and 31 euthyroid, and 33 (75%) and 14 (45%) of these patients, respectively, reverted to sinus rhythm (p less than 0.01). Of the 33 who became hypothyroid and reverted to sinus rhythm, 30 had developed the hypothyroidism within six months after treatment. These results are a strong case for increasing the dose of radioiodine in patients with Graves' disease complicated by atrial fibrillation in an effort to speed the onset of thyroid failure and thus maximise the rate of reversion to sinus rhythm. atrial fibrillation in a significant proportion of patients.Nakazawa HK, Handa S, Nakamura Y, Oyanagi H, Hasegawa M, Ishikawa N, Ozaki O, Ito KHigh maintenance rate of sinus rhythm after cardioversion in post- thyrotoxic chronic atrial fibrillation.Int J Cardiol Res] 1987INTERNATIONAL JOURNAL OF CARDIOLOGYSEARC16.1247-5569We performed rhythm conversion on 33 euthyroid patients with post- thyrotoxic atrial fibrillation who do not revert spontaneously to sinus rhythm from atrial fibrillation. The duration of atrial fibrillation ranged from 9 to 59 months (mean 25 +/- 14). The protocol of rhythm conversion was to first attempt pharmacological conversion with disopyramide and then to perform electrical cardioversion on the non-converters. Of 33 patients, 25 were converted to sinus rhythm (6 by disopyramide and 19 by electrical cardioversion), resulting in 8 non-converters. However, it was later discovered that cardioversion had been applied to 4 of the 8 non- converters when these patients had had a recurrence of thyrotoxicosis. These 4 patients were subjected to a second electrical cardioversion after attaining the euthyroid state. Sinus rhythm was restored in all 4 patients, giving a cardioversion rate of 88%. The sinus rhythm was maintained in 25 of the total 29 converters (86%) at the time of follow-up (10-68 months, mean 35 +/- 19 months). Our studies suggest that cardioversion should be encouraged for thyrotoxic atrial fibrillation, even if the duration of atrial fibrillation is long-standing, since there is excellent maintenance of sinus rhythm and even delayed application of cardioversion may improve its success rate.Epstein ND, Lin HJ, Fananapazir LGenetic evidence of dissociation (generational skips) of electrical from morphologic forms of hypertrophic cardiomyopathy.Am J Cardiol 1990AMERICAN JOURNAL OF CARDIOLOGY665627-31The diagnosis of hypertrophic cardiomyopathy (HC) is traditionally based on the demonstration by echocardiography of left ventricular hypertrophy in the absence of apparent cause. This study reports on 5 adults in 4 families who are obligate or highly probable carriers of the HC gene by virtue of their position in the pedigree, but who have normal echocardiographic findings. Four of these 5 patients had abnormal signal-averaged electrocardiograms, a finding suggesting the presence of electrical disease despite the absence of left ventricular hypertrophy. The fifth patient, an identical twin of a patient with familial HC, had neither left ventricular hypertrophy nor a myocardial electrical abnormality. These data indicate that the spectrum of HC includes patients who have a potentially arrhythmogenic left ventricular substrate but who have no evidence of left ventricular hypertrophy. Our data demonstrating generational skips also imply that some instances of HC previously judged to be sporadic may indeed by familial.