9
Volume 68 May 1975
327
Clinical Section President F B Gibberd FRCP
Meeting 10 May 1974 at the Royal Berkshire Hospital, Reading (continuedfrom February 'Proceedings' p 90)
Cases Thyrotoxic Cardiomyopathy Complicated by Systemic and Pulmonary Embolism W Hausmann MD FRCP (Battle Hospital, Oxford Road, Reading, RG3 JAG) D P, man aged 47 History: Illness started in 1971 with dyspnoea, palpitations and peripheral cedema. On examination: Evidence of congestive heart failure with fast fibrillation. Enlargement of right lobe of thyroid. Palms hot and moist. Investigations: Resin uptake of labelled T3 195 (normal 100±20). Protein bound iodine 12.5 ,g/ 100 ml. Chest X-ray showed cardiomegaly. ECG showed atrial fibrillation and nonspecific myocardial damage. Treatment was started with digoxin, frusemide and carbimazole. However, shortly afterwards he had a hemoptysis and right pleuritic pain and, 24 hours later, a right hemiparesis. Pulmonary and cerebral embolism was diagnosed and treatment with warfarin was started. The course of his illness was stormy; his heart failure was difficult to control, he was intolerant of digoxin, and lanatoside-C i.m. was substituted. He had a course of 'I'l therapy. He had to be admitted to hospital on four different occasions in four months and the outlook was considered extremely poor. However, in May 1972 he was sufficiently improved to start part-time work. His hyperthyroidism had been sufficiently controlled to stop carbimazole in July 1971 and in March 1972 the intramuscular lanatoside-C was replaced by the oral preparation. He is now working full-time and feels fit though still fibrillating at a controlled rate. No change in heart size since first attendance. Treatment still consists of lanatoside-C orally, frusemide and warfarin. Thyroid function tests have remained within normal limits.
Comment
It is not generally recognized that although the prognosis of thyrotoxic heart disease after successful treatment of hyperthyroidism is generally good, this is not universally so. Some features are irreversible in a few cases. This is especially true where cardiomegaly and atrial fibrillation are combined. If these features persist it may be presumed that the original diagnosis was mistaken and that the thyrotoxicosis was a purely accidental finding in a case of primary cardiomyopathy. This mistake was certainly made in the case described. A few months ago I saw a second case, a man aged 24 who presented with atrial fibrillation and cardiomegaly and thyrotoxicosis, successfully U treated with 1311. However, atrial fibrillation persisted and he suddenly collapsed and died. Postmortem showed that death was due to cardiomyopathy and that the thyrotoxicosis was purely coincidental. This was the opinion expressed by the pathologist, but I think that this explanation is erroneous and that cardiomyopathy was due to thyrotoxicosis and persisted in spite of the successful treatment of this condition. Cardiomyopathy secondary to thyrotoxicosis has been described by de Groot (1972). It is not well recognized that pulmonary and systemic embolism may complicate thyrotoxic heart disease. Parker & Lawson (1973) reported 33 patients dying from thyrotoxicosis of whom 6 had major emboli, either systemic or pulmonary, at post-mortem. It should be realized that patients with thyrotoxic heart disease and atrial fibrillation are liable to develop embolism and should be anticoagulated. REFERENCES de Groot W J (1972) In: Cardiomyopathy. Ed. G E Burch. Blackwell Scientific Publications, New York; pp 306-313 Parker J C & Lawson D H (1973) Lancet ii, 894
Volume 68 May 1975
327
Clinical Section President F B Gibberd FRCP
Meeting 10 May 1974 at the Royal Berkshire Hospital, Reading (continuedfrom February 'Proceedings' p 90)
Cases Thyrotoxic Cardiomyopathy Complicated by Systemic and Pulmonary Embolism W Hausmann MD FRCP (Battle Hospital, Oxford Road, Reading, RG3 JAG) D P, man aged 47 History: Illness started in 1971 with dyspnoea, palpitations and peripheral cedema. On examination: Evidence of congestive heart failure with fast fibrillation. Enlargement of right lobe of thyroid. Palms hot and moist. Investigations: Resin uptake of labelled T3 195 (normal 100±20). Protein bound iodine 12.5 ,g/ 100 ml. Chest X-ray showed cardiomegaly. ECG showed atrial fibrillation and nonspecific myocardial damage. Treatment was started with digoxin, frusemide and carbimazole. However, shortly afterwards he had a hemoptysis and right pleuritic pain and, 24 hours later, a right hemiparesis. Pulmonary and cerebral embolism was diagnosed and treatment with warfarin was started. The course of his illness was stormy; his heart failure was difficult to control, he was intolerant of digoxin, and lanatoside-C i.m. was substituted. He had a course of 'I'l therapy. He had to be admitted to hospital on four different occasions in four months and the outlook was considered extremely poor. However, in May 1972 he was sufficiently improved to start part-time work. His hyperthyroidism had been sufficiently controlled to stop carbimazole in July 1971 and in March 1972 the intramuscular lanatoside-C was replaced by the oral preparation. He is now working full-time and feels fit though still fibrillating at a controlled rate. No change in heart size since first attendance. Treatment still consists of lanatoside-C orally, frusemide and warfarin. Thyroid function tests have remained within normal limits.
Comment
It is not generally recognized that although the prognosis of thyrotoxic heart disease after successful treatment of hyperthyroidism is generally good, this is not universally so. Some features are irreversible in a few cases. This is especially true where cardiomegaly and atrial fibrillation are combined. If these features persist it may be presumed that the original diagnosis was mistaken and that the thyrotoxicosis was a purely accidental finding in a case of primary cardiomyopathy. This mistake was certainly made in the case described. A few months ago I saw a second case, a man aged 24 who presented with atrial fibrillation and cardiomegaly and thyrotoxicosis, successfully U treated with 1311. However, atrial fibrillation persisted and he suddenly collapsed and died. Postmortem showed that death was due to cardiomyopathy and that the thyrotoxicosis was purely coincidental. This was the opinion expressed by the pathologist, but I think that this explanation is erroneous and that cardiomyopathy was due to thyrotoxicosis and persisted in spite of the successful treatment of this condition. Cardiomyopathy secondary to thyrotoxicosis has been described by de Groot (1972). It is not well recognized that pulmonary and systemic embolism may complicate thyrotoxic heart disease. Parker & Lawson (1973) reported 33 patients dying from thyrotoxicosis of whom 6 had major emboli, either systemic or pulmonary, at post-mortem. It should be realized that patients with thyrotoxic heart disease and atrial fibrillation are liable to develop embolism and should be anticoagulated. REFERENCES de Groot W J (1972) In: Cardiomyopathy. Ed. G E Burch. Blackwell Scientific Publications, New York; pp 306-313 Parker J C & Lawson D H (1973) Lancet ii, 894
