| Abstract|| |
Cardiac function has long been known to be altered in patients with thyrotoxicosis and atrial fibrillation occurs in patients with hyperthyroidism. In addition to its disabling symptoms, atrial fibrillation is a strong risk factor for systemic embolism, especially with regard to cerebral circulation. A right atrial appendage thrombus formation in atrial fibrillation is a rare phenomenon. In this report, we describe a case of a 30-year-old female, who suffered from hyperthyroidism and subsequently developed atrial fibrillation and a right atrial appendage thrombus with infarction of right atrial appendage.
Keywords: Atrial appendage thrombus, atrial fibrillation, atrial infarction, hyperthyroidism
|How to cite this article:|
Lanjewar D N, Ramraje S, Lanjewar SD. Right atrial appendage thrombus with atrial infarct in a case of thyrotoxicosis: An autopsy report. Indian J Pathol Microbiol 2010;53:532-4
|How to cite this URL:|
Lanjewar D N, Ramraje S, Lanjewar SD. Right atrial appendage thrombus with atrial infarct in a case of thyrotoxicosis: An autopsy report. Indian J Pathol Microbiol [serial online] 2010 [cited 2021 Aug 1];53:532-4. Available from: https://www.ijpmonline.org/text.asp?2010/53/3/532/68295
| Introduction|| |
Thyroid hormones are essential to maintain normal function of many systems including the cardiovascular system. Long-standing thyrotoxicosis in a patient with heart disease may result in atrial fibrillation, deterioration of angina pectoris or congestive heart failure.  Atrial fibrillation is the most common cardiac complication of hyperthyroidism and occurs in 15% of patients. , It is associated with a higher risk of systemic thrombo-embolism that often involves the central nervous system.  Thrombosis in the left ventricle is observed in patients with thyrotoxicosis.  Thrombosis of right atrial appendage is extremely rare and to the best of our knowledge, is not described in patients with thyrotoxicosis. , In this report we describe a rare case of right atrial appendage thrombosis with infarction in a case of thyrotoxicosis.
| Case Report|| |
A 30-year-old female was admitted in March 2006 for cough with expectoration, breathlessness, palpitations and edema feet of 17 days duration. She was alright 17 days back, after which she started getting cough with expectoration. Her breathlessness gradually increased and she further developed pitting edema of feet. Patient was a known case of hyperthyroidism. In the past she was also diagnosed with mitral stenosis for which she was regularly followed up. She was treated with anti thyroid drugs nearly for a year and a half, however, 10 days before hospitalization for the present illness, she abruptly stopped anti thyroid medication.
Her clinical examination revealed that she was thin built. There was midline neck swelling which was moving with deglutition, her respiratory rate was 46 per minute, pulse was feeble and her blood pressure was 110/90 mm of Hg. She also had bilateral edema feet. Her jugular venous pressure was raised; apex beat was fast and showed mid-diastolic murmur. Respiratory system showed crackles and wheeze for which ventilatory support was given. Examination of the abdomen revealed tender hepatomegaly, however, there was no evidence of free fluid. Examination of central nervous system revealed fluctuating level of consciousness. The X-ray chest showed bilateral pleural effusion, electrocardiogram showed right ventricular hypertrophy.
Other laboratory investigations revealed: arterial blood gas- PO2-31.4 mm of Hg, PCO2-50.5 mm of Hg, pH-7.065, K-6.2 mEq/L, Na-137 mEq/l. The clinical condition of the patient worsened, she became unresponsive and the monitor showed ventricular tachycardia, heart rate was irregularly irregular, respiratory system showed decreased air entry. She developed severe bradycardia and suddenly went into cardiac arrest and died on 14/3/07 at 2.00 pm. She was provisionally diagnosed as rheumatic heart disease with mitral stenosis with atrial fibrillation with congestive cardiac failure with pulmonary hypertension in a case of hyperthyroidism. A clinical postmortem was performed to know the cause of death.
Significant findings at postmortem examination were identified in the following organs. The left lobe of thyroid showed diffuse enlargement (5 Χ 4 cm. in size), and the cut surface of it revealed homogenous grayish white appearance with areas of fibrosis and hemorrhages. The heart was enlarged due to biventricular enlargement. The right atrial appendage was enlarged, had intense red appearance and was firm to feel and cut surface showed that the entire right atrial appendage cavity was occupied by recent thrombus [Figure 1]. The tricuspid, pulmonary, mitral and aortic valves were thin and shiny. There was no evidence of mitral stenosis and or rheumatic activity in any valves [Figure 2]. The right and left ventricles were slightly dilated. The right and left coronary arteries and their branches were patent and did not show any evidence of atherosclerosis. The lungs showed presence of pulmonary edema and thromboemboli in pulmonary capillaries. The examination of liver and spleen showed features of chronic passive venous congestion. The gross examination of other organs did not show any significant pathology.
|Figure 1: Cut open heart showing right atrial appendage with occluding thrombus|
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The microscopic examination of diffusely enlarged thyroid gland showed features of toxic nodular goiter comprising of thyroid follicles lined by tall and crowded follicular epithelial cells with formation of small papillae projecting into the follicular lumina. Microscopic examination of heart showed muscle fiber hypertrophy and presence of mononuclear inflammatory cell infiltrate. The heart did not show any evidence of recent or old rheumatic activity. Histology of right atrial appendage showed infarction of right atrial appendicle and its lumen showed presence of recent thrombus. The age of the right atrial appendage infarct was less than 24 hours. Histology of lung showed features of pulmonary edema along with presence of recent thrombo-emboli in pulmonary vasculature. The microscopic examination of liver and spleen showed features of chronic passive venous congestion. The histology of other organs did not show any significant findings.
| Discussion|| |
It is well known that thyroid hormone action has profound consequences for the heart. The pathologic implications of thyroid-cardiac relationship range from atrial fibrillation in sub clinical thyrotoxicosis to hemodynamic collapse and death where severe thyrotoxicosis is superimposed on primary heart disease.  Atrial fibrillation (AF) is a common cardiac manifestation of hyperthyroidism. With AF, both atria are fibrillating yet the vast majority of thrombi are located in left atrial appendage. Occasional reports of persistent thrombi in right atrium in patients with thyrotoxicosis have been described.  In our case, atrial fibrillation is primarily caused by thyrotoxicosis which has further progressed to congestive cardiac failure and resulted in right atrial appendage thrombus. The larger right atrial appendage width, and lack of anatomic remodeling may partially explain the lower prevalence of right atrial appendage thrombus in patients with atrial fibrillation.  The myocardial histologic findings in hyperthyroidism include non-specific findings, such as histiocytic, lymphocytic and fibroblastic cellular accumulations, edema and necrosis, swollen fibers with indistinct striations and lipoid changes, hyaline replacement of muscle fibers, myocardial hypertrophy and in some cases no changes.  In our case, histology of heart showed muscle fiber hypertrophy and presence of mononuclear inflammatory cell infiltrate; these findings are non-specific and do not have any significance. Since right and left coronaries and their branches were patent; we assume that a finding of right atrial infarct in our case was secondary to a large thrombus in the atrial chamber; these findings are rarely described in the literature. 
Misdiagnosis of hyperthyroidism is possible and can be explained by errors in symptoms analysis. The various clinical masks of thyrotoxicosis are ischemic heart disease, active rheumatic fever with mitral and aortic defects, endogenic depression, and obesity, gastrointestinal and hepatic diseases. [ 12] In our case, diagnosis of mitral stenosis was suspected clinically and patient was treated accordingly; however at postmortem examination heart did not show any evidence of rheumatic heart disease and/or mitral stenosis. The findings described in this case emphasize the need to formally exclude hyperthyroidism in patients with atrial fibrillation whatever the apparent cause. Since involvement of right atrial appendage by thrombus is not described in literature, herein we describe a rare case of right atrial appendage thrombosis in a case of thyrotoxicosis.
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D N Lanjewar
Sir J. J. Group of Hospitals, Byculla, Mumbai-400 008
Source of Support: None, Conflict of Interest: None
[Figure 1], [Figure 2]