Why the study?
Does angiocardiography document the presence of pericardial effusion in patients with myxedema heart disease?
Does angiocardiography document the presence of pericardial effusion in patients with myxedema heart disease?
Angiocardiography may be a decisive imaging modality for documenting pericardial effusion in patients with myxedema heart disease.
Angiocardiography may document pericardial effusion in myxedema; single case report leaves open routine clinical adoption.
In 1918, Zondek (26) reported cardiac change in a number of patients with myxedema, emphasizing the increase in heart size as demonstrated by x-ray examination. In 1939, Scherf and Boyd (20) described 3 cases of pericardial effusion in myxedematous patients, offering this as a common cause of the enlarged cardiac silhouette. In recent years, there have been several reports of this association in the literature, usually in isolated cases (2, 3, 4, 6, 10, 12, 17, 21, 26). Most often, the diagnosis was established by pericardiocentesis (9); in other instances, by postmortem examination. Of interest is the report of Lerman et al. (14), who cited postmortem records showing 2 of 5 myxedematous patients to have pericardial effusions. In 1953, Marks and Roof (16) reviewed the literature on pericardial effusion in myxedema. In 13 of 44 cases of myxedema reported, there were associated pleural or peritoneal effusions, or both. The purpose of this paper is to show how angiocardiography may be decisive in documenting the presence of pericardial effusion in myxedema heart disease. Clinical Findings Myxedema heart disease usually occurs in a setting of classic hypothyroidism (1, 18, 25). The cardiovascular manifestations are nonspecific. It is important to note that the cardiac silhouette need not be markedly enlarged; 2 cases of pericardial effusion in myxedematous patients reported by Kern et al. (11) showed only mild enlargement. The increased size of the cardiac shadow in myxedema heart disease is often accompanied by faintness of the heart sounds on auscultation, feeble cardiac pulsations as seen fluoroscopically, prolonged circulation time, and decreased cardiac output. Pathological Findings White (24) has pointed out the three major factors that he believes contribute to the cardiac enlargement, namely, chamber dilatation, increased bulk of the heart muscle, and finally pericardial effusion. Pathologically, the heart muscle is thickened and edematous. Many have emphasized the frequent occurrence of pericardial effusion (2). This consists of a simple transudate, without evidence of pericardial inflammation. Effusions of as much as 4,000 c.c. have been demonstrated clinically and at postmortem examination (4, 7, 13, 16, 23). There is a tendency for fluid to accumulate in body cavities in myxedema; thus there are often associated pleural and peritoneal effusions (15, 19). Case Reports Case I: C. H., a 41-year-old white woman with known Marfan's syndrome, was admitted to St. Luke's Hospital, surgical service, in October, 1961, for repair of a diastasis recti. Eighteen years prior to admission, she had undergone a total thyroidectomy and postoperative irradiation for carcinoma of the thyroid with cervical node involvement. She had done well on maintenance doses of thyroid extract.
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Kittredge et al. (1963) studied this question.
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