The prevalence of mitral valve prolapse was investigated in 126 patients with hyperthyroidism due to Graves' disease or toxic nodular goitre and that of hyperthyroidism in 64 patients with mitral valve prolapse. One hundred and eleven asymptomatic healthy subjects comprised a control group. The patients with hyperthyroidism were divided into those with Graves' disease and those with toxic nodular goitre. Of the group as whole, 12 (9.5%) patients had mitral valve prolapse compared with six (5.4%) in the control group, but the difference was not statistically significant. The prevalence of mitral valve prolapse in the patients with toxic goitre was also not significantly different from that in the controls. When the prevalence in the group with Graves' disease was compared with that in the control group (16.3% vs 5.4%) the difference was significant. Only one patient with mitral valve prolapse had hyperthyroidism.

An increased prevalence of mitral valve prolapse has been found in Graves’ disease and a common autoimmune etiology has been suggested for both disorders. We investigated the prevalence of mitral valve prolapse in 87 patients with autoimmune chronic lymphocytic thyroiditis, 50 patients with nongoitrous hypothyroidism and 111 healthy control subjects. Mitral valve prolapse was found in 16.09% of patients with chronic lymphocytic thyroiditis compared to 6 and 5.4% in nongoitrous hypothyroidism and normal controls, respectively. The result is statistically significant, p < 0.02, and confirms that the prevalence of mitral valve prolapse is significantly increased in patients with autoimmune disorders of the thyroid gland, when compared to normals and nonautoimmune conditions.

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A case of Dressler’s syndrome with cardiac tamponade is presented. 19 days after an acute lateral myocardial infarction, the patient, 46 years old, was admitted the second time with a characteristic clinical picture of cardiac tamponade. The patient did not receive at any time during his admission an anticoagulant treatment. The clinical diagnosis was supported by fluoroscopic and echocardiographic findings. A pericardiocentesis performed immediately revealed a hemorrhagic pericardial fluid. After withdrawal of 60 ml, the patient’s clinical condition improved dramatically and this improvement continued further under treatment with corticosteroids. At the best of our knowledge this is the second case in the literature of Dressler’s syndrome with cardiac tamponade and hemorrhagic fluid in a patient not treated with anticoagulants.