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When primary amyloid infiltrates the my-oeaidium, there is a loss of distensibility and a resistance to contraction similar to that seen in constrictive pericardlitis. The clinical similarity between these two entities has been noted previously on only a few occasions and only one previous case of amynloid has had catheterization studies. A case of amyloid of the heart is presented with catheterization studies and the reasons for the clinical and physiologic similarity to constrictive pericarlditis are discussed.T HE essential pathology of constrictive pericarditis is the partial replacement of the epicardium and superficial myocardial layers by inelastic fibrous tissue. This interferes with diastolic filling of the ventricles and is recorded during right ventricular catheterization as a high end-diastolic plateau. In addition, the encasing and infiltrating lesion interferes with contractility and thereby reduces, somewhat, the systolic pressure anticipated in relation to the high diastolic filling pressure. This results in a pressure pattern in which the end-diastolic pressure is often greater than one-third the systolic pressure: a finding which has been considered diagnostic by some authors.' The early diastolic dip seen in the right ventricular curve is due to the "drag" effect of the fibrous exterior and its tendency to resist change and to reach the resting state more quickly. It is fairly sharply demarcated because of rapid filling caused by the high pressure within the auricle.Recently it has been shown by Hertzel, Wood and Burchell2 that similar pressure patterns can be found in other conditions and in amyloid of the heart specifically. In 1950, Fisher3 had showni the inability of the amyloid heart to augment its diastolic volume. Clinically this was not a new concept, for Couter and Reichert4 and Findley and Adams5 had noted the clinical

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