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The association of pericarditis and pulmonary embolism may be the source of diagnostic error and delay in the administration of anticoagulant therapy. Two cases are reported. Pericarditis occurred late in patients with severe, chronic pulmonary embolism with electrocardiographic changes of acute cor pulmonale. Two physiopathological mechanisms for this association have been proposed. The first, haemodynamic, suggests friction between the pericardium and distended right ventricle and pulmonary artery. The second, an immunological hypothesis, compares the association of pericarditis and pulmonary embolism to that of the Dressler syndrome after myocardial infarction. This assimilation would imply the constitution of an anatomical pulmonary infarction. It is not justifiable to accept this pathogenesis on the evidence of transient pulmonary opacities resulting from intra-alveolar haemorrhage or of linear opacities of pulmonary atelectasis secondary to hypocapnic pneumoconstriction which are radiological signs of anatomo-physiological stages of pre-infarction.

Cardiac output and haemodynamic volumetric values (stroke volume, stroke index, left ventricular end-diastolic volume, blood volume, mean corpuscular volume and packed red cell volume) were measured in a population of 69 very old subjects (80 to 102 years) whose heart was regarded as normal on the basis of criteria determined, by radiocardiography and radionuclide ventriculography. These harmless and non-invasive techniques provided reference values in subjects of a seldom explored age group. Altogether, these values were lower than those of younger adults, and they decreased with age. Their reliability is due to the fact that they were obtained by true measurement and not by extrapolation of results observed in adults.