Milk of calcium pericardial effusion confirmed with postmortem computed tomography and autopsy findings: A case report.

We present the postmortem computed tomography and autopsy findings of a 60-year-old man who developed milk of calcium pericardial effusion and died of constrictive epicarditis. He experienced out-of-hospital cardiopulmonary arrest, and spontaneous circulation returned at the hospital. However, 7 h after recovery, the patient died. He had a swollen neck, had been experiencing coughing from 4 to 5 days earlier, and had no significant medical or surgical history. On computed tomography (CT), highly dense pericardial fluid (CT value: 130-150 Hounsfield units) and multiple calcifications along the epicardium and pericardium were visualized. The epicardium and pericardium were thick, hard, rough, and widely calcified with mild adhesions on autopsy. The pericardial cavity contained a pale, reddish brown, turbid, and highly viscous liquid. Bacteriological tests of pericardial fluid cultures revealed the presence of group G ß-hemolytic streptococci. Hence, we diagnosed the patient's cause of death as heart failure due to constrictive epicarditis. We believe that this case of milk of calcium pericardial effusion is the first case confirmed with postmortem CT and autopsy findings.

Brothers with constrictive pericarditis - A novel mutation in a rare disease.

Familial constrictive pericarditis is extremely rare. We report a case of two brothers both suffering constrictive pericarditis along with having multiple painless joint deformities. Genetic workup confirmed the clinical diagnosis of camptodactyly-arthropathy-coxa vara-pericarditis (CACP) syndrome CACP syndrome and also revealed a rare mutation in the causative gene.

Collagen network remodelling and left ventricular function in constrictive pericarditis.

OBJECTIVE: To investigate whether patients with constrictive pericarditis have changes in collagen content and architecture that could influence left ventricular function. DESIGN: Cohort study. SETTING: University teaching hospital. PATIENTS: Biopsy specimens of myocardium from 13 patients admitted consecutively for treatment of chronic constrictive pericarditis were compared with normal heart tissue taken at necropsy from 15 patients free of cardiac disease. INTERVENTION: Pericardiectomy through median sternotomy. Biopsy specimens (4 or 5) were taken from the left ventricular free wall. MAIN OUTCOME MEASURES: Biochemical and histological assessment of total collagen content, relative proportion of type I and III collagen, and amount of orthogonal collagen fibre meshwork (crosshatching) in the left ventricular tissue. RESULTS: There was more collagen in the myocardium of patients with constrictive pericarditis than in controls when measured either biochemically by hydroxyproline content (89.4 v 50.4 mg/g dry weight) or by histological measurement of the collagen fraction of the myocardium (2.4% v 7.0%). Neither of these measurements, however, correlated with left ventricular ejection fraction, pulmonary wedge pressure, or right ventricular end diastolic pressure. The thickness of the fibrous trabeculae in the myocardium was, however, inversely related to both left ventricular ejection fraction (r = -0.76) and deceleration time (r = -0.68). Trabecular thickening was also related to NYHA class, with those in class III and IV having the greatest thickening. CONCLUSION: Changes in collagen content and architecture may contribute to impaired ventricular function in patients with chronic constrictive pericarditis.

Crystallographic identification of a calcium deposit in calcified pericarditis associated with articular chondrocalcinosis.

In a case of CPPD crystal deposition disease of the pseudorheumatoid type and of long duration, calcified constrictive pericarditis developed and was surgically treated. Analysis of the calcium deposit in the pericardium was carefully made by infrared absorption, x-ray diffraction, and thermogravimetry. It revealed that the deposit was composed of B-type carbonated apatite. Previously, both calcium pyrophosphate dihydrate (CPPD) and apatite crystals, either in the same place or in different tissues, have been reported in the same patient. These observations raise the possibility that the same metabolic error might lead to both types of crystal deposition.

Proteins of ascitic fluid in constrictive pericarditis.

A patient with chronic calcific pericarditis, hepatic congestion, and fibrosis had massive ascites with a protein concentration of 5.1 g/100 ml. This fluid was in all likelihood largely derived from hepatic interstitial fluid. The ascites-serum concentration ratio for several protein species and molecular exclusion chromatography of these fluids suggested two processes may be involved in the transfer of protein from serum to ascites, namely bulk transfer of all species and molecular sieving.

Maximal rate of fall of left ventricular pressure in cardiomyopathy and constrictive pericarditis.

The maximal rate of fall of left ventricular pressure (peak negative dp/dt) was measured in 4 patients with congestive cardiomyopathy (primary myocardial disease), in 5 patients with constrictive pericarditis and in 3 controls. Measurements were made at rest, with leg raising, after a bolus of 6 mug intravenous isoprenaline, and in patients with constrictive pericarditis during pulsus paradoxus. Peak negative dp/dt was 1810 +/- 234 mmHg/sec in controls; it was reduced in patients with constrictive pericarditis (1337 +/- 514 mmHg/sec) and greatly decreased in patients with congestive cardiomyopathy (812 +/- 190 mmHg/sec). There was close linear correlation between resting peak positive and peak negative dp/dt and there was little change with leg raising. Isoprenaline caused an increase in peak positive dp/dt, but there was only a small change in peak negative dp/dt. In patients with constrictive pericarditis, peak negative dp/dt varied during pulsus paradoxus: the linear relationship to peak positive dp/dt was maintained throughout the respiratory cycle. Peak negative dp/dt may be a useful index of myocardial function.