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Constrictive pericarditis and pyopericardium with tamponade in a patient and rheumatoid arthritis is described. No fever was recorded despite a litre of pus in the pericardial sac, perhaps because of previous treatment with hydrocortisone. Echocardiography is a diagnostic advance.
A 19 year old man presented with a six month history of chest pain, dyspnoea, and lethargy and was found on an echocardiogram to have a dilated left ventricle with a small pericardial effusion. Ramipril and a course of steroids were tried but serial echocardiograms showed a persistently thickened pericardium and slowly developing features of constriction. On computed tomography, a large mediastinal mass encasing the heart, along with para-aortic and paratracheal lymphadenopathy, was found. Right heart catheter studies showed equal pressures in all four chambers. His deteriorating clinical condition led to a pericardiectomy. Histology confirmed primary pericardial mesothelioma. The patient died soon after surgery.
A 63 year old man with a six year history of Parkinson's disease presented with signs of right heart failure following a knee replacement. Constrictive pericarditis was diagnosed and a radical pericardectomy performed. Six months later, the patient remained unwell with raised inflammatory markers. An inflammatory fibrotic reaction caused by cabergoline was diagnosed. He improved after cessation of cabergoline.
A case of chronic constrictive uraemic pericarditis successfully treated by pericardectomy is reported together with the pre- and postoperative haemodynamic data.
Constrictive pericarditis developed in a 55 year old man two years after transmural myocardial infarction complicated by severe acute pericarditis. Pericardiectomy was successful. Although this very rare late complication of myocardial infarction has been reported as a sequela of frank anticoagulant induced haemopericardium, in this case there was no clinical evidence of such an association.
Primary pericardial mesothelioma is an extremely rare tumour. This case illustrates the typical late presentation with symptoms and signs of constrictive pericarditis. An unusual feature was complete encasement of the heart by tumour. No satisfactory treatment is available.
A 34 year old woman with a history of self-mutilation developed severe constrictive pericarditis with sterile, calcified intrapericardial abscess cavities as a result of inserting sewing needles into her chest seven years previously. After pericardiectomy she made a good recovery.
Early constrictive pericarditis and anaemia developed in a 52 year old man after he had an inferior wall myocardial infarction complicated by Dressler's syndrome. Total pericardiectomy at the time of coronary artery bypass surgery resulted in complete resolution of signs and symptoms.
In order to test the regenerative capacity of atrophic axons, a constricting ligature was placed around the proximal tibial nerve of the rabbit, and the nerve crushed at the ankle one week later. Axonal atrophy with altered g ratios was subsequently confirmed in fibres distal to the site of ligature and proximal to the site of crush. In nerves with tight proximal ligatures the reinnervation of plantar muscles and the subsequent recovery of distal motor latency were delayed, indicating impaired regeneration. This result may be relevant to the "double-crush" theory of nerve damage.
Two months after a pericardectomy for constrictive pericarditis a 37-year-old man presented with diarrhoea, abdominal pain and weight loss. During the course of investigation he developed brisk rectal bleeding and emergency angiography revealed a bleeding site related to an area of abnormal vasculature in the caecum. At laparotomy, the small bowel was found to be inflamed and the mesenteric lymph nodes enlarged. The overall histological appearances, confirmed later on endoscopic duodenal biopsies, were those of Whipple's disease. His symptoms resolved promptly after starting tetracycline therapy. The clinical features of Whipple's disease are protean and often bizarre. We report here a case where the diagnosis was made after the onset of profuse rectal bleeding.
A patient with calcific constrictive pericarditis due to rheumatoid arthritis is presented: the literature reveals only one previous case which was attributed to the long duration of the rheumatoid arthritis.
We describe a 62-year-old woman in whom systemic lupus erythematosus presented as life-threatening effuso-constrictive pericarditis. Surgical drainage of the pericardium was required and the patient made a satisfactory recovery. At six-months follow-up, while taking hydroxychloroquine and a non-steroidal anti-inflammatory agent, she remains well.
A 30 year old man presented with symptoms of constrictive pericarditis. Echocardiography and computed tomography showed a mass extending from the pericardium to surround the heart and penetrating the left ventricular apex. An unresectable pleomorphic liposarcoma arising from the pericardium was found at thoracotomy.
Udder oedema was studied in eight Jersey cows with rectovaginal constriction (RVC) and three normal Jersey cows. A complete physical examination was performed at least two weeks before parturition, at parturition and two weeks after parturition. Jersey cows with RVC developed udder oedema as early as 14 days before parturition, and condition persisted for three to 10 days following parturition. Mammary blood flow and cranial superficial epigastric venous blood pressure were measured in three Jersey cows with RVC with udder oedema and three normal Jersey cows. The former with udder oedema had a significant decrease in mammary blood flow at parturition compared to the normal Jersey cows (P less than 0.05); there was no significant difference in mammary blood flow between Jersey cows with RVC and normal Jersey cows two weeks before parturition (P greater than 0.05). A significant mean increase in cranial superficial epigastric venous blood pressure occurred at parturition when compared to two weeks before parturition in Jersey cows with RVC (P less than 0.05), but normal Jersey cows had no significant increase in cranial superficial epigastric vein pressure during these two periods of measurement (P greater than 0.05). There was no significant increase in jugular vein blood pressure during the two periods of measurement in Jersey cows with RVC or normal Jersey cows (P greater than 0.05). There was a significant negative correlation between mammary blood flow and cranial superficial epigastric pressure at parturition (r = 0.733, P less than 0.05).
Coronary artery motion was evaluated in normal subjects and patients with constrictive pericarditis (CP), congestive cardiomyopathy, restrictive cardiomyopathy, and coronary artery disease. Seven of the 8 patients with CP had lack of motion of the major coronary arteries. Nine of the 10 patients with congestive cardiomyopathy and a markedly reduced ejection fraction showed normal motion, as did all 4 with restrictive cardiomyopathy and 9 of the 10 with segmental dysfunction due to coronary disease. Pericardial stripping in 5 patients with CP revealed epicardial involvement corresponding to regions of absent motion; one CP patient with normal motion had no epicardial involvement. Lack of motion may suggest CP when the diagnosis is unsuspected, right heart pressures are not obtained, or hemodynamics are atypical. This sign may also help to distinguish CP from restrictive cardiomyopathy, which produces similar hemodynamics.
PURPOSE: To assess ventricular septal motion and quantify the septal configuration in patients clinically suspected of having constrictive pericarditis (CP), and to compare these patients with healthy subjects and with patients who have other diastolic heart abnormalities such as restrictive cardiomyopathy (RCM). MATERIALS AND METHODS: In 41 patients clinically suspected of having CP and 12 healthy subjects, magnetic resonance (MR) imaging yielded information about cardiac morphology and function. On short-axis cine MR images, septal motion was assessed, and the septal and left ventricular free wall (LVFW) radii of curvature were quantified and normalized to end systole. Abnormal diastolic septal motion was expressed in terms of the largest difference in normalized radius between the septum and the LVFW. Analysis of variance was used to identify significant differences in septal shape among subject groups. RESULTS: Left-sided septal flattening was identified in 17 of the 21 patients with surgically proven CP, in none of the 20 patients without CP, and in none of the healthy subjects. CP without septal flattening was present on the left side (n = 1), on the right side (n = 1), and at the atrioventricular grooves (n = 2). Abnormal septal motion yielded a sensitivity of 81% (17 of 21 patients), specificity of 100% (20 of 20 patients), accuracy of 90% (37 of 41 patients), positive predictive value of 100% (17 of 17 patients), and negative predictive value of 83% (20 of 24 patients) in the detection of CP. The maximal difference in normalized radius of curvature between the septum and the LVFW in the patients with CP was significantly different from that in the patients without CP (P <.001) and that in the healthy subjects (P <.001). CONCLUSION: Abnormal diastolic septal motion is a frequent phenomenon of CP. If present in patients suspected of having CP, this finding is helpful in distinguishing CP from RCM.
Recent studies have found endothelin-1 (ET), a potent vasoconstrictor of endothelial cell origin, is increased in congestive heart failure (CHF) in plasma and correlates with increased atrial pressures. Additionally, it has been shown that, despite increased circulating ET concentrations in CHF, a decreased responsiveness to exogenous ET infusion exists in an experimental model of CHF induced by rapid pacing. The present study was designed to determine whether plasma ET would be increased in a model of low cardiac output congestive failure without elevated atrial pressures produced by thoracic inferior vena caval constriction (TIVCC). In addition, we sought to determine whether this model of low cardiac output would show a full vasoconstrictive response to exogenous ET infusion and whether atrial natriuretic factor (ANF) infused acutely to achieve pathophysiological concentrations would modulate the systemic and renal hemodynamic responses to exogenous ET. Dogs were studied in the anesthetized state at 8-9 days after the TIVCC or sham operation. Baseline ET levels were significantly increased in the TIVCC dogs (n = 14) compared with sham operated dogs (n = 6; 41.4 +/- 7.1 vs. 17.9 +/- 1.5 pg/ml, respectively; P less than 0.05). With exogenous ET infusion (5 ng.kg-1.min-1), an intact systemic and renal vasoconstrictor response in the TIVCC dogs was observed. ANF prevented the systemic vascular and arterial pressure responses to ET. However, the potent renal vasoconstricting action of ET was not prevented by ANF. These studies suggest that ET may play an important role in maintaining blood pressure in the setting of low cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)
In an attempt to elucidate the effects of two major risk factors of heart failure in humans, high blood pressure and coronary artery disease, renal hypertension and coronary artery constriction were induced singularly and in combination in rats, and the functional, structural, and biochemical alterations of the myocardium were examined 12-13 wk later. Renal hypertension (RH), coronary narrowing (CN), and their association (NH) resulted in left ventricular failure demonstrated by a significant increase in left ventricular end-diastolic pressure, a decrease in +dP/dt and -dP/dt, and a reduction in stroke volume and cardiac output. Measurements of ventricular loading documented that RH was characterized by elevations in systolic and diastolic wall stress of 42 and 160%, respectively. Corresponding changes with NH were 80 and 315%. CN was accompanied by an augmentation of diastolic wall stress only (280%). The abnormalities in mural stress were coupled with reductions in systolic and diastolic wall thickness-to-chamber radius ratios of 39 and 29% after CN. These anatomic parameters were preserved with RH, whereas the systolic wall thickness-to-chamber radius ratio was reduced 31% with NH. Structurally, multiple foci of replacement fibrosis were found with each intervention. The sites of tissue injury and their volume percent in the myocardium were comparable with CN and RH but were significantly more numerous and occupied a larger fraction of the ventricular wall in the presence of NH. Biochemically, the calcium dose-response curve of myofibrillar Mg2+ adenosinetriphosphatase (ATPase) activity did not vary with CN, RH, and NH. In contrast, a marked decrease in Ca2+ myosin ATPase activity was found in NH rats in association with a shift in myosin isoenzymes from V1 to V3. In conclusion, multiple physiological, morphological, and biochemical factors may participate in the generation of the abnormalities in ventricular loading with hypertension and/or coronary artery stenosis.