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Query: UMLS:C0018801 (heart failure)
72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

For reasons unknown, metastatic squamous-cell carcinoma is a rare cause of pleural effusions and is even less common in pericardial effusions. A review of all pericardial effusions examined in the Cytology Service at Montefiore Medical Center over a 15-year (1980-1994) period was undertaken (N = 251). Four cases with metastatic squamous-cell carcinoma were identified among 39 malignant effusions. Two patients with metastatic squamous-cell carcinoma presented with cardiac tamponade, and the other two cases had progressive cardiac failure. The diagnostic cells on cytology evaluation were scant in all four cases but exhibited classical features of metastatic squamous carcinoma, such as cytoplasmic keratinization, intercellular bridges, and occasional "pearl" formation. Pericardial biopsies available in three patients, two with cardiac failure and one with cardiac tamponade, were negative. In all four cases the primary tumor was a bronchogenic carcinoma. Metastatic squamous-cell carcinoma is an uncommon cause of pericardial effusion and usually indicates the presence of a bronchogenic carcinoma with a rapidly fatal outcome. Cytologic examination of pericardial fluid is essential in the evaluation of such patients.
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PMID:Metastatic squamous-cell carcinoma in pericardial effusion: report of four cases, two with cardiac tamponade. 962 14

A 45-year-old man with dry cough and dyspnea was referred by a medical practitioner for evaluation of heart failure on February 10, 1996. Chest X-ray revealed increased cardiothoracic ratio, and ultrasonographic echocardiography disclosed massive pericardial effusion with right ventricular collapse. Cardiac tamponade was diagnosed and pericardiocentesis was performed. Ten days after admission, the pleural effusion had become more pronounced, and thoracocentesis was performed. Carcinoembryonic antigen level was elevated in both the pericardial and pleural effusion, and cytology implicated adenocarcinoma, which suggested malignant effusion. Endoscopic study disclosed gastric cancer in the posterior wall of the upper body, and the histopathological diagnosis was signet-ring cell carcinoma. The patient died of respiratory failure on May 2, 1996, and autopsy was performed. The final diagnosis was gastric cancer with pulmonary lymphangitis, pericarditis, and pleuritis carcinomatosa, accompanied by enlargement of mediastinal and paraaortic lymph nodes. Interestingly, the primary signet-ring cell carcinoma of the stomach was situated mostly in the mucosa. Deep in the submucosal region, there was prominent invasion of the intralymphatic vessels, without direct destruction of the mucosa muscularis.
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PMID:Cardiac tamponade originating from primary gastric signet ring cell carcinoma. 1962 74

A six-year-old male crossbred dog was presented with clinical signs of right-sided heart failure. Echocardiography demonstrated a pericardial effusion with cardiac tamponade, while pericardiocentesis and cytology did not reveal any evidence of malignancy. Pericardial drainage was performed twice over a period of three months to resolve haemodynamic impairment before a subtotal pericardiectomy was performed. Biopsy of parietal and visceral pericardium confirmed the diagnosis of pericardial mesothelioma. Intrathoracic cisplatin combined with intravenous doxorubicin were administered, although neutropenia, mild azotaemia and alopecia were noted as adverse reactions to these drugs. Intravenous cisplatin was repeated 45 days later after the signs of nephrotoxicity had resolved. The dog was still free of disease after 27 months. Intrathoracic chemotherapy after pericardiectomy and early diagnosis are recommended to improve prognosis, having achieved long-term survival in the present case.
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PMID:Pericardial mesothelioma in a dog: long-term survival after pericardiectomy in combination with chemotherapy. 1047 26

Purulent pericarditis is rapidly fatal if untreated [1,2]. With increased development of bacterial resistance to antibiotics, severe bacterial infections in children are becoming more frequent [3,4]. We report two children with purulent pericarditis who presented in a 1-month period for evaluation of acute abdominal distention and signs of sepsis. In both, one evaluated with computed tomography (CT) and one with ultrasound, abdominal findings included periportal edema, gallbladder wall thickening, and ascites secondary to right heart failure from cardiac tamponade. Radiologists should be aware that children with purulent pericarditis may have a normal heart size on radiographs, present with acute abdominal symptoms, and demonstrate findings of right sided heart failure on abdominal imaging.
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PMID:Purulent pericarditis presenting as acute abdomen in children: abdominal imaging findings. 1054 98

Free wall rupture of the heart is the most common cause of death following pump failure. The incidence of death is 10-16% of all deaths because of acute myocardial infarction (AMI). In respect of time between the onset of AMI to Cardiac Rupture (CR), early (80%) and late CR are distinguished. Other clinical classification distinguishes acute and subacute CR. CR is considered subacute if the time between the onset of typical symptoms of CR and irreversible shock is longer as 30 min. There are three problems to solve: 1) selection of patient particularly threatened with CR, 2) defining the prodroms of CR and early diagnosis, 3) advancing the methods of surgical treatment. CR occurs more often in women, hypertensive patients and patient > 60 years old sustaining the first infarction. Thrombolytic agents diminish overall mortality in AMI, but do not influence frequency of CR. There are three mechanisms of CR incidence: 1) blood effusion into the ischemic zone resulting in the loss of tissue strength, 2) influence of thrombolytic therapy on degradation and inhibition collagen synthesis, 3) absorption of collagen by lymphocyte infiltration in infarction zone. Cardiac insufficiency with cardiogenic shock and rapid increase of pericardial effusion in echo examination and electro-mechanical discordance are considered to be clinical signs of CR and tamponade. CRP is an independent marker of subacute CR. Surgical treatment is possible only in case of subacute CR. Pericardiocentesis and bloodletting could temporary diminish cardiac tamponade and allow transfer to the operating room.
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PMID:[Cardiac rupture in acute myocardial infarction]. 1071 Sep 44

A 15-year-old man with end-stage heart failure due to dilated cardiomyopathy, underwent heart transplantation. In the second postoperative week, while being treated with monoclonal antibodies (OKT3), cyclosporine and azathioprine, he developed a postpericardiotomy syndrome and cardiac tamponade, which necessitated emergency pericardiocentesis. Corticosteroids, administered according to the immunosuppression protocol, resulted in the prompt subsidence of the syndrome. This is the first report of a large pericardial effusion and cardiac tamponade due to a postpericardiotomy syndrome in an adult cardiac recipient.
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PMID:Postpericardiotomy syndrome during intensive immunosuppression after cardiac transplantation. 1077 53

A 65-year-old woman was admitted to hospital because of orthopnea. She had been followed-up for chronic pericardial effusion detected by echocardiography 10 years previously. Initial echocardiography showed that the left ventricular diastolic diameter (LVDd) was 39 mm and percent fractional shortening (%FS) was 33.3%. Neither fluid samples nor a pericardial biopsy specimen identified the etiology. Cardiac tamponade was not evident, and C-reactive protein and creatine-kinase values were within normal limits. During follow-up, the %FS decreased gradually, but the LVDd remained unchanged. On admission, echocardiography showed that the %FS was 12.5% and LVDd was 40 mm. She developed intractable hyponatremic heart failure with bilateral pleural effusion. Autopsy findings revealed that infiltration of small lymphocytes in the epicardium had penetrated into the subepicardial myocardium. The subepicardial myocardium and the interventricular septal myocardium were diffusely replaced by fibrosis, which could have induced restrictive diastolic heart failure and reduced left ventricular contractility. The fibrosis was not detected in the epicardium itself nor the subendocardial myocardium. This is the first report describing diffuse subepicardial myocardial fibrosis in a patient with chronic pericardial effusion and progressive heart failure.
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PMID:Slowly progressive heart failure due to subepicardial myocardial fibrosis in a patient with chronic pericardial effusion. 1095 64

The treatment of sarcoid cardiomyopathy can be considered in part the treatment of the systemic disorder, and in part cardiac involvement, the manifestations of which may differ greatly. Therapy for the systemic disease is corticosteroid. Therapy for cardiac involvement includes prednisone, but because treatment must ameliorate or abolish many differing manifestations, therapy differs among patients. Asymptomatic patients (the majority) who are free from serious manifestations of the disease do not require pharmacologic or interventional treatment. Patients with dilated cardiomyopathy require treatment for congestive heart failure. High-grade atrioventricular conduction delay usually necessitates a permanent electronic pacemaker. Life-threatening arrhythmia usually requires implantation of an automatic implantable cardiac defibrillator (AICD). Antiarrhythmic drugs may also be needed. Cardiac tamponade should be treated by drainage of pericardial fluid. Pericardiectomy is usually the appropriate treatment for patients who develop significant constrictive pericarditis. Calcium channel blockers may be helpful for severe diastolic dysfunction that occurs in those with restrictive cardiomyopathy. Therapy should be given to those few patients who manifest hypertrophic cardiomyopathy to relieve left ventricular outflow obstruction. Cardiac transplantation for intractable heart failure or arrhythmia may be needed.
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PMID:Sarcoidosis and the Heart. 1109 43

Every acute dissection involving the ascending aorta (Stanford type A) must undergo emergency surgical repair. However, the surgical techniques must vary according to the clinical presentation of the patients or the anatomical patterns observed. Furthermore, surgery is generally difficult because of the poor condition of the aortic tissues. To reduce those difficulties many technical artifacts have been described. In 1977, we proposed the use of gelatin-resorcin-formalin (GRF) biological glue to reinforce the suture areas. From January 1977 to July 1999, 212 patients (pts) (152 males and 60 females) aged from 15 to 80 years (mean age: 54 +/- 11 years) underwent an emergency operation for type A aortic dissection. One-hundred-seventy-eight pts (84%) were operated on within 4 hours after being referred to the hospital. Twenty-eight pts (13.2%) had Marfan's syndrome. In 44 patients (20.7%), the aortic valve was replaced either independently (6 cases--2.8%) or by means of a composite graft (38 cases--17.9%). Because of the location of the intimal tear, the aortic replacement was extended to the transverse arch in 61 pts (28.7%). Hospital mortality amounts to 21.6% (46 pts), 25% in pts with arch replacement and 19.4% in pts without arch replacement (n.s). Analysis of hospital mortality demonstrates that the main causes of death were cardiac tamponade, neurologic disorders and visceral malperfusion. One-hundred-sixty-six pts were discharged and surveyed from 5 months to 22 years postoperatively (mean follow-up: 85 +/- 66 months). During this period of time, 25 pts (15%) had to be reoperated for a total of 33 reoperations. Seven pts (28%) died at reoperation. Using univariate analysis, the presence of Marfan's syndrome (p < 0.05) and absence of arch replacement (p < 0.02) were determinant risk factors for reoperation. Emergency (p < 0.01) and thoraco-abdominal replacement (p < 0.04) were determinant riskfactors for death at reoperation. The freedom from reoperation (Kaplan-Meier, CI: 95%) is 96% (90-98), 87% (79-92), 80% (70-88), 66% (51-78) at 1, 5, 10 and 15 years respectively. A total of 39 pts (24.3%) died during follow-up. The presence of Marfan's syndrome (p < 0.01), reoperation (p < 0.02), stroke (p < 0.05), and cardiac failure (p < 0.05) were determinant risk factors of late mortality. The late survival rate (K-M. C.I.: 95%), including hospital mortality, is 71% (64-77), 66% (58-73), 56% (47-64), 46% (36-56), 37% (28-44) at 1, 10, 15 and 20 years, respectively. From our experience extending over more than 23 years, GRF glue has proved to be extremely useful, making the procedure much easier and safer. Nevertheless, many factors are of importance in the pre-, intra- and postoperative management of the patients. Cardiac tamponade and visceral malperfusion must be properly diagnosed and treated. During aortic repair, the main intimal tear must be resected. The transverse arch must be checked and replaced whenever necessary. The aortic valve should be preserved whenever possible. During CPB, perfusing the aorta in the regular antegrade manner seems to dramatically reduce the rate of malperfusion. The quality of the first emergency operation seems to have a major influence on the late results, especially concerning the rate of late reoperations and aortic ruptures. However, those late results depend also on the patient's basic condition, particularly in Marfan patients.
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PMID:Surgery of acute type A dissection: what have we learned during the past 25 years? 1109 59

A three-year-old, female guinea pig (Cavia porcellus) presented for acute dyspnea and weakness. Radiographs and echocardiography were consistent with a diagnosis of pericardial effusion and heart failure secondary to cardiac tamponade. Ultrasound-guided pericardiocentesis was performed, and clinical signs rapidly improved. Serial echocardiography and radiographs demonstrated normalization of cardiac function over the subsequent six months.
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PMID:Pericardial effusion and pericardiocentesis in a guinea pig (Cavia porcellus). 1120 73


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