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

The causes of heart failure may be classified into three groups, hemodynamic causes, disturbances of cardiac rhythm and conduction and diseases of the myocardium. Accordingly the different causes of heart failure are discussed and the technics for diagnosis reviewed. Particular diagnostic problems are mentioned, which may arise in connection with cardiac echinococcosis, atrial myxoma, sarcoid heart disease and myocardial aneurysm.
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PMID:[The differential diagnosis of heart failure (author's transl)]. 36 78

The authors report an unusual case of chronic sarcoidosis with skin ulcerations and atrophic lesions simulating Pick-Herxheimer's disease. Other severe manifestations are found: cardiac involvement with conduction disturbances and myocardial failure, and muscular involvement which responded well to corticosteroid therapy.
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PMID:[Sarcoidosis with extensive ulcerating and atrophying cutaneous manifestations (of the Pick-Herxheimer type) and with cardiac and muscular involvement. About one case (author's transl)]. 61 47

A patient who presented with recurrent arrhythmias, including refractory ventricular tachycardia, and heart failure, was later found to have sarcoidosis with pulmonary and lymph node involvement.
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PMID:Systemic sarcoidosis with refractory ventricular tachycardia and heart failure. 68 94

Cardiac involvement by systemic sarcoidosis is well known, but occurs rarely. It usually manifests as either heart block, heart failure due to direct myocardial involvement, or cor pulmonale. We present the case of a patient with cardiac sarcoidosis who had ventricular tachycardia and congestive heart failure. Although there was other organ system involvement, the cardiac manifestation was the first to become clinically apparent. Therapy consisted of quinidine sulfate to control the arrhythmias and chronic diuretic therapy to control congestive heart failure. Steroid therapy was initially associated with recurrence of the ventricular tachycardia and was discontinued. It was reinstituted 18 months later when other organ system involvement developed with no recurrence of the ventricular tachyarrhythmia. The patient responded well to therapy and is currently doing well. This case is presented to illustrate a somewhat unusual, but nevertheless important, etiology of ventricular tachyarrhythmias. The recognition of underlying sarcoidosis is critical because of the propensity for other organ system involvement by this disease process.
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PMID:Ventricular tachyarrhythmia due to cardiac sarcoidosis in a child. 70 4

Although sarcoid may involve the myocardium, there is little information on its incidence or significance. We studied 84 consecutive autopsied patients with sarcoidosis. The patients ranged in age from 18--80 years (average 46 years) and 61% were women; 23 (27%) of them had myocardial granulomas. In eight (35%) these were clinically silent, and in 15 (65%) there was a history of heart failure and/or arrhythmias and conduction defects. Of the 23 patients, only four (17%) had grossly evident, widespread myocardial lesions: three of these four (75%) had documented arrhythmias. All four had sudden, unexpected death at an average age of 36 years; in only two had sarcoid been suspected during life. The other 19 patients (83%) had microscopically evident granulomatous involvement. Of these, eight (42%) had a thythm or conduction disturbance and three (16%) sudden death, although none of those who suffered sudden death had a recognized rhythm or conduction disturbance. Nine (15%) of those without cardiac sarcoidosis had a rhythm or conduction disturbance and eight (13%) suffered a sudden death. The results show that although myocardial involvement occurs in at least 25% of patients with sarcoid, it most often involves a small portion of myocardium and is clinically silent. Since some of the 61 patients in whom myocardial lesions were not identified may still have had small microscopic granulomas, the true incidence of myocardial sarcoid may be even greater than suggested here. Rhythm and conduction disturbances are more common in the cardiac sarcoid group, but the findings suggest that only the small subset of patients with severe, grossly evident myocardial sarcoid are at increased risk for sudden death.
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PMID:Cardiac sarcoid: a clinicopathologic study of 84 unselected patients with systemic sarcoidosis. 70 77

This study is to calculate a risk of lung cancer in a cohort of 1411 sarcoidosis cases which were followed for a 3 year period from 1984 to 1987. The physicians were requested to answer the questionnaire about progress of the disease by mail. Excess death was investigated using standardized mortality ratio (SMR). The expected number of deaths was calculated from Japanese sex-age specific mortality rate in 1985, using person-year method. Death from all causes and cancers did not show any excess. SMR being 0.98 and 0.97 respectively. The SMR of lung cancer was 3.26 (male: 5.56, female: 3.03), being statistically significant. The SMR of lung infection was 4.2, with statistical significance. The SMR of other main causes of death in Japan i.e., cerebrovascular accident, ischemic heart diseases and heart failure was less than 0.88. It is probably that sarcoidosis is a risk factor of lung cancer. The SMR of leukemia and uterine cancer was 5.88 and 8.70, respectively, though the observed number of leukemia was too small to conclude how high the cancer risk is among sarcoidosis patients. Gastric cancer, hepatic cancer and colon cancers were not observed.
Sarcoidosis 1991 Mar
PMID:Excess death of lung cancer among sarcoidosis patients. 166 41

Over the last 10 years, our knowledge of immunologically mediated processes involving the myocardium appears to have made quantum leaps. New and important disease entities such as AIDS have appeared and the cardiologist now becomes an important member of the "AIDS team." Our understanding of "older diseases" such as sarcoidosis, Lyme disease, systemic lupus and other connective tissue syndromes has significantly increased. The concept of high-dose steroid therapy for these processes may, in fact, turn out to be futile and more selective, as less dangerous immunosuppression is being introduced. This concept has significantly advanced in the field of cardiac transplantation where immunosuppression has now been usurped by specific immunotherapy aimed at selective aspects of the immune sequence. New and exciting concepts will emerge from the molecular biology laboratory that will have direct bearing on the management of patients with cardiovascular disorders. This information explosion will force the cardiovascular physician to become more in tune with the world of immunology and molecular biology. Many obvious, significant problems remain, such as accelerated atherosclerosis in the transplant patient and the role of myocarditis in the patient with heart failure. However, it will truly be an exciting decade in which to work and watch the unraveling of these mysteries and hopefully, the study of today's problems will give way to solutions and a clearer understanding of the heart as a target of immune injury.
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PMID:The heart as a target organ of immune injury. 191 12

A patient presented with severe heart failure due to myocardial sarcoidosis. Sarcoidosis was diagnosed by biopsy of the skin and uptake of gallium-67 in the heart. We treated the patient with corticosteroids and succeeded in improving her condition. We assume that this was a rare case in which severe heart failure improved following with steroid therapy.
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PMID:Improvement of severe heart failure with corticosteroid therapy in a patient with myocardial sarcoidosis. 204 45

We reported 4 cases diagnosed as myocardial sarcoidosis. One of them was diagnosed by endomyocardial biopsy, however, the others were diagnosed by cardiological findings and biopsy of the scalene node, liver or skin. Analysis of ECG findings showed conduction disturbances in all cases and disorders of impulse formation in two. Thallium 201 myocardial perfusion scans (T1 scan) revealed inferior and anteroseptal wall defects in case 4 and entire heterogenous defect in case 2. And also in case 2, left ventricular perfusion defect detected in T1 scan before steroid therapy changed to entire heterogenous defect. Thus, T1 scan was thought to be useful for the evaluation of therapy and for follow up study of myocardial sarcoidosis. In the cardiac echogram, thickening of the wall was seen in cases 3 and 4, and dilated ventricle in another case. Steroid was given in all cases and a pacemaker was implanted in two cases. The therapy was effective in all cases and ECG abnormalities were improved. In one case (Case 3) treated by a pacemaker steroid administration was halted and subsequently developed heart failure, but the other (Case 1) continued treatment with steroid caused return to a natural beat. Thus steroid therapy with a pacemaker implantation was considered to be effective for severe myocardial sarcoidosis.
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PMID:[Four cases of myocardial sarcoidosis]. 261 91

Although, the diagnosis of myocardial sarcoidosis is difficult to establish clinically, the heart may be involved at autopsy in upto a third of cases of sarcoidosis. Cardiac sarcoidosis may remain occult, may present with arrhythmia, or may even cause sudden death. In order to avoid a diagnostic oversight, sarcoid heart disease should be considered in any patient with unexplained heart block, cardiac arrhythmia, or heart failure.
Sarcoidosis 1989 Sep
PMID:Myocardial sarcoidosis: a review. 269 Feb 42


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