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

Fifty-nine patients between the ages of 13 and 88 with sinus node disease, who received a permanent ventricular pacemaker between 1965 and 1976 at one institution, were followed to determine the natural history of the disorder after permanent pacing. Nineteen had ischemic heart disease, six had primary myocardial disease, and eight valvular heart disease. In 26, no etiology for the arrhythmia was apparent. The one- and five-year survival was 85.5% and 73.1%, respectively. Patients with underlying heart disease had a significantly poorer survival when compared to those without (58% versus 94% at 36 months) and all but 3 of 13 deaths in the first 36 months were in those with ischemic heart disease. There was a distinct trend toward poor survival in those with heart failure prior to pacemaker implant and those over age 65. Patients with sinus bradycardia alone did best (91% survival three years after implant), while those with bradycardia-tachycardia syndrome and those with sinoatrial arrest alone did distinctly worse (76% and 65% survival at three years, respectively). Twelve of 18 deaths were due to progression of underlying heart disease. The long-term prognosis with symptomatic sinus node disease can be predicted in part by (1) etiology of the underlying heart disease, (2) pre-implant arrhythmia, and (3) ventricular function prior to implant.
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PMID:Symptomatic sinus node disease: natural history after permanent ventricular pacing. 9 95

Alcoholic cardiomyopathy is a consequence of toxic effects of ethyl alcohol. Acute effects must be distinguished from chronic effects over many years. Chronic abuse of alcohol of 1.5-2 g ethyl alcohol per kg body weight (i.e. about 100-150 g/70 kg) per day for years can cause congestive cardiomyopathy in predisposed persons, usually between 30 and 50 years of age. The diagnosis is associated with some criteria for exclusion, i.e. coronary heart disease, hypertension, valvular heart disease, in addition all obstructive and restrictive cardiomyopathy must be excluded. On the other hand, a specific constellation of findings can be considered characteristic of alcoholic cardiomyopathy, namely the coincidence of a radiologically established cardiomegaly in the form of a congestive cardiomyopathy with a raised serum concentration of immunoglobulin A and a negative myocardial immunofluorescence test. Therapeutically, in addition to the classical principles of the treatment of heart failure, absolute abstention from alcohol and physical stress seemed to be effective.
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PMID:[Alcoholic Cardiomyopathy (author's transl)]. 13 Dec 48

The authors report 25 cases of patients, average age 67 years with severe coronary or valvular heart disease, with conduction disorders. The conduction disorder occurred alone in 8 cases and was associated with a disorder of excitability in 17 cases. It was either obvious, as in 14 cases, or latent, as in 11 cases, and precipitated by various forms of treatment, the disadvantage of which was the negative dromotrope effect. This treatment was prescribed for permanent resting angina (amiodarone and prenylamine), heart failure (digitoxin) or excitability disorder (beta-blockaders or procainamide). 11 patients had one or several fainting attacks. Permanent electro-systolic pacing with stimulation on demand, is necessary in all patients to palliate the consequences of treatment. In 11 cases out of 25, prior temporary pacing permitted the authors to assess the efficacy of treatment. The high post-operative mortality (40%) is not due to the apparatus but depends on the severity of the coronary heart disease or heart failure in these patients, In 60% of cases, the result of stimulation was excellent and was maintained permanently.
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PMID:[Indications for permanent electrosystolic pacing in arrhythmia revealed or aggravated by treatment]. 17 99

Immediate emergency surgery is the accepted treatment of intractable pulmonary edema due to valvular heart disease. The presence of severe tissue hypoxia, acidosis, low cardiac output state and renal insufficiency results in a high operative risk. Delay of operation by several hours may prove advantageous in that it permits improvements of the patient's condition by means of intermittent positive pressure respiration with correction of acidosis and at the same time allows for treatment of the cardiac failure. Three illustrative cases are presented, all successfully managed by preoperative treatment in an intensive care unit. The pathophysiological basis of this therapeutic approach is discussed.
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PMID:Preoperative intermittent positive pressure respiration as preparation for emergency valvular surgery for pulmonary edema. 34 Apr 19

The haemodynamic effects of intravenous mexiletine have been studied in 16 patients with valvular heart disease without clinical evidence of heart failure. A bolus injection of 150 mg administered to 6 of the 16 patients resulted in a mean plasma concentration above the therapeutic range for at least 5 minutes after the drug was given. A small but significant rise in the mean pulmonary artery pressure occurred. In 10 patients, the effects of intravenous mexiletine were compared with those of intravenous saline in a double blind trial. No significant difference was found in the haemodynamic effects, though both saline and mexiletine produced a small rise in the mean pulmonary artery pressure. Mexiletine when administered to patients without heart failure in doses known to be clinically effective did not have important adverse haemodynamic effects.
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PMID:Observations on haemodynamic effects of mexiletine. 37 46

Overt liver disease caused by left-sided heart failure is seldom recognized unless there is obvious hypotension. We now report 4 patients whose initial diagnosis was hepatitis but who were later shown to have central hepatic necrosis associated with left ventricular failure. Signs of right-sided heart failure were absent. Hepatitis was initially suspected in 3 patients because of striking transaminase elevations and in 1 patient because of jaundice and symptoms compatible with hepatitis. Liver biopsies performed on all patients revealed central hepatic necrosis without evidence of acute or chronic hepatitis. Left ventricular failure was documented in all 4 patients. One patient had coronary artery disease, and the other three patients had valvular heart disease. Liver function tests became normal or improved in all cases as the underlying heart disease was treated. We believe that liver dysfunction secondary to left ventricular failure is not uncommon and can be seen in the absence of right-sided heart failure or hypotension.
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PMID:Left-sided heart failure presenting as hepatitis. 63 89

The present work was undertaken in order to study the role of monoamine oxidase (MAO) enzyme in the genesis of altered cardiac noradrenalin level in the human heart in various underlying pathologic conditions. The histochemical localization and the activity of MAO were studied in the right atrial appendage of man in ischemic heart disease, in valvular heart disease without or with congestive myocardial failure, and in hearts with an uncomplicated atrial septal defect. MAO was found to be localized mainly extraneuronally in the muscle cells, a little activity was detected in the connective tissue spaces, and nerves reacting positively were tentatively identified. There were no significant differences in MAO activity measured photometrically between the various heart disease groups. It seems that MAO activity measured photometrically between the various heart disease groups. It seems that MAO enzyme plays only a small or no role in the genesis of the latered noradrenalin level in the human heart observed in ischemic heart disease or congestive cardiac failure.
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PMID:Histochemically demonstrable monoamine oxidase activity in the adult human heart in various cardiac diseases. 82 12

Sixteen cases of chronic Q fever are described. In eight there was a history of exposure to infection from farms or farm products. All had valvular heart disease, involving the mitral valve in nine and the aortic valve in seven. Infection occurred on a prosthetic valve in two patients. Arterial embolism was common. Venous thrombosis occured in three patients, and pulmonary embolism occurred in three other patients. Complement fixing antibodies to phase 1 antigen were found in a titre of 1:200 or greater in all except two patients. In one of these post-mortem examination revealed rickettsial bodies in mitral valve vegetations, and in the other Coxiella burneti was isolated from heart valve tissue. The majority presented with infective endocarditis but two presented primarily with liver disease. All patients had evidence of liver involvement and in one this led to death from cirrhosis. Abnormal tests of liver function, particularly hyperglobulinaemia, raised alkaline phsophatase and abnormal bromsulphthalein retention were found in all patients. Hepatic histology was abnormal in all eight patients in whom it was studied. The commonest features were mononuclear cell infiltration of the portal tracts and prominence of the sinusoidal Kupffer cells. Patchy focal necrosis of parenchymal cells, granulomata, fatty change, and eosinophilia of the sinusoidal walls were also noted in several patients and cirrhosis developed in one. Six patients had a purpuric rash, and in 12 there was thrombocytopenia. It is suggested that the presence of hepatomegaly and liver involvement and thrombocytopenia may help to differentiate Q fever endocarditis from bacterial endocarditis. Raised serum IgM and IgA levels occured frequently, but with only a moderate dominance of IgM. Sheep cell agglutination and latex fixation tests for rheumatoid factor were occasionally positive. Several features of the disease suggest the possibility that immune-complex mechanisms may play a role in chronic Q fever. Treatment was with prolonged courses of tetracycline usually combined with lincomycin. Seven patients underwent valve replacement surgery for haemodynamic reasons. Five patients died; two from heart failure, one from cirrhosis, one seven days after valve replacement and one from intraperitoneal haemorrhage following percutaneous liver biopsy. Three patients have survived for more than five years, and another six for more than three and a half years after diagnosis. Of these nine patients, three received medical therapy alone and six required valve replacement as well. Antibiotics have been discontinued in four patients who have had valve surgery and three others. Six patients had received antibiotics for continuous periods varying from 29-62 months. In the period after stopping therapy varying from 15-21 months, no relapse has occured. A seventh patient, who had received antibiotics for four months prior to valve replacement, has survived 43 months after the withdrawal of antibiotics...
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PMID:Chronic Q fever. 94 Sep 18

The authors report a case of syncopal ventricular tachycardia in a patient with a respiratory-dependent rate responsive pacemaker, followed-up for valvular heart disease with severe left ventricular dysfunction and sustained atrial and ventricular arrhythmias. The introduction of low dose betablocker therapy with reinforcement of the treatment of cardiac failure controlled the ventricular arrhythmia, after suppression of the data responsive function had been shown to be ineffective. The authors discuss the role of the rate responsive function in the triggering of the ventricular tachycardias.
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PMID:[Ventricular tachycardia in a patient with rate-responsive cardiac pacemaker]. 130 Sep 59

Patients with different heart diseases, dilated cardiomyopathy, valvular heart disease, hypertension, ischemic heart disease or myocarditis showed manifestations of autoimmunity and down-regulation of beta-adrenergic receptors. Autoantibodies against beta-adrenergic receptors in these patients were detected with radioligand binding inhibition assay. The results suggested that the down-regulation of cardiac beta-adrenergic receptors in these patients may be mediated by autoimmunity. Autoantibodies against beta-adrenergic receptor were not related to any specific heart diseases, but to the severity of heart failure irrespective of its etiology. The significance of these autoantibodies in heart failure was discussed.
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PMID:[Circulating autoantibodies against beta-adrenergic receptors in patients with heart diseases]. 133 2


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