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

A case study in which propranolol hydrochloride was used as adjunct therapy in the treatment of atrial fibrillation with rapid ventricular response, thyrotoxicosis and high output heart failure is presented to illustrate the pharmacokinetics of this drug. The relationship of propranolol dosage to blood levels, the effect of blood levels on pharmacological response, the metabolism and elimination of propranolol, and determination of rational dosage of the drug, are discussed.
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PMID:Pharmacokinetics in drug therapy. I: Propranolol hydrochloride as adjunct therapy in the treatment of thyrotoxicosis. 5 90

The purpose of the work was to study some problems relating to the pathogenesis of cardiac insufficiency in patients with thyrotoxicosis. To do this a total of 108 patients suffering from thyrotoxicosis with varying degree of severity and aged from 17 to 59 were examined. In addition to the general clinical examination vectoro-, poly- and mechanocardiography was employed. The resulting findings ascertained two possible ways for the development of cardiac insufficiency in patients under consideration. One of them is cardiac hyperfunction that comes to the forefront. In this case the myocardial changes are of a stage-wise nature. The myocardial contractility at the onset of the affection is up, a slight hypertrophy is developing, chiefly, of the outflow passages. As the disease progresses further hypertrophy gains in intensity and dilation of the heart comes in as an intercurrent factor. At this time the contractile function of the myocardium is still unaffected and the patients are at a stage of compensation. With progressing dystrophy and wearing away of the myocardium its contractility is declining and signs of cardiac incompetence appear. Such a development is characteristic of patients with severe course of thyrotoxicosis, long-standing disease and frequent relapses. Of the other way is typical cardiac hyperfunction of low intensity. To the forefront come dystrophic alterations in the myocardium unaccompanied by hypertrophy, and in this case cardiac insufficiency is of latent nature. Such alterations are seen to occur with a milder course of thyrotoxicosis, with the disease of short duration. Dynamic observations bear proof to a reversible nature of hypertrophy and dystrophy of the myocardium.
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PMID:[Pathogenesis of cardiac insufficiency in thyrotoxicosis]. 13 9

In 70 patients with thyrotoxicosis and in 24--with ischemic heart disease with energy-dynamic cardiac insufficiency a study was made of electrolyte metabolism in the blood plasma, erythrocytes and 24-hour urine. The sodium and potassium content in erythrocytes rose, and sodium gradient diminished in the patients examined, this being related to the development of energy-dynamic cardiac insufficiency.
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PMID:[Electrolyte metabolism in thyrotoxicosis with energy-dynamic cardiac insufficiency]. 52 44

Congestive heart failure in neonatal thyrotoxicosis is attributed to sympathetic overstimulation of the myocardium with resulting high-output cardiac failure. An additional case of neonatal thyrotoxicosis with congestive heart failure is discussed; three possible causes (thyrotoxicosis, maternal propranolol therapy, and ventricular septal defect) were present. Along with the usual procedures, the echocardiogram is of value in separating these factors. In addition, we discuss the potential dangers to the newborn of a mother receiving long-term propranolol hydrochloride therapy during pregnancy.
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PMID:Neonatal hyperthyroidism and heart failure. A differential approach. 57 68

A series of 51 cases of thyrotoxicosis gathered during a period of 6 years in a department with a cardiological orientation is analysed. This peculiar form of thyrotoxicosis is often unrecognized in view of its frequent occurence in aged subjects (which is misdiagnosed as "senile heart") and of the incidence in its causality of a toxic adenoma, the endocrine semiology of which is often reduced. In front of any case of heart failure of unknown cause, one should systematically think of a thyroid aetiology. A persistent sinus rhythm is not enough to discard it. A low cholesterol rate should induce to continue the investigation. The subnormal character of the classical laboratory parameters (including the thyroid hormone assay) does not always make it possible to exclude definitely the diagnosis. When the clinical picture is suggestive, only the radio-isotope examination with dynamic tests is liable to provide decisive data.
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PMID:[Clinical considerations apropos of 51 cases of cardiothyrotoxicosis]. 81 8

Haemodynamic studies were performed in 10 patients with uncomplicated thyrotoxicosis and seven with thyrotoxic cardiac failure. The cardiac output of those with uncomplicated hyperthyroidism was higher than normal at rest. After 2 mg of intravenous propranolol there was a 13% fall but the level was still higher than normal. In patients with thyrotoxic cardiac failure the resting cardiac output was normal, but it fell after propranolol by 30% to subnormal levels. In both groups there was an increase in right heart pressures and fall in the rate of increase in arterial pressure, which indicated a decrease in myocardial contractility. These results indicate that increased autonomic activity is a compensatory phenomenon in hyperthyroid heart failure and that its abolition by beta-blocking drugs has a deleterious effect on cardiac function. They are therefore contraindicated in patients with thyrotoxic heart failure.
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PMID:Haemodynamic effects of beta-adrenergic blockade in hyperthyroid patients with and without heart failure. 87 33

All patients with unstable angina should be admitted to a coronary or an intensive care unit. There should be an attempt to classify the patient according to the proposed Braunwald nomenclature. If the patient has a secondary cause for unstable angina (e.g., tachyarrhythmia, heart failure, fever, thyrotoxicosis, severe hypertension, hypoxia, unusual emotional stress, or anemia), this condition should be treated initially with therapy specific for that etiology. If the patient does not have a secondary etiology, therapy should be initiated with nitrates, preferably intravenous nitroglycerin. Heparin should be concomitantly administered. If the patient cannot receive heparin, aspirin should be initiated. All patients should receive beta-blockers. If the patient cannot take a beta-blocker, a calcium antagonist (probably diltiazem) should be initiated. However, if the patient is refractory to beta-blockers, the dihydropyridine nifedipine should be added. Failure to all pharmacologic interventions necessitates a progressive invasive approach dictated by the potential surgical risk of the patient. Long-term aspirin and beta-blockers should be strongly considered.
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PMID:Pharmacotherapy of unstable angina. 158 55

The frequency, clinical characteristics, and outcome of patients admitted with heart failure to a district general hospital in North-West London serving a population of approximately 155,000 was assessed over a six-month period. The number of patients with heart failure was determined by both a prospective ward survey and a retrospective study of all patient records with diagnostic codes for heart failure or pulmonary oedema. During those six months, 2,877 patients were admitted to the medical and geriatric services of whom 140 (4.9%) had heart failure. Only 29 patients in heart failure were under the age of 65 years. In 86 patients the mode of presentation was acute pulmonary oedema. Fifty-two (37%) patients had an arrhythmia at the time of admission of whom 48 had atrial fibrillation. An electrocardiogram, a chest X-ray, and an echocardiogram were performed in 137, 136, and 81 patients respectively. The aetiology of heart failure was considered to be coronary artery disease (41%), valve disease (9%), hypertension (6%), cor pulmonale (4%), a dilated cardiomyopathy (1%), congenital heart disease (1%), thyrotoxicosis (1%), and unknown (36%). During the period of hospital stay 42 patients (30%) died; a further 20 patients (14%) died in a one-year follow-up. In a district general hospital heart failure is a common reason for admission and patients remain in hospital for a considerable time. Arrhythmias are commonly associated with heart failure. The prognosis is poor and the hospital mortality high. The management of heart failure is an important consideration in allocating hospital resources in a district general hospital.
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PMID:Heart failure in a district general hospital. 842 54

Six hundred and forty-nine patients with proven chronic atrial fibrillation were followed for a total of 1,436 patient-years without anticoagulation. The patient were divided into 7 disease groups with each having an average age ranging from 39 to 69 years. Eleven per cent of the patients had systemic embolism prior to being registered for the follow-up. The diseases which had the highest incidence of embolism prior to being followed were the same as those producing the highest rate of systemic embolism while under observation. The disease groups were rheumatic valvular (predominantly mitral stenosis) and ischemic heart diseases. Their embolic rate were 3.9 to 5.1 emboli per 100 pt-yr. Other disease groups with lower embolic rates of 0 to 0.9 per 100 pt-yr were heart failure, non-rheumatic mitral regurgitation, atrial septal defect and thyrotoxicosis. Since the incidence of systemic embolism varied according to the primary disease, and since the hemorrhagic complication of anticoagulant therapy is finite, it is advised that low risk group may not benefit greatly from anticoagulation. However, the true low risk group has still to be properly determined.
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PMID:Embolism and atrial fibrillation. A longitudinal follow-up. 164 52

In the present study: (a) physiopathology, (b) clinics, and (c) therapy of cardiothyreosis are discussed. (a) The hyperkinetic syndrome, the earliest clinical sign in thyrotoxicosis (vasodilatation, increase in inotropism, automatism, etc.), is mediated by a two-fold increase in the number of beta-receptors, and supported by an adequate synthesis of ATP and creatinphosphate (CP) in the young and, to a lesser extent, in the elderly. Genetical heart reserves are mobilized, thus significantly increasing the number and the size of mitochondria and also the enzymatic equipment (such as: the alpha-glycerophosphate-dehydrogenase, malic, pentosic cycles, etc.), a.s.o. Due to an excessive adrenergic action (glycogenolysis, an excessive oxygen consumption, up to necrosis, the ATP and CP syntheses dramatically drop; the phosphorus/oxygen ratio decreases to 2 (normal = 4). In this condition, the high functional cardiovascular performances are also impaired (the submaximal effort capacity is attained at a smaller and smaller oxygen consumption; Propranolol 2 mg i.v. decreased the cardiac output by above 30% (vs 10%--normal); electrocardiogram presents aspects of "coronary disease", tachycardia, etc.). An ultrastructural damage occurs: from "mitochondrial disease", partial lysis of myofibrils, to myofibrosis (revealed postmortem), in spite of a reduced degree of coronary atherosclerosis. Ultrastructural and biochemical experimental data support this point of view. (b) The incidence, precocity and severity of the thyrotoxic heart increase with age and the existence of a previous cardiovascular pathology. Cardiothyreosis is not present under 27 years; in 4,353 patients its incidence is of 25% (arrhythmia--21%, heart failure--12%, coronary insufficiency--1-3%). Of a major interest are tachyarrhythmias which may lead to a high mortality by hypodiastolic congestive heart failure, heart failure with secondary hyperaldosteronism, thromboembolic episodes and ventricular fibrillation. Thyrotoxicosis favours the disease of papillary muscles--mitral prolapse and insufficiency, reversible especially in children. (c) The treatment of thyrotoxic heart is an etiologic one (medical, surgical, radioactive--the last two being preferable after the adequate medical therapy). In particular, cardiothyreosis requires a reinforced irradiation (10,000 rads instead of 7,000 rads) in smaller 131I doses. The protection against the increased nocivity of catechols in thyrotoxicosis is very important (which explains the high mortality in the thyrotoxic "storm") and requires propranolol; doses above 2 mg/kilo body/day are recommended. In the elderly, the sensitivity to propranolol decreases: verapamil i.v. is more efficient in paroxysmal tachyarrhythmias (flutter, atrial fibrillation) and in those occurring intra-operatively during halothane narcosis. The anticoagulant therapy is administered in tachyarrhythmias with high ventricular rate, especially in the elderly, to avoid the embolic risk, higher in defibrillation condition.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cardiothyreosis. 182 Oct 70


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