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

Clonidine, propranolol, bethanidine and debrisoquine effectively decrease blood pressure by suppressing renin secretion or interfering with function of the sympathetic nervous system. In man these compounds exert an antihypertensive effect within several hours or days and their duration of action is sufficient to permit administration twice or thrice daily. Clonidine and propranolol are especially useful if sexual dysfunction or postural hypotension is undesirable. Although bethanidine and debrisoquine may produce these adverse effects, they are beneficial in severe hypertension and produce fewer side effects than guanethidine. Clonidine frequently causes sedation, and rebound hypertension may occur with sudden cessation of therapy. Injudicious use of propranolol may provoke heart failure or asthma in susceptible individuals. The combination of a thiazide diuretic with propranolol and one of hydralazine, bethanidine and debrisoquine may be used to treat severe or complicated hypertension.
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PMID:New drugs in hypertension. 34 94

The use of beta-adrenergic blocking drugs in angina pectoris was one of the original indications for these drugs suggested by Black. An anti-anginal effect was demonstrated with the first beta-adrenergic blocking drug, pronethalol, that was used clinically. This benefit in angina was confirmed in the early trials with propranolol in 1964-65. Although some definite anti-anginal effect can be demonstrated with low fixed dosage, evidence suggested that those trials which used a higher and a variable dose displayed a greater anti-anginal action of the drug. After a two dose trial (Gillam and Prichard, 1966,) demonstrated a dose dependent anti-anginal effect, a log-dose response study demonstrated a progressive reduction in angina attacks as dosage was increased (Prichard and Gillam, 1971). While a highly significant effect was found with an average dose of 52 mg a day a progressive reduction in angina attacks was found with logarithmic increases in dosage up to an average of 417 mg a day. Dosage in this trial was adjusted to produce a supine heart rate of 55-60 beats/minute provided this was not prevented by side effects. As the dosage of 417 mg a day was still on the straight line part of the dose response curve and therefore suboptimal, we not adjust dosage to produce a standing heart rate of 55-60. Fully meaningful comparative trials require that optimum dose of the drugs being compared are used. A variable dose comparative trial comparing propranolol and practolol, showed propranolol was the more effective agent. More recently a variable dose comparative trial of sotalol and propranolol indicated propranolol had greater anti-anginal action although sotalol, unlike practolol, was more effective than low dose propranolol. The use of beta-blocking agents in angina pectoris is relatively safe provided that the contraindications of asthma and cardiac insufficiency are observed and that treatment is commenced at a low dosage. The most dramatic change in the sympathetic environment of the heart takes place when treatment with a beta-blocking drug is commenced. The greatest danger of precipitating heart failure is therefore at the beginning of treatment even with a small starting dose. Once treatment has begun even an increase of 25% per dose represents a small pharmacological increment as there is no great change in the sympathetic drive to the heart. The larger dosage of beta-blocking drugs required for optimum treatment of angina may be gradually approached, but it has been my experience that heart failure is not likely to be precipitated at larger doses, provided they are not used initially. In other than mild angina pectoris the average optimum dosage of propranolol is 500-800 mg a day, similar, or perhaps more than the average dose in hypertension.
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PMID:Propranolol in the treatment of angina: a review. 78 54

Sixty-three patients with stable, severe typical angina pectoris (New York Heart Association functional class III or IV) were treated with propranolol and studied prospectively with a follow-up period of 5 to 8 years to assess the rate of complications and long-term effectiveness after an initial control period. The patients' mean age was 56 years; the mean daily dose of propranolol was 255 mg. The average yearly mortality rate was 3.8 percent with a cumulative 5 year mortality rate of 19 percent. Patients whose reduction of angina with propranolol was less than 50 percent had a nearly four-fold greater mortality rate than those whose reduction was 50 percent or more (P less than 0.01). Thirty-two percent of patients per year were angina-free with propranolol and 84 percent per year had 50 percent or more reduction in anginal episodes. There was no evidence for tachyphylaxis. Heart failure developed in 25 percent of patients, two thirds of whom had either congestive heart failure with an acute infarction or a prior history of congestive heart failure. All patients whose initial cardiothoracic ratio was greater than 0.5 had heart failure during the first 3 years of propranolol therapy. Of 12 patients who had an acute infarction during therapy, 7 died, 6 with cardiogenic shock; in contrast, 8 of 9 patients who had congestive heart failure without acute infarction survived. Eight percent of patients had other significant side effects, including gastrointestinal symptoms (three patients), hallucinations (one) and postural hypotension (one). The occurrence of asthma in three patients was dose-related and did not require drug discontinuation. Propanolol is an effective form of long-term therapy for severe angina pectoris; it does not induce tachyphylaxis or increase the overall mortality rate, although it may increase the risk of cardiogenic shock in acute myocardial infarction. Previous history of congestive heart failure, a cardiothoracic ratio of more than 0.5 without overt heart failure and mild asthma are relative contraindications. A 50 percent or greater reduction in anginal pain with propranolol predicts a low mortality group.
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PMID:Long-term propranolol therapy for angina pectoris. 81 88

Use of beta-adrenoceptor agonists in long-term treatment of patients with chronic asthma bronchiale or heart failure is of limited value because beta-adrenoceptor desensitization develops. The antiallergic drug ketotifen prevents beta-adrenoceptor agonist-induced desensitization of rat and human pulmonary and lymphocyte beta 2-adrenoceptors. In 10 healthy volunteers in a double-blind, placebo-controlled study, we investigated whether ketotifen also prevents beta-adrenoceptor agonist-induced desensitization of beta 1- and/or beta 2-adrenoceptor-mediated physiologic in vivo effects. beta 1-Adrenoceptor-mediated effects were isoprenaline (ISO) infusion-induced increase in systolic blood pressure (SBP) and bicycle exercise-induced increase in heart rate (HR); beta 2-adrenoceptor-mediated effects were ISO infusion-induced increase in plasma norepinephrine (NE) and decrease in diastolic blood pressure (DBP); ISO infusion-induced increase in HR was assessed as mixed beta 1- and beta 2-adrenoceptor-mediated effect. These parameters were assessed before and after a 14-day treatment with the beta 2-adrenoceptor agonist terbutaline (5 mg three times daily) with or without simultaneous administration of ketotifen (1 mg twice daily). Terbutaline desensitized all in vivo effects involving beta 2-adrenoceptors (ISO-induced decrease in DBP and increase in plasma NE and, to a minor extent, the mixed beta 1- and beta 2-adrenoceptor-mediated increase in HR), but did not affect beta 1-adrenoceptor-mediated in vivo effects; concomitant treatment of the volunteers with ketotifen markedly blunted terbutaline-induced desensitization of beta 2-adrenoceptor in vivo function. We conclude that ketotifen prevents, or at least attenuates, beta-adrenoceptor agonist-induced desensitization of beta 2-adrenoceptor in vivo function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Terbutaline-induced desensitization of beta 2-adrenoceptor in vivo function in humans: attenuation by ketotifen. 127 89

The past decade has seen a shift in the strategy for hypertension treatment from stepped therapy--a highly structured monolithic series of steps--to recommendations for a more individualized selection of treatment. Severe hypertension is a clear indicator to bypass traditional steps. Demographic factors, such as age, gender, and race, are often cited, but have proved to be less helpful. Concomitant medical conditions and problems are very common and are more often the crucial determinants in the selection of antihypertensive therapy. Coronary artery disease, diabetes mellitus, heart failure, azotemia, asthma, and chronic obstructive pulmonary artery disease, anxiety, and depression are all common, and each has implications for the selection of antihypertensive therapy. Blood pressure reduction is a surrogate for reduction of cardiovascular risk, and therefore, consideration of concomitant medical problems has extended to left ventricular hypertrophy, obesity, mild hyperlipidemia, and insulin resistance, as additional risk factors in hypertension. Consideration of all these factors makes it possible to individualize antihypertensive therapy in most patients today.
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PMID:Treatment of hypertension: the place of angiotensin-converting enzyme inhibitors in the nineties. 128 28

One hundred patients, admitted to the Emergency Unit for paroxysmal supraventricular tachycardia (SVT) with 1:1 AV conduction, atrial fibrillation (af) and flutter (AF) of recent onset (less than 72 hours) were treated with intravenous propafenone (P). The drug was administered at the dose of 70 mg over 5 min, repeated after 10 min if sinus rhythm (SR) was not restored and eventually followed by continuous infusion (0.35-0.50 mg/min) until conversion to SR or during the next 48 hours. Exclusion criteria were ventricular rate < 100/min, R-R intervals > 1 s, clinical signs of heart failure or asthma. Termination of SVT within 30 min was obtained in 94% of the patients, while reversion to SR occurred in 79% with af and in 55% with AF. For af and AF conversion was achieved within 30 min in 49% of overall responders (R), between 30 min and 6 hours in 27% and between 6 hours and 48 hours in 24%. The efficacy of P was significantly influenced by the duration of arrhythmia and left atrial size, measured by 2D-echocardiography. On the contrary, no difference was observed between R and non-R in mean age and in the percentage of primary or relapsing arrhythmias. Adverse effects were encountered in 7 patients: in 1 case worsened arrhythmia and in 6 patients, with long-lasting arrhythmias, congestive heart failure. Neither conduction disturbance nor extra-cardiac complications occurred. In conclusion, P provides effective and safe treatment for paroxysmal atrial tachyarrhythmias, so that it can be considered among the drugs of first choice even in non-intensive care units.
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PMID:[The emergency treatment of supraventricular tachyarrhythmias: the efficacy and safety of intravenous propafenone]. 129 66

Components of the intracellular mediators system: calmodulin in leukocytes, Ca2+ and cyclic nucleotides in leukocytes and blood plasma were studied in children with attack of bronchial asthma and heart failure. Alterations in content of these biologically active substances correlated with clinical manifestations of bronchial asthma: severity of the disease, duration of the attack, contractile activity of myocardium. Calmodulin, Ca2+ and cyclic nucleotides were demonstrated to be involved in development of the asthmatic attack. Alterations in the system calmodulin-Ca2+ were related to adaptation and contributed to realization of regulating effects responsible for a decrease of impairments in tissues.
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PMID:[The intracellular second messenger system and its regulatory effects in children with a bronchial asthma attack complicated by heart failure]. 132 49

The various antihypertensive agents reduce blood pressure by different mechanisms. Alpha-1 receptor blockers reduce vascular resistance and maintain cardiac output. Chronic treatment with beta blockers without intrinsic sympathomimetic activity produces a fall in blood pressure which is associated with a fall in cardiac index and heart rate. Beta blockers with strong intrinsic sympathomimetic activity showed reduced heart rate during exercise. Labetalol reduces cardiac output and peripheral vascular resistance with little or no reduction in peripheral blood flow. Alpha-1 blockers are suitable for patients with active life-styles, with peripheral vascular disorders, or with high blood-cholesterol levels. Beta blockers are useful in patients who have tachycardia, palpitation problems, or angina pectoris, or who have survived a heart attack. They should not be used in patients with bronchial asthma, reduced peripheral blood flow, or heart failure. Labetalol reduces blood pressure in a somewhat larger fraction of patients than the pure alpha- or beta-blocking agents. It is hoped that its long-term results will include regression of cardiovascular damage, improved quality of life, and increased life expectancy.
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PMID:The hemodynamic effects of adrenergic blocking agents. 135 Feb 35

A survey by parent questionnaire and interview was carried out to determine the frequency of health problems in 204 children with Down syndrome. Seventy-two children (35.3%) had a congenital heart defect. Refraction had been performed on 196 and 68 (34.6%) of these had a refractive error. A diagnosis of 'glue ear' had been made in 112 (54.9%) and in 12 (11%) of these permanent hearing loss was present. Significant ill-health over the previous 12 months consisted of cardiac failure (two children), more than three upper respiratory tract infections (24 children), bronchitis (eight children), pneumonia (two children) and asthma (seven children). A neck X-ray had been performed in 172 (84.3%) and had demonstrated the presence of atlanto-axial instability in 12 (7%) of these. One hundred and thirty-two (64.7%) of the children had been tested for hypothyroidism in the previous 18 months and this had been found in four (3%) of these children. The implications of these and other findings are discussed in relation to parental counselling and planning of routine health checks.
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PMID:Health problems and health checks in school-aged children with Down syndrome. 138 51

Asthma bronchiale (a.b.) is defined as paroxysmal or permanent, partly or completely reversible dyspnoea due to a bronchospasm resulting from pathological hyperreactivity of the bronchial system. In the pathogenesis participate allergic, immuno-infiltrative and genetic factors, irritating substances (environment) and infectious. The allergic constituent acts via sensitization and allergization of the mast cell, to its degranulation with release of mediators (histamine, serotonin, leukotrienes, thromboxane, PAF) with subsequent bronchoconstriction and production of viscous mucus. As to adrenergic factors, a block of beta-adrenergic receptors and reduced adrenal function is involved. As to non-adrenergic factors an increased sensitivity of the parasympathetic--vagus is involved which conditions bronchoconstriction and hyperkrinia. From the clinical aspect extrinsic (atopic) and intrinsic (cryptogenic) asthma bronchiale can be differentiated. The former is encountered more frequently in childhood and adolescence, in subjects with a positive family-history, high IgE and positive skin tests and a known allergen. The latter type of a.b. is found in adolescence, in subjects with a negative family-history, with eosinophilia; it is conditioned by infection (e.g. chronic bronchitis), strain, cold and takes a dangerous course (aspirin). As to the course, attacks of a.b. are involved with a symptom-free interval (extrinsic a.) easily controlled by treatment. Then there is the chronic form with a variable course and the necessity of permanent treatment. Status asthmaticus is in recent years with increasing frequency the cause of death and thus calls for maximal treatment. It is the third most serious form of a.b. Assessment of arterial blood gases is very important as a check of treatment as well as from the prognostic aspect (cross-over intubation). From the differential diagnostic aspect we must consider the asthmoid component in chronic bronchitis, pulmonary embolism, left-sided cardiac failure, tracheal or bronchial compression by an aortal aneurysm, tumour. The differential diagnosis is not always easy.
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PMID:[Bronchial asthma. Pathogenesis and clinical aspects]. 145 62


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