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

Beta blockers are drugs of first choice for the treatment of essential hypertension today and may be combined with other antihypertensive drugs or diuretics. Use of highly selective beta-1 receptor-blocking agents without intrinsic sympathomimetic activity is particularly recommended for hypertensive patients after transmural myocardial infarction who suffer from exercise-dependent myocardial ischemia. Highly selective beta-1 receptor-blocking agents have only little influence on the lipid metabolism; however, if prescribed in diabetic patients treated with insulin, in patients with cardiac failure or in asthmatic patients, close supervision is mandatory.
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PMID:[Beta blockers in antihypertensive treatment]. 789 48

Significant advances are emerging in what concerns the newer inotropic agents. Despite the ideal agent, whose sole action is to increase the sensitivity of contractile proteins to calcium is yet to be found, the identification of specific receptors of dopamine in the CNS and peripheral circulation, had stimulated the pharmacological research of dopaminergic receptors agonists, selective for the subtypes DA1 and DA2, selective DA1 and DA2 antagonists and the dopamine beta-hidroxilase inhibitors and represent an unequivocal value. Beta-adrenergic agonists have been extensively evaluated as positive inotropic agents in the patients with congestive heart failure. Although norepinephrine, epinephrine and isoproterenol are potent stimulators of myocardial beta-adrenergic receptors, the clinical use of these agents has been limited by their positive chronotropic actions and their tendency to exacerbate cardiac arrhythmias (epinephrine and isoproterenol); their potent effects on vascular alpha 1-adrenergic receptors, which cause vasoconstriction (norepinephrine); and their effects on vascular beta 2 receptors, which cause vasodilation (isoproterenol). Dopamine, endogenous precursor of norepinephrine, is a sympathomimetic amine that has been widely used clinically as a cardiac stimulant. The effects of this drug are due to a combination of its actions on alpha, beta, and dopaminergic receptors, as well as a tyramine-like effect that causes the release of endogenous norepinephrine. Dopamine's positive inotropic effects are due principally to stimulation of cardiac beta-adrenergic receptors. At low doses it also stimulates renal dopaminergic receptors, thereby increasing renal cortical blood flow and promotion diuresis; higher doses causes stimulation of alpha 1-adrenergic receptors, resulting in increasing systemic arterial and venous pressures and, potentially, decrease renal blood flow. This vasoconstrictor action is frequently undesirable in patients with severe heart failure, and limits the drug's usefulness as a positive inotropic agent. Despite this risk, the use of synthetically derived catecholamines, i.e. dobutamine, has gained wide acceptance for the treatment of low output state associated with systemic hypotension. Despite the well reported down regulation of beta 1-adrenergic receptors in patients with chronic congestive heart failure, dobutamine consistently exerts hemodynamic benefits in this clinical situation. An attenuation of these benefits may be observed at times, although new tachyphylaxis very rarely occurs. Since dobutamine does not preferentially dilate the renal vasculature, concomitant administration of dopamine, at a dose which only stimulates the dopaminergic receptors in the renal artery, had the advantage of increasing renal perfusion and improving renal function. Administration of dopamine is often prolonged after that of dobutamine, and may help the wearing off of dobutamine.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[New inotropic agents in the treatment of congestive heart failure]. 790 58

Topically administered beta blockers are the preferred medical therapy for glaucoma. These agents reduce intraocular pressure (IOP), thereby preventing damage to the optic nerve and the subsequent loss of vision. Timolol, betaxolol, levobunolol, metipranolol, and carteolol are the topical beta blockers available in the U.S. They have similar IOP-lowering efficacy, but differ in other pharmacological properties. Topically administered beta blockers are generally well tolerated. They undergo systemic absorption, however, and can adversely affect cardiovascular and bronchopulmonary function in patients with existing diseases such as heart failure, sinus bradycardia, chronic obstructive airways disease, or asthma. Betaxolol, which is beta 1-selective, and carteolol, which has intrinsic sympathomimetic activity (ISA), may have systemic tolerability profiles superior to the traditional nonselective, non-ISA beta blockers. These hypotheses require confirmation in controlled clinical trials. Local adverse effects associated with beta blockers include stinging, burning, red eye, itching, tearing and loss of corneal sensitivity. Stinging upon instillation is a particularly frequent finding with betaxolol (up to 30% to 40% of patients). Preliminary evidence suggests that carteolol has the best local tolerability profile of these drugs.
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PMID:Topical ophthalmic beta blockers: a comparative review. 790 96

Although prevention of heart failure recently has become a realistic issue, management of heart failure once the syndrome has developed, is mainly supportive, based on the various cardiac and peripheral changes which occur in the course of heart failure. Of these, abnormal neurohormonal activation is of major pathophysiologic and prognostic significance. Consequently, modulation of neuroendocrine activation is now recognized a prime target in the treatment of heart failure, besides diuretic therapy. In this respect, the value of converting enzyme inhibition is well established. Future developments in this area include dopaminergic agents, vasopressin antagonists, angiotensin II receptor antagonists, renin inhibitors, spironolactone and, possibly, ANF peptidase inhibitors. Besides diuretics, necessary when signs of fluid retention are present, the approach to heart failure management involves other pharmacologic issues. In view of abnormal vascular control with vasoconstriction prevailing during progressive heart failure, it clearly makes sense to vasodilate. However, of available vasodilators, only the combination of relatively high dose nitrates and hydralazine has proven to be of clinical significance, in terms of hemodynamics, exercise capacity and survival. It is possible, though, that novel generation dihydropyridine derivatives may prove beneficial as well. Thus far, there has been much debate concerning the usefulness and particularly the safety of positive inotrope therapy and inodilator treatment. Taken together, this concern relates to presence and predominance of cAMP-dependent mechanisms to induce these effects. Thus, sympathomimetic agents and phosphodiesterase inhibitors, such as milrinone or enoximone, are without beneficial effects, but instead shorten survival during long-term therapy. This may be different where compounds which act through cAMP-independent mechanisms, i.e., calcium sensitization or sodium channel stimulation, are concerned, but needs to be confirmed yet.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Congestive heart failure. Drug therapy: central or peripheral approach? 791 52

Selective beta-sympathomimetic drugs are frequently used for tocolysis. But, since these drugs exhibit some beta-1 activity as well, they may bring about pulmonary edema, myocardial ischemia, cardiac arrhythmia and others as side effects. A 29 year-old female with a triplet pregnancy had premature contraction at 26 weeks of gestation. High doses of IV ritodrine were given for tocolysis for 8 weeks until caesarean section. One hour after caesarean section at 35 weeks of gestation, she complained of dyspnea. Urinary output decreased and chest X-ray showed pulmonary edema. She was intubated and artificial ventilation with PEEP was performed in ICU. Echocardiogram showed left ventricular dilatation. ECG showed inverted T waves on all leads. We diagnosed her as suffering from acute heart failure, pulmonary edema and acute renal failure. Hemodialysis was performed for 6 hrs but PCWP was still 18 mmHg. So CVVH was added to hemodialysis. Five hrs after the start of CVVH, her symptoms gradually started to subside. Total fluid removal was 5.8 l over 16 hrs. Three days after admission she was extubated and five days later returned to her ward. We concluded that pulmonary edema, heart failure and renal failure were induced by the long-term high dose medication of ritodrine, resulting in volume overload and myocardial dysfunction.
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PMID:[Ritodrine induced pulmonary edema after caesarean section for a triplet pregnancy]. 793 76

Effect of three-week treatment with visken on renal and central haemodynamics, renin-angiotensin-aldosterone system (RAAS) and metabolism of electrolytes was studied in 88 elderly and old patients 45 of whom had hypertonic disease (HD) in the second stage and 43 suffered from atherosclerotic (isolated systolic) hypertension (AH). Visken is a highly effective hypotensive beta-adrenoblocker with partially retained sympathomimetic activity. It may be administered as monotherapy to elderly patients with HD as well as to the old and elderly with SH regardless of initial state of systemic and renal haemodynamics. The drug makes blood pressure fall due to its diuretic effect and decrease of general peripheral vascular resistance. It improves renal blood circulation, reduces renal vascular resistance, enhances compromised glomerular filtration but exert no influence upon RAAS. Efficacy of visken diminishes with age. This phenomenon is conditioned by increased refractivity rate and more frequent adverse effects in the old with HD. Latent heart failure, disorders of cardiac rhythm and conductivity (even if mentioned in anamnesis) as well as hypokalemia are contraindications to visken.
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PMID:[The characteristics of using visken in middle-aged and elderly patients with arterial hypertension]. 803 Mar 4

In patients with Thalassaemia Major the iron overload with alteration both of systolic and diastolic properties of left and right ventricles finally leads to symptoms of cardiac failure and is the most frequent cause of death in these patients. In the majority of asymptomatic thalassemic patients with normal myocardial mass it is possible to demonstrate an alteration of the diastolic function both with echocardiographic study and with radionuclide angiography (subclinical cardiac disease). We have also demonstrated in "ex thalassemics" with stable and heavy iron overload in the subclinical cardiac disease phase a subnormal systolic function and a slight impairment of the contractility state. Therefore our purpose was to evaluate cardiac performance emphasising the contractility properties of the left ventricle during moderate inotropic stimulation with dobutamine in thalassemic patients in subclinical cardiac disease. We are now also using this test to evaluate cardiac performance in adults thalassemic patients as a screening for marrow transplantation procedure. Dobutamine is a sympathomimetic drug (beta 1 agonist) that increases myocardial contractility and at high doses also systolic arterial blood pressure and heart rate. The half-life is extremely short and at low doses the drug has no major side effects. Continuous intravenous dobutamine infusion is largely used in the therapeutic field to treat cardiac failure and it is reported to be a very efficacious and safe therapeutic agent. Recently dobutamine stress echocardiography was reported to be an accurate non-invasive diagnostic technique for detecting cardiac dysfunction in adults with coronary artery disease (Dobutamine is used for this purpose at high dose to increase the myocardial oxygen consumption).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiac study by dobutamine stress echocardiography in thalassemic patients. 837 53

beta-Adrenergic receptor agonist tocolysis has been reported to cause noncardiogenic pulmonary edema. We report an association between chronic terbutaline therapy and cardiomyopathy in peripartum women. Among 15 gravidas who had peripartum heart failure, 4 had received prolonged terbutaline tocolysis. Although those four patients had completely normalized ventricular function, only 7 of the 11 others recovered. We suggest that gravidas receiving long-term beta-sympathomimetic tocolysis undergo close evaluation of cardiac function.
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PMID:Peripartum heart failure associated with prolonged tocolytic therapy. 843 16

Beta blockers may benefit patients with dilated cardiomyopathy but low output failure can be a problem. Thus a beta 1-selective beta blocker with about 45% intrinsic sympathomimetic activity (ISA), such as xamoterol, was thought to have a desirable pharmacologic profile. Long-term studies of xamoterol in patients with idiopathic dilated cardiomyopathy have shown improved cardiac performance and exercise tolerance, while exercise heart rate, left ventricular ejection fraction, and pulmonary artery wedge pressure were decreased. This improvement in exercise capacity and overall quality of life in patients treated with xamoterol has been confirmed in further controlled trials of patients with mild-to-moderate heart failure (NYHA class I and II). However, in patients with moderate-to-severe heart failure (NYHA class III and IV), mortality was unfavorably influenced by xamoterol. The therapeutic role of xamoterol in patients with heart disease needs further refinement.
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PMID:The xamoterol experience in the treatment of heart failure. 846

To study the physiological effect of the overexpression of myocardial Gsalpha (protein levels increased by approximately threefold in transgenic mice), we examined the responsiveness to sympathomimetic amines by echocardiography (9 MHz) in five transgenic mice and five control mice (both 10.3 +/- 0.2 months old). Myocardial contractility in transgenic mice, as assessed by left ventricular (LV) fractional shortening (LVFS) and LV ejection fraction (LVEF) was not different from that of control mice at baseline (LVFS, 40 +/- 3% versus 36 +/- 2%; LVEF, 78 +/- 3% versus 74 +/- 3%). LVFS and LVEF values in transgenic mice during isoproterenol (ISO, 0.02 micrograms/kg per minute) infusion were higher than the values in control mice (LVFS, 68 +/- 4% versus 48 +/- 3%; LVEF, 96 +/- 1% versus 86 +/- 3%; P < .05). Norepinephrine (NE, 0.2 micrograms/kg per minute) infusion also increased LVFS and LVEF in transgenic mice more than in control mice (LVFS, 59 +/- 4% versus 47 +/- 3%; LVEF, 93 +/- 2% versus 85 +/- 3%; P < .05). Heart rates of transgenic mice were higher than those of control mice during ISO and NE infusion. In three transgenic mice with heart rates held constant, LV dP/dt rose by 33 +/- 2% with ISO (0.02 micrograms/kg per minute) and by only 13 +/- 2% in three wild-type control mice (P < .01). NE (0.1 micrograms/kg per minute) also induced a greater effect on LV dP/dt in the three transgenic mice with heart rates held constant compared with three wild-type control mice (65 +/ 8% versus 28 +/- 4%, P < .05). Pathological and histological analyses of older transgenic mouse hearts (16.0 +/- 0.8 months old) revealed hypertrophy, degeneration, atrophy of cells, and replacement fibrosis reflected by significant increases in collagen volume in the subendocardium (5.2 +/- 1.4% versus 1.2 +/- 0.3%, P < .05) and in the cross-sectional area of myocytes (298 +/- 29 versus 187 +/- 12 micron2, P < .05) compared with control mouse hearts. These results suggest that Gsalpha overexpression enhances the efficacy of the beta-adrenergic receptor-Gs-adenylyl cyclase signaling pathway. This in turn leads to augmented inotropic and chronotropic responses to endogenous sympathetic stimulation. This action over the life of the animal results in myocardial damage characterized by cellular degeneration, necrosis, and replacement fibrosis, with the remaining cells undergoing compensatory hypertrophy. As a model, this transgenic mouse offers new insights into the mechanisms of cardiomyopathy and heart failure and provides a new tool for their study.
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PMID:Adverse effects of chronic endogenous sympathetic drive induced by cardiac GS alpha overexpression. 863 8


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