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

Measurement of vascular compliance has assumed increasing importance as a marker of early disease of the vascular wall, a predictor of future vascular disease, and a way to monitor the effects of vasoactive agents on arterial wall stiffness. Vascular compliance can be estimated by several methods: measurement of the pulse pressure, or pulse pressure-stroke volume ratio; analysis of the systolic pulse wave augmentation index and the diastolic pulse wave contour; ultrasonic echo-tracking; and MRI. Because few comparative studies have been done, the physiologic significance of the measures of compliance obtained by each method is uncertain. Antihypertensive drugs may improve vascular compliance by reducing blood pressure, relaxing vascular smooth muscle, or promoting long-term effects on vascular smooth muscle and cardiomyocyte growth and remodeling. Angiotensin converting enzyme (ACE) inhibitors have been reported to improve vascular compliance in nearly all studies, suggesting a beneficial class effect independent of blood pressure reduction. Favorable changes in the vascular wall-lumen ratio of small vessels from subcutaneous gluteal biopsy specimens after treatment with ACE inhibitors and the persistence of improved vascular compliance after withdrawal of therapy indicate that these agents may produce long-term vascular remodeling. Although few studies have been done, angiotensin II receptor antagonists improve vascular compliance, possibly by blocking angiotensin II-mediated cell proliferation and increasing apoptosis via unopposed AT1 receptor stimulation. In contrast, calcium antagonists and beta-blockers have variable effects on vascular compliance, although beta-blockers with intrinsic sympathomimetic activity improve vascular compliance. Diuretics have little effect on vascular compliance beyond their blood pressure-lowering actions, except for spironolactone, which by improving vascular compliance may have contributed to the reduction in heart failure mortality seen in the Randomized Aldactone Evaluation Study.
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PMID:The effect of antihypertensive drugs on vascular compliance. 1147 12

Congenital heart block (CHB) can result in intrauterine cardiac failure leading to fetal or neonatal loss. To establish perinatal hemodynamic factors which might predict adverse outcome, six fetuses with CHB diagnosed between 20 and 30 gestational weeks were examined by echocardiography at 2-week intervals. Neonatal morbidity and outcome in infancy are detailed. The fetuses showed a significant decrease in ventricular rate (VR) with advancing gestation (60 +/- 7 vs 51 +/- 4 beats/min, p = 0.03). Cardiac decompensation defined as hydrops or pericardial effusion was associated with VR of lower than 55 beats/min in two fetuses. Three mothers had a therapeutic trial with a sympathomimetic and digoxin. Salbutamol increased VR 10% in one of three fetuses treated. Digoxin decreased pericardial effusion in one hydropic fetus with autoimmune myocarditis. In this fetus, poor left ventricular fractional shortening (LVFS) was accompanied with high umbilical artery resistance index (RI). High amniotic fluid erythropoietin indicated severe hypoxia preceding death. Pacemaker was indicated in all the newborns. At the age of 2 weeks all the surviving infants had tricuspid regurgitation and a shunt through foramen ovale due to asynchronized atrioventricular contraction. During the 12-month follow-up two of five surviving infants had no symptoms. One had symptomatic neonatal lupus. Two infants had patent ductus arteriosus, one with dilated cardiomyopathy. In conclusion, poor fetal outcome was associated with low VR, low LVFS, and high RI. Despite early pacing, morbidity was high in infancy due to cardiomyopathy and associated heart defects. Regular echocardiographic monitoring during pregnancy and after delivery is required in order to optimize care and timing of any interventions.
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PMID:Congenital complete heart block in the fetus: hemodynamic features, antenatal treatment, and outcome in six cases. 1152 12

There are important pharmacodynamic differences between the various beta-adrenoceptor-blocking drugs, whereas the angiotensin-converting enzyme (ACE) inhibitors differ mainly in their pharmacokinetic properties. The differing properties of the beta-blocking drugs may contribute to their antihypertensive effect; possibly, the beta1-selective agents are slightly more effective. Comparisons between groups of drugs may not be fully applicable to all members of the group. Overall, however, beta-blocking drugs and ACE inhibitors appear to control the resting blood pressure to a similar degree, whereas on exercise the rise in blood pressure is inhibited to a greater extent by beta1-blockade. ACE inhibitors reverse the hemodynamic changes of hypertension in contrast to beta1-blocking drugs without intrinsic sympathomimetic activity (ISA). Neither group of drugs interferes with cardiovascular reflexes such as the response to posture. The beta-blocking drugs have specific contraindications such as asthma and heart failure. Although some earlier studies suggested otherwise, more recent smaller investigations suggest that overall patient acceptability of ACE inhibitors and beta-blockers is similar. In certain instances, particularly in the presence of diuretics, a large first-dose effect with a profound fall in blood pressure may be seen with ACE inhibitors. In contrast to other drugs, there is some evidence that beta-blocking drugs have a cardioprotective effect. ACE inhibitors and beta-blocking drugs have a similar spectrum of activity, with black patients responding less well. Although in dispute, drugs are often useful in the elderly. Both groups possess additional therapeutic indications that may influence the choice to treat hypertension.
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PMID:Comparison of beta-blockade and ACE inhibitors in the treatment of hypertension. 1152 41

We report a case of fetal congenital heart block treated with maternal administration of beta-sympathomimetics. The case was diagnosed as fetal complete heart block associated with maternal anti-Ro/SS-A antibody at 22 weeks of gestation. By fetal sonography, the ventricular rate was revealed to be 60 beats/min and mild cardiomegaly was shown. We initiated maternal administration of a sympathomimetic, specifically terbutaline, to prevent fetal heart failure. An increase in the fetal ventricular rate and an improvement in cardiac function were both achieved during the treatment. A viable infant was delivered by an elective cesarean section without complications at term. Maternal administration of the beta-adrenergic agent terbutaline is suggested to be effective for improving fetal congenital heart block in order to prevent heart failure in utero.
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PMID:Treatment of fetal congenital complete heart block with maternal administration of beta-sympathomimetics (terbutaline): a case report. 1158 45

In congestive heart failure patients, treatment with beta-adrenoceptor antagonists improves symptoms and decreases mortality. However, intrinsic sympathomimetic activity of beta-adrenoceptor antagonists might be disadvantageous in chronic heart failure. The nonselective beta1- and beta2-adrenoceptor antagonist bucindolol has failed to decrease mortality in clinical trials. A putative beta4-adrenoceptor, which mediates positive inotropic effects by activation of the adenylate cyclase has been described. Recently, this putative beta4-adrenoceptor has been identified to be a propranolol-insensitive state of the beta1-adrenoceptor. The present study aimed to characterize whether bucindolol exhibits agonistic activity on this atypical beta1-adrenoceptor state as one possible reason for clinical inefficiency. For comparison (S)-4-(3'-t-butylamino-1'-hydroxypropoxy)-benzimidozole-2 (CGP 12177), metoprolol, and nebivolol were investigated. Bucindolol did not reveal intrinsic sympathomimetic activity in electrically driven (1 Hz, 37 degrees C), forskolin-stimulated, left ventricular papillary muscle strips (donor hearts, nonfailing; n = 5) and in right auricular trabeculae (bypass operation; n = 4). Functional studies on the propranolol-insensitive state of beta1-adrenoceptors were performed in isolated muscle preparations after beta1- and beta2-adrenoceptor antagonism (propranolol, 1 microM), inhibition of beta3-mediated inotropic effects (N-nitro-L-arginine, 100 microM) and forskolin treatment (0.3 microM). Positive inotropic response to stimulation of atypical state beta1-adrenoceptors could be demonstrated in right auricular as well as left ventricular human myocardium (CGP 12177 treatment, 10 microM). Under these conditions, also bucindolol, but not metoprolol and nebivolol, significantly increased contractility (all 10 microM). In conclusion, bucindolol but not metoprolol or nebivolol mediate positive inotropic effects in human myocardium due to activation of atypical state beta1-adrenoceptors. Thus, the agonistic activity of bucindolol may influence outcome in heart failure patients.
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PMID:Bucindolol exerts agonistic activity on the propranolol-insensitive state of beta1-adrenoceptors in human myocardium. 1186 83

beta-Blockers have regained interest in the treatment of cardiovascular diseases after a period of decreasing importance due to the introduction of other cardiovascular treatment principles. beta-blockers expose the longest list of indications in cardiovascular therapy available and present positive mortality results for the treatment of arterial hypertension, the postinfarction situation and heart failure. There are three indications for the treatment of atrial fibrillation alone: slowing of AV-conductance, sinus rhythm restoration and atrial stabilization. Among the most recent developments there is the clear establishment of evidence for their life prolonging activity in heart failure treatment which has been proven for carvedilol, bisoprolol and metoprolol in NYHA (New York Heart Association) stages 2 and 3 and so far for carvedilol only in NYHA stage 4. Differences between beta-blocking agents are clinically most relevant for the presence of an intrinsic sympathomimetic activity (ISA) which should no longer be present in clinically used compounds. The ISA of bucindolol is the most likely reason for its failure in an outcome study for heart failure treatment. Other pharmacological distinctions relate to the selectivity in the beta-adrenergic system, activity in the alpha-adrenergic system and differences in metabolism and elimination.
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PMID:[Comparison beta-blockers and their relevance to pharmacologic therapy of cardiovascular diseases]. 1187 2

Clinical trials have shown that beta-blockers can produce symptomatic improvement and decrease the risk of death in chronic heart failure patients. However, the side effects of beta-blockers including worsening heart failure, AV-block, contracting peripheral vessels and unfavorable effects on glucose and cholesterol metabolism tend to make physicians hesitate to prescribe beta-blockers for elderly patients. Carvedilol is a novel non-selective beta-blocker without intrinsic sympathomimetic activity (ISA) and has vasodilating effect through blocking alpha 1 receptor. We examined the effects of carvedilol on cardiac parameters in order to clarify whether beta-blocker may affect left ventricular function in elderly Japanese patients with hypertension, angina pectoris, or both. We examined the hemodynamic effect of carvedilol in 16 patients with hypertension, angina patients or both, aged 65 and over (75.5 +/- 5.6 y.o.). After 12 weeks treatment with 10-20 mg daily oral administration, echocardiography was performed and hemodynamic parameters were calculated to evaluate their cardiac functions. Blood pressure was significantly decreased, especially in systolic pressure (163.8/87.6 +/- 15.6/11.2 mmHg to 141.6/76.9 +/- 16.6/11.7 mmHg, p < 0.001/p < 0.01, respectively). Ejection fraction increase (65.8 +/- 11.8% to 71.2 +/- 11.4%, p < 0.05) accompanied heart rate decrease (72.0 +/- 16.1 bpm to 63.9 +/- 11.4 bpm, p < 0.05). Carvedilol increased ejection fraction and decreased blood pressure safely in elderly patients with hypertension, angina pectoris, or both. Taking the condition of each patient into consideration, alpha-beta-blocker can be beneficial in elder patients.
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PMID:[Effects of carvedilol on the hemodynamics and its tolerance in elderly patients]. 1197 43

Nonglycosidic inotropic agents have been used for the short-term management of low output states and hypotension complicating acute myocardial infarction for several years. Without adequate reperfusion of the ischemic myocardium, inotropic agents are seldom effective in producing sustained hemodynamic responses. Furthermore, the potential exists for enhancement of ischemia and extension of myocardial necrosis. Thus, inotropic and vasopressors therapy should be regarded as temporary supportive treatment in patients with acute coronary syndrome and should be discontinued as soon as feasible. Parenteral sympathomimetic agents, usually dobutamine, and phosphodiesterase inhibitors, usually milrinone, are used for the management of exacerbations of chronic systolic heart failure. Although hemodynamics, and occasionally clinical status, improve, such therapy is associated with increased mortality and can potentially hasten a patient's demise. Nonparenteral sympathomimetics, such as ibopamine, phosphodiesterase-III inhibitors, such as milrinone and enoximone, calcium-sensitizing agents, such as pimobendan, and other novel inotropic agents, such as vesnarinone, all increase mortality of patients with chronic heart failure. Furthermore, newer noninotropic agents, such as B-natriuretic peptide, have been introduced for treatment of decompensated heart failure. New nonpharmacologic devices, such as biventricular pacing, are available for the treatment of advanced heart failure. Thus, indications for the use of presently available nonglycosidic inotropic agents are limited and should be considered only for short-term therapy or when no other treatment is available.
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PMID:Role of nonglycosidic inotropic agents: indications, ethics, and limitations. 1269 31

In 16 dog heart-lung preparations modified to permit a more accurate measurement of coronary flow, adrenaline or noradrenaline was infused at a rate of 4 mug. base/min. After a 30-min. pause during which the increased oxygen consumption and heart rate, but not the coronary flow, returned to pre-infusion levels, the other sympathomimetic amine was infused for the same length of time. It was found that, mole per mole, noradrenaline is as effective, and probably more so, than adrenaline in raising the oxygen consumption of the heart-lung preparation. The positive chronotropic and coronary dilating action of both amines appear to be equal. It was observed that in any one experiment the second dose of the sympathomimetic amine was slightly more effective than the first dose in raising the oxygen consumption. The level of high-energy phosphorus compounds does not change after adrenaline or noradrenaline administration even at the time when the oxygen consumption rises to as much as 200%. During this period there are no signs of cardiac hypoxia, as can be judged by the good oxygen saturation of coronary venous blood. Single doses of 5 mug. adrenaline or noradrenaline have a consistent positive inotropic effect that lasts about 15 min. when tested on a failing heart. In 12 experiments on non-failing modified heart-lung preparations, a single dose of 5 mug. adrenaline fails to cause a measurable increase in oxygen consumption after 1, 3, 6, or 11 min. in spite of a mild positive chronotropic action. The significance of these findings is discussed and the suggestion made that, when noradrenaline infusions are effective in treating cardiogenic shock in man, part of this effect may be due to its positive inotropic action, thus correcting an element of heart failure that might exist.
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PMID:The effect of adrenaline and noradrenaline on the metabolism and performance of the isolated dog heart. 1369 21

The principal drugs implicated in or disclosing cardiac insufficiency are drawn from a review of the literature and observations by the French national pharmacovigilance database, from 1984 to April 2003. Several pharmacological classes are identified: in addition to antimitotic drugs, such as anthracyclines, many drugs are implicated in cardiac insufficiency, e.g. immunomodulators, anti-inflammatory drugs (including coxibs), antiarrhythmic drugs, anaesthetic drugs, antipsychotic drugs, and antidiabetic drugs (including glitazones). It is usual to classify these drugs according to three categories: (i) drugs likely to cause cardiac insufficiency de novo (such as cyclophosphamide, paclitaxel, mitoxantrone, interferons, interleukin-2 etc.); (ii) drugs likely to worsen preexisting cardiac insufficiency (such as antiarrhythmics, beta-blockers, calcium antagonists, nonsteroidal and steroidal anti-inflammatory drugs, sympathomimetic drugs etc.); and (iii) drugs only occasionally causing cardiac insufficiency. This review shows that this classification is, in fact, artificial. If cardiac toxicity is a constant concern when using antimitotic drugs or some immunomodulator drugs, it is advisable to exercise caution in the use of many other drugs when treating patients with cardiac insufficiency, even if the clinical situation is well controlled. In particular, drug-drug interactions and patient medical history must be taken into account.
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PMID:[Drug-induced heart failure (excluding that caused by anthracyclines)]. 1519 79


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