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

Nine days following ingestion of 5 to 10 gm of thallium nitrate, a young man died with severe cranial and peripheral neuropathy, anuria, and heart failure. Ultrastructural examination of nerves obtained on days 7 and 9 demonstrated axonal degeneration with secondary myelin loss. Axons were swollen and contained distended mitochondria and vacuoles. Thallium levels in more than twenty organs and body fluids ranged from below 1.0 to 178 microgram/gm; concentrations in twenty areas of the nervous system ranged from 29 to 140 microgram/gm. The highest brain levels of thallium were found in gray matter. In the thalamus, 87% of the thallium was present in cell sap. Tissue concentrations of thallium did not parallel those reported for potassium, suggesting that thallium distribution differs from potassium distribution in human beings.
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PMID:Acute thallium poisoning: toxicological and morphological studies of the nervous system. 727 Dec 31

Oral pentaerythritol tetranitrate produces sustained beneficial hemodynamic effects in patients with cardiac failure of varied etiology. The principle action is a reduction of elevated left ventricular filling pressure. In a small group of angina patients, the oral nitrate in high dosage resulted in considerable increase in angina-limited exercise capacity compared to placebo for four hours following drug administration. No side effects were associated with ingestion of pentaerythritol tetranitrate in these investigations.
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PMID:Effects of oral pentaerythritol tetranitrate in cardiac failure and angina pectoris. Assessment by hemodynamic measurement and exercise capacity. 742 33

In addition to well-established roles in the management of stable angina, unstable angina and heart failure, nitrates are widely used in the management of acute infarction and the subacute period of recovery after infarction. A meta-analysis suggested that intravenous nitrate therapy in acute infarction reduced mortality by 35%. Subsequently, two recently reported 'mega' trials, GISSI-3 and ISIS-4, addressed the role of nitrates during and after infarction. The results of the mega trials have failed to substantiate a statistically significant benefit for nitrates. The contrast between the promising results of the meta-analysis and the disappointing results of the mega trials raises a number of issues considered in this paper. The role of nitrates in acute myocardial infarction remains unclear. The mega trials do offer some suggestive evidence of an early benefit of nitrate therapy. If any benefit does exist, it must be much smaller than the 35% reduction in mortality suggested by the meta-analysis. Further trials are required to assess the possibility of an early acute benefit. Any benefits will probably apply only to subgroups of infarcts.
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PMID:Nitrates in myocardial infarction: a current perspective. 772 51

The increased incidence and prevalence of congestive heart failure place a high priority on novel treatment strategies. Left ventricular ejection fraction remains the single most valuable measurement providing both diagnostic and prognostic insights. The most systematic approach to heart failure involves an objective assessment of functional disability, to include exercise tests such as a 6-minute walk under standardized conditions. Left ventricular dysfunction incites a host of neurohumoral compensations that are of fundamental importance in the heart failure syndrome expression. Both vasoconstrictor and vasodilator neurohormones are stimulated and provide new therapeutic opportunities. The therapeutic approach to heart failure begins with a strong emphasis on prevention, patient education, and self-participation in therapy with respect to both its monitoring and adjustment. Diuretics remain a mainstay of therapy but, in the face of severe heart failure, may become ineffectual, requiring constant infusion of loop-active diuretics, combination diuretics, or diuretics in association with concomitant low-dose dopamine infusion. Vasodilator therapy has been an important advance: combination hydralazine and nitrate therapy was initially shown to be efficacious in improving survival, and more recently, angiotensin-converting enzyme (ACE) inhibitors, in the form of enalapril, have shown incremental benefit on survival over this combination. Interestingly, there is now evidence from both SOLVD and SAVE to demonstrate an unexpected and, as yet, unexplained reduction in the frequency of both unstable angina and myocardial infarction. Although, on balance, the weight of evidence concerning the long-term efficacy of inotropic agents has been disappointing, especially as it relates to their unfavorable effects on survival, recent information on vesnarinone, an agent with a complex and diversified mechanism of action, suggests that with appropriate doses, improved symptoms and survival are possible. A substantial amount of new information from randomized placebo-controlled trials attests to the symptomatic relief, hemodynamic improvement, and gain in exercise performance achieved by digoxin. A long-term survival study is ongoing to assess its effects on mortality. beta-Blockers, especially metoprolol, appear beneficial in some patients with heart failure, possibly related to their reduction in sympathetic nervous activity and restoration of beta-receptor population, with resultant improved contractile performance, enhanced myocardial relaxation, and overall increase in cardiac efficiency. Based on available evidence, the best contemporary approach to treatment involves the use of ACE inhibitors coupled with diuretic therapy, either continuous or intermittent, to relieve central or peripheral congestion. The addition of digoxin or a hydralazine nitrate combination is a logical next step, with commencement of low-dose beta-blocker a reasonable option.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Medical advances in the treatment of congestive heart failure. 790 84

This study evaluated the relation between plasma cyclic guanosine monophosphate (cGMP) and hemodynamic and neurohormonal parameters in patients with chronic congestive heart failure and assessed the effect of organic nitrate on plasma cGMP levels. Plasma cGMP was fourfold higher in 18 patients with congestive heart failure compared with 15 control subjects (16.7 +/- 9.7 versus 4.0 +/- 1.0 pmol/ml; p < 0.0001) but did not correlate with plasma levels of catecholamines, renin, atrial natriuretic peptide, or with baseline hemodynamic values. The administration of a hemodynamically effective dose of oral isosorbide dinitrate (40 mg) resulted in a transient reduction in plasma cGMP from 16.7 +/- 9.7 pmol/ml at baseline to 13.0 +/- 6.6 pmol/ml at 1 hour (p < 0.05). This change was associated with small and statistically insignificant changes in neurohormonal values and had no relation to any of the hemodynamic changes. We concluded that (1) elevated plasma cGMP in congestive heart failure does not correlate with other neurohormonal or hemodynamic parameters and may be an independent parameter of heart failure, (2) in contrast to previously documented nitrate-mediated increases in intracellular cGMP, nitrate therapy results in a reduction in plasma cGMP, and (3) changes in plasma cGMP cannot serve as a surrogate measurement of changes in intracellular cGMP.
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PMID:Plasma cyclic guanosine monophosphate in chronic heart failure: hemodynamic and neurohormonal correlations and response to nitrate therapy. 790 16

The role of nitric oxide in heart failure is unknown. The high-capacity inducible isoform of nitric oxide synthase is present in the myocardium of patients with idiopathic dilated cardiomyopathy. Plasma nitrate, the stable end-product of nitric oxide production, was significantly increased in patients with heart failure compared with normal controls (means 51.3 and 24.6 mumol/L). Vasodilation caused by increased nitric oxide may compensate for the vasoconstrictor effect of neurohumoral adaptions to heart failure. Alternatively, excess production may be detrimental to the heart by a direct negative inotropic effect.
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PMID:Increased nitric oxide production in heart failure. 791 9

Recent studies have strengthened the arguments for the use of angiotensin-converting enzyme (ACE) inhibitors in the early postinfarct period. Those with clinically detectable heart failure, and hence at highest risk, will benefit most, as shown in the AIRE study, but those at lower risk with left ventricular dysfunction still have some benefit, theoretically through ventricular remodeling. In patients in the very early stages of acute myocardial infarction, three trials have shown discordant results. In CONSENSUS-II, intravenous enalaprilat followed by oral enalapril gave no benefit, rather causing excess hypotension and a possible increase in mortality. In ISIS-4 and GISSI-3, mortality improved by 0.46% and 0.8%, respectively, with risk reductions of 9% and 11%. Added transdermal nitrate in GISSI-3 gave a total reduction of 17%. In view of the risk of hypotension (20% in ISIS-4, compared with placebo 10%), very early ACE inhibition will probably only be used for selected patients. Logically, one target group would be those seen 7-24 hours after the onset of symptoms, particularly 7-12 hours, at which time captopril alone gave a reduction of 14.5% in risk. These mortality differences compare favorably with those recently found when comparing tPA and streptokinase in the GUSTO study.
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PMID:The new trials: AIRE, ISIS-4, and GISSI-3. Is the dossier on ACE inhibitors and myocardial infarction now complete? 794 63

Patients with heart failure have reduced forearm vasodilator responses when endothelial cell nitric oxide production is stimulated by muscarinic agonists. The aim of this study was to determine if activity of the nitric oxide pathway was also abnormal under basal conditions. Forearm blood flow (FBF) was measured with strain-gauge plethysmography in response to the intraarterial infusion of a subsystemic dose range of L-N-monomethylarginine (L-NMMA), a competitive inhibitor of nitric oxide synthase. In 18 normal subjects, the baseline FBF of 3.6 +/- 1.4 was decreased by 0.3 +/- 0.5 (p < 0.01), 1.0 +/- 0.7 (p < 0.01), 1.4 +/- 0.9 (p < 0.01), and 1.3 +/- 1.3 (p < 0.01) ml/min/100 ml forearm volume during infusions of 1, 4, 8, and 16 mumol/min of L-NMMA, respectively. In 10 patients with heart failure, the baseline FBF of 2.6 +/- 0.9 was decreased by 0.4 +/- 0.5 (p < 0.05), 0.4 +/- 0.5 (p < 0.05), 0.9 +/- 0.8 (p < 0.01), and 0.9 +/- 0.7 (p < 0.01) ml/min/100 ml forearm volume with the 4 doses of L-NMMA, respectively. There was no difference in the L-NMMA response between the 2 groups in terms of absolute flow, percent change, or with analysis of covariance to adjust for different baselines. The stable end products of nitric oxide (nitrite and nitrate) were measured in the forearm venous effluent. Nitrite and nitrate levels at baseline were not reduced in patients with heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lack of contribution of nitric oxide to basal vasomotor tone in heart failure. 797 73

Vasodilator drugs, particularly intravenously infused nitroprusside and an orally administered combination of hydralazine and isosorbide dinitrate, exert a profoundly favorable hemodynamic effect in the setting of heart failure complicating a prior myocardial infarction. Although these oral drugs also may relieve symptoms and improve exercise tolerance, the long-term benefits appear to be related to inhibition or reversal of the left ventricular dilation that results in a progressive fall in left ventricular ejection fraction. The long-term efficacy of both ACE inhibitors and hydralazine-nitrate in symptomatic heart failure makes the vasodilator combination a rational alternative to an ACE inhibitor and possibly an effective agent for cotherapy with an ACE inhibitor. Trials are needed to test the additive efficacy of this vasodilator combination and to develop other safe and effective drugs that target the progressive remodeling process in heart failure.
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PMID:Treatment of infarct related heart failure: vasodilators other than ACE inhibitors. 808 21

It is a common opinion that nitrate therapy may have a harmful effect on cardiac output in patients with congestive heart failure when left ventricular filling pressure is markedly reduced. In this study, we evaluated, using hemodynamic monitoring with Swan-Ganz catheterization, the effects on cardiac output and filling pressures of high-dose intravenous nitroglycerin in 8 patients with dilated cardiomyopathy and severe heart failure. At maximal doses of nitroglycerin utilized (350 +/- 220 micrograms/m, range 100-800), a significant reduction in right atrial pressure (from 4 +/- 3.5 to -1 +/- 4 mm Hg, p < 0.001) and pulmonary capillary wedge pressure (from 16 +/- 5 to 7 +/- 3 mm Hg, p < 0.001) was observed. Furthermore, we found neither a significant reduction in systemic vascular resistances (from 1,500 +/- 329 to 1,320 +/- 330 dynes/s/cm-5) nor changes in heart rate or blood pressure. Finally, stroke volume and cardiac index increased slightly although not significantly (from 62 +/- 18 to 70 +/- 16 ml and from 2.3 +/- 0.45 to 2.65 +/- 0.4 l/m/m2). The preservation of stroke volume despite a marked reduction in left ventricular filling pressure can be explained by a reduction in pericardial constraint and of mitral regurgitation induced by nitroglycerin. The clinical implications of these hemodynamic results are discussed with emphasis on the short- and long-term use of nitrates in congestive heart failure.
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PMID:[Nitrates in heart failure: the hemodynamic effects and clinical implications]. 808 25


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