Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As lignocaine clearance is influenced by factors such as cardiac failure and liver impairment, clinical pharmacokinetic principles should be used to account for kinetic variability so that target concentrations are achieved consistently throughout the course of intravenous therapy. Two groups of patients with ischaemic heart disease, who received lignocaine, were studied: a control group with no feedback or intervention from therapeutic drug monitoring, and an intervention group in which strict guidelines for lignocaine administration were introduced. Lignocaine plasma concentrations were measured by EMIT (Syva), and rapid feedback of concentration data in the intervention group allowed adjustment of infusion rates using the Chiou equation. The mean concentration in the intervention group remained within the therapeutic range (2-5 micrograms/ml) at all times, whereas it exceeded 5 micrograms/ml after the first 7 h in the control group. The distribution of concentrations in the intervention group was always narrower than that in the control group. The study also included a comparison of the ability of the Chiou equation and a Bayesian optimisation procedure to estimate pharmacokinetic parameters and to forecast lignocaine concentrations over various periods of time. There was no significant difference between prediction errors determined by the two methods at various points throughout a 32-h period; both methods were associated with a negative prediction bias beyond the first 12 h of infusion. It is likely that this reflects assumptions made about lignocaine clearance and indicates the need for more sophisticated kinetic models.
Ther Drug Monit 1983
PMID:Kinetic predictive techniques applied to lignocaine therapeutic drug monitoring. 663 55

A decrease in hepatic clearance and volume of distribution in patients with congestive heart failure frequently leads to toxicity when drugs such as lidocaine are administered. To determine the effect of adjusted dosing of lidocaine in patients with myocardial infarction, we studied 32 patients receiving lidocaine either by a conventional method (control group: 1-2 mg/kg bolus, then 1 to 4 mg/min) or by an adjusted regimen based on the presence or absence of heart failure [experimental group: 1-2 mg/kg bolus; then, class I (no heart failure), 35 to 88 micrograms/kg/min; class II (heart failure), 12 to 35 micrograms/kg/min]. Plasma lidocaine levels were determined at 2 and 5 h of the infusion by enzyme multiplied immunoassay technique (EMIT) and gas liquid chromatography (GLC). Ten of 33 determinations in the control group were in the toxic range, i.e., greater than 6 micrograms/ml, and four others were subtherapeutic, i.e., less than 2 micrograms/ml. In contrast, 13 of 16 determinations in the experimental group were in the therapeutic range, and none were in the toxic range. These data show that administration of lidocaine by a conventional method may produce diverse plasma levels that may occasionally be in the toxic range. Modified dosing based on cardiac status may result in optimal levels in most patients.
Ther Drug Monit 1982
PMID:Optimal lidocaine dosing in patients with myocardial infarction. 675 54

Effective treatment of hypertension with permanent achievement of normal blood pressure readings is the most effective prevention of organ manifestations of hypertension. Treatment must, however, affect also other risk factors, in particular hyperlipoproteinaemia, smoking and diabetes. Treatment of hypertension is individually adjusted and depends on: a) age, b) the presence of complications of hypertension and c) the presence of associated diseases. In elderly hypertensive patients small doses of diuretics and beta-blockers are the drugs of choice. The most frequent complication of hypertension is hypertrophy of the heart and IHD. The drug of choice in patients with IHD, and in particular in patients after myocardial infarction, are beta-blockers, in patients with cardiac hypertrophy which substantially influences the prognosis in an adverse way ACE inhibitors are recommended. In patients with cardiac failure as well as in patients with asymptomatic dysfunction of the left ventricle the drugs of choice are ACE inhibitors. The author indicates therapeutic approaches used in the most frequent associated diseases--diabetes and hyperlipoproteinaemia.
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PMID:[Manifestations in cardiovascular organs of essential hypertension-- possibilities of directed therapy and prevention]. 767 62

To identify any differences in inhibitory G protein (Gi) attributable to species or the cause of heart failure, we studied the changes in this protein in different animal models of heart failure: 1) different species; rats vs. hamsters (F1B) with cardiomyopathy induced by adriamycin (ADR) and 2) different etiologies; rats with ischemic heart failure (IHD) due to coronary artery ligation vs. rats with cardiomyopathy induced by ADR and F1B (20-week-old) hamsters with cardiomyopathy induced by ADR vs Syrian hamsters BIO 14.6 (40-week-old) with genetic cardiomyopathy, using Western blotting methods and ADP-ribosylation. We also sought to determine whether changes in the amount of Gi protein reflected the regulation of adenylate cyclase. The amount of immunodetectable Gi rose by 35% (p < 0.05) in ADR rats, 25% (p < 0.05) in ADR hamsters, 15% (p < 0.05) in IHD rats, and 28% (p < 0.05) in BIO 14.6 hamsters, as compared with control rats, F1B (20-week-old) hamsters, sham-operated control rats, and F1B (40-week-old) hamsters, respectively. Assessment of Gi by pertussis toxin-catalyzed ADP-ribosylation revealed increases in Gi of 24% (p < 0.05) in ADR rats and of 44% (p < 0.05) in BIO 14.6 hamsters, as compared with their respective controls. Gi function, as assayed by the acetylcholine-induced inhibition of adenylate cyclase, also increased. Thus, Gi protein appears to contribute to the changes in signal transduction in myocardium with heart failure.
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PMID:Increased levels of inhibitory G protein in myocardium with heart failure. 769 38

Use of sodium nitroprusside aerosol in association with ultrasound in 51 patients with IHD plus cardiac failure (stage I-IIA) allowed to reduce the dosage and side-effects of drugs as compared with a group of patients by routine complex methods. The method may be used for treatment and prophylaxis of initial stages of cardiac failure in IHD patients including those with contraindications to cardiac glycosides.
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PMID:[The use of sodium nitroprusside aerosols combined with ultrasound in the combined treatment of patients with ischemic heart disease and heart failure]. 820 64

There are very few contemporary studies on the frequency and cause of congestive heart failure (CHF) in a general population. In western Sweden, inhabited by 1.64 million people, a retrospective survey was performed. All hospital records of patients with CHF, ages 16 through 65 years, were examined in all hospitals in the region. During the study period 2711 patients fulfilled the criteria for CHF or cardiomyopathy. Patients were monitored for 37 +/- 28 months. The most common cause of heart failure was coronary artery disease (IHD) (40%). Other common causes were hypertension (17%), valvular disease (13%), alcohol (11%), diabetes mellitus (10%), and systemic diseases (10%). There were positive correlations between the male sex and IHD, alcohol, and dilated cardiomyopathy; the female sex was associated with systemic diseases, valvular heart disease, and diabetes. The incidence of CHF requiring hospitalization per 100,000 in the population was 1.2 to 263 men and 1.1 to 129 women, in the youngest (age 16 to 30 years) and oldest (61 to 65 years) age groups, respectively. The 5-year survival rate was 50%. Analysis of causes performed with Cox's proportional hazards model for survival showed that age, IHD, alcohol, and diabetes were independent and powerful predictors of mortality (p < 0.001). The mode of death was progressive heart failure in 54% and sudden death in 26%. We concluded that the prognosis in patients with CHF was still very poor, even among this young population. The most common cause of CHF was IHD, and the second was hypertension.
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PMID:Spectrum and outcome of congestive heart failure in a hospitalized population. 836 19

Treatment of hypertension reduced markedly (by more than 40%) the prevalence of cerebrovascular attacks, the prevalence of cardiac failure, malignant hypertension and ophthalmological complications of hypertension. The impact of antihypertensive treatment on the incidence of ischaemic heart disease is less marked. The wide use of diuretics and beta-blockers is supported by the fact that large studies of antihypertensive treatment revealed that they reduced the cardiovascular mortality and morbidity in a marked way. On the other hand, diuretics exert a negative effect on insulin resistance, glucose tolerance, cholesterol and may lead to hypokalaemia and hyperuricaemia. Non-selective beta-blockers are not optimal from the aspect of the risk profile of hypertensive patients. Therefore there is justified hope that wider use of calcium antagonists, beta-blockers of the third generation, ACE inhibitors and selective alpha 1 blockers will have a greater impact on IHD, as these drugs do not exert a negative effect on metabolic risk factors. At present an individual approach to treatment which takes into account other diseases present or complications of hypertension, in particular diabetes and hyperlipoproteinaemia, is the basic approach so far and the basis of therapeutic tactics.
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PMID:[Current trends in antihypertensive therapy: pro and con]. 837 69

Recently, a significant activity of inducible nitric oxide synthase (iNOS) has been reported in biopsies from failing hearts due to idiopathic dilated cardiomyopathy (IDC). Thus, a potential pathophysiological role of iNOS in IDC has been stated. In order to investigate, whether iNOS expression is of pathophysiological relevance in human heart failure, we measured iNOS protein expression and cGMP content in left ventricular myocardium from non-failing and failing human hearts. Immunoblot analysis revealed iNOS protein expression in four out of six failing hearts from septic patients, whereas no iNOS-protein expression was detected in either non-failing human hearts (n = 6) or failing hearts due to IDC (n = 9), ischemic heart disease (IHD, n = 7), Becker muscular dystrophy (BMD, n = 2) and mitoxantrone-induced toxic cardiomyopathy TCM, n = 1). cGMP content was increased by 130% in septic hearts, whereas there was no cGMP increase in hearts with IDC. IHD and BMD compared to non-failing hearts. We conclude, that the induction of iNOS may play a role in contractile dysfunction observed in septic shock, but is unlikely to be of major pathophysiological importance in end-stage heart failure due to IDC, IHD, BMD and TCM.
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PMID:Expression of inducible nitric oxide synthase in failing and non-failing human heart. 874 24

The lidocaine-monoethylglycinexylidide (MEGX) test is used to monitor liver function in liver transplant recipients. Serial studies have been undertaken after 155 allografts. The initial MEGX concentration is significantly correlated with the donor MEGX concentration. It is also influenced by the recipient's pretransplant bilirubin concentration, being lowest among patients with very high bilirubin levels. Use of segmental grafts is also accompanied by low MEGX concentrations. The flow-dependent clearance of lidocaine makes it a sensitive indicator of disturbed liver blood flow, with decreased MEGX concentrations occurring in hepatic artery thrombosis and rejection and as a result of cardiac failure and pulmonary effusions. Significant hepatic ischemia resulting in delayed initial function or cholestasis also is associated with low MEGX concentrations. The initial median MEGX concentrations were lowest among patients who required retransplantation or who died within 2 months of allografting.
Ther Drug Monit 1996 Aug
PMID:The use of the lidocaine-monoethylglycinexylidide test in the liver transplant recipient. 885 55

Cardiac failure is a syndrome which comprises ventricular dysfunction (confirmed by echocardiography) and compensating mechanisms (immediate activation of the sympathetic nerve and functioning of Starling's mechanism, within hours or days activation of RAAS within days or weeks hypertrophy of the heart). Cardiac failure develops rapidly either in a previously healthy subject (first extensive IM, diffuse myocarditis, acute aortic or mitral regurgitation) or in a damaged heart (IHD, KMP, defect) as a result of sudden excessive burdening (ischaemia, arrythmia, infection, surgery etc.) or spontaneously (end-stage). It is manifested above all by "backward" failure (pulmonary oedema). The pulmonary pressure must be rapidly reduced: i.v. nitrovasodilators act immediately, i.v. furosemide acts within 10-15 min. (in can, however, reduce the circulating volume which has not increased during the first failure). Also O2, anodynes. In the subacute stage (without any precise time limits) which may develop in serious cases from acute failure, or develop as a result of deterioration of chronic failure, in addition to congestion, symptoms caused by "forward" failure are in the foreground. These are symptoms caused by a reduced minute output and hyperfusion of tissue. It is indicated to administer substances which improve work tolerance, i.e. positive inotropics (digitalis, beta-agonist or phosphodiesterase inhibitors). If the blood pressure drops, a combination of dopamine and dobutamine should be administered; if the respiratory volume drops, artificial pulmonary ventilation, in case of persisting oedema continuous arteriovenous haemofiltration, in severe failure intraaorrtic balloon contrapulsation etc. In an irreversible state urgent or elective orthoptic transplantation of the heart should be considered. In chronic heart failure an important component of comprehensive treatment is in addition to treatment of congestion and hypoperfusion, prevention of "cardiovascular remodelling" by means of angiotensin convertase inhibitors etc. Which improve the quality of life and survival. Arrhythmias are an independent prognostic factor.
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PMID:[Acute and chronic heart failure]. 924 65


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