UMLS:C0018801 - FACTA Search

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

The efficacy of the phosphodiesterase inhibitor enoximone for reversal of severe postcardiotomy low cardiac output syndrome was investigated in 13 cases of cardiogenic shock refractory to conventional treatment consisting of beta-adrenergic agonists (n = 13) combined with vasodilators (n = 7), and intra-aortic balloon counterpulsation (n = 5). Following a bolus of 1 mg/kg enoximone, cardiac and stroke volume indices increased from 1.56 +/- 0.27 l/min/m2 and 16.3 +/- 3.3 ml/m2, respectively, to 2.72 +/- 0.67 and 27.8 +/- 7.1 (both p < 0.001). Mean arterial pressure fell, from 77 +/- 11 to 68 +/- 9 mmHg (p < 0.05), as did atrial filling pressures (LAP and RAP), LAP from 21.3 +/- 5.5 to 15.9 +/- 2.9 and RAP from 16.6 +/- 2.3 to 13.7 +/- 2.1 mmHg (both p < 0.01). The heart rate rose by only 5%. Enoximone therapy was maintained by a continuous infusion (5-7.5 micrograms/kg/min) for 40.6 +/- 8.6 hours (range 14-92). All hemodynamic parameters remained stable throughout treatment. Six patients died of sepsis and/or multiorgan failure but seven were discharged from hospital. Enoximone thus improved hemodynamic performance significantly in cardiogenic shock after open-heart surgery. It also has proved valuable in cardiac failure when conventional therapy was unsuccessful.
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PMID:Efficacy of phosphodiesterase inhibitor enoximone in management of postcardiotomy cardiogenic shock. 143 45

We studied the effect of a volume load induced by a 45 degrees Trendelenburg position on atrial natriuretic peptide (ANP) secretion in awake and anaesthetized patients with coronary artery disease undergoing aortocoronary bypass surgery. ANP was measured in different parts of the circulation before and after induction of high dose fentanyl anaesthesia at fixed times prior to and after extracorporeal circulation. METHOD. In eight patients with coronary artery disease (NYHA classification II-III), who received neither diuretic nor positive inotropic therapy, ANP was measured in the various parts of the circulation: in a peripheral vein, a radial artery, in the pulmonary artery and in the coronary sinus. The measurements were made in the supine and 45 degrees Trendelenburg position. Measurements of mean arterial pressure (MAP), central venous pressure (RAP), pulmonary arterial pressure (PAP), pulmonary capillary wedge pressure (PCWP), cardiac index (CI) and heart rate (HR) were taken simultaneously. The measurements were taken in the awake patient, during steady-state high-dose fentanyl anaesthesia with 50% O2 in N2O and after extracorporeal circulation. RESULTS. Compared to measurements in a control group, ANP levels were significantly higher in all parts of the circulation in patients with coronary artery disease, although clinical symptoms of heart failure were absent. After extracorporeal circulation, significantly higher levels of ANP were found at all measurement sites; however the concentration gradient of ANP between coronary sinus and arterial or venous blood was reduced. In awake and anaesthetized patients a change in body position, causing a significant increase in filling pressures, did not produce an increase in ANP levels at all measurement sites. The induction of high-dose fentanyl anaesthesia did not have an influence on plasmatic ANP levels. CONCLUSION. The results of this study lead to the following conclusions: 1. ANP levels in patients with CAD are increased, even if clinical heart failure symptoms are absent. 2. ANP is secreted in the coronary vessels. Following dilution in the atrial blood, it is metabolized to inactive compounds in the periphery. 3. Basic ANP levels are not changed by high-dose fentanyl anaesthesia. Marked increases of the filling pressures do not correlate with atrial ANP levels either before or after induction of anaesthesia. 4. After extracorporeal circulation ANP levels are significantly increased in all parts of the circulation. The concentration gradient between coronary sinus blood, on the one hand, and arterial and venous blood on the other hand is reduced. This phenomenon is probably caused by an alteration in the metabolism of ANP during hypothermic extracorporeal circulation.
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PMID:[The concentration of atrial natriuretic peptides (ANP). ANP in different sections of the circulation during atrial volume load with and without anesthesia]. 148 72

To test the efficacy of exogenous prostaglandins for vasodilator therapy in heart failure, we studied the effects of the prostacyclin-derivative iloprost (1.5-150 ng/kg/min) in seven conscious dogs before and after induction of heart failure by right ventricular pacing (250/min. 10 days). In healthy dogs, iloprost (150 ng/kg/min) decreased mean arterial blood pressure (MAP) (-45%) by a decrease in total peripheral resistance (TPR) (-55%), and increased cardiac output (CO) (+24%) and heart rate (HR) (+20%) with no effect on right atrial and pulmonary arterial pressures (RAP, PAP). Plasma norepinephrine (NE) (+47%), renin (+351%), and aldosterone (+126%) were increased. Urine flow (-70%) and Na excretion (-53%) were decreased. Iloprost (15 ng/kg/min) increased renal blood flow (RBF) (+29%), but did not change glomerular filtration rate (GFR). In dogs with heart failure, iloprost decreased arterial BP (-31%), TPR (-42%) and pulmonary vascular resistance (-28%) and increased CO (+29%), with no change in RAP and PAP. Plasma NE (+34%), renin (+385%), and aldosterone (+146%) were increased. RBF was unchanged. GFR (-24%) and filtration fraction (FF) (-30%) were decreased, as was urine flow (-65%). In experimental heart failure, iloprost is a potent arteriolar dilator, increasing CO with no preload effect. These beneficial effects are limited, however, by further neurohumoral activation and deterioration of renal function.
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PMID:Hemodynamic, hormonal, and renal effects of the prostacyclin analogue iloprost in conscious dogs with and without heart failure. 170 1

The hemodynamic effects of IS-5-MN were studied in 18 patients with acute myocardial infarction (AMI) complicated with left ventricular failure. Before treatment, 13 patients were in Forrester's hemodynamic class II and 5 in class IV. Hemodynamic monitoring was performed for 3 days, and the following parameters were measured: heart rate (HR), blood pressures (BP), right atrial (RAP), pulmonary artery and pulmonary capillary (PCP) pressures, cardiac index (CI), systemic (SVR) and pulmonary (PVR) vascular resistances, and coronary perfusion pressure (CPP). Patients with clinical symptoms of acute pulmonary edema or systolic BP (BPs) less than 90 mmHg were not included. Twenty mg of 5-IS-MN per os were administered every 8 h. Hemodynamic measurements and IS-5-MN plasma levels were obtained in basal conditions and 1/2, 1, 2, 6 and 8 h after the first and seventh dose of IS-5-MN. A significant decrease of systolic and diastolic BPs, RAP, PCP, SVR and PVR was observed after 1/2 of IS-5-MN administration and was maintained through the study, while CI and CPP increased and HR remained unchanged. The hemodynamic effect was maintained after the seventh dose, with a further decrease of the following parameters: BP, RAC, PCP and PVR. However, 2 patients were withdrawn from the study due to severe symptoms of heart failure. One patient presented headache. IS-5-MN plasma levels were identified after 1/2 h, with a peak level after 1 h, and were similar after the seventh dose. A significant correlation was found between the IS-5-MN levels and the delta RAP and delta PCP after the seventh dose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hemodynamic effect of isosorbide-5-mononitrate in acute cardiac insufficiency secondary to myocardial infarct]. 281 84

We investigated the role of atrial natriuretic peptide (ANP) in a rat model of chronic heart failure (CHF) (coronary ligation) by four different studies: (1) stimulation of secretion of ANP by volume loading, (2) infusion of 1 micrograms/min of rat ANP (99-126), (3) correlations of pressure measurements of right atrium (RAP) and LVEDP versus plasma ANP levels and ANP mRNS versus infarct size, (4) blocking endogenous plasma levels of ANP with monoclonal ANP antibody. In severe CHF, volume loading did not exert a significant increase in plasma ANP, in contrast to moderate CHF or to normal animals. Infusion of ANP reduced RAP and LVEDP without significant increase in renal blood flow (radioactive microspheres) in rats with severe cardiac failure, in contrast to normal animals. A close relationship was found between LVEDP and atrial plasma levels. After injection of ANP antibody, filling pressures and systemic vascular resistance increased, indicating that removal of ANP may enhance arterial vasoconstriction or elevated endogenous ANP to exert a vasodilatory action in severe heart failure. Nevertheless, the cardiocirculatory effects, primarily on renal blood flow, appear to be limited.
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PMID:[Significance of atrial natriuretic peptide in heart failure: experimental findings]. 297 Jan 72

The purpose of the study was to compare the haemodynamic effect of new antiarrhythmic preparations - ethmozine and its diethylamine analogue etacizine in 22 patients with heart failure (HF), stage IIa, of different etiology. The patients were given for one week ethmozine and then again for one week etacizine, during which periods they were followed echocardiographically, with pressure measurement in the pulmonary artery (PAP) and in the right atrium (RAP). Ethmozine in a daily dosis of 600-800 mg did not induce changes in left ventricular dimensions, percentual shortening of the anteroposterior left ventricular dimension (% delta S), in PAP, RAP, arterial pressure and heart rate. With application of etacizine in a dose of 150-200 mg/day, a clinically insignificant decrease was observed in % delta S (by 19.7%; p less than 0.05), which was not accompanied by a more marked augmentation of left ventricular dimensions, PAP, RAP or an intensification of clinical signs of heart failure. In spite of this, on administration of etacizine to patients with HF it is necessary to control haemodynamics, the most suitable method for this being echocardiography.
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PMID:Echocardiographic assessment of the haemodynamic effect of ethmozine and its diethylamine analogue etacizine in patients with heart failure. 354 57

Amrinone, a positive inotropic-vasodilator agent, was administered to anaesthetised dogs in an attempt to reverse heart failure induced by drugs possessing negative inotropic properties. Propranolol, a beta-adrenergic blocker; verapamil, a calcium slow-channel blocker procainamide, a type 1 antiarrhythmic agent; or sodium pentobarbital, a barbituate; administered as a bolus injection and/or infusion, produced a sustained depression in canine cardiac function. Cardiac depression was characterised by a greater than 40% reduction in cardiac contractile force (CF) and maximum left ventricular pressure development (LV dp/dtmax), a 30 to 50% reduction in cardiac output (CO) and concomitant increases in mean central venous or mean right atrial blood pressures (CVP, RAP, respectively). Amrinone, when administered intravenously as a bolus injection (1 or 3 mg X kg-1) plus an infusion (0.03 or 0.1 mg X kg-1 X min-1) reversed the depression in cardiac function by increasing CF, CO and LV dp/dtmax and decreasing preload CVP or RAP in all four drug-induced failure models. Due to the vasodilator properties of amrinone, afterload, total peripheral resistance (TPR), was reduced in verapamil and procainamide failures as well as in propranolol failure, the only model where TPR increases. In another model of heart failure, in which ouabain-induced arrhythmias preceded procainamide toxicity, amrinone was also an effective cardiotonic agent. Ouabain's inotropic effect was studied in propranolol-induced heart failure. Although an increase in LV dp/dtmax and a decrease in CVP were noted, ouabain (40 micrograms X kg-1 iv) increased TPR and had little effect on the depression in CF and CO. Drug-induced models of heart failure were useful pharmacological tools for evaluating the cardiotonic agent's ability to overcome severe cardiac depression. In propranolol-, verapamil-, procainamide-, and pentobarbital-induced cardiac toxicity, amrinone could be of therapeutic value.
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PMID:The beneficial effect of amrinone on acute drug-induced heart failure in the anaesthetised dog. 404 15

In 13 patients with heart failure colloid osmotic pressure in plasma (IIp) and in subcutaneous interstitial fluid from thorax (IIi) (wick technique), plasma volume (PV) and interstitial fluid volume (IFV) were measured and correlated to haemodynamic parameters (cardiac index (CI) and right atrial pressure (RAP]. In seven patients with anasarca measurements of IIp, IIi, PV and IFV were repeated after fluid withdrawal (mean 7786 ml) by ultrafiltration. In the patients, IIi was reduced compared with normal subjects (11.5 +/- 3.4 versus 15.8 +/- 2.7 mmHg, p less than 0.01 (mean +/- SD] and transcapillary colloid osmotic gradient (IIp - IIi) increased (14.6 +/- 2.3 versus 12.8 +/- 2.7 mmHg, p less than 0.05). The IFV in the patients was increased to 137% of values in normal subjects (p less than 0.01) and the ratio PV/IFV significantly reduced. Correlations were found between IIi and CI (r = 0.69, p less than 0.01) and IIi and RAP (r = 0.78, p less than 0.01). Ultrafiltration led to a parallel decrease in PV and IFV and increase in IIp. The results indicate that reduced IIi is an important factor limiting peripheral oedema in heart failure and the reduction is more pronounced in severe heart failure. The reduction of IIi is due to both dilution of interstitial proteins and to reduction of interstitial protein mass by lymphatic wash-out.
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PMID:Colloid osmotic pressures, plasma volume and interstitial fluid volume in patients with heart failure. 408 22

Recent studies suggest that plasma levels of alpha-hANP may reflect the severity of heart failure, but mechanism whereby ANP secretion increase is not known. Changes in alpha-hANP concentration in the arterial (A-ANP) and coronary sinus blood (CS-ANP) during and after the cardiopulmonary bypass (CPB) were measured to investigate the role of ANP in patients undergoing cardiac surgery. Fifteen patients were divided into 2 group; Group I, valvular heart disease (n = 9), Group II, coronary artery disease (n = 6). Both A-ANP and CS-ANP were significantly higher in the Group I than Group II before and during CPB. The difference between two groups decreased and was insignificant after CPB. The CS-ANP was twice as high as A-ANP at simultaneous sampling point. Significant correlations between the changes in PCWP (delta PCWP) and delta A-ANP (p < 0.01), delta RAP and delta A-ANP (p < 0.02) and an inverse linear correlation between CI and A-ANP (p < 0.01) were observed. Not a significant correlation was found between ANP and urine volume, urinary sodium excretion and other renal functional parameters during and after CPB. Hypothermia and the use of mannitol in large quantities were considered to be factors. In the Group I, A-ANPs were also measured in the postoperative follow-up period. A-ANP remained elevated above 100 pg/ml in patients with poor and decreased below 100 pg/ml with good prognostic signs 3 to 6 months postoperatively. From these results, it is suggested that alpha hANP is secreted from the atrial wall to the coronary sinus vein and the levels of alpha-hANP in the perioperative and follow-up period after heart surgery, especially in the valvular heart disease, are considered to reflect the cardiac performance.
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PMID:[Changes of alpha hANP concentration in arterial and coronary sinus blood during and after cardiopulmonary bypass]. 851 51

Human BNP serves to compensate for deteriorating cardiac function causing preload and afterload reductions, natriuresis, diuresis, suppression of the renin-angiotensin-aldosterone system (RAAS) and endothelin-1, and lowering of norepinephrine. Based on its unique pharmacologic profile, nesiritide results in clinically significant balanced vasodilation of arteries and veins, and may be well suited for patients presenting with various scenarios of decompensated CHF usually due to volume overload (NYHA classes II-IV). More than 1000 subjects have participated in clinical trials with nesiritide and more than 55,000 patients have been treated with nesiritide since it was approved for use in August 2001. Unlike nitroglycerin, tachyphylaxis did not appear to occur with Natrecor. The complete efficacy profile of nesiritide included preload reduction (PCWP and RAP), reductions in pulmonary artery pressures, afterload reduction (systemic vascular resistance), and increases in cardiac index and stroke volume index (which are dose-dependent and not the result of a direct inotropic effect), without increasing heart rate. Unlike inotropes, the beneficial hemodynamic effects produced by nesiritide do not cause an increase in myocardial oxygen consumption (MVO(2)), an important consideration for patients with acutely decompensated heart failure. Because Nesiritide is not an inotrope, it does not affect myocardial contractility, as does a beta-adrenergic receptor agonist, or a phosphodiesterase III inhibitor. As a result, nesiritide is not arrhythmogenic. Nesiritide should be considered for patients presenting with acutely typical or useful decompensated heart failure, especially those with dyspnea at rest or with minimal activity.
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PMID:Nesiritide: a new therapy for the treatment of heart failure. 1266 89

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