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)

An analysis of heart rate (HR) variability (HRV) was based on quantifying the number and amplitude of HR fluctuations over long (8-30 cycles) and short (2-4 cycles) sequences of acceleration and deceleration-forming oscillations. The 'product' (number times amplitude) is an equivalent of the power spectrum in the frequency domain. In the time domain, positive correlations with HR were found for the number of long (L) sympathetic-mediated oscillations, whereas they were negative for short (S) vagally-mediated oscillations. The L/S ratio, an index of the autonomic nervous system (ANS) balance, closely paralleled the circadian HR values. HRV was studied in the ambulatory ECG of three groups of 15 normal adults (group I), 13 patients with left ventricular hypertrophy (LVH, group II) and 13 patients with heart failure (HF, group III). In basic conditions the mean HR was 77.1 +/- 1.9 beats min-1 (mean +/- SEM) in group I, 76.8 +/- 3.3 in II, 79.5 +/- 3.5 in III (P = NS). The different types of oscillations had smaller 24-h average values of the product in groups II and III than in group I, but the trends did not reach significance. However, the pooled 24 hourly values of the L/S ratio in group I (1.17 +/- 0.09) were lower than in group II (1.33 +/- 0.06, P less than 0.05 at Ancova) and higher than in group III (1.06 +/- 0.09, P less than 0.001). A 3-day treatment with acebutolol non-uniformly slowed the mean HR:--9.5% in group I, --18.1% in II and -19.1% in III (P less than 0.001), and uniformly diminished the L/S ratio by 17% to 20% (P less than 0.01). In conclusion, the sympathetic predominance of the ANS balance in LVH and HF is reflected by the beta-blockade induced HR decrease that is twice as marked in patients as in controls. In basic conditions HRV tends to be depressed in LVH and even more in HF. The ANS imbalance, however, has different modalities depending on the presence of HF, probably because of the different status of beta-adrenergic receptors in this condition.
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PMID:Heart rate variability in left ventricular hypertrophy and heart failure, and the effects of beta-blockade. A non-spectral analysis of heart rate variability in the frequency domain and in the time domain. 182 32

To characterize renal transport of Na+ in heart failure, urinary Na+ excretion (UNaV), aldosterone levels, and Na,K-ATPase activity in isolated nephron segments were determined in three groups: control rats, rats with heart failure and moderate sodium retention, and rats with heart failure and severe sodium retention. Heart failure was induced by a fistula between the aorta and vena cava. For the control group, UNaV was 0.66 +/- 0.04 (mean +/- SEM) mueq/min, and aldosterone was 18.4 +/- 3.5 ng%. Na,K-ATPase activity (in 10(-11) mol/mm/min) was 28.4 +/- 1.1 in the proximal convoluted tubule, 23.3 +/- 1.0 in the proximal straight tubule, 37.4 +/- 1.9 in the medullary thick ascending limb, 40.2 +/- 1.9 in the cortical thick ascending limb, 43.2 +/- 2.2 in the distal convoluted tubule, and 20.5 +/- 0.9 in the cortical collecting duct. For the group with moderate heart failure, UNaV was 0.35 +/- 0.02 (p less than 0.001 versus control), and aldosterone was 15.9 +/- 4.4 (p = NS versus control). Na,K-ATPase activity was unchanged in the proximal convoluted tubule, proximal straight tubule, medullary thick ascending limb, and cortical collecting duct, but it increased in the cortical thick ascending limb to 57.7 +/- 3.1 (p less than 0.001 versus control) and decreased in the distal convoluted tubule to 35.3 +/- 1.2 (p less than 0.005 versus control). For the group with severe heart failure, UNaV was 0.029 +/- 0.016 (p less than 0.001 versus control), and aldosterone was 186.0 +/- 14.8 (p less than 0.001 versus control).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Na,K-ATPase in isolated nephron segments in rats with experimental heart failure. 184 57

This investigation was conducted to study the incidence and the causes of sow mortality in breeding herds. Data were obtained from 24 swine breeding herds with an average inventory of 3755 sows and served gilts for the total sample. Producers were involved for 12 consecutive months and agreed to submit to the diagnostic laboratory every dead or moribund sow and served gilt. The average herd death rate was 3.3% +/- 0.5 (SEM), but varied considerably among herds, ranging from 0% to 9.2%. A total of 137 sows and mated gilts died during the year, and these females had produced an average of 4.2 litters +/- 0.2 (SEM). The number of deaths was significantly higher during the months of July, August and October. The peripartum period appeared to be when sows were most at risk, with 42% of all deaths occurring during this short period of the reproductive cycle. The three major causes of death were heart failure (31.4%), torsions and accidents of abdominal organs (15.3%) and cystitis-pyelonephritis (8.0%). Other causes included endometritis (6.6%), uterine prolapses (6.6%), pneumonia (3.6%), gastric ulcers (3.6%), downer sow syndrome (2.2%), miscellaneous (8.0%) and unknown (14.6%).
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PMID:A prospective study of sow mortality in breeding herds. 188 99

Eleven patients with chronic heart failure secondary to ischaemic heart disease (mean [SEM] age 63.0 [2.3] years; left ventricular ejection fraction 19 [8]% undertook 8 weeks of home-based bicycle exercise training and 8 weeks of activity restriction (rest) in a physician-blind, random-order, crossover trial. Training increased exercise duration from 14.2 (1.1) min to 16.8 (1.3) min and peak oxygen consumption from 14.3 (1.1) ml.min-1.kg-1 to 16.7 (1.3) ml.min-1.kg-1. Heart rates at submaximum workloads and rate-pressure products were significantly reduced by training, and there was also a significant improvement in patient-rated symptom scores. No adverse events occurred during the training phase. Thus home-based physical training programmes are feasible even in severe chronic heart failure and have a beneficial effect on exercise tolerance, peak oxygen consumption, and symptoms. The commonly held belief that rest is the mainstay of treatment of chronic heart failure should no longer be accepted.
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PMID:Effects of physical training in chronic heart failure. 196 55

This study compared the pharmacokinetics of orally administered isosorbide-5-mononitrate (20 mg) in patients with and without signs of ischemic heart failure after acute myocardial infarction. The central venous pressure was used as a parameter of global myocardial function and to separate 17 patients into two groups with normal (group I: CVP less than 6 cmH2O; Killip class I; n = 9) and elevated (group II: CVP greater than or equal to 6 cmH2O; Killip class II-III; n = 8) pressure. As compared to subjects with normal CVP patients with hemodynamic impairment showed a markedly lower peak concentration of isosorbide-5-mononitrate levels (475 +/- 32 vs 663 +/- 38 ngml-1; p less than 0.01; mean +/- SEM) which occurred delayed (32 +/- 6 vs 55 +/- 9 s; p less than 0.05). Reduced cardiac function also resulted in a prolonged elimination of isosorbide-5-mononitrate as was suggested by the diminished elimination rate constant (0.14 +/- 0.01 vs 0.18 +/- 0.01 h-1; p less than 0.05). Thus, in patients with ischemic heart failure cardiac performance influences both the absorption and apparent elimination phase of oral isosorbide-5-mononitrate.
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PMID:Pharmacokinetics of oral isosorbide-5-mononitrate in patients with ischemic heart failure. 203 15

The purpose of this study is to clarify fetal cardiovascular effects of four popular analgesics administered to a maternal animal model. Clinical doses of aspirin (14 mg/kg), acetaminophen (14 mg/kg), ibuprofen (6 mg/kg), or indomethacin (0.7 mg/kg) were administered orally to near-term rats. At 1, 4, 8, or 24 hours later fetuses were delivered by cesarean section, and were fixed immediately by the whole-body freezing technique. The ductus diameter, pericardial effusion, and volume and mass of the ventricles were studied by photographing multiple planes of the heart. Fetal ductal constriction was most remarkable with ibuprofen, with the diameter decreased 70% +/- 5% (mean +/- SEM) at 1 to 8 hours. Both ventricles were dilated 60% +/- 27%, and pericardial fluid was increased 120% +/- 20%. These changes partly disappeared at 24 hours. Milder but more persistent effects were observed with indomethacin. The fetal ductus was constricted 30% at 4 to 24 hours. Pericardial fluid was increased 140% +/- 30% at 24 hours. Aspirin and acetaminophen constricted the fetal ductus 10%. In conclusion, clinical doses of ibuprofen and indomethacin constricted the fetal rat ductus and caused cardiac failure. The effects of aspirin and acetaminophen were much milder.
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PMID:Transplacental cardiovascular effects of four popular analgesics in rats. 214 Feb 40

The response of atrial natriuretic factor to an acute increase in atrial pressures produced by changing from a 45 degrees upright to a -15 degrees Trendelenburg tilt was examined in 21 patients with heart failure and 8 control subjects with normal hemodynamics. In the control subjects, baseline (45 degrees upright tilt) pulmonary capillary wedge and right atrial pressures increased from 3.1 +/- 0.9 (mean +/- SEM) and 4.4 +/- 0.3 mm Hg to 6.9 +/- 1.9 and 8.5 +/- 0.4 mm Hg, respectively (p less than 0.05 for both), 30 min after the -15 degrees tilt. Baseline arterial plasma atrial natriuretic factor concentration increased from 34 +/- 4 to 44 +/- 1 pg/ml (p less than 0.05) 30 min after the tilt, with an increase observed in every patient. In the group with heart failure, baseline pulmonary capillary wedge and right atrial pressures increased from 17.5 +/- 2.0 and 5.3 +/- 1.2 mm Hg to 24.6 +/- 1.8 and 9.7 +/- 1.3 mm Hg, respectively (p less than 0.01 for both), 30 min after the tilt. Plasma atrial natriuretic factor concentration was 326 +/- 38 pg/ml at baseline and 347 +/- 34 pg/ml (p = NS) 30 min after tilt. Compared with the 7 patients with heart failure who had increased atrial natriuretic factor concentrations after the tilt (responders), the 14 patients with unchanged or decreased atrial natriuretic factor concentrations after the tilt (nonresponders) had a higher baseline right atrial pressure and atrial natriuretic factor concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Response of atrial natriuretic factor to postural change in patients with heart failure versus subjects with normal hemodynamics. 214 66

To characterize the neural excitatory state of heart failure, simultaneous measurements of efferent sympathetic nerve activity to muscle (by microneurography) and rest hemodynamics were obtained in 10 normal subjects (age 25 +/- 2 years, mean +/- SEM) and 29 patients with heart failure (age 49 +/- 2 years; New York Heart Association functional class II to IV; left ventricular ejection fraction 21 +/- 1%; cardiac index = 2.16 +/- 0.13 liters/min per m2; pulmonary capillary wedge pressure 23 +/- 2 mm Hg). Sympathetic nerve activity was significantly higher in the patients with heart failure (54.7 +/- 4.5 bursts/min) than in normal subjects (16.7 +/- 2.2 bursts/min, p less than 0.001). Multiple linear regression analyses indicated that sympathetic activity in these human subjects was most strongly and inversely correlated with left ventricular stroke work index (r = -0.86, p less than 0.0001) and stroke volume index (r = -0.85, p less than 0.0001). There was a strong positive correlation between sympathetic nerve activity and pulmonary artery diastolic (r = 0.82, p less than 0.0001) and mean (r = 0.81, p less than 0.0001) pressures. Similar correlations were seen when patients with heart failure were analyzed separately. There was no significant correlation between sympathetic nerve activity and mean arterial pressure, left ventricular ejection fraction (by radionuclide ventriculography), cardiac chamber size (by echocardiography) or arterial oxygen tension in the patients with heart failure. Direct measurements of sympathetic nerve activity correlated closely with plasma norepinephrine (r = 0.72, p less than 0.0001) in patients with heart failure. Thus, sympathetic nerve activity at rest parallels impairment of cardiac performance in patients with heart failure.
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PMID:Clinical and hemodynamic correlates of sympathetic nerve activity in normal humans and patients with heart failure: evidence from direct microneurographic recordings. 222 59

OPC-8212 is a newly synthesized, orally effective inotropic agent. Previous studies have shown short-term hemodynamic and symptomatic improvement in patients with congestive heart failure. However, the long-term efficacy of this agent remains to be established. Eighty-three patients with chronic heart failure were randomly assigned to treatment with either OPC-8212 (n = 45) or matching placebo (n = 38). Of the placebo-treated patients, two patients died and another six patients were withdrawn from the study because of a deterioration of heart failure, while only 1 out of 45 OPC-8212-treated patients were withdrawn because of increased congestive symptoms. After 12 weeks of treatment, the OPC-8212 group showed a significant improvement in their numerical scores in sense of well-being as judged by the patients subscale A (p less than 0.01) and their physicians' general impression of the patients' status (p less than 0.01). The ejection fraction obtained from echocardiography increased from a mean (+/- SEM) baseline value of 42.8 +/- 2.6% to 46.6 +/- 2.9% (p less than 0.05) in the OPC-8212 group and 44.4 +/- 3.7% to 45.5 +/- 4.1% in the placebo group. These effects were not associated with an increase in the heart rate. The treatment was well tolerated without any limiting side effects. Thus, OPC-8212 is effective in patients with chronic heart failure, providing significant hemodynamic and symptomatic benefit in chronic treatment, together with a possible improvement of the prognosis of patients with heart failure.
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PMID:A placebo-controlled, randomized, double-blind study of OPC-8212 in patients with mild chronic heart failure. OPC-8212 Multicenter Research Group. 228 26

The clinical outcome of 18 patients, who presented with a Coxsackie virus myopericarditis in 1965, was evaluated 23 years later. Five patients had died, two of them had had heart failure. Thirteen patients and 23 healthy control subjects underwent exercise testing with gas exchange analysis. Left ventricular (LV) peak filling rate (PFR) was estimated by digitized M-mode echocardiography. Left ventricular ejection fraction was measured at rest and during exercise by radionuclide angiography. All patients were free of cardiac symptoms. Their clinical examination and the chest X-ray were normal. Peak oxygen consumption was not decreased in the patient group compared with the control group. PFR was significantly lower in the patient group than in the control group, 10.2 +/- 0.4 vs 13.2 +/- 0.4 cm s-1, P less than 0.001 (mean +/- SEM). LV ejection fraction was normal at rest in all patients (58 +/- 1%). An abnormal LV ejection fraction response to exercise was observed in two patients. Our data indicate that long-term prognosis after acute Coxsackie virus myopericarditis is good in a majority of patients.
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PMID:Clinical outcome and left ventricular function 23 years after acute coxsackie virus myopericarditis. 231 17


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