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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although it has been demonstrated that during isotonic grip exercise patients with chronic congestive heart failure have an abnormally reduced forearm oxygen consumption resulting from a depressed forearm flood flow, there may be additional etiologies of this abnormality. To explore this possibility biopsies of the pronator teres muscle were taken in eight control subjects with normal cardiac hemodynamics and in seven severely decompensated chronic congestive heart failure subjects. Each sample was fixed, stained, and photomicrographs of the sections were obtained and the capillary basement membrane thickness determined. The control capillary basement membrane thickness was 3028 plus or minus 187 A (mean plus or minus SEM) compared to the congestive heart failure thickness of 4924 plus or minus 538 A (pless than .01). It is possible that the increased basement membrane thickness in congestive heart failure may result from or actually cause the depressed oxygen consumption by altering diffusion.
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PMID:Evaluation of skeletal muscle capillary basement membrane thickness in congestive heart failure. 111 95

We studied the effects of inhaled and intravenous furosemide (40 mg) on bronchial responsiveness to acetylcholine (ACh) in patients with chronic congestive heart failure. The measurement of bronchial responsiveness was performed by inhaling doses of ACh and calculating the provocative concentration of ACh needed to cause a 20% fall in FEV1.0 (PC20-ACh). Intravenous furosemide (N = 11) had a marked diuretic effect (urine output 1014 ml (SEM 156) in 2 hours), but had no effect on resting pulmonary function and PC20-ACh. In contrast, inhaled furosemide (N = 10) had no effect on urine output and resting pulmonary function, but caused significant increase in PC20-ACh from 2.74 (GSEM 1.28) to 8.47 (GSEM 1.22) mg/ml (p less than 0.05). We conclude that inhaled furosemide, but not intravenous furosemide reduces bronchial hyperresponsiveness to ACh in patients with chronic congestive heart failure. The mechanism of this effect appears to be related to the ion transport system of airway epithelium.
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PMID:[Effects of inhaled and intravenous furosemide on bronchial hyperresponsiveness in patients with chronic congestive heart failure]. 140 95

Measurement of energy expenditure with indirect calorimetry allows determination of caloric balance. The present study was done to determine the predictive value of caloric and nitrogen balances for nutritional outcome. Energy expenditure was obtained weekly and interpolated between measurements for daily caloric balance. Nitrogen balance was obtained weekly. Because nitrogen output fluctuated, interpolation of daily values was not possible. Nutritional outcome was defined by whether body weight was lost or maintained and by levels of visceral proteins (albumin, prealbumin, and transferrin). The study group included 12 patients with 7% to 82.5% total body surface area burns. Eleven patients survived their burn injuries, and one died of congestive heart failure at 38 days, after her burn wounds had healed. Nine patients had good nutritional outcomes (group 1) and three had poor nutritional outcomes (group 2) (including the one who died). Nitrogen balance was 1.3 +/- 1.0 gm/day in group 1 and 4.5 +/- 1.7 gm/day in group 2 (mean +/- SEM; p > 0.10). Caloric balance was 515 +/- 130 kcal/day in group 1 and -667 +/- 140 in group 2 (p < 0.001). Caloric balance was significantly different between the two groups, whereas nitrogen balance was not. Caloric intake correlated positively with nitrogen intake (r = 0.92). Nitrogen intake was 16% of total caloric intake. Nitrogen intake from blood products was appreciable and averaged 15% of total nitrogen intake (range, 0% to 47%); 11.3 +/- 1.6 gm/day in group 1 and 14.8 +/- 3 gm/day in group 2 (p > 0.10).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Caloric and nitrogen balances as predictors of nutritional outcome in patients with burns. 146 36

Clentiazem, 8-chloro diltiazem, is a calcium channel blocker currently undergoing evaluation for the treatment of stable angina and hypertension. As patients with ischaemic disorders often present some degree of heart failure, the aim of this study was to investigate the effect of congestive heart failure on clentiazem (200 micrograms kg-1, i.v. bolus) pharmacokinetics in a canine model. Congestive heart failure was induced in six dogs by rapid ventricular pacing (240 beats min-1) for 3-5 weeks. Clentiazem pharmacokinetics was studied in each dog under the control condition and after the development of clinical signs of heart failure (ascites, dyspnea, fatigue). Blood samples were collected up to 480 min post-dose. Clentiazem plasma concentrations were determined by high performance liquid chromatography. The area under the plasma concentration versus time curves (AUC0-infinity) was significantly increased in congestive heart failure dogs (8.8 +/- 1.6 vs 21.8 +/- 1.4 micrograms min ml-1) (mean +/- SEM). These changes were related to a reduction of the volume of distribution of the central compartment (0.9 +/- 0.1 vs 0.2 +/- 0.11 kg-1) and total body clearance (1.9 +/- 0.4 vs 0.7 +/- 0.21 h-1 kg-1). It is concluded that, in our model, congestive heart failure significantly modifies clentiazem disposition. These results suggest that caution should be exercised when clentiazem is given to patients with a low ejection fraction and a compromised cardiac function. Reduced loading and maintenance doses might be recommended in patients with severe congestive heart failure.
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PMID:Effect of congestive heart failure on clentiazem pharmacokinetics in a dog model. 148 42

To investigate the influence of the presence of oedema on the pharmacokinetics and pharmacodynamics of furosemide (frusemide) we selected 9 hospitalised patients (mean age 70.3 years, range 59 to 84 years) with severe congestive heart failure (NYHA III to IV) and an assessed amount of peripheral oedema of at least 5 kg. In these patients the absorption of a single oral dose of furosemide 250 mg was studied when their heart failure was decompensated and again, after intensive therapy, when it was clinically compensated. The mean (+/- SEM) weight loss after clinical treatment was 12.0 +/- 2.2 kg. Individual furosemide plasma concentration-time curves could be fitted adequately to a 1-compartment model with 1 first-order absorption and elimination process, in which absorption took place in 2 parts with different lag times. Comparing the decompensated state with the compensated state we did not find significant differences in pharmacodynamics, absorption half-life, elimination half-life, time to peak serum concentration, peak serum concentration itself and area under the plasma concentration-time curve. However, the relative amount of furosemide absorbed in the first fraction was significantly increased after compensation. We conclude that the presence of massive oedema in patients with congestive heart failure has a minor influence on the pharmacokinetics and pharmacodynamics of high dose oral furosemide.
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PMID:Absorption of high dose furosemide (frusemide) in congestive heart failure. 160 90

The effects of the long-acting angiotensin-converting enzyme inhibitor benazepril hydrochloride on exercise tolerance and signs and symptoms of congestive heart failure (CHF) were evaluated in a double-blind, multicenter, placebo-controlled clinical trial. Patients with chronic New York Heart Association class II to IV symptoms of CHF and an ejection fraction by radionuclide scanning of less than or equal to 35% were randomized in a 2:1 ratio to treatment with ascending doses of oral benazepril (n = 114) or placebo (n = 58) once daily, while continuing to receive background therapy with digoxin and diuretics. After randomization, patients were evaluated clinically every 2 weeks during a 12-week, double-blind treatment period. Maximal exercise tolerance was measured before and at specified time points after randomization by graded treadmill exercise testing. At week 12, mean exercise time increased 95 +/- 12 (SEM) seconds in the group receiving benazepril, whereas the increase was 37 +/- 18 seconds in the group receiving placebo (p less than 0.01 for the difference between the groups). There was also greater improvement in overall clinical status and in the signs and symptoms of CHF in benazepril-treated patients than in control subjects. There were 3 deaths in placebo-treated patients and none in benazepril-treated patients (p less than 0.05); the overall incidence of adverse effects was identical in the 2 groups. Benazepril is a well-tolerated angiotensin-converting enzyme inhibitor that provides clinically important improvement in exercise tolerance and in signs and symptoms when given once daily to patients with CHF receiving background therapy with digoxin and a diuretic.
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PMID:Effects of once-daily benazepril therapy on exercise tolerance and manifestations of chronic congestive heart failure. The Benazepril Heart Failure Study Group. 163 2

Eighteen patients with New York Heart Association class III congestive heart failure were given single 100 mg oral doses of fenoldopam with food or fasting in a random-order single-blind crossover trial. Before and after each fenoldopam dose, thermodilution cardiac output, right atrial pressure, pulmonary artery pressure, and pulmonary capillary wedge pressure (PCWP) were measured with a balloon-tipped pulmonary artery catheter, and heart rates and blood pressures were recorded with an automated sphygmomanometer. Compared with fasting, bioavailability of fenoldopam was decreased significantly when administered with food: mean peak plasma fenoldopam level decreased from 26.5 (+/- 4.1 SEM) ng/ml to 10.9 (+/- 1.7 SEM) ng/ml (p = 0.0004) and mean area under the concentration-time curve was decreased from 44.7 (+/- 5.8 SEM) ng.hr/ml to 26.8 (+/- 4.1 SEM) ng.hr/ml (p = 0.0001). Fenoldopam administration to fasting patients resulted in decreases in mean arterial pressure, systemic vascular resistance, and PCWP and significant increases in cardiac index without change in heart rate. The maximum changes in mean cardiac index, systemic vascular resistance, and PCWP were greatest 1 hour after oral administration and did not persist beyond 3 hours after administration. In fasting patients, changes in cardiac index were correlated with plasma fenoldopam levels, whereas changes in PCWP and mean arterial pressure did not correlate significantly with the observed fenoldopam level.
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PMID:The effect of food on pharmacokinetics and pharmacodynamics of fenoldopam in class III heart failure. 167 97

The effect of captopril on steady-state pharmacokinetics of digoxin was studied in 12 patients with mild congestive heart failure (CHF; New York Heart Association functional class 1 or 2). Serum and urine digoxin concentrations were determined before and after a repeated administration of captopril in the patients on chronic digoxin therapy. The patients were taking digoxin, 0.25-0.375 mg/day, once daily, and were concurrently administered captopril, 37.5 mg/day, three times daily, for seven days. Peak serum concentration of digoxin (SCD) before and after captopril was 2.1 +/- 0.2, mean +/- SEM, and 2.0 +/- 0.1 ng/ml; the time to peak was 1.1 +/- 0.2 and 1.8 +/- 0.3 h; the terminal half-life (t1/2 alpha) was 10.9 +/- 1.0 and 8.7 +/- 0.9 h, and the area under the concentration-time curve to 24 h was 26.9 +/- 2.4 and 27.6 +/- 2.0 ng.h/ml. There was no significant difference between patients without and with captopril in SCD and its pharmacokinetic parameters. Renal digoxin clearance and creatinine clearance also showed no significant difference. After an administration of captopril, angiotensin-converting-enzyme (ACE) activity was well suppressed. These results suggest that captopril does not increase SCD in patients with CHF, and effectively suppresses ACE activity. Thus, modification in the dosage regimen of digoxin may be unnecessary in the case of coadministration with captopril.
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PMID:The effect of captopril on pharmacokinetics of digoxin in patients with mild congestive heart failure. 171 23

The effects of nasal continuous positive airway pressure (CPAP) were examined during cardiac catheterization in 22 patients with congestive heart failure (CHF). CPAP was applied at a level of 5 cm H2O pressure. Hemodynamic measurements were made at baseline and while on CPAP. We hypothesized that patients with high left ventricular (LV) diastolic pressures would experience an increase in cardiac index (CI). To test this hypothesis, patients were divided into two groups based on their baseline pulmonary capillary wedge pressure (PCWP): one group of 11 whose PCWP was greater than or equal to 12 mm Hg (high-PCWP group) and a second group of 11 whose PCWP was less than 12 mm Hg (low-PCWP group). Among the high-PCWP group (mean PCWP +/- SEM = 19.0 +/- 2.7 mm Hg), CI rose significantly while on CPAP (from 2.48 +/- 0.26 to 2.82 +/- 0.26 L/min/m2, p less than 0.01). Stroke volume index (SVI) also rose significantly (from 52.6 +/- 7.0 to 64.1 +/- 8.0 ml/m2, p less than 0.001). In contrast, among the low-PCWP group (PCWP = 8.3 +/- 0.6 mm Hg), CI decreased significantly while on CPAP (from 3.14 +/- 0.44 to 2.89 +/- 0.62 ml/m2, p less than 0.025). SVI fell but not significantly while on CPAP (from 75.5 +/- 8.4 to 74.2 +/- 8.5 ml/m2). Multiple stepwise linear regression analysis revealed that the only significant correlate of the magnitude of change in CI in response to CPAP was baseline PCWP (r = 0.50, p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiac output response to continuous positive airway pressure in congestive heart failure. 173 45

We demonstrated in previous works that the circadian rhythms of blood pressure (BP) and atrial natriuretic peptide (ANP) are antiphasic in normal subjects and in essential hypertension. The aim of the present study was to assess the circadian rhythms of BP and ANP in 20 patients with stable congestive heart failure (CHF), divided into two groups of 10 according to their New York Heart Association functional class. A matched control group of 10 normal volunteers was also studied. Noninvasive BP monitoring at 15-min intervals was performed for 24 h. Peripheral blood samples were also obtained at 4-h intervals starting from 08:00 h. The mean (+/- SEM) circadian mesors of ANP plasma levels were 13.4 +/- 1.7 pmol/L in the control group, 28.6 +/- 2.4 pmol/L in the group of 10 patients in class II, and 81.5 +/- 12 pmol/L in the group of 10 patients in class III-IV. In normal subjects, plasma ANP concentration was highest at 04:00 h (21.5 +/- 2.7 pmol/L) and lowest at 16:00 h (8.8 +/- 2.4 pmol/L; p less than 0.01). Both groups of patients with CHF showed no significant circadian change in the plasma levels of ANP and also a significantly blunted circadian rhythm of BP. Cosinor analysis confirmed the loss of the circadian rhythms of ANP and BP in CHF patients. Our findings support the existence of a causal relationship between the circadian rhythms of ANP and BP.
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PMID:Consistent changes in the circadian rhythms of blood pressure and atrial natriuretic peptide in congestive heart failure. 184 Jan 79


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