Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

7 consecutive patients with congestive heart failure refractory to standard therapy were treated with nitroglycerin ointment (GTNO). The pulmonary wedge pressure decreased from a control value of 30+/-1 to 15+/-1 mm Hg (mean +/-SEM), and the arteriovenous oxygen difference narrowed from 6.8+/-0.5 to 5.5+/-0.3 ml%, after GTNO therapy. The heart rate decreased in 5 patients and the systolic blood pressure was either unchanged or decreased slightly. A reduction in the echocardiographic end diastolic dimension was noted in all patients. The transmyocardial gradient (systemic artery diastolic pressure - pulmonary artery wedge pressure) increased in all except 1 subject. The double product decreased in 5 of the 7 patients. Hemodynamic improvement was maintained for 4.5-7 h. All patients were symptomatically improved on chronic GTNO treatment. Our results indicate that GTNO is a useful agent in the management of heart failure which is unresponsive to standard therapy.
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PMID:Use of nitroglycerin ointment in congestive heart failure. Results of acute and chronic therapy. 10 Feb 19

Ten patients with severe congestive heart failure after acute myocardial infarction were treated with 40 mg isosorbiddinitrate-retard every 4 hours and additional sublingual nitroglycerine. There was a prompt improvement of hemodynamic parameters which was maintained for 24 hours: pulmonary capillary wedge pressure (PCW) decreased within 10 min from 26 +/- 5 (X +/- SEM) to 17 +/- 2 mm Hg (p less than 0.01) and mean arterial pressure from 109 +/- 7 to 98 +/- 6 mm Hg. The heart rate remained constant, and the cardiac index improved from 2.3 +/- 0.2 to 2.5 +/- 0.21/min/m2. The fall in blood pressure was dependent on the pretreatment pressure: it was significantly greater in patients with elevated blood pressure and only slight in those with a low pretreatment blood pressure. In the presented series of patients neither adverse effects or symptoms nor a critical reduction of blood pressure were observed. Combined oral treatment with isosorbiddinitrate and nitroglycerine can therefore be carried out without invasive blood pressure monitoring.
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PMID:[Peroral nitrate therapy in severe cardiac insufficiency following acute myocardial infarct]. 10 29

Isosorbide dinitrate is an effective vasodilator that improves resting left ventricular performance in patients with congestive heart failure, but little is known of the effect of the drug on the response to exercise. Bicycle exercise to symptomatic maximum was performed by 18 patients with class II to IV congestive heart failure before and 90 minutes after administration of isosorbide dinitrate, 40 mg orally. Although resting pulmonary wedge pressure and systemic vascular resistance were significantly reduced after isosorbide dinitrate, exercise duration was not altered and maximal oxygen consumption was not significantly changed (13.6 +/- 1.3 [SEM] standard error of the mean versus 13.8 +/- 1.2 ml/kg per min). At peak exercise pulmonary wedge pressure of 37.1 +/- 1.7 mm Hg, cardiac index of 4.19 +/- 0.35 liters/min per m2, and systemic vascular resistance of 14.7 +/- 1.3 units were not significantly different after nitrate administration. However, at submaximal loads, pulmonary wedge pressure was reduced from 33.6 +/- 1.7 to 27.9 +/- 1.8 mm Hg (P less than 0.01), and systemic resistance from 16.5 +/- 1.5 to 13.7 +/- 1.0 units (P less than 0.01) after administration of isosorbide dinitrate. Thus, short-term administration of nitrates does not improve maximal exercise capacity or left ventricular performance at maximal exercise in patients with congestive heart failure, but it does appear to improve pump function at submaximal work loads and may therefore enable patients to perform limited exercise more comfortably.
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PMID:Effect of isosorbide dinitrate on response to submaximal and maximal exercise in patients with congestive heart failure. 43 62

Resting hemodynamics improve during vasodilator administration in patients, with congestive heart failure (CHF), but the effects of these agents on exercise is unknown. Twenty-two patients with class II or III CHF performed bicycle exercise to symptomatic maximum before and 90 minutes after random double-blind administration of oral hydralazine (100 mg) and isosorbide dinitrate (40 mg) (11 patients, group 1) or placebo (11 patients, group 2). Exercise duration was unchanged after treatment in either group. Maximal oxygen consumption changed insignificantly in both groups, from 12.6 +/- 1.2 (SEM) to 13.6 +/- 1.6 ml/kg/min in group 1, and from 11.7 +/- 1.4 to 13.4 +/- 1.7 ml/kg/min in group 2. Maximal cardiac index was unchanged in both group 1 (4.00 +/- 0.33 to 4.41 +/- 0.29 l/min/m2) and group 2 (4.11 +/- 0.43 to 4.14 +/- 0.42 l/min/m2). Systemic vascular resistance at peak exercise was also unchanged in both group 1 (14.1 +/- 1.6 to 11.8 +/- 1.0 units) and group 2 (14.7 +/- 1.6 to 13.5 +/- 1.6 units). at submaximal exercise (300 kilopond-meters/min), however, cardiac index after treatment increased in group 1 (0.51 +/- 0.18 l/min/m2, p less than 0.05) and systemic vascular resistance decreased (-3.3 +/- 1.3 units, p less than 0.05), but were unchanged in group 2. Thus, although vasodilators do not improve maximal exercise capacity acutely, they can improve hemodynamics at lower work loads which may, therefore, be better tolerated in patients with CHF.
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PMID:Immediate effects of hydralazine-isosorbide dinitrate combination on exercise capacity and exercise hemodynamics in patients with left ventricular failure. 43

Eighty-six of 452 patients (19%) with chronic bifascicular block were found to have no clinically apparent associated organic heart disease (OHD) and were defined as having primary conduction disease (PCD). Comparison of patients with PCD and OHD revealed a significantly lower incidence of the following clinical variables in the PCD patients (p less than 0.001): exertional angina, dyspnea, congestive heart failure, cardiomegaly, functional class I (all by study design), left bundle branch block and premature ventricular contractions. Both mean AH and HV intervals were significantly shorter in patients with PCD (p less than 0.01). The incidence of HV prolongation was 21% in PCD and 41% in OHD patients (p less than 0.001). All patients were prospectively followed for 21-2998 days with a mean +/- SEM of 1209 +/- 66 days for PCD and 1172 +/- 36 days for OHD. Atrioventricular (AV) block developed in three patients from the PCD group and 26 from the OHD group (NS), with spontaneous block occurring in one (1%) PCD patient and 19 (5%) OHD patients (p less than 0.05). Annual mortality due to sudden death as well as total cardiovascular mortality (including sudden death) for the 5-year follow-up was significantly lower in patients with PCD. Patients with PCD have significantly lower incidence of electrophysiologic abnormalities and subsequent spontaneous AV block as well as cardiovascular and sudden death mortality. The diagnosis of PCD based on clinical criteria probably underestimates the presence of underlying OHD, as suggested by a small but definite risk of cardiovascular mortality.
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PMID:Significance of chronic bifascicular block without apparent organic heart disease. 44 30

The kinetics of oral prazosin was studied in 10 healthy normal subjects (NS) and in 9 patients with congestive heart failure (CHF). NS received a single 5-mg dose, and blood concentrations of prazosin (CB) were measured, using a specific HPLC assay, during an 8-hr period. CHF patients received a 2-mg dose after which CB was measured for 10 hr. These patients then received 2 to 5 mg prazosin every 8 hr for 48 hr. After the last dose of prazosin, CB was measured for 24 hr. After the initial dose, time to peak CB did not differ significantly between that of the NS (123 +/- 19 SEM min) and of patients with CHF (132 +/- 31.3 min). AUC/mg prazosin was greater (p less than 0.001) in patients with CHF (3,385 +/- 380 Ng x min/ml) than in NS (1,603 +/- 208 ng x min/ml). Elimination of prazosin from blood was slower in CHF patients (t1/2 = 374 +/- 33.4 min) than in NS (t1/2 = 144.5 +/- 4.3 min) (p less than 0.001). These data suggest that in patients with CHF the elimination of prazosin is substantially slower than in NS and therefore higher steady-state prazosin concentrations can be expected in CHF patients than in NS.
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PMID:Influence of congestive heart failure on prazosin kinetics. 44 45

Trimazosin is a new quinazoline derivative vasodilator previously thought to act primarily on resistance vessels. Vasodilators characteristically improve hemodynamics in patients with left ventricular failure. Trimazosin in single oral doses of 100 to 300 mg was given to 6 patients with class III-IV congestive heart failure due to ischemic or primary cardiomyopathy and hemodynamics were monitored for 4 hr. Onset of action was apparent at 1 hr, with peak effects occurring at 1 to 3 hr and significant effects persisting at 4 hr. At peak, mean systemic arterial pressure fell from 91.2 +/- 4.8 (SEM) to 82.5 +/- 2.5 mm Hg (p less than 0.05), heart rate was unchanged, and cardiac index (by dye dilution) was up to 2.12 +/- 0.27 from 1.76 +/- 0.33 L/min/m2 (NS). Right heart pressures (by Swan-Ganz catheterization) were reduced, right atrial, 11.3 +/- 2.1 to 8.7 +/- 1.6 mm Hg (p less than 0.02), mean pulmonary arterial pressure, 40.7 +/- 4.6 to 33.8 +/- 4.8 mm Hg (p less than 0.01), and pulmonary arterial wedge, 30.7 +/- 4.5 to 23.8 +/- 5.0 mm Hg (p less than 0.01). Forearm venous capacitance, by occlusion plethysmography, increased from 0.83 +/- 0.18 ml/100 gm to 1.12 +/- 0.22 ml/100 gm after trimazosin (p less than 0.01). Trimazosin is an orally effective vasodilator that acts on both resistance and capacitance vessels in patients with congestive heart failure.
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PMID:Hemodynamic effects of trimazosin in patients with left ventricular failure. 61 5

Aminopyrine disposition was studied in 11 patients with congestive heart failure (CHF) and 15 control patients. The aminopyrine metabolic clearance rate was 29.7 +/- 7.1 ml/min (mean +/- SEM) in the patients with CHF and 125.1 +/- 5.7 ml/min (mean +/- SEM) in the control patients (p less than 0.01). The aminopyrine breath test was 2.6 +/- 0.4 per cent (mean +/- SEM) in the patients with CHF and 5.6 +/- 0.3 per cent (mean +/- SEM) in the control subjects (p less than 0.01). Probably due to fluid retention in CHF, the apparent volume of distribution of aminopyrine increased to 63.3 +/- 4.9 liters (mean +/- SEM) in patients with CHF from 43.1 +/- 1.9 liters (mean +/- SEM) in control patients, thereby further impairing aminopyrine elimination in patients with CHF (p less than 0.01). The aminopyrine breath test was measured in a group of eight patients before treatment for an acute episode of CHF and seven to 10 days after initiation of therapy: in each patient clinical improvement was associated with an increased aminopyrine breath test, mean values of aminopyrine breath test increasing from 2.8 per cent before treatment to 5.2 per cent after initiation of treatment (p less than 0.01). These results suggest that in patients with CHF hepatic drug-metabolizing activity is imparied, and the volume of distribution of drugs is increased, with consequent retardation in rates of drug elimination.
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PMID:Reduced drug elimination in congestive heart failure. Studies using aminopyrine as a model drug. 68 23

Severe constriction of the suprarenal abdominal aorta of 3-kg rabbits to 3.7+/-0.2 mm2 and maintenance of a daily sodium intake of 10 mE q by infusion of 0.9% sodium chloride resulted in a progressive increase in central ear arterial pressure to 106+/-3 (SEM) mm Hg (control=79+/-1). This was accompanied by a progressive increase in left ventricular end-diastolic pressure to 22+/-2 mm Hg (control=3+/-1), plasma renin activity to 21+/-5 ng of angiotensin/hour per ml (control=5+/-1), plasma aldosterone concentration to 99+/-23 pg/ml (control=14+/-4), and plasma sodium concentration to 142+/-1 mEq/liter (control=136+/-1). Urinary excretion of sodium decreased to 3.9+/-0.7 mEq/day and marked fluid retention occurred. We also found that these changes were accompanied by a decrease in hematocrit to 24+/-2% (control=40+/-1), formation of 36+/-9 ml of fluid in the thoracic cavity, 33+/-9 ml of ascites, pulmonary congestion and edema, hepatic congestion, and enlargement and hypertrophy of both the left and right ventricles. All rabbits died of ventricular failure at a time that was partly related to the degree of aortic constriction and that ranged from 2 to 12 days. The model we have established is chronic, highly reproducible, easy to produce, and inexpensive, and resembles the clinical syndrome of right and left congestive heart failure in man. Furthermore, the studies provide evidence for an important role of the renin-angiotensin-aldosterone system in the fluid retention that leads to pulmonary and systemic venous congestion after suprarenal aortic constriction.
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PMID:The renin-angiotensin-aldosterone system in rabbits with congestive heart failure produced by aortic constriction. 83 74

The renin-aldosterone system was studied in cardiomyopathic hamsters (CMH) before and after the onset of untreated clinical congestive heart failure. Age-matched random-bred hamsters (RB) served as controls. Before heart failure, there were no differences in body weight accretion, sodium balance, plasma renin activity or in vitro aldosterone production. After the onset of heart failure in CMH, body weight increased at a greater rate than in RB and positive sodium balance was nearly twice control levels. Although plasma renin activity was greater (P less than 0.005) in CMH than in RB (23.4+/-4.2 (mean+/-SEM) vs. 3.8+/-1.8 ng/ml/h), aldosterone production (101+/-15 vs. 95+/-16 ng/h) did not differ. Plasma aldosterone was low or undetectable in RB and in CMH in heart failure. In response to angiotensin stimulation, aldosterone production increased in both strains and did not differ. No difference in muscle potassium content, potassium balance or excretion was detected. Thus, in CMH, congestive heart failure is attended by increased plasma renin activity without a significant increase in aldosterone production, a dissociation which does not appear to be due to adrenal unresponsiveness to angiotensin II or to potassium depletion.
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PMID:Renin and aldosterone in the cardiomyopathic hamster in congestive heart failure. 88 11


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