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

Hemodynamic changes during exercise were evaluated in 20 patients with severe, chronic congestive heart failure. Two groups were identified by their stroke work response to maximal exercise. Group I (eight patients) showed an increase in stroke work index. This occurred because the stroke volume increased and the difference between mean systolic pressure and left ventricular filling pressure increased. Group II (12 patients) showed a decrease in stroke work index. This occurred because stroke volume decreased while the difference between mean systolic pressure and left ventricular filling pressure did not change. Despite hemodynamic differences, the groups could not be distinguished by the usual clinical criteria for heart failure including etiology, New York Heart Association functional class, heart size on chest X-ray film or duration of heart failure. Clinical criteria are relatively insensitive in predicting the exercise hemodynamics of any given patient with chronic severe heart failure. Determining the exercise hemodynamics may be helpful as a means of assessing left ventricular functional reserve in heart failure. Prognostic implications, drug therapy and prescription of activities may require adjustment based on this spectrum of hemodynamic response to exercise in patients with chronic heart failure.
Am J Cardiol 1979 Nov
PMID:Detection of left ventricular functional reserve by supine exercise hemodynamics in patients with severe, chronic heart failure. 49 99

Hemodynamic response to exercise before and 10 minutes after propranolol (5 mg intravenously) was studied in 10 young patients with pure mitral stenosis who had normal sinus rhythm and no cardiac failure. After propranolol the mean heart rate and cardiac index at rest were lower than during the control state (respectively, 95 +/- 4 versus 82 +/- 3 beats/min, P less than 0.005; 3.4 +/- 0.2 versus 2.8 +/- 0.1 liters/min per m2, P less than 0.025). As a result, the mean pulmonary wedge pressure and mean mitral valve gradient at rest were lower (respectively, 22 +/- 2 versus 18 +/- 2 mm Hg, P less than 0.005; 24 +/- 2 versus 17 +/- 2 mm Hg, P less than 0.001). During exercise after propranolol the values of pulmonary wedge pressure and mitral valve gradient were lower than control values during exercise (respectively, 39 +/- 3 versus 30 +/- 2 mm Hg, P less than 0.005; 44 +/- 3 versus 32 +/- 3 mm Hg, P less than 0.005), again because of the lower heart rate and cardiac index (130 +/- 6 versus 104 +/- 6 beats/min, P less than 0.001; 4.6 +/- 3 versus 3.7 +/- 2 liters/min per m2, P less than 0.01). Left ventricular end-diastolic pressure and stroke index showed no significant changes. Thus, propranolol may benefit patients with pure mitral stenosis with sinus rhythm and no cardiac failure whose symptoms occur during those reversible conditions characterized by an increase in heart rate or cardiac output, or both.
Am J Cardiol 1979 Nov
PMID:Hemodynamic response to exercise after propranolol in patients with mitral stenosis. 49 1

In order to determine and compare the pharmacodynamic responses to single and multiple dose prazosin therapy in cardiac failure, 14 patients with severe low-output heart failure underwent central and regional hemodynamic measurements after random placement in one of two prazosin dosing schedules. A single 5 mg oral dose of prazosin (Group A, no. = 7) significantly increased the cardiac index and stroke volume index while significantly decreasing systemic, pulmonary and pulmonary capillary wedge pressures and vascular resistances. Hepatic plasma flow and limb blood flow increased after the single dose. Striking attenuation of these hemodynamic effects occurred when the same dose was administered after 24 hours of pretreatment with oral prazosin, 2 mg every 8 hours (Group B, no. = 7). The plasma prazosin levels of the two groups, drawn 2 hours after administration, were 24.5 and 30.5 ng/ml, respectively. Repeated administration of prazosin in patients with congestive heart failure results in rapid attenuation of its beneficial central and regional hemodynamic effects. The usefulness of this vasodilator as a preload- and afterload-reducing agent in the clinical setting of chronic congestive heart failure may be limited by the development of pharmacodynamic tolerance.
Am J Cardiol 1979 Nov
PMID:Development of pharmacodynamic tolerance to prozosin in congestive heart failure. 49 12

Changes in left ventricular performance were evaluated in 14 patients with functional New York Heart Association class III or IV chronic heart failure before and after the addition of oral hydralazine to conventional therapy. With conventional therapy, cardiac output increased from 3.4 +/- 0.8 (mean +/- 1 standard deviation) at rest to 4.7 +/- 1.4 liters/min during exercise. This increase in cardiac output on exercise during conventional therapy was mainly due to an increase in heart rate. After the addition of hydralazine, cardiac output at rest increased to 5.0 +/- 1.4 liters/min. The increase in cardiac output was essentially due to an increase in stroke volume. This enhanced stroke volume after hydralazine therapy was maintained during exercise. Hydralazine therapy did not change either the left ventricular filling pressure at rest or the magnitude of increase in left ventricular filling pressure during exercise. Nevertheless, increased cardiac output and stroke volume with similar changes in left ventricular filling pressure during exercise indicated improved left ventricular performance after hydralazine therapy. After short-term hydralazine therapy, symptom-limited peak exercise work load, duration of exercise and maximal oxygen consumption during exercise did not increase. Clinical follow-up at 2 months after long-term therapy revealed subjective improvement in exercise tolerance in 13 of the 14 patients.
Am J Cardiol 1979 Nov
PMID:Influence of short-term oral hydralazine therapy on exercise hemodynamics in patients with severe chronic heart failure. 49 13

The effects of acute myocardial infarction on the pharmacokinetics of digoxin were studied. Digoxin, 0.75 mg, was given orally to 12 patients with left-sided cardiac failure due to acute myocardial infarction and to 9 healthy control subjects. Serum concentration of digoxin in the first 4 hours and the area under the serum concentration-time curve in the first 12 hours after administration of the drug were lower in patients with infarction than in control subjects (P less than 0.01). The 24 hour area under the concentration curve, the amount excreted in urine and the renal clearance did not differ between the groups. The 24 hour area under the concentration curve correlated with the predigoxin pulmonary capillary wedge pressure and with heart rate (P less than 0.01). The decrease of renal clearance of digoxin was related to the serum activity of MB isoenzyme of creatine kinase (P less than 0.001). Morphine reduced and delayed the peak serum concentrations of digoxin (P less than 0.001). Thus, the absorption of oral digoxin was slower and the peak concentrations remained lower in patients with acute myocardial infarction than in healthy control subjects. However, the total amount of digoxin absorbed was unchanged.
Am J Cardiol 1979 Nov
PMID:Pharmacokinetics of digoxin in patients with acute myocardial infarction. 49 14

After the acute onset of heart failure and in the absence of acute myocardial infarction, plasma volume may occasionally be depleted to the extent that the patient presents with clinical signs of circulatory shock. In five patients, the acute onset of clinical and radiographic signs of cardiogenic pulmonary edema were associated with reduction in arterial blood pressure and cardiac output. The pulmonary arterial wedge pressure was within normal limits but a reduction in plasma volume was demonstrated, which is best explained by the rapid translocation of plasma water that represented pulmonary (and most likely also peripheral) edema fluid. The infusion of 5 percent albumin solution significantly increased cardiac output, mean arterial pressure and cardiac work, reversed lactic acidosis, enhanced furosemide-induced diuresis and was followed by a decrease in both clinical and radiographic signs of pulmonary edema. These observations confirm that volume expansion may constitute appropriate treatment for some patients with cardiogenic pulmonary edema who may present with hypotension and who are unresponsive to conventional therapy.
Am J Cardiol 1979 Dec
PMID:Hypovolemia and hypotension complicating management of acute cardiogenic pulmonary edema. 50 39

A new multivariate stepwise linear regression analysis (Cox's model) with survival time as prognostic endpoint was utilized in 281 patients with acute myocardial infarction. From 18 prognostic factors occurring during the first 5 days in the Coronary Care Unit a new prognostic index was calculated for the chance of survival in the first 36 days after admission. The significant prognostic variables were heart failure, cardiogenic shock, atrioventricular block and age. The total group of patients was classified in 6 subgroups with different mean indices and prognosis. There were 2 large groups of patients with relative bad and good prognosis (with and without heart failure). Over half of the patients had no prognostic variables. There was a trend of overestimating the expected deaths. A definite cardiac cause of death was shown by 23 patients (82%). This prognostic index based on the 4 variables can for the individual patient predict the chance of survival, which can be the basis of an individualized duration of hospital stay.
Eur J Cardiol 1979 Nov
PMID:Short-term prognostic index in acute myocardial infarction. Multivariate analysis by Cox model. 51 Mar 46

Thirteen patients out of 42 affected by acute myocardial infarction complicated by atrio-ventricular block survived the illness and were discharged from hospital. Eight of these patients (60%) died, all in the first six months of follow up: 3 suddenly and 5 in consequence of progressive heart failure. Dead patients were all in III or IV class of the N.Y.H.A. Three had been previously submitted to permanent pacing, one of these died suddenly. Five patients survive at the end of follow up that varies from 2 to 56 months. Of these five survivors 1 patient belong to the I class of the N.Y.H.A., 1 to the II class and 3 to the III class. Among survivors there is only 1 patient with permanent pacing. This is also the only one who had syncopal attacks during a period of pacing failure. Prognosis of patients with myocardial infarction complicated by atrio-ventricular block who survive illness is dependent on functional class and seems to be not considerably modified by permanent pacing.
G Ital Cardiol 1979
PMID:[Long-term prognosis of survivors from anterior myocardial infarction complicatedy by complete atrio-ventricular block (author's transl)]. 54 Jun 90

Tienilic acid (TA) is a common new diuretic agent with a potent uricosuric action. In a double-blind cross-over study its antihypertensive effect was compared to that of hydrochlorothiazide (HCT). 20 patients with essential hypertension were studied: after I weeks of placebo wash-out 10 patients received TA (dose range 250-750 mg/die) and 10 HCT (dose range 50-150 mg/die), for 5 weeks. Systolic and diastolic blood pressures were significantly and equally reduced (p < 0.001) after the first week of treatment in both groups. While serum uric acid concentration increased after HCT, it was significantly reduced (p < 0.001) after TA treatment. Serum potassium was slightly reduced with both treatments. Serum tryglicerides, unchanged after HCT, showed a slight tendency to reduction on TA treatment. Ten patients with congestive heart failure, on full digitalis treatment, were given TA (dose range 250-1000 mg/die): in each patient a prompt diuretic effect was observed, associated to a significant reduction of body weight and to a marked improvement of the clinical signs of heart failure. Therefore, TA is an effective diuretic agent which may be conveniently used in the treatment of arterial hypertension and congestive heart failure, as it induces a diuretic effect comparable to that obtained with HCT, reducing at the same time, serum uric acid levels.
G Ital Cardiol 1979
PMID:[Tienilic acid in the treatment of arterial hypertension and congestive cardiac insufficiency]. 54 82

A new oral vasodilator, prazosin, was evaluated in twenty patients with refractory congestive heart in a double blind non cross-over trial. Patients were divided into two groups. The first (group A) was treated by prazosin (40-50 microgram/Kg/pro die) for 20 days, the second was given placebo for the same period. Ventricular performance was assessed by measurement of the systolic time intervals, the peak time of the first derivative of the apexcardiogram (delta ACG), pressure-rate product and clinical evaluation. After ten days of prazosin left ventricular ejection time (LVET) increased (P < 0.01), pre-ejection period (PEP) and relation PEP/LVET were reduced (respectively: P < 0.05 and P < 0.01). Similarly the peak of delta ACG and pressure-rate product decreased significantly (respectively: P < 0.05 and P < 0.01). Symptomatology improved in NYHA functional class (3.7 to 2.4, P < 0.001). After twenty days of prazosin there was no further significant improvement in myocardial performance. No significant changes of clinical course and of the same parameters were observed in patients of group B. It is concluded that prazosin is effective in improving cardiac performance in refractory heart failure for its balanced dilator action on the arteriolar and venous vessels.
G Ital Cardiol 1979
PMID:[Efficacy of prazosin in severe cardiac insufficiency]. 54 85


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>