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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

24 patients with severe heart failure (NYHA III) were randomly assigned to an additional therapy with captopril or enalapril. The mean daily dose of captopril was 56 +/- 2 mg and of enalapril, 9.6 +/- 0.9 mg. After a mean of 9 days, the influence of both inhibitors of the angiotensin converting enzyme (ACE-inhibitors) on hemodynamics and renal function was evaluated. The mean arterial pressure in the group treated with captopril (group A) fell by 11 +/- 2 mm Hg (p less than 0.001), with enalapril (group B) by 13 +/- 3 mm Hg (p less than 0.01), the difference between the groups not being significant. Heart rate decreased in both groups to a similar degree. The change was significant only in the patients treated with enalapril (13 +/- 4/min; p less than 0.05 vs. 11 +/- 5/min in group A). Stroke volume index increased by 10 +/- 2 ml/m2 in group A vs. 12 +/- 2 ml/m2 in group B; both increases were highly significant (p less than 0.001). Mean decreases in pulmonary artery and right atrial pressure were comparable in both groups. The hemodynamic improvement was not different with both ACE-inhibitors. Serum sodium and potassium before therapy were 137 +/- 1 mmol/l and 4.1 +/- 0.2 mmol/l in group A and 139 +/- 1 mmol/l and 3.8 +/- 0.1 mmol/l in group B and serum creatinine was 1.2 +/- 0.1 mg/dl in both groups. Neither serum electrolytes nor serum creatinin were changed significantly by therapy with captopril or enalapril.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Comparison of captopril with enalapril in the therapy of heart failure: effect on hemodynamics and kidney function]. 285 Jun 82

Nisoldipine, a calcium entry blocker, was given to 10 patients with congestive heart failure. During a 2 month follow-up period, 7 of the 10 patients were readmitted with pulmonary edema; daily furosemide doses were increased (128 +/- 87 to 192 +/- 135 mg/day, p less than 0.01), and plasma creatinine increased (1.5 +/- 0.5 to 1.8 +/- 0.6 mg/dl, p less than 0.05) (all values mean +/- SD). Despite this unfavorable clinical course, nisoldipine caused some beneficial chronic (1 month) hemodynamic effects. It decreased systemic vascular resistance (from 1,781 +/- 229 to 1,306 +/- 345 dynes X s X cm-5, p less than 0.01), decreased mean arterial pressure (from 88 +/- 0 to 74 +/- 4 mm Hg, p less than 0.001) and increased stroke volume index (from 27 +/- 6 to 33 +/- 9 ml/min per m2, p less than 0.02). Heart rate, pulmonary capillary wedge pressure and stroke work index did not change. However, nisoldipine's chronic renal and neurohumoral effects were not as favorable. These were assessed during a 5 hour water load (15 ml/kg body weight of 5% dextrose in water) and compared with the effects of a water load before therapy. Nisoldipine did not change creatinine clearance or sodium excretion, but decreased water excretion (from 58 +/- 35 to 46 +/- 40% of water load in 5 hours). Over this 5 hour study, mean plasma vasopressin was also higher with nisoldipine (1.9 +/- 2.3 versus 2.7 +/- 3.2 pg/ml, p less than 0.05), but mean plasma aldosterone was lower (67 +/- 31 to 47 +/- 27 mg/dl, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic renal and neurohumoral effects of the calcium entry blocker nisoldipine in patients with congestive heart failure. 288 Aug 84

The risks of complications like death, myocardial infarction and stroke increase continuously with increasing age. Therefore, the chances of detecting effects of treatment in trials also increase when patients get older. The relationships between different end-points change with age, e.g. the ratio between stroke and MI increases with age. However, interventions not related to the interventions under study may also increase, causing dilution of effects. The older subject may also be more vulnerable to the side-effects of treatment. Side-effects, and quality-of-life measures, which indeed may vary with age, must be properly balanced against effects on 'hard' end-points. A review of trials in patients with hypertension and myocardial infarction shows that effects of various interventions have been at least as great in older as in younger patients. However, metabolic side effects such as impaired glucose metabolism, increased serum creatinine, and increased uric acid levels have not been negligible, and such effects may turn out to be more hazardous in the elderly than in younger patients. The balance between positive and negative effects must be properly assessed in relation to the prognosis of the untreated condition. Patients who have suffered a myocardial infarction have, in general, a more serious prognosis than most hypertensives, and more side-effects of treatment may therefore be accepted in patients with myocardial infarction.
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PMID:Trials in coronary heart disease and hypertension with special reference to the elderly. 289 91

The mechanisms by which variations in blood ionized calcium (Ca2+) influence systemic arterial pressures independent of changes in extracellular fluid volume, pH, and electrolytes are unknown. To study this issue, we dialyzed eight stable hemodialysis patients on three separate occasions during 1 week with dialysates differing only in calcium concentration. Ultrafiltration was adjusted to achieve the patient's estimated dry weight. Postdialysis Ca2+ was measured, as were arterial blood gases, electrolytes, magnesium, blood urea nitrogen, creatinine, and hematocrit. Blood pressures and two-dimensional, targeted M-mode echocardiograms were recorded with the patient in the supine position after 15 minutes of rest. Postdialysis, three different levels of Ca2+ were achieved. Other measured biochemical variables and body weight did not differ among the three study periods. Changes in Ca2+ correlated directly with changes in systolic, diastolic, and mean blood pressures, left ventricular stroke volume, and cardiac output. In contrast, heart rate, left ventricular end-diastolic dimension, and total systemic vascular resistance were not altered significantly by changes in Ca2+. Thus, alterations in Ca2+ within the physiological range affect systemic blood pressure primarily through changes in left ventricular output rather than in peripheral vascular tone in stable dialysis patients.
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PMID:Physiological mechanisms for calcium-induced changes in systemic arterial pressure in stable dialysis patients. 292 Oct 76

To evaluate the influence of renal function on the efficacy of converting-enzyme inhibition in patients with severe chronic heart failure, we measured the long-term hemodynamic and clinical responses to captopril in 101 consecutive patients with heart failure grouped according to pretreatment serum creatinine concentration (group I, less than 1.4 mg/dL; group II, 1.4 to 2.8 mg/dL; and group III, greater than 2.8 mg/dL). After 1 to 3 months of treatment, patients with preserved renal function (group I) had greater increases in stroke volume index and greater decreases in left ventricular filling pressure and systemic vascular resistance than did patients with renal impairment (groups II and III) (p less than 0.05). Clinical improvement paralleled these hemodynamic benefits; only 2 of 12 patients with severe renal insufficiency (group III) improved clinically compared with 29 of 40 patients with preserved renal function (group I) and 29 of 49 patients with mild-to-moderate renal impairment (group II), (p less than 0.005). Therapy-limiting rash and dysgeusia occurred most frequently in patients with renal impairment. Our findings support an important role for the kidneys in mediating the beneficial actions of captopril in patients with severe congestive heart failure.
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PMID:Influence of renal function on the hemodynamic and clinical responses to long-term captopril therapy in severe chronic heart failure. 293 91

Alpha-human atrial natriuretic polypeptide (alpha-hANP) was applied to 16 clinical patients, 6 patients with essential hypertension, 7 patients with congestive heart failure and 3 patients with cirrhosis. Following intravenous bolus injection of 400 micrograms of synthetic alpha-hANP, a hypotensive effect of very rapid onset was found, which was more potent in the hypertensive patients than in the normotensive cases. Cardiac functions were improved significantly with a similar time course as the depressor response in the cases of heart failure or hypertension. Hemodynamic observations showed a marked increase in cardiac output, cardiac index, stroke volume, ejection fraction and ejection rate, and a concomitant decrease of the pressure in the right side of the heart and pulmonary circulation in these subjects. In addition, the renal response to alpha-hANP induced obvious increases in urine volume, electrolytes and creatinine excretions in all the subjects. Finally, plasma levels of aldosterone, Arg-vasopressin and noradrenaline were also altered by alpha-hANP. No significant side effects were registered. The above result confirms the therapeutic actions of alpha-hANP in human subjects and opens the possibility to research alpha-hANP as a powerful pharmacological tool as well as potential new medicine for human disorders.
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PMID:Therapeutic actions of alpha-human atrial natriuretic polypeptide in 16 clinical cases. 295 43

Synthetic alpha-human atrial natriuretic polypeptide was infused in patients with congestive heart failure (CHF) (New York Heart Association class III or IV) and in those without CHF. The infusion of atrial natriuretic polypeptide (ANP) at a rate of 0.1 microgram/kg/min significantly decreased pulmonary capillary wedge pressure and increased stroke volume index in all of the patients with CHF, whereas it decreased pulmonary capillary wedge pressure but caused no significant change in stroke volume index in the patients without CHF. Concomitant significant reductions in total systemic resistance were observed in both groups of patients. The ANP infusion significantly increased the urine volume, the excretion of sodium, and endogenous creatinine clearance in the patients without CHF. In the patients with CHF, it also showed a tendency to increase all these variables, but the urine volume did not correlate with the reduction in pulmonary capillary wedge pressure. The ANP infusion also decreased plasma aldosterone concentrations in these patients, although no significant difference was observed in the decrement of the plasma aldosterone concentration in the patients with and those without CHF. These findings indicate that the ANP infusion improves left ventricular function in patients with CHF, and suggest that this improvement results mainly from the vasodilating activity of ANP.
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PMID:Clinical application of atrial natriuretic polypeptide in patients with congestive heart failure: beneficial effects on left ventricular function. 295 23

Hemodynamic, renal, and hormonal effects of intravenous bolus injection of 50 micrograms synthetic alpha-human atrial natriuretic peptide (alpha-hANP) were studied in eight patients with congestive heart failure. alpha-hANP caused significant reductions in mean blood pressure and systemic vascular resistance. These responses were sustained up to 90 minutes and not accompanied by reflex tachycardia. Cardiac index and stroke volume index increased significantly at 90 minutes and pulmonary capillary wedge pressure, pulmonary arterial pressure, and mean right atrial pressure remained unchanged. Urine volume, urinary sodium excretion, creatinine clearance, and fractional excretion of sodium increased significantly, but fractional excretion of potassium and phosphate did not change. Elevated plasma renin activity, plasma aldosterone, and norepinephrine were suppressed after the injection of alpha-hANP. The bolus injection of this peptide has moderately hypotensive, vasorelaxant, and natriuretic effects in patients with congestive heart failure.
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PMID:Hemodynamic, renal, and hormonal responses to alpha-human atrial natriuretic peptide in patients with congestive heart failure. 295 95

The impact of microalbuminuria on mortality as well as other risk factors was investigated in a 10-year follow-up study of 503 predominantly non-insulin-dependent diabetic patients of whom 265 had died. Using Cox's regression analysis the prognostic influence of age, sex, age at diagnosis, known diabetes duration, blood pressure, fasting plasma glucose, relative weight, serum creatinine, retinopathy, and treatment was evaluated as well as morning urine albumin concentration (UAC) in four categories, i.e. UAC less than or equal to 15 micrograms/ml (normal), 15 micrograms/ml less than UAC less than or equal to 40 micrograms/ml, 40 micrograms/ml less than UAC less than or equal to 200 micrograms/ml and UAC greater than 200 micrograms/ml. Age, UAC, known duration, and serum creatinine were the only significant risk factors. After correction for the other three independent risk factors, the hazard ratios in the elevated UAC categories relative to the group with UAC less than or equal to 15 micrograms/ml were 1.53 (p = 0.007), 2.28 (p = 0.000002), and 1.82 (p = 0.02). The statistically significant correlations with UAC were: age (r = 0.09, p less than 0.05), duration (r = 0.14, p less than 0.01), systolic blood pressure (r = 0.12, p less than 0.01), serum creatinine (r = 0.33, p less than 0.001), and fasting plasma glucose (r = 0.12, p less than 0.01). Increased UAC was associated also with retinopathy (p = 0.01). Fifty-eight per cent of the deaths were caused by cardiovascular disease or stroke; only 3% died from uraemia. A reinvestigation including blood pressure, fasting plasma glucose, and UAC was made on 208 survivors.
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PMID:Microalbuminuria: a major risk factor in non-insulin-dependent diabetes. A 10-year follow-up study of 503 patients. 296 77

To evaluate the long-term effects of orally administered levodopa, 11 patients with chronic congestive heart failure (NYHA III-IV) were studied during maintenance therapy (30 +/- 1 days) and after withdrawal from levodopa. The daily levodopa dose was 4 g in six patients; because of side effects the levodopa dose was reduced to 2-3 g in the remaining patients. After withdrawal of levodopa, mean pulmonary capillary wedge pressure and mean right atrial pressure increased significantly (from 19 +/- 2 to 24 +/- 3 and from 7 +/- 2 to 9 +/- 2 mmHg, respectively). Effective renal plasma flow was 329 +/- 57 during levodopa therapy and decreased significantly to 252 +/- 27 ml/min after withdrawal of levodopa. The number of ventricular premature contractions and couplets increased during levodopa therapy and decreased again significantly after withdrawal of levodopa. No significant differences between on and off levodopa were observed in resting heart rate, arterial blood pressure, cardiac index, stroke work index, systemic vascular resistance, sodium and water excretion, or creatinine clearance. Seven patients improved on levodopa therapy by one NYHA class; four of these seven patients deteriorated again by one NYHA class after withdrawal of levodopa. Regarding both clinical and hemodynamic changes after withdrawal of levodopa, three patients were classified as responders to long-term levodopa therapy. All three responders received 4 g levodopa per day. Average dopamine plasma level was 5.3 +/- 0.8 ng/ml in the responder group and 2.0 +/- 0.5 ng/ml in the nonresponder group. Long-term administration of oral levodopa is associated with beneficial clinical and hemodynamic response in only a minority of patients with chronic congestive heart failure.
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PMID:Evaluation of long-term oral levodopa therapy in chronic congestive heart failure. 312 9


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