Objective evidence of DD was found in two-thirds of HF-PSF patients. Moderate and severe DD, which were found in less than one-half of the patients, were important predictors of adverse outcome. The results demonstrate the prognostic significance and need for objective evidence of DD in HF-PSF patients.

Objective-Angiotensin II (AII) and aldosterone are not always fully suppressed during chronic angiotensin converting enzyme (ACE) inhibitor treatment. In congestive heart failure (CHF) such failure of hormonal suppression is associated with increased mortality. This study examined how common AII and aldosterone increases are observed during routine clinical practice. Patients and methods-91 patients with symptomatic (mean New York Heart Association class 2.7) CHF (mean (SD) left ventricular ejection fraction 29.9 (8)%, range 9-46%) were studied 4-6 hours after ACE inhibitor dosing. A representative range of ACE inhibitors (enalapril, lisinopril, captopril, perindopril, and fosinopril) was examined. Results-Supine measurements showed a wide range of AII (10.5 (25.5) pg/ml), aldosterone (130.8 (136) pg/ml), and serum ACE (12.1 (13.3) EU/l; excludes captopril data) concentrations on diuretics. AII concentrations > 10 pg/ml were seen in 15% of patients, and aldosterone concentrations > 144 pg/ml were seen in 38% of patients. AII concentrations were significantly correlated (p < 0.001) with ACE but not with aldosterone concentrations. Aldosterone concentrations were not significantly correlated with ACE concentrations. Conclusions-AII"reactivation" occurred in 15% and failure of aldosterone suppression in 38% of routine CHF patients taking ACE inhibitor treatment. AII "reactivation" was associated with both low and high levels of ACE activity, which suggests that multiple diVerent mechanisms are at play. In patients with high plasma ACE concentrations, noncompliance should be considered along with inadequate dose titration. In patients with low plasma ACE and high AII concentrations, non-ACE mediated production of AII may be operative. Raised aldosterone concentrations appear to be more common than AII "reactivation". It is important to establish the cause of detectable or increased AII concentrations in a heart failure patient treated with an ACE inhibitor. The measurement of serum ACE may help to identify the likely cause as poor compliance or inadequate dose.(Heart 1999;82:57-61)

The effect of the converting enzyme inhibitor captopril as long term treatment was investigated in 14 patients with severe congestive heart failure in a double blind trial. Captopril reduced plasma concentrations of angiotensin II and noradrenaline, with a converse increase in active renin concentration. Effective renal plasma flow increased and renal vascular resistance fell; glomerular filtration rate did not change. Serum urea and creatinine concentrations rose. Both serum and total body potassium contents increased; there were no long term changes in serum concentration or total body content of sodium. Exercise tolerance was appreciably improved, and dyspnoea and fatigue lessened. Left ventricular end systolic and end diastolic dimensions were reduced. There was an appreciable reduction in complex ventricular ectopic rhythms. Adverse effects were few: weight gain and fluid retention were evident in five patients when captopril was introduced and two patients initially experienced mild postural dizziness; rashes in two patients did not recur when the drug was reintroduced at a lower dose; there was a significant reduction in white cell count overall, but the lowest individual white cell count was 4000 X 10(6)/l. Captopril thus seemed to be of considerable value in the long term treatment of severe cardiac failure.

Background -The activity of the reninangiotensin system in asthma has not been studied previously and the effect of angiotensin II (AII) on bronchomotor tone in vivo is unknown. Methods -Plasma levels of renin and AII levels were measured in 20 patients with acute severe asthma, nine with mild asthma, 10 with severe chronic asthma, and 16 normal volunteers. The effect of AII, given as an intravenous infusion, on bronchomotor tone was also investigated in eight mild asthmatic patients. Results -In acute severe asthma plasma levels of renin [median (interquartile range)] were elevated on days 1, 2, and 5 after admission [48-7 (24-79), 44-2 (15-75), and 45 5 (21-70) ,uU/ml, respectively].Plasma AII levels were significantly elevated at day 5 [56 (12-109) Plasma levels of renin and AII were measured in four groups of subjects. Group 1 comprised 20 patients (six men) of mean (SD) age 34 (12 9) years admitted non-consecutively (two patients admitted twice) to Accident and Emergency with acute severe asthma (PEF 125 (38) 1/min, Pao2 9 2 (3 3) kPa (on air), pulse rate 120 (15) beats/min on admission). Venous blood was withdrawn shortly after admission for estimation of plasma renin and AII levels and measurements were repeated on days 2 and 5 after admission. All had received nebulised 02 agonists (salbutamol) and four were given intravenous hydrocortisone in Accident and Emergency prior to venesection. Seventeen patients were taking regular inhaled corticosteroids, five oral theophylline, and 10 were on oral prednisolone. All used as required inhaled P2 agonists via a metered dose inhaler (six were also taking 02 agonists via home nebuliser), four inhaled salmeterol, and four inhaled ipratropium bromide. No patients were on oral I agonists. Only one patient was on regular oral diuretic therapy. Group 2 comprised nine patients (two men) of mean (SD) age 40 3 (13) years with mild chronic asthma (PEF 450 (59)

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1. Diurnal changes in plasma concentrations of atrial natriuretic peptide (ANP), renin, angiotensin II, aldosterone, cortisol and antidiuretic hormone were investigated in seven normal volunteers studied under standardized conditions of dietary sodium, posture and physical activity. After completion of the diurnal study serial measurements of these variables were continued during, and on recovery from, a 2 day period of severe sodium depletion. 2. Clear diurnal variations in plasma concentrations of renin, angiotensin II, aldosterone, cortisol and antidiuretic hormone were observed. 3. Plasma ANP concentrations also varied significantly over 24 h. Values peaked about mid-day and a distinct trough in peptide concentrations occurred in the early evening. However, variations in plasma ANP values were of relatively small amplitude and not clearly independent of modest parallel shifts in sodium balance. 4. Changes in plasma ANP concentrations both within the diurnal study period and during sodium deprivation were closely and positively correlated with concomitant changes in cumulative sodium balance. 5. No simple parallel or reciprocal relationships between plasma concentrations of ANP, on the one hand, and concurrent plasma concentrations of other hormones or in the rate of urinary sodium excretion, on the other, were observed during the 25 h of the diurnal study.

The materials used in the fabrication of self-retained internal ureteral stents should provide strength, flexibility, low surface friction, radiopacity, biodurability, biocompatibility, and reasonable unit cost. Polymeric biomaterials currently used for stent construction include polyurethane, silicone, Silitek, C-Flex, and Percuflex. Comparative evaluation of these materials in the context of the requirements for stent structure and function suggests advantages and disadvantages for all of them. We believe that the most important attributes for an internal ureteral stent are ease of insertion, effective restoration and maintenance of flow, resistance to migration, significant biodurability, and biocompatibility. Based on our physical testing of stents fabricated from these materials, as well as clinical and laboratory experience, we believe that C-Flex and Percuflex are the most suitable materials for stent construction.