Aim

To assess the effect of changing clinical practice on the costs and outcomes of percutaneous coronary intervention (PCI) between 1998 and 2002.

Setting

Two tertiary interventional centres.

Patients

Consecutive patients undergoing PCI over a 12‐month period between 1998 and 2002.

Design

Comparative observational study of costs and 12‐month clinical outcomes of consecutive PCI procedures in 1998 (n = 1047) and 2002 (n = 1346). Clinical data were recorded in the Scottish PCI register. Repeat PCI, coronary artery bypass graft and mortality were obtained by record linkage. Costs of equipment were calculated using a computerised bar‐code system and standard National Health Service reference costs.

Results

Between 1998 and 2002, the use of bare metal stents increased from 44% to 81%, and the use of glycoprotein IIB/IIIA inhibitors increased from 0% to 14% of cases. During this time, a significant reduction was observed in repeat target‐vessel PCI (from 8.4% to 5.1%, p = 0.001), any repeat PCI (from 11.7% to 9.2%, p = 0.05) and any repeat revascularisation (from 15.1% to 11.3%, p = 0.009) within 12 months. Significantly higher cost per case in 2002 compared with 1998 (mean (standard deviation) £2311 (1158) v £1785 (907), p<0.001) was mainly due to increased contribution from bed‐day costs in 2002 (45.0% (16.3%) v 26.2% (12.6%), p = 0.01) associated with non‐elective cases spending significantly longer in hospital (6.22 (4.3) v 4.6 (4.3) days, p = 0.01).

Conclusions

Greater use of stents and glycoprotein IIb/IIIa inhibitors between 1998 and 2002 has been accompanied by a marked reduction in the need for repeat revascularisation. Longer duration of hospital stay for non‐elective cases is mainly responsible for increasing costs. Strategies to reduce the length of stay could considerably reduce the costs of PCI.

Objectives

To determine whether socioeconomic status (SES) influences clinical outcomes and quality of life after percutaneous coronary intervention (PCI).

Design

Prospective observational study.

Setting

Two interventional cardiac centres.

Participants

1346 consecutive patients undergoing PCI over a 12‐month period.

Outcomes

Self reported health‐related quality of life (HRQoL; EuroQol‐5 Dimensions (EQ‐5D); EuroQol Visual Analogue Scale (EQ‐VAS)), repeat angiography, revascularisation, hospital admission, myocardial infarction and death within 12 months, by SES derived using postal address code.

Main results

No significant differences were found between patients with high and low SES in the occurrence of repeat angiography (p = 0.55), repeat revascularisation (PCI, p = 0.81, CAEG, p = 0.27), total cardiac hospitalisation (p = 0.10), myocardial infarction (p = 0.97) or death 12 months after PCI (p = 0.88). Non‐procedure‐related readmissions were higher in patients with low SES (18.6% v 13.7%; p = 0.025). After adjustment for confounding factors, patients with low SES had lower HRQoL scores at baseline (95% CI for difference 0.01 to 0.14; p = 0.003) and at 12 months (95% CI 0.07 to 0.17; p<0.001) compared with those with high SES.

Conclusions

Clinical outcomes were similar for patients in different SES groups. Patients with low SES had considerably more non‐procedure‐related readmissions and lower quality‐of‐life scores. Future studies on HRQoL after coronary revascularisation should take account of these important differences related to SES.

Objective: To investigate the potential differential effects of selective endothelin (ET) A and dual ET-A/B receptor blockade in patients with chronic heart failure.

Methods: Nine patients with chronic heart failure (New York Heart Association class II–III) each received intravenous infusions of BQ-123 alone (selective ET-A blockade) and combined BQ-123 and BQ-788 (dual ET-A/B blockade) in a randomised, placebo controlled, three way crossover study.

Results: Selective ET-A blockade increased cardiac output (maximum mean (SEM) 33 (12)%, p < 0.001) and reduced mean arterial pressure (maximum −13 (4)%, p < 0.001) and systemic vascular resistance (maximum −26 (8)%, p < 0.001), without changing heart rate (p  =  0.38). Dual ET-A/B blockade significantly reduced the changes in all these haemodynamic variables compared with selective ET-A blockade (p < 0.05). Selective ET-A blockade reduced pulmonary artery pressure (maximum 25 (7)%, p  =  0.01) and pulmonary vascular resistance (maximum 72 (39)%, p < 0.001). However, there was no difference between these effects and those seen with dual ET-A/B blockade. Unlike selective ET-A blockade, dual ET-A/B blockade increased plasma ET-1 concentrations (by 47 (4)% with low dose and 61 (8)% with high dose, both p < 0.05).

Conclusions: While there appeared to be similar reductions in pulmonary pressures with selective ET-A and dual ET-A/B blockade, selective ET-A blockade caused greater systemic vasodilatation and did not affect ET-1 clearance. In conclusion, there are significant haemodynamic differences between selective ET-A and dual ET-A/B blockade, which may determine responses in individual patients.

Background: Despite the existence of several chronic heart failure (CHF) guidelines the treatment of patients with CHF is suboptimal. The new general medical services (GMS) contract in primary care has only three specific performance indicators for patients with left ventricular dysfunction. The aim of this current questionnaire survey was to assess the views of general practitioners (GPs) on CHF treatments and services in light of the new GMS contract.

Methods and Results: All local GPs (717) were sent a questionnaire. Fifty three per cent were returned. Forty five per cent of GPs had access to a community CHF nurse. Having read a national guideline (SIGN) and having the support of a CHF nurse did not seem to affect the knowledge of GPs in terms of perceived benefits of drug treatments. GPs with access to a specialist CHF nurse service attached more importance to it than those with no specialist nurse (p = 0.003).

Conclusions: Most GPs were aware of the existence of a national guideline but many had not read it. There was little or no difference in the knowledge level for various evidence based treatments between GPs who had or had not read the guideline suggesting that reading guidelines may not be a key factor in determining knowledge. Support for a specialist CHF nurse was higher among GPs who already had this service, suggesting that this service is valued. The new GMS contract may improve identification and diagnosis of patients with CHF but there is a danger that it may fall short of ensuring optimal treatment for patients with CHF.

Coronary revascularisation continues to be underused despite evidence that this results in poorer outcomes

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BACKGROUND--Endogenous opioids have a tonic inhibitory effect on sympathetic tone and have been implicated in the pathophysiology of vasodepressor syncope. Plasma beta endorphin concentrations increase after vasodepressor syncope induced by exercise or by fasting. AIMS--To take frequent samples for plasma beta endorphin estimation during tilt testing, and to determine whether plasma beta endorphin increased before the start of syncope. PATIENTS--24 patients undergoing tilt testing for investigation of unexplained syncope. SETTING--Tertiary referral centre. METHODS--Blood samples were obtained during 70 degrees head up tilt testing. Plasma beta endorphin concentrations were estimated by radioimmunoassay (mean(SD) pmol/l). RESULTS--Patients with a positive test showed a rise in beta endorphin concentrations before syncope (baseline 4.4(1.5) v start of syncope 8.5(3.1), p < 0.002). In contrast, patients with a negative test showed no change in beta endorphin concentrations (baseline 3.4(1.0) v end of test 4.5(2.3), NS). After syncope all patients showed a large secondary increase in beta endorphins (32.3(18.6)). CONCLUSION--An increase in plasma beta endorphins precedes vasodepressor syncope. This finding supports a pathophysiological role for endogenous opioids.

BACKGROUND--Endogenous opioids have a tonic inhibitory effect on sympathetic tone and have been implicated in the pathophysiology of vasodepressor syncope. Plasma beta endorphin concentrations increase after vasodepressor syncope induced by exercise or by fasting. AIMS--To take frequent samples for plasma beta endorphin estimation during tilt testing, and to determine whether plasma beta endorphin increased before the start of syncope. PATIENTS--24 patients undergoing tilt testing for investigation of unexplained syncope. SETTING--Tertiary referral centre. METHODS--Blood samples were obtained during 70 degrees head up tilt testing. Plasma beta endorphin concentrations were estimated by radioimmunoassay (mean(SD) pmol/l). RESULTS--Patients with a positive test showed a rise in beta endorphin concentrations before syncope baseline 4.4(1.5) v start of syncope 8.5(3.1), p < 0.002). In contrast, patients with a negative test showed no change in beta endorphin concentrations (baseline 3.4(1.0) v end of test 4.5(2.3), NS). After syncope all patients showed a large secondary increase in beta endorphins (32.3(18.6)). CONCLUSION--An increase in plasma beta endorphins precedes vasodepressor syncope. This finding supports a pathophysiological role for endogenous opioids.