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Since only a few standard benthic test species are available for sediment quality, our study aimed to employ multiple test species representing different sensitivity categories in the quality assessment of contaminated sediments. To this end three macroinvertebrate species, Sericostoma personatum (caddisfly, sensitivity category 10), Asellus aquaticus (isopod, category 3) and Chironomus riparius (chironomid, category 2), were exposed to sediments originating from various contamination sources in whole sediment bioassays using intact sediment cores. The agricultural sediment caused insect mortality, the agricultural and urban sediment caused isopod growth reduction and the urban and Wastewater Treatment Plant (WWTP) sediment affected chironomid emergence time. It is concluded that the arsenal of standard species can be successfully expanded by non-standard species, reducing over- or underestimation of the risks of contaminated sediments. [ABSTRACT FROM AUTHOR]

Objectives: To assess the influence of smoking on restenosis after coronary angioplasty.Design and Patients: The incidence of smoking on restenosis was investigated in 2948 patients. They were prospectively enrolled in four major restenosis trials in which quantitative angiography was used before and immediately after successful angioplasty and again at six months.Results: Within the study population there were 530 current smokers, 1690 ex-smokers, and 728 non-smokers. Smokers were more likely to be men (85.9% v 87. 5% v 65.3%, current v ex- v non-, p < 0.001), to be younger (54.0 (9. 0) v 57.0 (9.1) v 59.9 (9.4) years, p < 0.001), to have peripheral vascular disease (7.2% v 5.5% v 2.3%, p < 0.001), and have sustained a previous myocardial infarction (42.9% v 43.9% v 37.9%, p = 0.022), but were less likely to be diabetic (9.1% v 9.5% v 12.6%, p = 0.043) or hypertensive (24.9% v 29.3% v 37.2, p < 0.001). There was no significant difference in the categorical restenosis rate (> 50% diameter stenosis) at six months (35.28% v 35.33% v 37.09%, current v ex- v non-), or the absolute loss (0.29 (0.54) v 0.33 (0.52) v 0. 35 (0.55) mm, respectively; p = 0.172).Conclusions: Although smokers have a lower incidence of known predisposing risk factors for atherosclerosis, they require coronary intervention almost six years earlier than non-smokers and three years earlier than ex-smokers. Once they undergo successful coronary angioplasty, there appears to be no evidence that smoking influences their short term (six month) outcome, but because of the known long term effects of smoking, patients should still be encouraged to discontinue the habit. [ABSTRACT FROM AUTHOR]

Aims A randomized trial was performed to assess the safety and efficacy of a laser guidewire, in the treatment of chronic coronary occlusions.Methods and Results In 18 European centres, 303 patients with a chronic coronary occlusion were randomized to treatment with either the laser guidewire (n=144) or conventional guidewires (mechanical guidewire, n=159). The primary end-point of the study was treatment success, defined as reaching the true lumen distal to the occlusion by the allocated wire within 30min of fluoroscopic time: laser guidewire vs mechanical guidewire; 52·8% (n=76) vs 47·2% (n=75), P=0·33. Serious adverse events following the initial guidewire attempt were 0% (laser guidewire) and 0·6% (mechanical guidewire), respectively. Angioplasty (performed following successful guidewire crossing) was successful in 179 patients (91%, laser guidewire n=79, mechanical guidewire n=100), followed by stent implantation in 149 (79%). At the 6-month angiographic follow-up, the difference in binary restenosis rate (laser guidewire vs mechanical guidewire; 45·5% vs 38·3 %, P=0·72) or reocclusion rate (25·8% vs 16·1%, P=0·15) did not reach statistical significance. At 1, 6 and 12 months, angina and event-free survival were 69%, 35% and 24% (laser guidewire) vs 74%, 40% and 31% (mechanical guidewire).Conclusion Although laser guidewire technology was safe, the increase in crossing success did not reach statistical significance. [ABSTRACT FROM PUBLISHER]

Aims Thrombin plays a key role in the clinical syndrome of unstable angina. We investigated the safety and efficacy of five dose levels of efegatran sulphate, a direct thrombin inhibitor, compared to heparin in patients with unstable angina.Methods Four hundred and thirty-two patients with unstable angina were enrolled. Five dose levels of efegatran were studied sequentially, ranging from 0·105mg.kg−1.h−1to 1·2mg.kg−1.h−1over 48h. Safety was assessed clinically, with reference to bleeding and by measuring clinical laboratory parameters. Efficacy was assessed by the number of patients experiencing any episode of recurrent ischaemia as measured by computer-assisted continuous ECG ischaemia monitoring. Clinical end-points were: episodes of recurrent angina, myocardial infarction, coronary intervention (PTCA or CABG), and death.Results Efegatran demonstrated dose dependent ex-vivo anticoagulant activity with the highest dose level of 1·2mg.kg−1.h−1resulting in steady state mean activated partial thromboplastin time values of approximately three times baseline. Thrombin time was also increased. Neither of the efegatran doses studied were able to suppress myocardial ischaemia during continuous ECG ischaemia monitoring to a greater extent than that seen with heparin. There were no statistically significant differences in clinical outcome or major bleeding between the efegatran and heparin groups. Minor bleeding and thrombophlebitis occurred more frequently in the efegatran treated patients.Conclusion Administration of efegatran sulphate at levels of at least 0·63mg.kg−1.h−1provided an anti-thrombotic effect which is at least comparable to an activated partial thromboplastin time adjusted heparin infusion. There was no excess of major bleeding. The level of thrombin inhibition by efegatran, as measured by activated partial thromboplastin time, appeared to be more stable than with heparin. Thus, like other thrombin inhibitors, efegatran sulphate is easier to administer than heparin. However, no clinical benefits of efegatran over heparin were apparent. [ABSTRACT FROM PUBLISHER]

Background The 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors competitively inhibit biosynthesis of mevalonate, a precursor of non-sterol compounds involved in cell proliferation. Experimental evidence suggests that fluvastatin may, independent of any lipid lowering action, exert a greater direct inhibitory effect on proliferating vascular myocytes than other statins. The FLARE (Fluvastatin Angioplasty Restenosis) Trial was conceived to evaluate the ability of fluvastatin 40mg twice daily to reduce restenosis after successful coronary balloon angioplasty (PTCA). Methods Patients were randomized to either placebo or fluvastatin 40mg twice daily beginning 2–4 weeks prior to planned PTCA and continuing after a successful PTCA (without the use of a stent), to follow-up angiography at 26±2 weeks. Clinical follow-up was completed at 40 weeks. The primary end-point was angiographic restenosis, measured by quantitative coronary angiography at a core laboratory, as the loss in minimal luminal diameter during follow-up. Clinical end-points were death, myocardial infarction, coronary artery bypass graft surgery or re-intervetion, up to 40 weeks after PTCA. Results Of 1054 patients randomized, 526 were allocated to fluvastatin and 528 to placebo. Among these, 409 in the fluvastatin group and 427 in the placebo group were included in the intention-to-treat analysis, having undergone a successful PTCA after a minimum of 2 weeks of pre-treatment. At the time of PTCA, fluvastatin had reduced LDL cholesterol by 37% and this was maintained at 33% at 26 weeks. There was no difference in the primary end-point between the treatment groups (fluvastatin 0·23±0·49mm vs placebo 0·23±0·52mm,P=0·95) or in the angiographic restenosis rate (fluvastatin 28%, placebo 31%, chi-squareP=0·42), or in the incidence of the composite clinical end-point at 40 weeks (22·4% vs 23·3%; logrankP=0·74). However, a significantly lower incidence of total death and myocardial infarction was observed in six patients (1·4%) in the fluvastatin group and 17 (4·0%) in the placebo group (log rankP=0·025). Conclusion Treatment with fluvastatin 80mg daily did not affect the process of restenosis and is therefore not indicated for this purpose. However, the observed reduction in mortality and myocardial infarction 40 weeks after PTCA in the fluvastatin treated group has not been previously reported with statin therapy. Accordingly, a priori investigation of this finding is indicated and a new clinical trial with this intention is already underway. [ABSTRACT FROM PUBLISHER]

With the increasing clinical application of new devices for percutaneous coronary revascularization, maximization of the acute angiographic result has become widely recognized as a key factor in maintained clinical and angiographic success. What is unclear, however, is whether the specific mode of action of different devices might exert an additional independent effect on late luminal renarrowing. The purpose of this study was to investigate such a difference in the degree of provocation of luminal renarrowing (or ‘restenosis propensity’) by different devices, among 3660 patients, who had 4342 lesions successfully treated by balloon angioplasty (n=θ3797), directional coronary atherectomy (n= θ200), Palmaz-Schatz stent implantation (n= θ229) or excimer laser coronary angioplasty (n= θ116) and who also underwent quantitative angiographic analysis pre- and post-intervention and at 6-month follow-up. To allow valid comparisons between the groups, because of significant differences in coronary vessel size (balloon angioplasty=θ2.62±0.55 mm, directional coronary atherectomy= θ3.28±0.62 mm, excimer laser coronary angioplasty= θ2.51±0.47 mm, Palmaz-Schatz=θ3.01±0.44mm; P<0.0001), the comparative measurements of interest selected were the ‘relative loss’ in luminal diameter (RLoss= θlosslvessel size) to denote the restenosis process, and the ‘relative lumen at follow-up’ (RLfup= θminimal luminal diameter at follow uplvessel size) to represent the angiographic outcome. For consistency, lesion severity pre-intervention was represented by the ‘relative lumen pre’ (RLpre= θminimal luminal diameter prelvessel size) and the luminal increase at intervention was measured as ‘relative gain’ (relative gain= θgainl vessel size). Differences in restenosis propensity between devices was evaluated by univariate and multivariate analysis. Multivariate models were constructed to determine relative loss and relative lumen at follow-up, taking account of relative lumen pre-intervention, lesion location, relative gain, vessel size and the device used. In addition, model-estimated relative loss and relative lumen at follow-up at given relative lumen pre-intervention relative gain and vessel size, were compared among the four groups. Significant differences were detected among the groups both with respect to these estimates, as well as in the degree of influence of progressively increasing relative gain, on the extent of renarrowing (relative loss) and angiographic outcome (relative lumen at follow-up), particularly at higher levels of luminal increase (relative gain). Specifically, lesions treated by balloon angioplasty or Palmaz-Schatz stent implantation (the predominantly ‘dilating’ interventions) were associated with more favourable angiographic profiles than directional atherectomy or excimer laser (the mainly ‘debulking’ interventions). Significant effects of lesion severity and location, as well as the well known influence of luminal increase on both luminal renarrowing and late angiographic outcome were also noted. These findings indicate that propensity to restenosis after apparently successful intervention is influenced not only by the degree of luminal enlargement achieved at intervention, but by the device used to achieve it. In view of the clinical implications of such findings, further evaluation in larger randomized patient populations is warranted. [ABSTRACT FROM PUBLISHER]