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Aims  The aim of this study was to determine the contemporary use of reperfusion therapy in the European Society of Cardiology (ESC) member and affiliated countries and adherence to ESC clinical practice guidelines in patients with ST-elevation myocardial infarction (STEMI). Methods and results  Prospective cohort (EURObservational Research Programme STEMI Registry) of hospitalized STEMI patients with symptom onset <24 h in 196 centres across 29 countries. A total of 11 462 patients were enrolled, for whom primary percutaneous coronary intervention (PCI) (total cohort frequency: 72.2%, country frequency range 0–100%), fibrinolysis (18.8%; 0–100%), and no reperfusion therapy (9.0%; 0–75%) were performed. Corresponding in-hospital mortality rates from any cause were 3.1%, 4.4%, and 14.1% and overall mortality was 4.4% (country range 2.5–5.9%). Achievement of quality indicators for reperfusion was reported for 92.7% (region range 84.8–97.5%) for the performance of reperfusion therapy of all patients with STEMI <12 h and 54.4% (region range 37.1–70.1%) for timely reperfusion. Conclusions  The use of reperfusion therapy for STEMI in the ESC member and affiliated countries was high. Primary PCI was the most frequently used treatment and associated total in-hospital mortality was below 5%. However, there was geographic variation in the use of primary PCI, which was associated with differences in in-hospital mortality.

The present study showed that levosimendan may beneficially affect ECM remodeling in patients with acutely decompensated CHF. Whether these effects translate into added clinical benefits, as suggested by an improved ejection fraction in the levosimendan group, deserves further investigation.

Objectives-To examine the eVect of isoprenaline on slow and fast pathway properties and tachycardia initiation. Design-Consecutive patients, prospective study. Setting-Referral centre for cardiology, academic hospital. Patients-24 patients suVering from common type atrioventricular nodal reentrant tachycardia (AVNRT). interval shortened significantly after isoprenaline administration. Conclusions-In group 1 isoprenaline did not aVect inducibility of AVNRT because it prolonged the fast pathway refractory period without aVecting slow pathway conduction. In group 2 isoprenaline shortened the fast pathway refractory period and appeared to abolish slow pathway conduction. Consequencely, isoprenaline prevented induction of AVNRT. In group 3 isoprenaline facilitated induction of AVNRT. This eVect seemed primarily to be the result of shortening of retrograde refractoriness of the fast pathway with prolongation of slow pathway anterograde conduction and refractory period. (Heart 1998;79:165-168) Interventions-Programmed