Eine kritische Durchsicht der wissenschaftlichen Literatur zeigt diskrepante und in bedeutsamem Umfang methodisch unzureichende Befunde zur Wirkung von Mg2+ bei akuten infarktbedingten Herzrhythmusstörungen und bei infarktbedingten Todesfällen. Nach derzeitiger Datenlage kann weder eine antiarrhythmische Wirkung von Magnesium noch eine prophylaktische Wirkung im Sinne einer Mortalitätsverminderung bei akutem Myokardinfarkt als zweifelsfrei gesichert gelten. Im Gegensatz hierzu sollte bei Patienten mit akutem Myokardinfarkt und dokumentierter Hypokaliämie (Kalium <3,5 mmol/l) eine Kaliumsubstitution erfolgen, um der Entwicklung ventrikulärer Arrhythmien entgegenzuwirken. Der therapeutische Einsatz von Magnesium bei akutem Myokardinfarkt kommt dagegen nur im Rahmen klinisch kontrollierter Studien in Betracht.

A critical role analysis of literature concerning the effects of intravenous magnesium on arrhythmias and mortality in acute myocardial infarction shows discrepant results and often inappropriate methods. So far neither an antiarrhythmic efficacy nor prophylactic effects with respect to mortality could be demonstrated. In contrast, potassium substitution should be performed in the setting of acute myocardial infarction with documented hypokalemia (K+ < 3.5 mmol/l) because of increased risk of ventricular arrhythmias. According to the documented results of the trials reviewed in this article no recommendations for the routine use of magnesium in myocardial infarction can be given.

In recent years, stress echocardiography has gained broad acceptance as a non-invasive method for the diagnosis of coronary artery disease. Facing different protocols, dosages and instrumentation, official guidelines for the performance, standardization and quality control of stress echocardiograms are needed; however, so far they are not available. This paper recommends the type of personnel and technical equipment needed for stress echocardiography laboratories, based on experience gained during more than 2000 stress echocardiographic procedures. To perform stress echocardiography, a cardiologist and a technical assistant--both well trained over a large number of tests--should be involved. The laboratory must have basic equipment such as a 12-lead ECG, blood pressure monitoring capacity, a treadmill or bicycle for ergometry, a precision intravenous delivery system for pharmacological stress testing as well as an adequate echo table; additionally, emergency equipment is mandatory. The ultrasound machine should contain transducers with high 2-D resolution; most important is a digital image acquisition system which facilitates performance and interpretation through side-by-side display of synchronized rest and stress images. Finally, there is a need for proper patient preparation and the obtaining of informed consent.

Arbutamine, a new potent non-selective beta-adrenoceptor agonist with mild alpha 1-sympathomimetic activity, has been developed specifically for pharmacological stress testing. The drug acts like physical exercise, increasing both heart rate and myocardial contractility. Sensitivity, specificity and accuracy in detecting significant stenotic coronary artery disease are 76%, 96%, and 82%, respectively, again similar to those of exercise echocardiography. The drug is delivered by a computerized drug delivery and monitoring device (GenESA) which adjusts the infusion rate according to the patient's heart rate data feedback. The drug is generally well tolerated and has an acceptable safety profile. This article describes recent clinical experience with arbutamine and presents preliminary results of a multicentre multinational study which evaluates the clinical utility and safety of the GenESA system in diagnosing coronary artery disease.

Accurate heparin anticoagulation assessment is important to prevent complications (hemorrhage, thrombotic coronary occlusion) during and after coronary angioplasty (PTCA). Paired ACT-, aPTT- and prothrombin time (PT) measurements have not been studied after PTCA using a high dose heparin management. For that reason we analyzed in 150 consecutive patients (115 m., 35 f., 61 +/- 10 y.) immediately after PTCA and at the time of arterial sheath removal aPTT-(Neothromtin, Behring), PT- (Thromborel S, Behring) and ACT-(HR-ACT, HemoTec) values after application of 20,000 U of heparin (5,000 U intravenous, 15,000 U intracoronary) followed by a heparin-infusion (15,000-25,000 U/24 h). Immediately after PTCA in all patients a aPTT above the upper limit of >180 s was found. The average postprocedural ACT was 330 +/- 82 s. Only 9 patients showed an ACT below 200 s. All coronary reocclusions (n = 3) immediately after PTCA occurred in this group. Arterial sheaths were removed 13 +/- 3 h after PTCA. The incidence of minor peripheral bleeding complications at that time was 21% and was related to the anticoagulation level. Major bleeding complications requiring transfusion were noted in only one case. Our findings suggest that after high dose heparinization for PTCA the ACT test provides a reliable and broad range for the assessment of heparin anticoagulation. In contrast to the aPTT the ACT is ideally suited to determine the dosage of heparin infusion and the time of arterial sheath removal after PTCA. ACT measurements are superior to aPTT measurements in heparin anticoagulation assessment during and direct after PTCA.

Accurate heparina anticoagulation assessment is important to prevent complications (hemorrhage, thrombotic coronary occlusion) during and after coronary angioplasty (PTCA). Paired ACT-, aPTT- and prothrombin time (PT) measurements have not been studied after PTCA using a high dose heparin management. Fur that reason we analyzed in 150 consecutive patients (115 m., 35 f,, 61 +/- 10 V.) immediately after PTCA and at the time of arterial sheath removal aPTT- (Neothromtin, Behring), PT- (Thromborel S. Behring) and ACT- (HR-ACT, HemoTec) values after application of 20 000 U of heparin (5000 U intravenous, 15 000 U intracoronary) followed by a heparin-infusion (15 000-25 000 U/24 h). Immediately after PTCA in all patients a aPTT above the uppper limit of > 180 s was found. The average postprocedural ACT was 330 +/- 82 s. Only 9 patients showed an ACT below 200 s. All coronary reocclusions (n = 3) immediately after PTCA occurred in this group, Arterial sheaths were removed 13 +/- 3 h after PTCA. The incidence of minor peripheral bleeding complications at that time was 21% and was related to the anticoagulation level. Major bleeding complications requiring transfusion were noted in only one case, Our findings suggest that after high dose heparinization for PTCA the ACT test provides a reliable and broad range for the assessment of heparin anticoagulation. In contrast to the aPTT the ACT is ideally suited to determine the dosage of heparin infusion and the time of arterial sheath removal after PTCA. ACT measurements art: superior to aPTT measurements in heparin anticoagulation assessment during and direct after PTCA.

Heparin is always used in conjugation with primary PTCA to prevent thrombotic coronary occlusion. Experimental findings suggest antiproliferative heparin effects. For that reason we examined in a retrospective clinical study the relationship between heparin anticoagulation level during primary PTCA and incidence of restenosis 3 months after PTCA.45 patients (34 m.,11 f., 61 +/- 11 y.) with acute myocardial infarction and successful primary PTCA (TIMI flow 0 --> TIMI flow III) were divided in two groups according to their measured ACT values immediately after PTCA: group 1 with high heparin anticoagulation level (mean ACT 397 +/- 95 sec), group 2 with low heparin anticoagulation level (mean ACT 272 +/- 31 sec,). The incidence of restenosis (NHLBI IV) was obtained angiographically 3 months after PTCA. No differences in the incidence of restenosis could be found between both groups (group I = 29,6%, group II = 30%).Our findings suggest that there is no relationship between heparin anticoagulation level immediately after primary PTCA and incidence of post-PTCA restenosis.