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Objective—To study the circumstances and medical profile of out-of-hospital sudden cardiac arrest (SCA) patients in whom resuscitation was attempted by the ambulance service, and to identify causes of SCA in survivors and factors that influence resuscitation success rate. Methods—During a five year period (1991-95) all cases of out-of-hospital SCA between the ages of 20 and 75 years and living in the Maastricht area in the Netherlands were studied. Information was gathered about the circumstances of SCA, as well as medical history for all patients in whom resuscitation was attempted by the ambulance personnel. Causes of SCA in survivors were studied and logistic regression analysis was performed to identify factors associated with survival. Results—Of 288 SCA patients in whom cardiopulmonary resuscitation (CPR) and advanced life support were applied, 47 (16%) were discharged alive from the hospital. Their mean (SD) age was 58 (11) years, 37 (79%) were men, and 24 (51%) had a history of cardiac disease. Acute myocardial infarction was diagnosed in 24 (51%) of the survivors; seven with and 17 without a history of cardiac disease. Ventricular fibrillation (VF) or ventricular tachycardia (VT) as the first documented rhythm was significantly positively associated with survival (odds ratio (OR) 5.7, 95% confidence interval (CI) 2.1 to 15.9). A time interval of less than four minutes between the moment of collapse and the start of resuscitation, and an ambulance delay time of less than eight minutes were significantly positively associated with survival (OR 3.3, 95% CI 1.3 to 8.6, and OR, 3.6, 95% CI 1.3 to 10.5, respectively). A history of cardiac disease was negatively associated with survival (OR 0.46, 95% CI 0.21 to 0.98). Conclusions—Acute myocardial infarction was the underlying mechanism of SCA in most of the survivors, especially in those without a history of cardiac disease. CPR within four minutes, an ambulance delay time less than eight minutes, and VT or VF diagnosed by the paramedics were positively associated with success. Keywords: cardiac arrest; sudden death; cardiopulmonary resuscitation; paramedics

Any physician treating cardiac arrhythmias should be aware of a possible worsening of the arrhythmia (so-called arrhythmogenesis) after the start of antiarrhythmic drug treatment. To facilitate the recognition of that complication the type and possible mechanisms of arrhythmogenesis are reviewed. Recognition also requires an understanding of (a) the time of appearance of arrhythmogenic effects after different drugs, (b) the value of non-invasive and invasive tests, and (c) the profile of the patient most likely to develop this problem. Guidelines are given to reduce the incidence of the arrhythmogenic effects of antiarrhythmic drugs and a plea is made that the physician should be always on the alert for this complication.

Prediction of atrial fibrillation (AF) is usually based on anatomical and functional characterisation of the atrial substrate, such as left atrial diameter, ejection fraction, and P wave duration.1 In this respect, triggers such as atrial extrasystoles are often neglected.2 Atrial extrasystoles may occur during or shortly after exercise as a result of acute atrial stretch, especially in patients with left ventricular hypertrophy (LVH) and diastolic dysfunction. As LVH may induce the atrial substrate and atrial extrasystoles are the trigger for AF, we reasoned that these exercise induced atrial extrasystoles may predict AF in patients with LVH. Patients with LVH (interventricular septal diameter ⩾ 11 mm) and ejection fraction ⩾ 55% who underwent an exercise test between 1994 and 2004 were studied. Patients with prior AF or flutter or pacemaker rhythm, patients without at least one follow up ECG, and those with an incomplete exercise test were excluded. Of 864 screened patients 258 were selected. The exercise tests (Case Exercise Testing System; GE Medical Systems, Milwaukee, USA) were performed according to standard protocols.3 Each test was manually reviewed for atrial extrasystoles and supraventricular tachycardia (SVT; three or more consecutive supraventricular extrasystoles). Follow up ECG data were retrieved from an electronic storage system containing all ECGs recorded in our institution since 1994. The follow up period lasted from the date of the exercise test …

The electrophysiological effects of the intravenous administration of a new antiarrhythmic drug, lorcainide, were evaluated by programmed electrical stimulation of the heart in 23 patients with atrioventricular conduction disturbances (four patients), ventricular tachycardia (five patients), and accessory atrioventricular pathway (14 patients). Lorcainide did not affect the refractory period of the atrium, ventricle, atrioventricular node, or the AH interval. It lengthened the duration of the HV interval, the refractory period of the accessory pathway, and the width of the QRS complex. The drug terminated ventricular tachycardia in four of five patients. It is concluded that the drug may be of potential benefit in patients with ventricular tachycardia or accessory atrioventricular pathways (especially those with a short refractory period). Lorcainide is contraindicated in patients with bundle-branch block and prolonged HV interval.