Serial measurements of creatine kinase (CK) and its MB isoenzyme (CK-MB) and calculation of area under the curve (AUC) or peak value can be used to estimate infarct size. Peak values usually occur 20–24 hours postinfarction but release kinetics are affected by reperfusion (spontaneous or therapeutic). Regular, frequent samples must be obtained following admission, not a convenient approach for busy clinical or nursing staff. In a previous retrospective study1 we demonstrated that an angiographically determined left ventricular ejection fraction (LVEF) < 40 % could be identified by a single cardiac troponin T (cTnT) measurement at the diagnostically efficient time point of 12–24 hours from admission. We performed a larger prospective study and compared the measurement of cTnT and peak CK with early estimation of LVEF by echocardiography. Consecutive admissions to a typical UK district general hospital (DGH) with suspected acute coronary syndromes (ACS) and a final diagnosis of acute myocardial infarction (AMI) had measurement of cTnT and LVEF performed. Myocardial infarction was diagnosed according to World Health Organization criteria2 if two of the following were present: cardiac chest pain; S-T segment elevation of at least 2 mm in chest leads or 1 mm in limb leads or new …

Aim To determine whether elective direct current (dc) cardioversion of atrial fibrillation/flutter causes myocardial damage. Methods and results Cardiac troponin T and creatine kinase were estimated 20–28 hours after dc cardioversion in 51 patients who received dc shocks for elective cardioversion of chronic atrial fibrillation/flutter. Although creatine kinase was raised in 44 patients, cardiac troponin T was undetectable in all patients. Conclusion Cardiac damage does not occur as a result of cardioversion.

Sir,—Two recent papers in Heart showed that direct admission of patients with acute myocardial infarction to the coronary care unit (CCU) by ambulance staff reduced time delays in administering thrombolytic treatment.1 2The approach is novel; however, because it involves training a large number of ambulance personnel in reading ECGs as well as …

Sophisticated pacemakers now afford greater benefit than only relief of syncope for patients with symptomatic bradyarrhythmia. For clinical reasons it is inappropriate to implant ventricular demand (VVI) pacemakers in every patient, but for both clinical and economic reasons it is also undesirable to use dual-lead or rate-responsive systems indiscriminately. However, the published guidelines for pacemaker choice and investigation are inadequate. We have analysed the clinical assessment and the investigations required in a series of 150 patients with various electrophysiological disorders, considered consecutively for pacemaker implantation using an algorithm to assist decisions. Holter electrocardiography in 77.3%, exercise testing--formal (in 9.3%) or informal (during Holter electrocardiography), electrophysiology study (EPS)--full in 15.3% and partial in 29.3%, and trial of pacing (10.7%) were all used to characterize dysfunction and to define appropriate pacing mode. 142 patients were paced--57.0% with single lead modes (12.7%) AAI, 44.3% VVI) and 43.0% dual-lead (2.8% DVI, 23.9% VDD or VAT, 16.2% DDD). Three patients received rate-responsive systems (VVIR) which, if available, would have been used in nine; four would have been suitable for AAIR and four for dual-lead responsive pacing (DVIR, DDIR or DDDR). We offer a rational approach based on published data for investigation and pacemaker choice in the management of patients with bradyarrhythmia.