Body surface maps and the conventional 12-lead ECG compared by studying their performances in classification of old myocardial infarction.

The performance of body surface potential maps and the 12-lead ECG in the detection of old myocardial infarction has been compared in a two-group (54 normals; 52 infarctions) classification procedure (linear discriminant analysis). Three methods for data reduction of body surface maps were compared: 1) time integration, 2) one-step reduction in eigenvectors and 3) two-step reduction in spatial and temporal eigenvectors. Features were taken from the reduction variables by a stepwise selection procedure. From 90% to 93% correct classifications could be obtained using three features from the map data over the initial 30 ms (Q interval) of the QRS wave for all three methods considered. Using the 100 ms (QRS) interval 86% correct classifications were obtained using method 1, and up to 90% and 87% for methods 2 and 3, respectively. In a further analysis the classification based on body surface maps was compared to the one based on the 12-lead ECG. The 12-lead ECG was treated as a restricted set of the body surface mapping leads, so the same methods of data reduction, feature extraction and classification could be applied to both sets of data. Applying method 1 (time integration) 89% correct classifications were obtained using data taken from the 30 ms interval of the 12-lead ECG and a subsequent reduction to three features. When using the 100 ms interval the result was 79% also using three features. The results of method 2 applied to the 12-lead ECG were 89% (30 ms interval, three features) and 78% (100 ms interval, three features).

Substrate dependence of reoxygenation arrhythmias in the isolated rat heart.

Isolated rat hearts perfused with various substrates were subjected to oxygen restriction followed by sudden reoxygenation. The incidence of ventricular arrhythmias occurring after reoxygenation appeared to be dependent on the substrate present during oxygen restriction; it was low with glucose (11 mM) and significantly higher with oleic acid (FFA to albumin molar ratio 4), with beta-hydroxy butyrate (11 mM), with acetate (11 mM) or without added substrate. When verapamil (1 muM) was also present in the medium, these arrhythmias were largely prevented. When glucose or verapamil were present during the reoxygenation period only, the incidence of reoxygenation arrhythmias was high. Tissue levels of long-chain acyl-CoA increased during oxygen restriction under all substrate conditions tested. At the moment when reoxygenation was started they were most elevated in hearts perfused with oleic acid. Verapamil did not influence levels of long-chain acyl-CoA. The amount of creatine-kinase (CK) released from the heart after reoxygenation did not correlate with the observed arrhythmias and was greatest in hearts perfused with oleic acid. Verapamil protected against CK release in the absence of added substrate, but not when oleic acid was present. It is concluded that ventricular arrhythmias after reoxygenation are not necessarily caused by FFA or long-chain acyl-CoA.

[Surgical interruption of the accessory pathway in a case of WPW-syndrome with persistent supraventricular tachycardia provoked by sinus node suppression (author's transl)]. / Chirurgische Unterbrechung des akzessorischen Bündels bei einem Fall von WPW-Syndrom mit permanenter supraventrikulärer Tachykardie durch Sinusknoten-Suppression.

This is a case report of a 60-year-old woman with a WPW-syndrome Type A developing persistent supraventricular tachycardia refractory to medical treatment. The re-entry mechanism was based on av-junction escape beats leading to retrograde conduction through the accessory pathway in presence of sinus node dysfunction i.e. long periods of sinus arrest probably enhanced through antiarrhythmic drug therapy and/or digitalis. With the aid of electrophysiological examinations and intraoperative epicardial mapping the accessory pathway was located in the upper lateral region of the left ventricle and interrupted by an incision in the av-groove from inside of the lfet atrium. Although an additional accessory pathway, not interrupted by surgery was suggested by the postoperative electrophysiological study, the patient remained free from tachycardia over more than 18 months, except for one episode terminated promptly by overdrive pacing from the right atrium. Postoperatively sinus bradycardia and av-junctional escape rhythm prevailed.

Electrical activation of ventricles and interventricular septum in hypertrophic obstructive cardiomyopathy.

In 10 cases with proven left ventricular outflow obstruction, we studied the time sequence of activation at the epicardial surface, in the left ventricular wall, and in the interventricular septum by means of epicardial exploration and intramural needle electrodes carrying 10 to 20 terminals, during surgical exposure. A variable delay (15-40 msec) was found in subendocardial activation of the anterior paraseptal left ventricular wall, probably caused by a block in the anterior division of the left bundle-branch. Epicardial excitation is additionally retarded by the increased diameter of the left ventricular wall because of hypertrophy. Conduction velocity in the left ventricular wall and in the interventricular septum was found to be approximately normal: +/-45 cm/sec; activation of the hypertrophic interventricular septum starts at normal times and proceeds mainly from left to right, with a smaller contribution from right to left; both fronts meet to the right of the middle of the interventricular septum; total septal activation time is prolonged because of hypertrophy.