Search

Experimental reinvestigation of the mechanism and spread of ventricular activation by Prinzmetal and his co-workers 1 has stimulated interest in the clinical correlation between subendocardial infarction and its electrocardiographic manifestations. In this regard, cases of particular importance are those in which the infarction is widespread circumferentially, but limited to the inner half or less of the left ventricular myocardium. Because of conflicting statements in the recent literature concerning the presence or absence of QRS alterations with this specific type of infarction, we were encouraged to review our autopsied cases of extensive subendocardial infarction that had had recent electrocardiograms. Seventeen such cases were available for study. From the case material available at the Rhode Island Hospital during the decade 1950-1960, we excluded those cases of subendocardial infarction combined with transmural extensions or those having significant conduction disturbances prior to the onset of the infarction. Thus, two cases with previous left and

The electrocardiographic abnormalities associated with bundle-branch block (BBB) are based on a delay in the transmission of impulses to one of the ventricles, causing its asymmetrical activation. It is customary to divide such blocks into complete and incomplete forms, the former arbitrarily based on duration of the QRS complexes of more than 0.1 seconds, and the latter on QRS duration of 0.1 seconds or less. Left Bundle-Branch Block Left BBB usually shifts the extremity leads 1 axis to the left and superiorly and produces deep QS-waves in right precordial leads and broad R-waves in left precordial leads. Left BBB completely rearranges the mode of ventricular activation, so that if preblock tracings showed such abnormalities as ventricular hypertrophy or myocardial infarction, these are no longer identifiable in the presence of BBB. Incomplete left BBB resembles pronounced forms of left ventricular hypertrophy; according to some views 1 a conduction defect causing incomplete left

Background: Long term asynchronous ventricular activation from right ventricular apex results in increased wall stress and hypertrophy of the left ventricle (LV), leading to reduced systolic and diastolic function. The purpose of this study is to assess in the peripheral blood alterations of the expression of genes related to LV contractile function and hypertrophy, after right ventricular apical pacing in patients with preserved LV systolic function.

Background Pace-mapping is a commonly used electrophysiological (EP) procedure which aims to identify exit sites of ventricular tachycardia (VT) by matching ventricular activation patterns (assessed by QRS morphology) at specific pacing locations with activation during VT. However, long procedure durations and the need for VT induction render this technique non-optimal. To demonstrate the potential of in-silico pace-mapping, using stored electrogram (EGM) recordings of clinical VT from implanted devices to guide pre-procedural ablation planning. Method Six scar-related VT episodes were simulated in a 3D torso model reconstructed from computed tomography (CT) imaging data, including three different infarct anatomies mapped from infarcted porcine imaging data. In-silico pace-mapping was performed to localise VT exit sites and isthmuses by using 12-lead electrocardiogram (ECG) signals and different combinations of EGM sensing vectors from implanted devices, through the creation of conventional correlation maps and reference-less maps. Results Our in-silico platform was successful in identifying VT exit sites for a variety of different VT morphologies from both ECG correlation maps and corresponding EGM maps, with the latter dependent upon the number of sensing vectors used. We also showed the added utility of both ECG and EGM reference-less pace-mapping for the identification of slow-conducting isthmuses, uncovering the optimal algorithm parameters. Finally, EGM-based pace-mapping was shown to be more dependent upon the mapped surface (epicardial/endocardial), relative to the VT origin. Conclusions In-silico pace-mapping can be used along with EGMs from implanted devices to localise VT ablation targets in pre-procedural planning.