kBSTRACT A custom-made probe, consisting of four electrodes arranged so that two orthogonal )ipolar electrograms could be recorded from a single site, was used to record epicardial activity during itrial and ventricular pacing in five normal and five anesthetized open-chest mongrel dogs with nyocardial infarction. Unfiltered bipolar electrograms recorded with a 2 mm interelectrode distance iveraged 36 + 15 mV in amplitude and 16 5 msec in duration in normal areas and 14 ± 11 mV and 13 ± 12 msec in infarcted areas (p < .01 infarct vs normal). The bipolar electrograms were vector ,ummed so that a vector loop could be generated at each site. The direction of epicardial impulse )ropagation as determined by multipoint isochronal activation mapping was compared with that ndicated by maximum x,y deflection of the vector loop. At 203 sites (141 normal and 62 infarcted) :here was a median error of only 13 degrees and an excellent correlation by linear regression (r2 = .95).[n normal myocardium vector loops were straight (60%), open (21%), or hooked (19%). In infarcted Tnyocardium, notched and irregular loops were occasionally seen. However, a clear maximum x,y leflection was still obtained from 98% of infarcted sites. During ventricular pacing in normal dogs, iniform epicardial conduction was observed for up to 4 cm longitudinal to fiber orientation but only 1 -m transverse to it. At selected sites longitudinal to fiber orientation conduction velocity was 0.618 n/sec, electrogram duration 12 msec, and vector amplitude 76 mV compared with 0.304 m/sec, 18 nsec, and 38 mV during conduction transverse to fiber orientation (p < .05 for all comparisons). Vector mapping of epicardial activation was performed during ventricular tachycardia induced by )rogrammed stimulation in two of five 2-week-old canine myocardial infarcts. Aside from minor .rregularities caused by impulse spread around areas of block, vector loops indicated when impulses were spreading away from the area of early epicardial activity and thus directed mapping to the region f earliest activation. We conclude that vector loops generated by summing orthogonal local bipolar -lectrograms accurately represent the direction of epicardial activation in both normal and infarcted Tnyocardium. Such loops may prove useful in mapping tachycardias and in clarifying details about :ardiac activation processes. Circulation 74, No. 3, 603-615, 1986. MAPPING of the sequence of ventricular activation with single or multiple epicardial, transmural, or endocardial electrodes has provided basic information about the mechanism and origin of both experimental and clinical arrhythmias.'-1 However, a limitation of these studies is that they either require sophisticated recording techniques with expensive computerized analysis systems3' 6 or large numbers of recording sites using a single probe electrode to define areas such as the site of origin of ventricular tachycardia (VT

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High-energy electrical ablation is a new experimental approach to control arrhythmias. In this study, the cellular electrophysiologic effects of high-energy shocks (5 to 40 J) delivered in vitro to 14 epicardial tissues from 11 dogs were studied in an attempt to understand the nature and extent of injury as well as potential arrhythmogenic mechanisms. In addition, this preparation was used to test the importance of cathode-anode configuration, current density, and fiber orientation in the induction of tissue injury in vitro. Electrophysiologic abnormalities were noted up to 10 mm from the electrode wall, and their extent was determined in part by current density and the cathode-anode orientation. A decrease in resting membrane potential, action potential amplitude, and dV/dT occurred in all tissues after high-energy shocks, which was worst nearest the cathode and of graded severity at increasing distances from the cathode. The most severe effects were noted with high current densities and in tissues located between the cathode and anode. In addition, impaired impulse conduction and abnormal repolarization were documented. Histologic study demonstrated contraction band necrosis immediately after delivery of high-energy shocks. The extent and distribution of the contraction bands was in part dependent on the energy delivered and the cathode-anode configuration. These findings suggest potential mechanisms for arrhythmogenesis and altered regional hemodynamic abnormalities that occur in vivo.

Direct mechanical ventricular actuation (DMVA) is an experimental procedure that provides biventricular cardiac assistance by intracorporeal pneumatic compression of the heart. The advantages this technique has over other assist devices are biventricular assistance, no direct blood contact, pulsatile blood flow, and rapid, less complicated application. Prior studies of nonsynchronized DMVA support have demonstrated that a subject can be maintained for up to 7 days. The purpose of this study was to determine the acute hemodynamic effects of cardiac synchronized, partial DMVA support in a canine model (RVP) of left ventricular (LV) dysfunction. The study consisted of rapidly pacing seven dogs for 4 weeks to create LV dysfunction. At the conclusion of the pacing period, the DMVA device was positioned around the heart by means of a median sternotomy. The animals were then imaged in a 1.5 T whole body high speed clinical MR system, with simultaneous LV pressure recording. Left ventricular pressure-volume (PV) loops of the nonassisted and DMVA assisted heart were generated and demonstrated that DMVA assist shifted the loops leftward. In addition, assist significantly improved pressure dependent LV systolic parameters (left ventricular peak pressure and dp/dt max, p < 0.05), with no diastolic impairment. This study demonstrates that DMVA can provide synchronized partial assist, resulting in a decrease in the workload of the native heart, thus having a potential application for heart failure patients.

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