Antonio Guill

Analyzing the electrophysiological effects of local epicardial temperature in experimental studies with isolated hearts.

As a result of their modulating effects upon myocardial electrophysiology, both hypo- and hyperthermia can be used to study the mechanisms that generate or sustain cardiac arrhythmias. The present study describes an original electrode developed with thick-film technology and capable of controlling regional temperature variations in the epicardium while simultaneously registering its electrical activity. In this way, it is possible to measure electrophysiological parameters of the heart at different temperatures. The results obtained with this device in a study with isolated and perfused rabbit hearts are reported. An exploration has been made of the effects of local temperature changes upon the electrophysiological parameters implicated in myocardial conduction. Likewise, an analysis has been made of the influence of local temperature upon ventricular fibrillation activation frequency. It is concluded that both regional hypo- and hyperthermia exert reversible and opposite effects upon myocardial refractoriness and conduction velocity in the altered zone. The ventricular activation wavelength determined during constant pacing at 250 ms cycles is not significantly modified, however. During ventricular fibrillation, the changes in the fibrillatory frequency do not seem to be transmitted to normal temperature zones.

New epicardial mapping electrode with warming/cooling function for experimental electrophysiology studies.

Cardiac electrical activity is influenced by temperature. In experimental models, the induction of hypothermia and/or hyperthermia has been used for the study of mechanisms of cardiac arrhythmia. A system that allows for localized, controlled induction, besides simultaneously recording electrical activity in the same induced area, needs to be developed ad hoc. This article describes the construction and application of a new system capable of locally modifying the epicardial temperature of isolated hearts and of carrying out cardiac mapping with sufficient spatial resolution. The system is based on a thermoelectric refrigerator and an array of 128 stainless steel unipolar electrodes in encapsulated epoxy of good thermal conductivity. The surface of the electrode is shaped to match the ventricular curvature. The electrode-device was tested on 7 isolated perfused rabbit hearts following the Langendorff technique. Quality recordings were obtained for the left ventricle at temperatures of 37° C, 22° C and 42° C. The effects of temperature were explored in relation to two electrophysiological parameters: the QT interval during sinus rhythm and the VV interval during ventricular fibrillation. The results indicate that this is a suitable method for creating and analyzing electrophysiological heterogeneities induced by temperature in the experimental model.

QT Interval Heterogeneities Induced Through Local Epicardial Warming/Cooling. An Experimental Study

INTRODUCTION AND OBJECTIVES Abnormal QT interval durations and dispersions have been associated with increased risk of ventricular arrhythmias. The present study examines the possible arrhythmogenic effect of inducing QT interval variations through local epicardial cooling and warming. METHODS In 10 isolated rabbit hearts, the temperatures of epicardial regions of the left ventricle were modified in a stepwise manner (from 22°C to 42°C) with simultaneous electrogram recording in these regions and in others of the same ventricle. QT and activation-recovery intervals were determined during sinus rhythm, whereas conduction velocity and ventricular arrhythmia induction were determined during programmed stimulation. RESULTS In the area modified from baseline temperature (37°C), the QT (standard deviation) was prolonged with maximum hypothermia (195 [47] vs 149 [12] ms; P<.05) and shortened with hyperthermia (143 [18] vs 152 [27] ms; P<.05). The same behavior was displayed for the activation-recovery interval. The conduction velocity decreased with hypothermia and increased with hyperthermia. No changes were seen in the other unmodified area. Repetitive responses were seen in 5 experiments, but no relationship was found between their occurrence and hypothermia or hyperthermia (P>.34). CONCLUSIONS In the experimental model employed, local variations in the epicardial temperature modulate the QT interval, activation-recovery interval, and conduction velocity. Induction of heterogeneities did not promote ventricular arrhythmia occurrence.

2D Isochronal Correlation Method to Detect Pacing Capture during Ventricular Fibrillation

During ventricular fibrillation (VF), a portion of myocardial tissue can be captured by pacing at a rate near the fibrillation rate. Interruption of ventricular fibrillation can be favored by achieving stable myocardial capture, lowering the energy required for electrical cardioversion. Existence of myocardial capture during electrical stimulation is determined by visual inspection of electrograms (EGM) by an experienced observer. The objective of this work is the development of a semi-automatic method for the detection of myocardial capture based on the 2D correlation of isochronal maps. In 4 isolated rabbit hearts VF was induced by ventricular pacing with an increasing rate. An array of 128 sensing electrodes plus a central electrode for pacing was used. For each experiment, an isochronal capture template (TImap) was computed by using isochronal maps corresponding to pacing before the induction of VF. After VF induction, epicardial pacing was delivered during 15 seconds at the same rate of the spontaneous fibrillatory rate and 10% higher. An experienced observer visually inspected the recordings and identified which stimulations resulted in capture. Isochronal maps were generated by automatically detecting the myocardial activation during VF. Detections of the algorithm were compared with captures previously identified by the observer. Our algorithm discarded 73.35% of non-capture cases and missed only one capture case reducing the time required for analyzing myocardial capture experiments. This is the first method that makes use of 2D correlation to detect myocardial capture during VF.

QT dispersion induced by local temperature variations

Abnormally long and short QT intervals (QTi) have been shown to be associated with an increased risk for life-threatening ventricular arrhythmias and sudden cardiac death. Because of its electrophysiological effects temperature can influence this parameter. Therefore hypothermia or/and hyperthermia can be used for modulate QTi in studies with experimental models. In this work, a novel electrode-device to perform epicardial mapping and simultaneous thermal modifications is presented. In ten preparations of isolated rabbit hearts (Langendorff-perfused) changes in QTi was analyzed in two different left ventricular areas. One area was thermally modified, while the other remained in basal conditions, the QTi were measured in both areas. During hypothermia the differences between them increased mainly due to the prolongation of the QTi in altered area. hyperthermia had the opposite effect.

Epicardial-limited electrophysiological heterogeneities do not facilitate ventricular arrhythmia induction. An experimental study

The electrophysiological heterogeneities of the myocardium are associated with vulnerability to arrhythmias. This study presents an experimental heterogeneity model based on local epicardial cooling/warming. The ventricular activation-recovery interval (ARl), conduction velocity (CV) and arrhythmogenic response to electrical pacing were determined. Electrical mapping was carried out on isolated rabbit hearts (n=8), using a specific electrode device for epicardial temperature control. With respect to baseline, ARl in the modified zone was prolonged (137 ± 22 ms vs 111 ± 13 ms, p<;0.05) under maximum hypothermia (22.3 ± 0.6 °C vs 36.7 ± 0.8 DC), and was shortened (98 ± 13 ms vs 107 ± 16 ms, p<;0.05) under conditions of hyperthermia (41.8 ± 0.3 °C vs 37.3 ± 0.4 DC). CV decreased (70 ± 17 cm/s vs 76 ± 17 cm/s, p<;0.05) under hypothermia and increased (79 ± 20 cm/s vs 75 ± 21 cm/s, p<;0.05) under hyperthermia. There were no changes in the unmodified zone. Repetitive responses were observed in four hearts, with no dependency between the appearance of responses and the induced modifications. Thermally induced dispersion of ARl and CV did not favor the induction of ventricular arrhythmias, probably because only a limited zone of the ventricular epicardium was affected.