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Warren M Jackman

Publications and source records attributed to Warren M Jackman.

24 records · Page 2Linked to original sources
PubMed2003

High incidence of thrombus formation without impedance rise during radiofrequency ablation using electrode temperature control.

The authors hypothesized that during RF ablation, the electrode to tissue interface temperature may significantly exceed electrode temperature in the presence of cooling blood flow and produce thrombus. In 12 anesthetized dogs, the skin over the thigh muscle was incised and raised to form a cradle that was superfused with heparinized canine blood (ACT > 350 s) at 37 degrees C. A 7 Fr, 4-mm or 8-mm ablation electrode containing a thermocouple was held perpendicular to the thigh muscle at 10-g contact weight. Interface temperature was measured at opposite sides of the electrode using tiny optical probes. RF applications (n = 157) were delivered at an electrode temperature of 45 degrees C, 55 degrees C, 65 degrees C, and 75 degrees C for 60 seconds, with or without pulsatile blood flow (150 mL/min). Without blood flow, the interface temperature was similar to the electrode temperature. With blood flow, the interface temperature (side opposite blood flow) was up to 36 degrees C and 57 degrees C higher than the electrode temperature using the 4- and 8-mm electrodes, respectively. After each RF, the cradle was emptied and the electrode and interface were examined. Thrombus developed without impedance rise at an interface temperature as low as 73 degrees C without blood flow and 80 degrees C with blood flow (11/16 RFs at 65 degrees C electrode temperature using 4 mm and 13/13 RFs at an electrode temperature of 55 degrees C using an 8-mm electrode with blood flow). With blood flow, interface temperature markedly exceeded the electrode temperature and the difference was greater with an 8-mm electrode (due to greater electrode cooling). In the presence of blood flow, thrombus occurred without an impedance rise at an electrode temperature as low as 65 degrees C with a 4-mm electrode and 55 degrees C with an 8-mm electrode.

Analysis of Variance↗
PubMed2003

Endovascular stimulation of autonomic neural elements in the superior vena cava using a flexible loop catheter.

It has been previously shown that parasympathetic nerve stimulation (PNS) can be achieved via basket electrode catheters (BEC) positioned in the superior vena cava (SVC). Since questions have been raised regarding formation of thrombi between and/or on the splines of the BECs, we investigated the use of a flexible loop "Lasso" catheter (LC) to achieve autonomic nerve stimulation in the SVC without clot formation. In 5 dogs, anesthetized with Na-pentobarbital, standard ECG leads II and aVR, blood pressure and right atrial electrograms were continuously monitored. The LC is a 7-French catheter at the end of which is a circular ring, 25 mm in diameter, equipped with ten 1-mm electrodes. The circular loop is made of a flexible, shape retaining, covered metal, which can be straightened in order to be inserted transvenously. The catheter was inserted through a sheath in the external jugular vein and positioned in the SVC. Stimulation was performed sequentially across each of the five bipolar pairs of electrodes, and consisted of square wave stimuli, each 0.1 msec duration, frequency 20 Hz at voltages from 1-40 V. The average voltage required to produce a 50% decrease in heart rate was 15 +/- 7 V, compared to 22 +/- 12 V with the standard BEC and 10 +/- 5 V with a modified BEC. We did not observe any thrombus formation at the end of a four-hour period during which the catheter was stabilized in the SVC. PNS can be achieved safely and effectively by the LC in the SVC in dogs.

Animals↗
PubMed2002

Endovascular stimulation within the left pulmonary artery to induce slowing of heart rate and paroxysmal atrial fibrillation.

OBJECTIVE: In recent years there have been many reports dealing with basic models for sustained atrial fibrillation (AF), however few animal models exist for paroxysmal AF which closely simulate that seen clinically. METHODS: In 12 dogs, anesthetized with sodium pentobarbital, a right thoracotomy was performed. We stabilized a basket electrode catheter within the left pulmonary artery (LPA) through a purse string suture in the right ventricle. Electrode catheters were sutured to multiple atrial sites including the four pulmonary veins and the right and left atrial appendages, along Bachman's bundle and the coronary sinus. RESULTS: Continuous pulses of electrical stimulation (20 Hz square wave stimuli, each 0.1 ms in duration, voltage range 1-40 V) across adjacent splines of the five arms of the basket induced slow heart rates (at lower voltages) and then initiated atrial premature depolarizations (APDs), atrial tachycardia (AT) and AF (at higher voltages). To avoid possible direct activation of atrial myocardium, we also applied a train (50-100 ms duration) of high frequency stimuli (200 Hz) coupled to each atrial paced beat so that the train fell within the atrial refractory period. Stimulation in the LPA at an average of 14+/-7 V induced heart rate slowing, APDs were seen followed by AT/AF at a voltage of 20+/-6 V, P=0.002. Stimulation in the LPA resulted in APDs arising from a variety of sites including the left pulmonary veins (superior or inferior) and the left atrial appendage. After beta-blockade (intravenous esmolol or propranolol, 1 mg/kg) the voltage threshold for induction of AF rose from 14+/-7 to 25+/-10 V, P=0.02. Upon the addition of intravenous atropine (1-2 mg) the arrhythmic response (AF) to stimulation was completely abolished. Atrial pacing threshold was unchanged after autonomic blockade. Local application of radiofrequency energy (average number=3+/-2) across the metallic splines of the basket catheter in the LPA (70-80 V for 60 s) caused abolition of both the slowing and the arrhythmic response to LPA stimulation. CONCLUSION: These data suggest that stimulation of autonomic nerves in the LPA causes slowing of the heart rate followed by paroxysmal APD/AT/AF simulating the spontaneously occurring paroxysmal AF syndrome, associated with bradycardia, reported in patients.

Acute Disease↗
PubMed2002

The elusive extracellular AV nodal potential: studies from the canine heart, ex vivo.

Various forms of extracellular recordings from the AV node (AVN) have been reported. However, lack of consistent validation have precluded the use of such recordings in experimental and clinical studies. In 14 Langendorff perfused dog hearts, the triangle of Koch (TOK) was exposed and an octapolar electrode catheter (2 mm rings, 2 mm spacing) was inserted under the endocardium so that the bipolar pairs recorded electrograms from the apex to the base of the TOK. All recording were filtered between 0.05 and 250 Hz, except for a His bundle (Hb) recording (30-250 Hz) made from another bipolar electrode catheter placed in the aortic root. Transmembrane action potentials (AP) were recorded close to the sites of extracellular electrograms. Pin electrodes at the periphery of the bath were arranged to register two ECG leads from the volume conductor. During recovery of electrical activity 11 of 14 preparations developed a junctional rhythm that initially manifested only an AV nodal extracellular and corresponding intracellular AV nodal potentials followed gradually by conduction to the Hb and ventricles but no retrograde atrial activation; 3 preparations initially produced Hb rhythms based on extracellular and transmembrane AP recordings from the AVN and Hb. The amplitude and duration of the AVN extracellular potentials (average: 97 +/- 26 microV and 92 +/- 25 msec, respectively) during AVN rhythms, significantly differed from those during atrial pacing (262 +/- 185 microV and 78 +/- 26 msec, p < 0.05). Histologic sections of the sites underlying the electrodes recording AVN potentials showed AVN tissue throughout. We conclude that extracellular AV nodal potentials are independent waveforms with specific qualitative and quantitative characteristics that distinguish them from adjacent atrial, transitional, Hb or ventricular potentials.

Action Potentials↗
PubMedDate not supplied

Magnetism and cardiac arrhythmias.

Low-level electromagnetic fields (EMFs) have been used to treat various neurologic disorders. In the present study, we applied micro Gauss (microG) levels of EMFs either to the vagosympathetic nerve trunks, dissected in the neck, or across the chest in anesthetized dogs. Based on theoretical and empiric grounds, we compared EMFs (2.87 microG at 0.043 Hz) delivered to the vagosympathetic trunks in an experimental set (n = 5) with a sham control group (n = 6). Over a period of 2 to 3 hours, heart rate decreased after an initial 5-minute EMF exposure. The maximal heart rate changes in the experimental versus control groups was 29% versus 12% (P = 0.03). The voltage applied to the autonomic nerves required to induce atrioventricular (AV) conduction block decreased by 60% in the experimental group versus a 5% increase in the control group (P = 0.005). This effect also lasted 2 to 3 hours. Another EMF setting (amplitude 0.34 microG, frequency 2 kHz) applied for 5 minutes to the vagosympathetic trunks was associated with a significant increase in the occurrence of atrial premature depolarizations (APDs), atrial tachycardia (AT), and atrial fibrillation (AF) in response to autonomic nerve stimulation compared with control states before EMF exposure. No atrial arrhythmias could be induced after propranolol and atropine, even at the highest voltage used to stimulate the autonomic nervous input to the heart (n = 11). Only 2 dogs showed no response to this EMF application. In 3 dogs in whom atrial pacing (cycle length = 250 ms) and autonomic nerve stimulation induced AF, an EMF (2.87 microG at 0.043 Hz) delivered for 35 minutes across the chest suppressed AF for up to 3 to 4 hours, after which the same protocol again induced AF. We conclude that in these preliminary experiments, specific low-level EMFs alter heart rate, AV conduction, and heart rhythm. These effects were mediated through the autonomic nervous system inputs to the heart based on adjunctive effect of autonomic nerve stimulation and the inhibitory action of autonomic blockers.

Animals↗