Search PubMed⌕ Search

Biomedical subjects

Benjamin J Scherlag

Publications and source records attributed to Benjamin J Scherlag.

26 records · Page 2Linked to original sources
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↗
PubMed2002

Decremental conduction in the posterior and anterior AV nodal inputs.

UNLABELLED: The role for fiber orientation as a determinant of conduction and block in the posterior (slow pathway, SP) and anterior (fast pathway, FP) AV nodal inputs was examined using multiple extracellular bipolar and intracellular microelectrode recordings in the superfused canine AV junction (N = 14). RESULTS: In both inputs, antegrade longitudinal conduction velocity decremented in association with decreased action potential amplitude and dV/dt(max). A similar decrement was also present in the SP transverse to fiber orientation. SP conduction block occurred preferentially near its insertion into the compact AV node with very slow conduction (0.05 +/- 0.01 M/sec) preceding conduction block. Distal antegrade FP conduction block occurred before conduction block occurred at more proximal FP sites. Conduction in the distal FP was maintained at a higher velocity (0.11 +/- 0.01 M/sec, p < 0.05 vs. SP) before 2:1 conduction block was observed. Conduction velocity, action potential amplitude, and dV/dt(max) were not different at any SP or FP site for paired activation transverse and longitudinal to fiber orientation. CONCLUSIONS: The data do not demonstrate a role for fiber orientation determining decremental conduction and block in transitional cell AV nodal inputs. Decremental conduction in both the SP and FP inputs is consistent with a proximal-to-distal gradient in resting membrane potential, action potential amplitude, dV/dt(max), and intracellular excitability in transitional cells during antegrade activation.

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↗