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Biomedical subjects

Ralph Lazzara

Publications and source records attributed to Ralph Lazzara.

At least 19 recordsLinked to original sources
PubMed2007

Gradients of atrial refractoriness and inducibility of atrial fibrillation due to stimulation of ganglionated plexi.

INTRODUCTION: The mechanism(s) whereby atrial ectopy induces atrial fibrillation (AF) is still poorly understood. METHODS AND RESULTS: In 12 dogs, we determined the refractory period (RP) along the right atrium (RA) and right superior pulmonary vein (RSPV), and AF inducibility with and without concurrent stimulation of the anterior right ganglionated plexi (ARGP) at the base of the RSPV. Multielectrode catheters were attached to the RSPV and RA with the distal electrodes close to ARGP. The RP and window of vulnerability (WOV), i.e., the longest S1-S2 minus the shortest S1-S2 at which AF was induced, were measured before and during incremental levels of ARGP stimulation. Mapping of the onset of AF was performed using the EnSite mapping system (St. Jude Medical, St. Paul, MN, USA) positioned in the RA. A single premature depolarization (PD) from the RSPV that did not induce AF without ARGP stimulation could do so with ARGP stimulation. The onset of AF consistently arose at the myocardium subtending the ARGP. With GP stimulation, the average WOV at the RSPV-atrial junction was significantly wider than at the RA appendage (65 +/- 27 vs. 8 +/- 17 msec, P < 0.05) or further along the RSPV sleeve (48 +/- 39 vs. 10 +/- 20 msec, P < 0.05). Even without GP stimulation, high intensity (10-20 mA) premature stimuli delivered at the RA appendage induced AF, originating from atrial tissue subtending the ARGP, presumably due to axonal conduction that activated the ARGP. CONCLUSION: GP stimulation, subthreshold for atrial excitation, converts isolated PDs into AF-inducing PDs, suggesting that autonomic tone may play a critical role in the initiation of paroxysmal AF.

Animals↗
PubMed2006

Interactive atrial neural network: Determining the connections between ganglionated plexi.

BACKGROUND: The electrophysiologic functions of the intrinsic cardiac autonomic nervous system (ANS) are not well understood. OBJECTIVES: The purpose of this study was to investigate the functional interactions between ganglionated plexi within the intrinsic cardiac ANS. METHODS: The hearts of 21 dogs were exposed via right and/or left thoracotomy to expose the (1) anterior right ganglionated plexi near the caudal end of the sinoatrial node, (2) inferior right ganglionated plexi at the junction of inferior vena cava and atria, and (3) superior left ganglionated plexi near the junction of left superior pulmonary vein and left pulmonary artery. Ganglionated plexi were stimulated at 0.6 to 8.0 V (square waves, 20 Hz, 0.1-ms duration). Sinus rate, AH interval during atrial pacing, and ventricular rate during atrial fibrillation were compared before and after ganglionated plexi stimulation and after their ablation. RESULTS: Anterior right ganglionated plexi stimulation induced significant AH prolongation and slowing of ventricular rate and sinus rate. When inferior right ganglionated plexi was ablated, slowing of sinus rate by anterior right ganglionated plexi stimulation was unaltered, but inhibition of AV conduction was eliminated. Superior left ganglionated plexi stimulation induced similar effects on sinus and AV nodal function, and sinus rate slowing was markedly attenuated by anterior right ganglionated plexi ablation. Ablation of both anterior right ganglionated plexi and inferior right ganglionated plexi eliminated AV conduction inhibition but not sinus rate slowing by superior left ganglionated plexi stimulation. CONCLUSION: This study provides functional evidence for the interconnections between ganglionated plexi to modulate sinus and AV nodal function, supporting clinical evidence that interconnections within the intrinsic cardiac ANS are critical elements in identifying the targets for atrial fibrillation ablation.

Animals↗
PubMed2006

Sodium-calcium exchange initiated by the Ca2+ transient: an arrhythmia trigger within pulmonary veins.

OBJECTIVES: The hypothesis that an increased or prolonged Ca2+ transient during an abbreviated action potential can give rise to early afterdepolarizations (EADs) and triggered arrhythmia by enhanced forward sodium-calcium (Na-Ca) exchange was examined. BACKGROUND: Because pulmonary veins have the shortest action potential of any cardiac tissue, we examined this hypothesis in canine pulmonary vein sleeves during interventions further shortening the action potential and increasing the calcium transient. METHODS: Extracellular bipolar electrode, intracellular microelectrode, and isometric force (a surrogate marker for the Ca2+ transient) recordings were obtained from superfused canine pulmonary veins. RESULTS: An elevation and prolongation of the terminal phase of repolarization (EADs) were observed during interventions increasing contractile force; isoproterenol or norepinephrine (3.2 x 10(-11) to 3.2 x 10(-7)M), hypothermia, and pacing (post-extrasystolic potentiation, post-pacing pause). The EAD formation was prevented by ryanodine (10 microM) or reversed by transiently increasing [Ca2+](o) from 1.35 to 5 mM (inhibition of forward Na-Ca exchange). Pacing-induced EADs were enhanced by re-introduction of normal Tyrode solution (Na+ = 130 mM) after substitution of 30 mM NaCl with 30 mM LiCl (stimulation of forward Na-Ca exchange). With norepinephrine or isoproterenol (3.2 x 10(-8)M) + acetylcholine (10(-7)M) (to enhance the Ca2+ transient and further shorten the abbreviated action potential, respectively), tachycardia-pause initiated arrhythmia (1,132 +/- 153 beats/min) lasting >1 s was observed. Rapid firing was prevented by either suppression of the Ca2+ transient (ryanodine) or transiently increasing [Ca2+](o). CONCLUSIONS: The data show EAD formation in superfused canine pulmonary veins, enhanced by an increased Ca2+ transient and increased Na-Ca exchange current. With subsequent shortening of the action potential with acetylcholine, tachycardia-pause triggers rapid firing within the PV sleeve.

Action Potentials↗
PubMed2006

Experimental model for paroxysmal atrial fibrillation arising at the pulmonary vein-atrial junctions.

BACKGROUND: The mechanism(s) by which pulmonary veins (PVs) become ectopically active and subsequently initiate and sustain atrial fibrillation (AF) remains poorly understood. OBJECTIVES: The purpose of this study was to produce an acute canine model of paroxysmal AF arising from the PVs. METHODS: In 11 dogs, a thoracotomy was performed and a 26-gauge needle with a polyethylene tube attached was inserted into a fat pad containing autonomic ganglia at the base of the PV. The 11 dogs were divided into two groups: acetylcholine (ACh) 1-10 mM (group I, n = 5) or carbachol (CARB) 1-10 mM (group II, n = 6) injected (0.5 mL) into the fat pad. RESULTS: Within 2 to 5 minutes after injection of parasympathomimetics into the fat pad, a sequence of heart rate slowing, spontaneous premature depolarizations, and spontaneous AF was observed in four of 11 dogs. In seven dogs, single premature extrastimuli easily induced AF. AF was sustained for an average of 10 minutes (ACh) and 38 minutes (CARB), with the shortest AF cycle length seen at the PV-atrial junction adjacent to the fat pad (AF cycle length 75 +/- 41 ms for ACh and 37 +/- 12 ms for CARB). CONCLUSION: Acute autonomic remodeling produced by injection of parasympathomimetics into the fat pad resulted in spontaneous or easily induced sustained AF with short AF cycle length; the most rapid firing rate was observed in the PV and atria adjacent to the injected fat pad. These findings resemble paroxysmal AF in patients, suggesting that hyperactive autonomic ganglia may be a critical element in patients exhibiting focal AF arising from the PV.

Acetylcholine↗
PubMed2006

Abnormal intra-QRS potentials associated with percutaneous transluminal coronary angiography-induced transient myocardial ischemia.

This article introduces a novel concept of abnormal intra-QRS potentials (AIQPs) associated with myocardial ischemia. AIQPs are microvolt-level potentials--subtle alterations in the QRS of the high-resolution electrocardiogram (ECG)--isolated from the unfiltered signal-averaged ECG (SAECG) by a method of mathematical modeling. The aims of the study were (1) to determine the characteristics of potentials in the SAECG related to ischemically altered activation during percutaneous transluminal coronary angiography (PTCA), (2) to determine their relationship with standard 12-lead ECG variables, and (3) to investigate whether AIQPs have a specific pathophysiologic basis in myocardial ischemia. Continuous high-resolution ECG data were acquired from 12 patients before, during, and after PTCA. SAECGs were computed every 60 seconds using an enhanced method of signal averaging. AIQP, ST-segment deviation, and changes in standard ECG QRS duration were measured in each 1-minute SAECG. AIQP amplitudes increased significantly during balloon inflation, compared with the preinflation state. AIQPs exhibited a greater prevalence (12 of 12 patients) than ST-segment deviation changes of more than 100 microV (7 of 12 patients), or measurable changes in standard QRS duration (4 of 12 patients). In patients with significant changes in 12-lead ECG variables during balloon inflation, AIQPs were strongly correlated with both ST-segment and QRS-duration changes. AIQP timing was correlated with the artery occluded, suggesting a specific, ischemia-influenced origin of the signal. AIQPs show promise as a time-localized, sensitive new ECG marker of ischemically altered ventricular activation.

Angioplasty, Balloon, Coronary↗
PubMed2006

Experimental model simulating right ventricular outflow tract tachycardia: a novel technique to initiate RVOT-VT.

BACKGROUND: The mechanism(s) whereby a discrete area of myocardium in the RVOT becomes arrhythmogenic remains unknown. METHODS: In 13 dogs, a circular catheter was placed in the proximal pulmonary artery (PA) to contact the endovascular circumference of the PA. A 50-msec train of high-frequency stimulation (HFS, 200 Hz), coupled to atrial pacing, was applied at each bipolar pair of the circular catheter. The coupling interval was adjusted so that the 50-msec train occurred during the ventricular refractory period, that is, the QRS complex, in order to prevent stimulation of the myocardial sleeve within the proximal PA. RESULTS: In all dogs, HFS induced ventricular premature depolarizations and VTs with a left bundle branch block (LBBB) morphology and inferior axis (average 6.8 +/- 1.6 V). Earliest activation was consistently recorded from the proximal PA. Esmolol, a short-acting beta-blocker (1 mg/kg), was administered intravenously in 11 dogs. The inducible ventricular ectopy was abolished in 10 dogs (>12 V, P < 0.05) and the response to HFS was blunted in one dog (10-11 V). After 30 minutes, the response to HFS returned to pre-esmolol levels. CONCLUSIONS: Stimulation of the sympathetic input to the proximal PA induces ventricular ectopy and VTs exhibiting a left bundle branch block morphology and inferior axis, closely simulating clinical RVOT-VT. Beta-blockade either abolishes or blunts this response, corroborating the sympathetic etiology in this model and in some clinical cases of RVOT tachycardias.

Animals↗
PubMed2005

Comparison of electrode cooling between internal and open irrigation in radiofrequency ablation lesion depth and incidence of thrombus and steam pop.

BACKGROUND: Electrode cooling by circulating fluid within the electrode (closed loop) or open irrigation facilitates radiofrequency (RF) ablation. This study compared lesion parameters between closed loop and open irrigation with the use of a canine model. METHODS AND RESULTS: In 8 anesthetized dogs, the skin over the thigh muscle was incised and raised, forming a cradle superfused with heparinized blood (activated clotting time >350 seconds) at 37 degrees C. A 7F 4-mm closed loop electrode (irrigation 36 mL/min) and 7.5F 3.5-mm open irrigation electrode (irrigation 17 mL/min) were positioned perpendicular to the thigh muscle at 10 g contact weight. RF was applied (n=121) at 20 or 30 W for 60 seconds in low (0.1 m/s) or high (0.5 m/s) pulsatile blood flow. Temperatures were measured in the electrode, electrode-tissue interface, and within the tissue at 3- and 7-mm depths. After each RF, the cradle was emptied to examine the electrode and interface for thrombus. There was no difference between closed loop and open irrigation in impedance, lesion depth, or tissue temperature at 20 or 30 W. Interface temperature and electrode temperature were greater in the closed loop application. Thrombus occurred in 32 of 63 closed loop versus 0 of 58 open irrigation RF applications (P<0.05) with interface temperature > or =80 degrees C in all 32 (electrode temperature <40 degrees C in 1, 40 degrees C to 50 degrees C in 26, and >50 degrees C in 5). With closed loop, interface temperature and thrombus incidence were greater at 30 W and low blood flow. With open irrigation, interface temperature remained low (< or =71 degrees C) with no difference between 20 and 30 W or between low and high blood flow. Steam pop occurred at 20 W in 4 of 35 closed loop and 0 of 30 open irrigation and at 30 W in 15 of 28 closed loop and 4 of 28 open irrigation applications (P<0.05). CONCLUSIONS: Lower interface temperature, thrombus, and steam pop, especially in low blood flow, indicate greater interface cooling with open irrigation.

Animals↗
PubMed2005

Autonomically induced conversion of pulmonary vein focal firing into atrial fibrillation.

OBJECTIVES: This study was designed to determine the mechanism(s) whereby focal firing from pulmonary veins (PVs) is converted into atrial fibrillation (AF). BACKGROUND: The mechanism(s) whereby PV focal firing or even a single PV depolarization is converted into AF is unknown. METHODS: In 14 anesthetized dogs a right thoracotomy was performed to expose the right superior pulmonary vein (RSPV). An octapolar electrode catheter was sutured alongside the RSPV so that the distal electrode pair was adjacent to the fat pad containing autonomic ganglia (AG) at the veno-left atrial (LA) junction. An acrylic plaque electrode on the fat pad allowed AG stimulation at voltages ranging from 0.6 to 4.0 V. Multi-electrode catheters were sutured to the atria with their distal electrode pairs at the fat pad-atrial junctions. Right superior pulmonary vein focal firing consisted of S(1)-S(1) = 330 ms followed by as many as 11 atrial premature depolarizations (APDs) (A(2)-A(12)) whose coupling interval just exceeded RSPV refractoriness. RESULTS: Autonomic ganglia stimulation, without atrial excitation, caused a reduction in heart rate (HR): control 142 +/- 15/min, 4.0 V; 75 +/- 30/min, p </=0.05. The fewest number of APDs from the RSPV required to induce AF during AG stimulation was as follows: control (no stimulation) 7 +/- 4, 2.4 V; 3 +/- 1, p </=0.05. In seven dogs, lidocaine (2%, 0.4 cc), a neuronal blocker, was injected into the fat pad, resulting in the loss of AF inducibility in six of seven dogs at the same AG stimulation levels. Three of seven dogs showed AF inducibility only with AG stimulation >/=9.3 V. CONCLUSIONS: The effects of AG stimulation at the base of the RSPV can provide a substrate for the conversion of PV firing into AF.

Animals↗
PubMed2005

Rapid and stable re-entry within the pulmonary vein as a mechanism initiating paroxysmal atrial fibrillation.

OBJECTIVES: We investigated the hypothesis that re-entrant pulmonary vein (PV) tachycardias may serve as a mechanism for initiating and sustaining paroxysmal atrial fibrillation (PAF). BACKGROUND: The mechanisms of rapid repetitive discharges from the PV initiating PAF remain incompletely understood. Pulmonary vein myocardial sleeves appear to provide a favorable substrate for re-entry formation. METHODS: The electrophysiologic properties of canine PV sleeves were investigated using a combination of high-resolution optical mapping (n = 5) and extracellular bipolar and intracellular microelectrode recordings (n = 56) in a superfused PV preparation. RESULTS: From the left atrium to distal PV, there was progressive shortening of the action potential (AP) duration, reduction in AP and bipolar electrogram amplitude, and depolarization of resting membrane potentials. Sustained PV tachycardias were induced exclusively in the presence of acetylcholine (10(-7) to 10(-6) mol/l, n = 12). Sustained PV tachycardias were rapid (mean cycle length = 93 +/- 15 ms), regular, and capable of induction, termination, and resetting by single extrastimuli. Re-entry as the mechanism underlying PV tachycardias was confirmed by optical mapping (n = 5). Acetylcholine also reduced the slope of the AP restitution curve and suppressed AP alternans (n = 6). Importantly, PV tachycardias exhibited 1:1 conduction into the atrium at short cycle lengths (<100 ms), emphasizing the potential role of re-entrant PV tachycardia in atrial fibrillation. CONCLUSIONS: Pulmonary veins provide a favorable substrate for re-entry formation. Heterogeneity of the electrophysiologic properties and marked abbreviation of action potential duration and refractoriness by acetylcholine combine to produce rapid and stable re-entrant PV tachycardias. Elevated parasympathetic tone and re-entrant PV tachycardia may serve as a mechanism underlying the perpetuation of PAF.

Acetylcholine↗
PubMed2005

Experimental model of inappropriate sinus tachycardia: initiation and ablation.

OBJECTIVE: The purpose of the present study was to develop an experimental model of inappropriate sinus tachycardia (IST) by injecting a catecholamine into a fat pad containing autonomic ganglia (AG) innervating the sinus node (SN). METHODS: Initial protocols in 3 groups of pentobarbital anesthetized dogs consisted of (1) slowing the heart rate (HR) by electrical stimulation of AG in the fat pad; (2) the effect of intravenous injection of epinephrine (0.1-0.3 mg) on the HR and systolic blood pressure (BP); (3) the response of SN rate to intravenously injected isoproterenol (1 microgm/kg). These studies established a reference for the response to epinephrine injection (mean dose 0.2 +/- 0.9 mg, n = 14) into the fat pad at the base of the right superior pulmonary vein (RSPV). ECG leads, right atrial and His bundle electrograms, BP and core body temperature were continuously monitored. RESULTS: Epinephrine, injected into the fat pad, caused a significant increase in heart rate (HR, average: 211 +/- 11/min, p < 0.05 compared to control) but little change in systolic BP, 149 +/- 10 mmHg, p = NS (Group I, N = 8). The tachycardia lasted >30 minutes. Ice mapping and P wave morphology showed the tachycardia origin in the SN in 6/8 and in the crista terminalis (CT) in 2. Injection of 0.4 cc of formaldehyde into the FP restored HR (159 +/- 16) toward baseline (154 +/- 18). In Group II (N = 6), the same regimen induced a significant increase in both HR and systolic BP (194 +/- 17/min and 230 +/- 24 mmHg, respectively) compared to control values (143 +/- 23/min, 162 +/- 24 mmHg) which lasted for > 30 minutes. Ice mapping and P wave morphology showed that the pacemaker was in the SN (1), overlying the CT (2), or atrioventricular junction (2). Formaldehyde (0.4 cc) injected into the FP restored both HR and systolic BP toward baseline values (148 +/- 29/min and 152 +/- 24 mmHg, p = NS) and prevented, slowing of the HR by electrical stimulation of the AG; moreover, the same dose of epinephrine injected intravenously increased HR and SBP but only for 2-5 minutes; Isoproterenol (1 microg/kg) injected intravenously induced essentially the same increase in sinus rate after AG ablation as in the control state (194 +/- 15/min vs 193 +/- 23/min, p = NS). CONCLUSION: Experimental IST is mainly localized in the SN or CT. Ablation of the AG terminates IST without impairing the SN response to an adrenergic challenge.

Animals↗
PubMed2005

Electrical stimulation to identify neural elements on the heart: their role in atrial fibrillation.

EXPERIMENTAL STUDIES: Anesthetized dogs were subjected to a right then left thoracotomy. Two modes of electrical stimulation were used to activate ganglionated plexi (GP) on the epicardium of the atria: (1) Near the base of each pulmonary vein (PV), trains of high frequency stimuli (HFS) were coupled to each atrial paced beat so as to fall within the refractory period to achieve nerve stimulation without atrial excitation; and (2) Continuous HFS was applied via plaque electrodes sutured to epicardial fat pads (containing a GP) near the right superior (RS) and left superior (LS) PVs. The chest was then closed. An ablation catheter, inserted percutaneously, was positioned fluoroscopically in the right atrium across from the epicardial plaque electrode near the RSPV. Transeptal puncture was used to place an ablation catheter at the LSPV-left atrial junction. HFS applied to each of the epicardial fat pads induced atrial fibrillation (AF) and also caused high grade AV block due to a strong parasympathetic effect on the AV node. Radiofrequency ablation from the right and left atrial endocardium abolished the vagal response to HFS delivered to the plaque electrodes on the fat pads close to the RSPV and LSPV, respectively. CLINICAL STUDIES: Sixty (60) patients with paroxysmal or persistent AF underwent PV antrum isolation (27 patients) or PV antrum isolation plus left atrial GP ablation (33 patients). Endocardial HFS at the border of the PV antra near the 4 GPs produced AF and high grade AV block (vagal response) during AF. RFA at these sites abolished the vagal response. Testing in a small number of patients with very short follow-up suggests that adding GP ablation to PV antrum isolation may increase ablation success (absence of AF recurrence) from 70% to 91%. CONCLUSIONS: These basic and clinical studies suggest that localized cardiac autonomic ganglia (GPs) may play a critical role in the initiation and maintenance of AF.

Animals↗
PubMed2005

Triggered firing in pulmonary veins initiated by in vitro autonomic nerve stimulation.

BACKGROUND: Rapid firing within pulmonary vein sleeves frequently initiates atrial fibrillation. The role of the autonomic nervous system in facilitating spontaneous firing is unknown. OBJECTIVES: The purpose of this study was to determine if autonomic nerve stimulation within canine atrium and pulmonary vein sleeves initiates arrhythmia formation. METHODS: Extracellular bipolar and intracellular microelectrode recordings were obtained from isolated superfused canine pulmonary veins (N = 28) and right atrium (N = 5) during local autonomic nerve stimulation. RESULTS: Autonomic nerve stimulation decreased pulmonary vein sleeve action potential duration (APD90 = 160 +/- 17 to 92 +/- 24 ms; P < .01) and initiated rapid (782 +/- 158 bpm) firing from early afterdepolarizations in 22 of 28 pulmonary vein preparations. The initial spontaneous beat had a coupling interval of 97 +/- 26 ms. Failure to induce arrhythmia was associated with a failure to shorten APD90 (151 +/- 18 to 142 +/- 8 ms; P = .39). Muscarinic receptor blockade (atropine: 3.2 x 10(-8) M) prevented APD90 shortening in 8 of 8 preparations and suppressed firing in 6 of 8 preparations, whereas beta1-adrenergic receptor blockade (atenolol: 3.2 x 10(-8) M) suppressed firing in 8 of 8 preparations. Suppression of the Ca transient with ryanodine (10(-5) M) completely suppressed firing in 6 of 6 preparations. Inhibition of forward Na/Ca exchange by a transient increase in [Ca+2]o completely suppressed firing in 4 of 6 preparations. The same stimulus trains produce atropine-suppressed APD90 shortening in superfused right atrial free wall but fail to produce triggered arrhythmia. CONCLUSIONS: The data demonstrate triggered firing within canine pulmonary veins with combined parasympathetic and sympathetic nerve stimulation. Both an enhanced Ca transient and increased Na/Ca exchange may be required for arrhythmia formation.

Animals↗
PubMed2005

Comparison of cryothermia and radiofrequency current in safety and efficacy of catheter ablation within the canine coronary sinus close to the left circumflex coronary artery.

INTRODUCTION: A canine model was used to compare cryoablation and radiofrequency ablation (RFA) within the coronary sinus (CS) in the ability to create a transmural CS myocardial (Trans-CSM) lesion and risk of coronary artery stenosis. METHODS: After CS and left circumflex (LCx) coronary angiography, an intravascular ultrasound (IVUS) probe was placed in LCx in 29 dogs. An irrigated RFA catheter (8 dogs) or N(2)O cryoablation catheter (21 dogs) was inserted into the CS and positioned within 2 mm of LCx, confirmed by IVUS. RF (30-50W) was applied for 60 seconds at 10 CS sites. Cryoablation (-75 degrees C) was performed with one (n = 7) or two (n = 14) 4-minute applications. Dogs were sacrificed at 1 week (8 RFA and 13 cryoablation) or 3 months (8 cryoablation). RESULTS: During RFA, IVUS showed wall thickening and LCx narrowing in 9 of 10 sites. Angiography at 5-minute post-RFA identified LCx narrowing (25-90%) at 6 of 10 sites and 25-75% narrowing at 4 of 9 sites at 1-week post-RFA. During cryoablation, IVUS showed reversible ice ball compression of LCx, and no LCx narrowing by angiography at 5 minutes, 1 week, or 3 months. Histology showed Trans-CSM lesion at 10 of 10 RFA sites and 20 of 21 cryoablation sites. RFA produced LCx medial necrosis at 7 of 10 sites, involving 20-50%(median 32.5%) of LCx circumference with loss of intima at 5 of 7 sites. Single and twice 4-minute cryoablation produced LCx medial necrosis at 2 of 7 and 8 of 14 sites (5-40%, median 25% circumference). Intima was preserved at 1 week (13/13) with minor proliferation (without narrowing) at 2 of 8 sites at 3 months. CONCLUSIONS: Cryoablation in CS within 2 mm of LCx produces Trans-CSM lesions similar to RFA with lower risk of LCx stenosis than RFA.

Animals↗
PubMed2004

Relation between pulmonary vein firing and extent of left atrial-pulmonary vein connection in patients with atrial fibrillation.

BACKGROUND: The purpose of this study was to measure the extent of left atrial-pulmonary vein (LA-PV) connections and determine the relation to PV firing in patients with atrial fibrillation (AF). METHODS AND RESULTS: Ten close-bipolar (1 mm-spacing) Lasso electrograms were recorded circumferentially around 210 PVs (excluding 2 right middle PVs and 4 left common trunks) in 62 patients with AF. PV firing was provoked by isoproterenol (4 microg/min) and cardioversion of pacing-induced AF. The width of each LA-PV connection was measured in tenths of PV circumference, based on number of continuous close-bipolar Lasso electrode sites required for ablation (10% for each close-bipolar electrode site). One, 2, or 3 to 4 discrete LA-PV connections (discrete connection defined by ablation along 10% to 30% of PV circumference) were present in 18 (9%), 31 (14%), and 32 (15%) of 210 PVs, respectively: 1 broad connection (ablation along continuous 40% to 80% circumference) in 46 (22%) PVs; 1 broad plus other broad or discrete connections in 54 (26%) PVs; and a circumferential connection (ablation along 90% to 100%) in 29 (14%) PVs. Circumferential LA-PV connections were more common in superior than in inferior PVs (20% versus 7%, P<0.01). There was no major difference in distribution of the other types of LA-PV connections between the four PVs. PV firing occurred in 27%, 47%, and 72% of PVs with discrete only, broad and circumferential connections, respectively (P<0.01). Dissociated PV potentials after isolation were more common in arrhythmogenic (firing) PVs (32% versus 8%, P<0.01). CONCLUSIONS: The extent of LA-PV connections corresponds with arrhythmognesis. The incidence of PV firing increases with progressively wider LA-PV connections (discrete versus broad versus circumferential).

Action Potentials↗
PubMed2004

Variability of AV nodal potentials recorded, in vivo: direct demonstration of dual AV nodal physiology.

OBJECTIVES OF STUDY: We developed a method to record extracellular A-V nodal potentials in the beating dog heart, in vivo. METHODS: In eleven Na-pentobarbital anesthetized, open-chest dogs, an octapolar electrode catheter (2 mm rings, 2 mm spacing) was inserted through a purse-string suture in the coronary sinus (CS) distal to the ostium and positioned electrographically so that the tip electrode recorded a His bundle (Hb) potential. RESULTS: Stable recordings of A-V nodal potentials (amplitude, 178 +/- 94 microV; duration 78 +/- 26 msec) were consistently made during sinus rhythm from the second and/or third bipolar pairs of electrodes. Programmed atrial stimulation and vagal stimulation resulted in loss of amplitude and increased duration of the A-V nodal potentials associated with A-H prolongation. In another series of experiments, crushing the sinus node in 6 dogs resulted in AV nodal rhythms with AV nodal potentials of varying amplitudes (132 to 840 microV) and durations (range 25 to 71 msec) as the earliest activation which preceded the Hb, atrial and ventricular deflections. One dog, showing dual AV nodal physiology as documented from the AV nodal function curve, had two distinctly different AV nodal potentials. The low-level, longer duration potentials were associated with longer (slow pathway) A-H intervals; whereas the shorter higher amplitude potentials (fast pathway) showed shorter A-H intervals, each occurring at a critical paced cycle length. CONCLUSION: We conclude that consistent extracellular AV nodal electrograms can be recorded in vivo although the configuration of these potentials varies depending on heart rate, autonomic stimulation and different arrhythmic conditions such as AV nodal escape rhythms and dual AV nodal physiology.

Action Potentials↗
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↗