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Biomedical subjects

R Lazzara

Publications and source records attributed to R Lazzara.

At least 37 records · Page 2Linked to original sources
PubMed2000

Conditioning of beta(1)-adrenoceptor effect via beta(2)-subtype on L-type Ca(2+) current in canine ventricular myocytes.

We investigated the roles of beta(1)- and beta(2)-receptors (beta-AR) in adrenergic enhancement of L-type Ca(2+) current (I(CaL)) in canine ventricular myocytes. Isoproterenol and l-norepinephrine produced a monophasic and a biphasic concentration-I(CaL) relationship (CR), respectively. alpha(1)-AR inhibition with prazosin and beta(2)-AR stimulation with zinterol or l-epinephrine shifted the CR of l-norepinephrine leftward. Zinterol (50 nM) and l-epinephrine (10 nM), but not prazosin, altered the biphasic CR of l-norepinephrine to a monophasic CR. Zinterol and l-epinephrine applied after l-norepinephrine had no effect on I(CaL). beta(2)-AR inhibition with ICI-118551 reduced the E(max) of isoproterenol and l-norepinephrine by 60% and abolished the augmentation of l-norepinephrine by zinterol and l-epinephrine. Carbachol (100 nM) modestly reduced the I(CaL) response to beta(1)-AR stimulation but abolished the enhancement via beta(2)-AR. Zinterol augmented the enhancement of I(CaL) by forskolin, IBMX, and theophylline, but not in the presence of CGP-20712A. We conclude that selective beta(2)-AR stimulation does not increase I(CaL) but enhances adenylyl cyclase activity when stimulated via beta(1)-AR and with forskolin. beta(2)-AR activity preconditions adenylyl cyclase for beta(1)-AR stimulation.

Adrenergic Agonists↗
PubMed1999

Ventricular rate control during atrial fibrillation by cardiac parasympathetic nerve stimulation: a transvenous approach.

OBJECTIVES: To identify intravascular sites for continuous, stable parasympathetic stimulation (PS) in order to control the ventricular rate during atrial fibrillation (AF). BACKGROUND: Ventricular rate control during AF in patients with congestive heart failure is a significant clinical problem because many drugs that slow the ventricular rate may depress ventricular function and cause hypotension. Parasympathetic stimulation can exert negative dromotropic effects without significantly affecting the ventricles. METHODS: In 22 dogs, PS was performed using rectangular stimuli (0.05 ms duration, 20 Hz) delivered through a catheter with an expandable electrode-basket at its end. The catheter was positioned either in the superior vena cava (SVC, n = 6), coronary sinus (CS, n = 10) or right pulmonary artery (RPA, n = 6). The basket was then expanded to obtain long-term catheter stability. Atrial fibrillation was induced and maintained by rapid atrial pacing. RESULTS: Nonfluoroscopic (SVC) and fluoroscopic (CS/RPA) identification of effective intravascular PS sites was achieved within 3 to 10 min. The ventricular rate slowing effect during AF started and ceased immediately after on-offset of PS, respectively, and could be maintained over 20 h. In the SVC, at least a 50% increase of ventricular rate (R-R) intervals occurred at 22 +/- 11 V (331 +/- 139 ms to 653 +/- 286 ms, p < 0.001), in the CS at 16 +/- 10 V (312 +/- 102 ms vs. 561 +/- 172 ms, p < 0.001) and in the RPA at 18 +/- 7 V (307 +/- 62 ms to 681 +/- 151 ms, p < 0.001). Parasympathetic stimulation did not change ventricular refractory periods. CONCLUSIONS: Intravascular PS results in a significant ventricular rate slowing during AF in dogs. This may be beneficial in patients with AF and rapid ventricular response since many drugs that decrease atrioventricular conduction have negative inotropic effects which could worsen concomitant congestive heart failure.

Animals↗
PubMed1999

Transvenous parasympathetic cardiac nerve stimulation: an approach for stable sinus rate control.

INTRODUCTION: Epicardial electrical stimulation of parasympathetic nerves innervating the sinus node has been shown to decrease sinus rate. We investigated whether intravascular parasympathetic cardiac nerve stimulation (IPS) can be achieved over a relatively long-term period to slow the supraventricular rate. METHODS AND RESULTS: Fifteen dogs were investigated. IPS was performed with rectangular stimuli (0.05-msec duration, 20 Hz) using a catheter with an expandable electrode basket. The catheter was positioned in the superior vena cava (SVC; n = 9) or right pulmonary artery (RPA; n = 6). The basket then was expanded to hold the catheter in place. Nonfluoroscopic identification of effective IPS sites was achieved within 5 minutes in the SVC. Increasing IPS voltage resulted in a graded response of supraventricular rate slowing. A 50% prolongation of the baseline atrial cycle length was achieved with 28 V in the SVC (1,056 +/- 355 msec vs 489 +/- 154 msec; P < 0.001) and 25 V in the RPA (1,181 +/- 306 msec vs 518 +/- 138 msec; P < 0.01). The rate slowing started immediately after IPS onset, terminated abruptly after IPS cessation, and could be maintained over 10 hours. A rate slowing effect also was observed when the sinus rate was increased by isoproterenol (SVC: 304 +/- 8 msec/RPA: 341 +/- 9 msec with isoproterenol vs SVC: 635 +/- 12 msec with isoproterenol + IPS at 39 V/ RPA: 584 +/- 16 msec with isoproterenol + IPS at 38 V; n = 6). CONCLUSION: IPS results in a significant supraventricular rate slowing that is stable over a relatively long period and may be applied to slow undesirable sinus tachycardia in acute ischemic syndromes or to counteract undesirable chronotropic effects of catecholamines during treatment of cardiogenic or septic shock and acute congestive heart failure.

Animals↗
PubMed1999

Canine ventricular myocyte beta2-adrenoceptors are not functionally coupled to L-type calcium current.

INTRODUCTION: To establish the functional coupling of beta adrenoceptor (betaAR) subtypes beta1AR and beta2AR to L-type calcium current (I(CaL)), we investigated the nonselective agonist isoproterenol (ISO) and the relatively selective beta2AR agonists zinterol (ZIN) and salbutamol (SAL) on I(CaL) in isolated canine ventricular myocytes in the presence and absence of CGP 20712A (CGP) and atenolol (AT), selective beta1AR antagonists, and ICI 118,551 (ICI) a selective beta2AR antagonist. METHODS AND RESULTS: Peak I(CaL) was determined using "patch type" microelectrodes and whole cell voltage clamp. ISO (0.5 microM) increased I(CaL) maximally 3.5 +/- 0.67 fold. ZIN (10.0 microM) and SAL (10.0 microM) increased I(CaL) maximally 1.5 +/- 0.2 fold (n = 5) and 1.4 +/- 0.1 fold (n = 5), respectively. These effects were fully inhibited by CGP (0.3 microM) and AT (1.0 microM), which are inhibitors of beta1AR, but not by ICI (0.1 microM), which is a beta2AR inhibitor. ZIN at relatively lower concentrations (< or = 0.1 microM) did not increase I(CaL). CGP (0.3 microM) but not AT and ICI inhibited I(CaL) in the absence of betaAR agonists. CGP inhibition of I(CaL) was absent in the presence of forskolin (1.0 microM), which increases cAMP levels and I(CaL) by directly stimulating the adenylate cyclase. These data indicate that none of the antagonists affect I(CaL) through an action downstream of betaAR. CONCLUSION: Beta-adrenergic agonists increase I(CaL) via beta1AR but not beta2AR in canine ventricular myocytes.

Animals↗
PubMed1999

[The coupling of canine ventricular myocyte beta2-adrenoceptors to L-type calcium current].

UNLABELLED: To establish the functional coupling of beta adrenoceptor (beta AR) subtypes of beta 1AR and beta 2AR to L-type calcium current (ICaL), we investigated the non-selective agonist isoproterenol (ISO), and the relatively selective beta 2AR agonists zinterol (ZIN) and salbutamol (SAL) on ICaL in isolated canine ventricular myocytes in the presence and absence of CGP 20712A (CGP) and atenolol (AT), selective beta 1AR antagonists, and ICI 118,551 (ICI) a selective beta 2AR antagonist. Peak ICaL was determined using "patch type" microelectrodes and whole cell voltage clamp. ISO (0.5 microM) increased ICaL maximally 3.5 +/- 0.67 fold. ZIN (10.0 microM) and SAL (10.0 microM) increased ICaL maximally 1.5 +/- 0.2 (n = 5) fold and 1.4 +/- 0.1 (n = 5) fold, respectively. These effects were fully inhibited by CGP (0.3 microM) and AT (1.0 microM), inhibitors of beta 1AR but not by ICI (0.1 microM) a beta 2AR inhibitor. ZIN at relatively lower concentrations (< or = 0.1 microM) did not increase ICaL. CGP (0.3 microM) but not AT and ICI inhibited ICaL in the absence of beta AR agonists. CGP inhibition of ICaL was absent in the presence of forskolin (FK, 1.0 microM) that increases cAMP levels and ICaL by directly stimulating the adenylate cyclase. These indicate that none of the antagonists affect ICaL through an action downstream of beta AR. CONCLUSION: beta-adrenergic agonists increase ICaL via beta 1AR but not beta 2AR in canine ventricular myocytes.

Adrenergic beta-Agonists↗
PubMed1998

Electrical conduction between the right atrium and the left atrium via the musculature of the coronary sinus.

BACKGROUND: The purpose of this study was to determine whether the coronary sinus (CS) musculature has electrical connections to the right atrium (RA) and left atrium (LA) and forms an RA-LA connection. METHODS AND RESULTS: Six excised dog hearts were perfused in a Langendorff preparation. A 20-electrode catheter (2-4-2-mm spacing center to center) was placed along the CS. Excision of the pulmonary veins provided access to the LA, and a second 20-electrode catheter was placed along the LA endocardium opposite the CS catheter. An incision opened the CS longitudinally, and microelectrodes were inserted into the CS musculature and adjacent LA myocardium. Continuous CS musculature was visible along a 35+/-9-mm length of the CS beginning at the ostium. During lateral LA pacing, CS electrodes recorded double potentials, a rounded, low-frequency potential followed by a sharp potential. The rounded initial potential propagated in the lateral-to-septal direction and represented "far-field" LA activation (timing coincided with adjacent LA potentials and with action potentials recorded from microelectrodes in adjacent LA cells). The sharp potential represented CS activation (timing coincided with action potentials recorded from CS musculature). A distal LA-CS connection (earliest sharp potential in the CS during lateral LA pacing) was located 26+/-7 mm from the ostium. During RA pacing posterior to the CS ostium, CS electrodes recorded septal-to-lateral activation of the high-frequency potential, with slightly later activation of the rounded potential (LA activation). Incisions surrounding the CS ostium isolating the ostium from the RA had no effect on the CS musculature and LA potentials during RA pacing within the isolated segment containing the CS ostium. RA pacing outside the isolated segment delayed activation of the CS musculature until after LA activation, confirming that the RA-CS connection was located in the region of the CS ostium as well as confirming the presence of the LA-CS connection. CONCLUSIONS: In canine hearts, the CS musculature is electrically connected to the RA and the LA and forms an RA-LA connection.

Animals↗
PubMed1998

Inverse relationship between electrode size and lesion size during radiofrequency ablation with active electrode cooling.

BACKGROUND: Clinical efficacy has driven the use of larger electrodes (7F, length > or =4 mm) for radiofrequency ablation, which reduces electrogram resolution and causes variability in tissue contact depending on electrode orientation. With active cooling, ablation electrode size may be reduced. The purpose of this study was to examine the effect of electrode length on tissue temperature and lesion size with saline irrigation used for active cooling. METHODS AND RESULTS: In 11 anesthetized dogs, the thigh muscle was exposed and bathed with heparinized canine blood. A 7F ablation catheter with a 2- or 5-mm irrigated tip electrode was positioned perpendicular or parallel to the thigh muscle. Radiofrequency current was delivered at constant voltage (50 V) for 30 seconds during saline irrigation (20 mL/min) to 148 sites. Tissue temperature at depths of 3.5 and 7 mm and lesion size were measured. In the perpendicular electrode-tissue orientation, radiofrequency applications at 50 V with the 2-mm electrode compared with the 5-mm electrode resulted in lower power at 50 V (26 versus 36 W) but higher tissue temperatures, larger lesion depth (8.0 versus 5.4 mm), and greater diameter (12.4 mm versus 8.4 mm). Also, in the parallel orientation, overall power was lower with the 2-mm electrode (25 versus 33 W), but tissue temperatures were higher and lesions were deeper (7.3 versus 6.9 mm). Lesion diameter was similar (11.1 versus 11.3 mm) for both electrodes. CONCLUSIONS: The smaller electrode resulted in transmission of a greater fraction of the radiofrequency power to the tissue and resulted in higher tissue temperature, larger lesions, and lower dependency of lesion size on the electrode orientation.

Animals↗
PubMed1998

Development and validation of an ECG algorithm for identifying accessory pathway ablation site in Wolff-Parkinson-White syndrome.

INTRODUCTION: Delta wave morphology correlates with the site of ventricular insertion of accessory AV pathways. Because lesions due to radiofrequency (RF) current are small and well defined, it may allow precise localization of accessory pathways. The purpose of this study was to use RF catheter ablation to develop an ECG algorithm to predict accessory pathway location. METHODS AND RESULTS: An algorithm was developed by correlating a resting 12-lead ECG with the successful RF ablation site in 135 consecutive patients with a single, anterogradely conducting accessory pathway (Retrospective phase). This algorithm was subsequently tested prospectively in 121 consecutive patients (Prospective phase). The ECG findings included the initial 20 msec of the delta wave in leads I, II, aVF, and V1 [classified as positive (+), negative (-), or isoelectric (+/-)] and the ratio of R and S wave amplitudes in leads III and V1 (classified as R > or = S or R < S). When tested prospectively, the ECG algorithm accurately localized the accessory pathway to 1 of 10 sites around the tricuspid and mitral annuli or at subepicardial locations within the venous system of the heart. Overall sensitivity was 90% and specificity was 99%. The algorithm was particularly useful in correctly localizing anteroseptal (sensitivity 75%, specificity 99%), and mid-septal (sensitivity 100%, specificity 98%) accessory pathways as well as pathways requiring ablation from within ventricular venous branches or anomalies of the coronary sinus (sensitivity 100%, specificity 100%). CONCLUSION: A simple ECG algorithm identifies accessory pathway ablation site in Wolff-Parkinson-White syndrome. A truly negative delta wave in lead II predicts ablation within the coronary venous system.

Adolescent↗
PubMed1998

Why a large tip electrode makes a deeper radiofrequency lesion: effects of increase in electrode cooling and electrode-tissue interface area.

INTRODUCTION: Increasing electrode size allows an increase in radiofrequency lesion depth. The purpose of this study was to examine the roles of added electrode cooling and electrode-tissue interface area in producing deeper lesions. METHODS AND RESULTS: In 10 dogs, the thigh muscle was exposed and superfused with heparinized blood. An 8-French catheter with 4- or 8-mm tip electrode was positioned against the muscle with a blood flow of 350 mL/min directed around the electrode. Radiofrequency current was delivered using four methods: (1) electrode perpendicular to the muscle, using variable voltage to maintain the electrode-tissue interface temperature at 60 degrees C; (2) same except the surrounding blood was stationary; (3) perpendicular electrode position, maintaining tissue temperature (3.5-mm depth) at 90 degrees C; and (4) electrode parallel to the muscle, maintaining tissue temperature at 90 degrees C. Electrode-tissue interface temperature, tissue temperature (3.5- and 7.0-mm depths), and lesion size were compared between the 4- and 8-mm electrodes in each method. In Methods 1 and 2, the tissue temperatures and lesion depth were greater with the 8-mm electrode. These differences were smaller without blood flow, suggesting the improved convective cooling of the larger electrode resulted in greater power delivered to the tissue at the same electrode-tissue interface temperature. In Method 3 (same tissue current density), the electrode-tissue interface temperature was significantly lower with the 8-mm electrode. With parallel orientation and same tissue temperature at 3.5-mm depth (Method 4), the tissue temperature at 7.0-mm depth and lesion depth were greater with the 8-mm electrode, suggesting increased conductive heating due to larger volume of resistive heating because of the larger electrode-tissue interface area. CONCLUSION: With a larger electrode, both increased cooling and increased electrode-tissue interface area increase volume of resistive heating and lesion depth.

Animals↗
PubMed1998

Evidence for multiple atrio-AV nodal inputs in the normal dog heart.

INTRODUCTION: Complete AV block after combined fast pathway (FP) and slow pathway (SP) ablation is uncommon. The purpose of this study was to interrupt activation of these and additional inputs by placing a radiofrequency lesion across the interatrial septum between the FP and SP ablation sites. METHODS AND RESULTS: In eight anesthetized open chest dogs, FP ablation induced significant A-H prolongation (deltaA-H: 51 +/- 14 msec; P < 0.001) and a shift of earliest retrograde atrial activation from the anterior septum to the region of the coronary sinus (CS) os. Subsequently, ablation of the interatrial septum across the fossa ovalis was successful in 5 of 8 dogs, changing the sequence of atrial activation (A) so that A at the His-bundle electrogram, which initially preceded A at the CS os (18 +/- 4 msec vs 46 +/- 7 msec, P < 0.01), now followed CS os A (81 +/- 31 msec vs 59 +/- 20 msec, P < 0.05). Additional ablation of the SP caused a type II Mobitz AV block or complete AV block in 5 of 8 dogs. The four dogs with complete AV block showed a stable, high junctional escape rhythm at a rate of 64 +/- 16 beats/min. Pacing between the ablation lesions and the AV node in one dog showed 1:1 AV conduction and Wenckebach-type AV block indicating preserved AV nodal function. Histology showed necrotic changes in the FP and SP transitional cell zones and in the atrial tissue of the interatrial septum. However, the compact AV node, His bundle, and adjacent atria and transitional cells were undamaged. CONCLUSION: There are additional AV nodal inputs in the interatrial septum in addition to the anterior FP and posterior SP inputs. Ablation of all of these may be required, if the aim is production of complete AV block proximal to the AV node with a high junctional escape rhythm.

Animals↗
PubMed1997

Analysis of abnormal intra-QRS potentials. Improved predictive value for arrhythmic events with the signal-averaged electrocardiogram.

BACKGROUND: Using the signal-averaged ECG (SAECG), this study developed a new electrical index for predicting arrhythmic events: abnormal intra-QRS potentials (AIQP). METHODS AND RESULTS: We studied 173 patients followed after myocardial infarction for a mean duration of 14 +/- 7 months. Sixteen arrhythmic events occurred, defined as sudden cardiac death, documented sustained ventricular tachycardia, or non-fatal cardiac arrest. Noninvasive indices of arrhythmia risk were measured, including AIQP, conventional SAECG, Holter, and left ventricular ejection fraction (LVEF). Abnormal intra-QRS potentials were defined as abnormal signals occurring anywhere within the QRS period. They were estimated with a lead-specific, parametric modeling method that removed the smooth, predictable part of the QRS. AIQPs are characterized by the remaining transient, unpredictable component of the QRS and manifest as low-amplitude notches and slurs. A combined XYZ-lead AIQP index exhibited higher specificity (95%) and predictive value (PV) (+PV, 47%; -PV, 94%) than the conventional SAECG in combination with Holter and LVEF (specificity, 89%; +PV, 25%; -PV, 93%). CONCLUSIONS: AIQP improved specificity and predictive value, compared with conventional tests, for prediction of arrhythmic events. AIQP emerged as the best noninvasive univariate predictor of arrhythmic events after myocardial infarction in this study. A review of several other reports shows that AIQP in the present study outperformed the conventional predictive indices reported in those other data sets.

Arrhythmias, Cardiac↗
PubMed1997

Similarities between early and delayed afterdepolarizations induced by isoproterenol in canine ventricular myocytes.

OBJECTIVES: This study aims at clarifying the role of cellular Ca2+ overload and spontaneous sarcoplasmic reticulum (SR) Ca2+ release in the generation of early afterdepolarizations (EAD) by isoproterenol. The involvement of a Ca(2+)-activated membrane current in isoproterenol-induced EAD is investigated. METHODS: Membrane potential and contraction (an indicator of SR Ca2+ release) were recorded in canine left ventricular myocytes at pacing cycle lengths (CL) of 300-4000 ms. Threshold concentration for EAD was 20-50 mmol/l isoproterenol. Ni2+ (2.0-5.0 mmol/l) was used at normal and high (5.4 mmol/l) [Ca2+]o to examine the role of Ca2+ current and/or Na(+)-Ca2+ exchange (1Na-Ca) in EAD. RESULTS: In all cells delayed afterdepolarizations (DAD) appeared during isoproterenol. In most (approximately equal to 70%) cells EAD were also generated, which were fast-pacing dependent, occurring only at CL of 400-1000 ms. EAD were always initiated by a delay in repolarization. Early aftercontractions preceded the EAD upstrokes, often occurring without them. They coincided with the initial delays in repolarization. During treatment with isoproterenol, Ni2+ and high [Ca2+]o, EAD and DAD were suppressed despite the continued presence of early and delayed aftercontractions. CONCLUSIONS: Our data indicate that beta-adrenergic EAD share a common ionic mechanism with DAD in terms of cellular Ca2+ overload and spontaneous SR Ca2+ release. beta-Adrenergic EAD consist of two phases: (1) a conditional phase coinciding with the onset of an early aftercontraction, often followed by (2) an EAD upstroke. A Ca2(+)-activated membrane current, probably I Na-Ca, is necessary at least for the initiation of these EAD.

Action Potentials↗
PubMed1997

Facilitation of epinephrine-induced afterdepolarizations by class III antiarrhythmic drugs.

The electrophysiologic actions of epinephrine (10(-9) M, 10(-8) M, and 10(-7) M) were evaluated in canine Purkinje fibers pretreated with the class III antiarrhythmic drugs clofilium (10(-7) M) or d,l-sotalol (10(-6) M). Clofilium and d,l-sotalol prolonged action potential duration at 50% and 90% of repolarization without provoking early afterdepolarization (EAD) or delayed afterdepolarization (DAD). Subsequent administration of epinephrine provoked both bradycardia-dependent EADs and tachycardia-dependent DADs in clofilium-treated Purkinje fibers, with predominantly EADs observed in d,l-sotalol-treated Purkinje fibers. A temporary increase in Ca0(+2) from 1.35 mM to 5 mM suppressed both EADs and DADs. The data demonstrate facilitation of epinephrine-induced EADs and DADs by class III antiarrhythmic drugs. The acute suppression of both EADs and DADs observed following an acute increase in Ca0(+2) suggests inward Na(+)-Ca0(+2) exchange current as a basis for both EADs and DADs observed in the presence of class III antiarrhythmic drugs and epinephrine.

Action Potentials↗
PubMed1997

Electrophysiology of the right anterior approach to the atrioventricular node: studies in vivo and in the isolated perfused dog heart.

INTRODUCTION: Previous reports have described electrophysiologic properties and rate-dependent responses in the transitional cell zone of the posterior AV nodal input (slow pathway). The purpose of this study was to investigate the electrophysiology of the anterior transitional cell zone (fast pathway) in vivo and in a Langendorff preparation perfused with a nonblood solution containing butanedionemonoxime to inhibit contraction. METHODS AND RESULTS: In five anesthetized dogs, the His-bundle electrogram recorded from the aortic root included atrial activity in close proximity to the anterior limbus of the fossa ovalis. During decremental atrial pacing, the atrial potential exhibited amplitude alternans at a pacing cycle length (CL) of 135 +/- 14 msec. In ten isolated perfused canine hearts, a bipolar electrode catheter was positioned with its tip against the right anterior interatrial septum just superior to the tendon of Todaro. The AV Wenckebach CL (WCL) averaged 262 +/- 21 msec. During further decreases in pacing CL, the bipolar atrial potential developed a 2:1 amplitude alternans (9/10 dogs) at CL = 168 +/- 15 msec and then split into two components with subsequent 2:1 block between these components (10/10 dogs) at CL = 152 +/- 19 msec. Radiofrequency ablation at this site in six dogs prolonged the stimulus to HB interval from 113 +/- 19 to 151 +/- 30 msec (P < 0.01) without changing the WCL, consistent with ablation of the fast AV nodal pathway. In six other isolated perfused canine hearts, an octapolar catheter (2-mm spacing) was positioned along the anterior limbus of the fossa ovalis with the tip electrode located over the anterior portion (apex) of the triangle of Koch. The aforementioned 2:1 amplitude alternans occurred at a longer CL in the distal electrodes located at the tendon of Todaro than in the proximal electrodes at farther distances from the tendon of Todaro (185 +/- 25 vs 171 +/- 20 msec, P < 0.05), as did the 2:1 block between the two components (161 +/- 18 vs 150 +/- 18 msec, P < 0.05). Microelectrode recordings obtained adjacent to the catheter demonstrated 2:1 alternans and block patterns in the action potentials of transitional cells but not in atrial cells, which exhibited 1:1 conduction at all CL. CONCLUSIONS: The transitional cell zone in the anterior interatrial septum exhibits a specific rate-dependent, spatial gradient of conduction block, which can be recorded in bipolar electrograms as well as microelectrode recordings. Electrophysiologic changes induced by radiofrequency ablation of this anterior atrial/transitional cell zone (corroborated by histology) provide strong presumptive evidence that this area constitutes all or a major part of the fast AV nodal pathway.

Animals↗
PubMed1997

Electrophysiology of the atrio-AV nodal inputs and exits in the normal dog heart: radiofrequency ablation using an epicardial approach.

INTRODUCTION: We studied the effects of selective and combined ablation of the fast (FP) and slow pathway (SP) on AV and VA conduction in the normal dog heart using a novel epicardial ablation technique. METHODS AND RESULTS: For FP ablation, radiofrequency current (RFC) was applied to a catheter tip that was held epicardially against the base of the right atrial wall. SP ablation was performed epicardially at the crux the heart. Twenty-three dogs were assigned to two ablation protocols: FP/SP ablation group (n = 17) and SP/FP ablation group (n = 6). In 12 of 17 dogs, FP ablation prolonged the PR interval (97 +/- 10 to 149 +/- 22 msec, P < 0.005) with no significant change in anterograde Wenckebach cycle length (WBCL). Subsequent SP ablation performed in 8 dogs further prolonged the PR interval and the anterograde WBCL (117 +/- 22 to 193 +/- 27, P < 0.005). Complete AV block was seen in 1 of 8 dogs, whereas complete or high-grade VA block was seen in 6 of 8 dogs. In the SP/FP ablation group, SP ablation significantly increased WBCL with no PR changes. Combined SP/FP ablation in 6 dogs prolonged the PR interval significantly, but no instance of complete AV block was seen. VA block was found in 50% of these cases. Histologic studies revealed that RFC ablation affected the anterior and posterior atrium adjacent to the undamaged AV node and His bundle. CONCLUSION: Using an epicardial approach, combined ablation of the FP and SP AV nodal inputs can be achieved with an unexpectedly low incidence of complete AV block, although retrograde VA conduction was significantly compromised.

Animals↗