bluuebunny/crossref_metadata_2025_split huggingface dataset:
Differential Effects of Parasympathetic Blockade and Parasympathetic Withdrawal on Heart Rate Variability
Authors: CHALLAPALLI SRIDEVI , KADISH ALAN H. , HORVATH GEORGE , GOLDBERGER JEEFREY J. 
Published: April 2007

Parasympathetic Withdrawal and Blockade Effects on HRV. introduction: Low heart rate variability (HRV) has been shown to have important prognostic significance in multiple settings. Although this is believed to reflect reduced parasympathetic tone, the physiology of reduced parasympathetic tone has not been elucidated. Methods and Results: To evaluate whether parasympathetic withdrawal and partial parasympathetic blockade result in similar changes in HRV, 27 normal volunteers underwent complete β‐adrenergic blockade and then were given (1) graded doses of nitroprusside to achieve baroreflex‐mediated parasympathetic withdrawal and (2) low‐dose atropine (0.01 mg/kg) to achieve partial parasympathetic blockade. Five‐minute ECG recordings were obtained for HRV analysis. In 19 subjects, paired 5‐minute recordings from each condition were available with mean RR intervals that differed by < 50 msec (low‐dose atropine: 869 ± 96 msec and nitroprusside 875 ± 99 msec). The root mean square of the successive RR interval differences was lower following low‐dose atropine than following parasympathetic withdrawal with nitroprusside (16 ± 11 msec vs 22 ± 15 msec; P < 0.02). During parasympathetic withdrawal, the low‐frequency (LF) power was 0.917 ± 0.602 bpm2 and the high‐frequency (HF) power was 0.501 ± 0.521 bpm2. During partial parasympathetic blockade, the LF and HF powers were significantly lower (0.443 ± 0.474 bpm2, P < 0.005; and 0.198 ± 0.207 bpm2, P < 0.02). Conclusion: These data confirm that HRV reflects the character of parasympathetic modulation of the heart rate rather than parasympathetic tone per se. Furthermore, this study identifies two distinct physiologic explanations for the finding of low HRV, namely, diminished vagal discharge and resistance of cardiac muscarinic receptors to vagal discharge. Further delineation of the relationships between parasympathetic tone and HRV will allow for better understanding of the pathophysiologic derangements associated with low HRV.
Effects of Mibefradil, a T‐Type Calcium Current Antagonist, on Electrophysiology of Purkinje Fibers that Survived in the Infarcted Canine Heart
Authors: PINTO JUDITH M.B. , SOSUNOV EUGENE A. , GAINULLIN RAVIL Z. , ROSEN MICHAEL R. , BOYDEN PENELOPE A. 
Published: April 2007

Mibefradil's Effects on Canine Purkinje Myocytes.Introduction: We studied the effects of mibefradil (MIB), a nondihydropyridine T‐type Ca2+channel antagonist, on T‐ and L‐type Ca2+(ICaT, ICaL) currents in Purkinje myocytes dispersed from the subendocardium of the left ventricle of normal (NZPC) and 48‐hour infarcted (IZPC) hearts.Methods and Results: Currents were recorded with Cs*‐ and EGTA‐rich pipettes and in Na+‐K+‐free external solutions to eliminate overlapping currents. In all cells, ICawas reduced by MIB (0.1 to 10 μM). No change in the time course of decay of peak ICawas noted. Average peak T/L ratio decreased in NZPCs hut not IZPCs with 1 μM MIB. Steady‐state availability of ICaLwas altered with I μM MIB in both cell types (mean ± SEM) (V0.5= ‐22 ± 4 mV for NZPC and ‐25 ± 5 mV for IZPC before drug; ‐63 ± 9 mV for NZPC and ‐67 ± 6 mV for IZPC after drug: P < 0.05). For ICaTV0.5(‐50 ± 3 mV for NZPC and ‐52 ± 1 mV for IZPC before drug) shifted 10 ‐60 ± 2 mV (NZPC) and ‐62 ± 3 mV (IZPC) (P < 0.05) after drug. We also determined the effects of MIB on spontaneously heating Purkinje normal fibers and on depolarized abnormally automatic fibers from the infarcted heart using standard microelectrode techniques. When NZPC and IZPC fibers were superfused with [K+]0= 2.7 mM, MIB 3 μM and 10 μM had no effect on rate or the maximum diastolic potential, but action potential plateau shifted to more negative values, the slope of repolarization phase 3 decreased, and action potential duration increased.Conclusion: MIB blocks L‐ and T‐type Ca2+currents in Purkinje myocytes hut lacks an effect on either normal or abnormal automaticity in Purkinje fibers.
Sequential Change in Action Potential of Rabbit Epicardium During and Following Radiofrequency Ablation
Authors: WU CHAU‐CHUNG , FASCIANO ROBERT W. , CALKINS HUGH , TUNG LESLIE 
Published: April 2007

Action Potential Change During RF Ablation. introduction: Although radiofrequency (RF) catheter ablation is used to treat certain cardiac arrhythmias, little is known regarding transient changes in cellular electrophysiology during and following RF delivery. Optical recordings of action potential (OAP) with voltage‐sensitive dyes allow immunity from electrical noise during RF delivery. The purpose of this study was to clarify the possible synergistic effects of both the thermal and electrotonic components of RF ablation. Methods and Results: In this study, OAPs were recorded on the epicardium of 16 isolated Langendorff‐perfused rabbit hearts within or adjacent to lesions made by RF catheters. Hearts were perfused at room temperature with Tyrode's solution containing 2,3‐butanedione monoxime and stained by the voltage‐sensitive dye di‐4‐ANEPPS. OAPs were recorded before, during, and after RF pulses. Within the lesion, the action potential duration at 80% repolarization (APD80) of OAP decreased rapidly during the RF pulse, without recovery following the pulse. In the border zone surrounding the lesion, the RF energy resulted in a rapid decrease in APD80, which recovered promptly after the pulse (recovery time constant: 82 ± 37 sec). APD80 was nonlinearly related to temperature during the RF ablation and responded faster to RF ablation than to purely thermal injury. Conclusion: The application of RF energy results in significant changes in myocardial cellular electrophysiologic properties. The RF energy bas a combination of thermal and electrotonic effects on the myocardial tissue. The results of this in vitro study may illustrate the cellular basis for commonly observed phenomena in clinical practice.
Cardiac Parasympathetic Stimulation via QRS‐Synchronous Low‐Energy Shocks In Humans
Authors: FRIEDMAN PAUL A. , HILL MICHAEL R.S. , STANTON MARSHALL S. 
Published: April 2007

Parasympathetic Stimulation via Intracardiac Shocks. Introduction: In patients receiving test shocks to verify lead connections at implantation, we anecdotally have observed postshock delay. The purpose of this study was to determine whether QRS‐synchronous low‐energy shocks delivered by implantable defibrillators result in postshock cycle length prolongation, and to determine the mechanism of this phenomenon. Methods and Results: Twenty‐five patients undergoing defibrillator testing were studied, three with epicardial patches and 22 with transvenous leads. Each patient received QRSsynchronous shocks of 0.2, 0.4, 0.6, and 2.0 J in random order. Patients were further randomized to receive either saline or 2.0 mg atropine intravenously, and then given a second sequence of shocks. At baseline, the postshock cycle length (1, 035 ± 245 msec) was significantly longer than the preshock cycle length (968 ± 177 msec, P = 0.01). In patients with a coronary sinus (CS) or superior vena cava (SVC) lead, the mean prolongation was 91 ± 160 msec, compared with 12 ± 106 msec for patients without such a lead (P < 0.0001). All energy levels resulted in significant postshock prolongation compared with preshock cycle lengths (P < 0.05). Postshock prolongation before atropine was 76 ± 162 msec, compared with −13 ± 52 msec afterward (P < 0.00001). Biphasic shocks resulted in greater postshock prolongation than monophasic shocks of equal energy. Conclusion: Low‐energy shocks delivered during the QRS complex cause postshock cycle length prolongation in man. This effect required the presence of a CS or SVC lead. Atropine inhibited this effect, suggesting the phenomenon was mediated by direct cardiac parasympathetic nerve stimulation by the intracardiac shock.
Catecholamine Facilitated Reentrant Ventricular Tachycardia: Uncoupling of Adenosine's Antiadrenergic Effects
Authors: LERMAN BRUCE B. , STEIN KENNETH M. , MARKOWITZ STEVEN M. , MITTAL SUNEET , SLOTWINER DAVID 
Published: April 2007

Catecholamine Facilitated Reentry. Introduction: Adenosine has no direct electrophysiologic function in ventricular tissue, but in the presence of cyclic adenosine monophosphate (cAMP), stimulation exerts a potent antiadrenergic effect. This effect has been exploited in the recognition and treatment of ventricular tachycardia (VT) due to cAMP‐mediated triggered activity and automaticity, which are respectively terminated and suppressed by adenosine. However, the effects of adenosine on catecholamine‐facilitated reentrant VT are unknown. A pivotal issue is whether termination of VT with adenosine is mechanism specific, or whether it represents a nonspecific antiadrenergic effect. The purpose of this study, therefore, was to define the effects of adenosine in a well‐characterized group of patients with catecholamine‐facilitated reentrant VT. Methods and Results: Fourteen patients with catecholamine‐facilitated reentry were studied. In the 12 patients with structural heart disease (including two with arrhythmogenic right ventricular dysplasia), adenosine (260 to 550 μ/kg) failed to slow or terminate VT. Two patients without structural heart disease had intrafascicular tachycardia confined to the left posterior fascicle, a calcium‐dependent, verapamil‐sensitive arrhythmia. In the absence of isoproterenol, verapamil terminated VT but adenosine did not. However, when isoproterenol was subsequently required for facilitation of tachycardia, adenosine terminated VT in both patients. Conclusion: Adenosine has no antiadrenergic (antiarrhythmic) effect in patients with catecholamine‐ facilitated VT due to structural heart disease. Patients with verapamil‐sensitive, left posterior intrafascicular reentry have an unusual dual response to adenosine. In the unstimulated state, adenosine has no effect on basal inward calcium current and, therefore, no effect on VT. However, when induction of VT requires amplification of the inward calcium current through stimulation of cAMP, adenosine sensitivity of VT becomes manifest. These results indicate that with few exceptions, termination of VT with adenosine is strongly suggestive of a cAMP‐mediated triggered mechanism rather than reentry.
Bezold‐Jarisch‐Like Reflex During Radiofrequency Ablation of the Pulmonary Vein Tissues in Patients with Paroxysmal Focal Atrial Fibrillation
Authors: TSAI CHIN‐FENG , CHEN SHIH‐ANN , TAI CHING‐TAI , CHIOU CHUEN‐WANG , PRAKASH V.S. , YU WEN‐CHUNG , HSIEH MING‐HSIUNG , DING YU‐AN , CHANG MAU‐SONG 
Published: April 2007

Pulmonary Vein Ablation‐Induced Bradycardia. Introduction: Information is lacking about the occurrence of radiation‐related proarrhythmic events during application of radiofrequency (RF) energy at (he pulmonary veins in patients with paroxysmal focal atrial fibrillation. The purpose of this study was to assess the theoretical risk of reflex bradycardia and hypotension response during RF ablation of these regions rich in endocardial nerve terminals. Methods and Results: Among the 40 consecutive patients (29 men, 11 women; mean age 65 ± 12 years) with clinically documented frequent attacks of paroxysmal atrial fibrillation who underwent superior pulmonary vein ablation for left local atrial fibrillation, 6 patients (15%) developed bradycardia‐hypotension syndrome during energy delivery. A single atrial fibrillation trigger focus in the left or right superior pulmonary vein was found in 3 and 1 patients, respectively. Two patients had two trigger foci originating from the orifice or proximal part of both superior pulmonary veins. After RF current was applied for a period of 14 ± 10 seconds, 2 patients developed functional rhythm and sinus bradycardia, another 2 patients had profound sinus bradycardia, I patient had two episodes of sudden onset of complete AV block with resultant 9.5‐second a systole, and I patient showed profound sinus bradycardia, transient AV block, and an K‐second asystole due to sinus arrest. Blood pressure fell when any substantial bradyarrhythmias occurred. All 6 patients were free of rhythm disturbances during The postablation follow‐up period (mean 8 ± 2 months). Conclusion: RF catheter ablation of the pulmonary vein tissues could evoke a variety of profound bradycardia‐hypotension responses. The Bezold‐Jarisch‐like reflex might be the underlying mechanism.
Preexcitation Secondary to Fasciculoventricular Pathways in Children: A Report of Three Cases
Authors: SALLEE DENVER , Van HARE GEORGE F. 
Published: April 2007

Fasciculoventricular Pathways in Children. Introduction: Fasciculoventricular connections are the rarest form of accessory pathways leading to preexcitation. Electrophysiologic characteristics of these pathways include ventricular preexcitation with normal PR and AH intervals and short HV intervals during sinus rhythm. In addition, atrial overdrive pacing prolongs the PR interval without affecting the HV interval or the degree of preexcitation. Methods and Results: From March 1994 through February 1997, 3 of 59 pediatric patients referred for electrophysiologic study for preexcitation on surface ECGs were found to have iasciculoventricular pathways. Two patients had no inducible supraventricular tachycardia. One patient had successful ablation of both a left lateral pathway and a concealed antentlateral pathway that had facilitated antidromic and orthodromic supraventricuiar tachycardias, respectively. Conclusion: Children often manifest minimal preexcitation via accessory AV pathways due to rapid AV conduction and/or left lateral pathway location. Fasciculoventricular pathways may masquerade as Wolff‐Parkinson‐White syndrome. Separation of the two diagnoses depends on the demonstration of specific electrophysiologic criteria.
Heterogeneous Loss of Connexin43 Protein in Ischemic Dog Hearts
Authors: HUANG XIAO‐DI , SANDUSKY GEORGE E. , ZIPES DOUGLES P. 
Published: April 2007

Heterogeneous Loss of Connexin43 Protein in Ischemic Dog Hearts. Introduction: Ischemia causes cell decoupling in the myocardium. Prolonged ischemia activates proteases and causes degradation of structural proteins as well as gap junctions. There is little information about the degradation of gap junction protein during the early time period after acute ischemia. The purpose of the present study was to investigate connexin43 (Cx43) protein degradation and distribution patterns in (he canine left ventricular wall during 1 to 6 hours of ischemia. Methods and Results: Ischemia of canine left ventricular myocardium was induced by ligation of the left anterior descending coronary artery. Following a period of in situ ischemia of up to 6 hours, samples were harvested, and standard paraffin slides were prepared for Cx43 and wheat germ agglutinin double labeling. Cx43 distribution was visualized by confocal microscopy. In controls, homogeneous distribution of Cx43 staining was determined. Ischemia caused a loss of Cx43 with a heterogeneous pattern by mixing foci of infarcted cells among normal cardiac myocytes. To determine if the changes were induced by heterogeneous reduction in the blood supply, an in vitro ischemic model was studied to induce more homogeneous ischemia. Western blot analysis of these in vitro ischemic tissue samples revealed a reduction of Cx43 protein concentration with a 50% decay time of 4.8 hours. Cx43 dephosphorylation was detected after 1 hour of in vitro ischemia. Heterogeneous loss of Cx43 was found in the in vitro ischemic tissue. There were no. significant changes in Cx43 staining density during the first hour of ischemia at a time when dephospharylation of the protein was observed. After 1 hour of ischemia, Cx43 was reduced at intercalated disk areas, and. after 6 hours, most Cx43 disappeared at intercalated disk areas, while small amounts of Cx43 remained at side‐to‐side junctions. Conclusion: Cx43 undergoes both distribution and concentration changes following acute cardiac Ischemia. The loss of Cx43 protein is heterogeneous. Cx43 dephosphorylation occurred within 1 hour following ischemia.
Field Stimulation of Isolated Chick Heart Cells
Authors: STONE BRADLEY A. , LIEBERMAN MELVYN , KRASSOWSKA WANDA 
Published: April 2007

Activation Thresholds for Chick Heart Cells. Introduction: This study examines the accuracy of using membrane models to predict activation thresholds for chick heart cells during field stimulation. Methods and Results: Activation thresholds were measured experimentally in ten embryonic chick heart cells at 37°C for stimulus durations 0.2 to 40 msec. Activation was assessed by observing the mechanical twitch of the cell. The heart cells ranged in diameter from 15.0 to 26.7μm. Since the electric field required for activation depends on diameter, the thresholds were expressed as the maximum field‐induced transmembrane potential, Vth= 1.5 a Eth where a is the cell radius and Eth is the strength of the electric field at threshold. A cell model was created using a singular perturbation method and membrane models describing the ionic currents of a heart cell. The study used membrane models of Ebihara and Johnsim (1980), Luo and Rudy (1991), Shrier and Clay (1994), and their combinations. The results show that for stimuli longer than 1 msec, theoretical activation thresholds were within one standard deviation of experimental thresholds. For shorter stimuli, the models failed to predict thresholds because of a premature deactivation of the sodium current. The modification of the in gates dynamics, so that they closed with a time constant of 1.4 msec, allowed to predict thresholds for all durations. The root mean square error between experimental and theoretical thresholds was 6.14%. Conclusions: The existing membrane models can predict thresholds for field stimulation only for stimuli longer than 1 msec. For shorter stimuli, the models need a more accurate representation of the sodium tail current.
Heterogeneous Changes in Electrophysiologic Properties in the Paroxysmal and Chronically Fibrillating Human Atrium
Authors: TSE HUNG‐FAT , LAU CHU‐PAK , AYERS GREGORY M. 
Published: April 2007

Heterogeneous Changes in Atrial Electrophysiologic Properties. Introduction: The regional changes in atrial elettrophysiologic properties related to atrial fibrillation (AF) in patients with paroxysmal AF (PAF) and chronic AF (CAF) remain unclear. The purpose of this study was to investigate the regional changes in atrial electrophysiology in patients with AF. Methods and Results: We evaluated the atrial electrophysiology at different sites (high right atrium, low right atrium [LRAJ, and distal coronary sinus [DCS]) in 11 patients with CAF, 8 patients with PAF, and 10 controls. Patients with CAF had significantly prolonged interatrial conduction and corrected sinus node recovery time, and shortened atrial effective refractory period (ERP) with loss of rate‐related adaptation in the DCS, hut had paradoxic prolongation of atrial ERP in the LRA, as compared with patients with PAF and the controls. As a result, the spatial distribution of atrial ERP that was observed in the controls and in patients with PAF was reversed in patients with CAF, without an increase in the dispersion of atrial refractoriness. Patients with PAF showed intermediate changes in atrial conduction times and atrial refractoriness as compared with patients with CAF and controls. Conclusion: There was a regional heterogeneity on the changes of atrial electrophysiology in different parts of the atrium, and the “normal” spatial distribution of atrial refractoriness was reversed in patients with CAF. The electrophysiologic changes observed in patients with PAF appear to behave as if in transition from the control state to CAF, suggesting progressive changes in atrial electropbysiologic properties.
Double Multielectrode Mapping Catheters Facilitate Radiofrequency Catheter Ablation of Focal Atrial Fibrillation Originating from Pulmonary Veins
Authors: HSIEH MING‐HSIUNG , CHEN SHIH‐ANN , TAI CHING‐TAI , TSAI CHIN‐FENG , PRAKASH V.S. , YU WEN‐CHUNG , LIU CHUEN‐CHIA , DING YU‐AN , CHANG MAU‐SONG 
Published: April 2007

Ablation of Focal AF. Introduction: Several reports have demonstrated that focal atrial fibrillation (AF) may arise from pulmonary veins (PVs). The purpose of this study was to investigate the safety and efficacy of using double multielectrode mapping catheters in ablation of focal AF. Methods and Results: Forty‐two patients (30 men, 12 women, age 65 ± 14 years) with frequent attacks of paroxysmal AF were referred for catheter ablation. After atrial transseptal procedure, two long sheaths were put into the left atrium. Two decapolar catheters were put into the right superior PV (RSPV) and left superior PV (LSPV), or inferior PVs if necessary, guided by pulmonary venography. All the patients had spontaneous initiation of AF either during baseline (2 patients), after isoproterenol infusion (8 patients) or high‐dose adenosine (2 patients), after short duration burst pacing under isoproterenol (14 patients), or after cardioversion of pacinginduced AF (16 patients). The trigger points of AF were from the LSPV (12 patients), RSPV (8 patients), and both superior PVs (19 patients). The trigger points from PVs (total 61 points) were 18 (30%) in the ostium of PVs and 43 inside the PVs (9 to 40 mm). After 6 ± 3 applications of radiofrequency energy, 57 of 61 triggers were completely eliminated, and the other 4 triggers were partially eliminated. During a follow‐up period of 8 ± 2 months, 37 patients (88%) were free of symptomatic AF without any antiarrhythmic drugs. Twenty patients received a transesophageal echocardiogram, and 19 showed small atrial septal defects (2.8 ± 1.2 mm) with trivial shunt. Fifteen defects closed spontaneously 1 month later. Conclusion: The technique using double multielectrode mapping catheters is a relatively safe and highly effective method for mapping and ablation of focal AF originating from PVs.
Efficacy and Safety of the Initial Use of Stability and Onset Criteria in Implantable Cardioverter Defibrillators
Authors: WEBER MAX , BÖCKER DIRK , BÁNSCH DIETMAR , BRUNN JÜRGEN , CASTRUCCI MARCO , GRADAUS RAINER , BREITHARDT GÜNTER , BLOCK MICHAEL 
Published: April 2007

Primary Programming of Stability and Onset Criteria. Introduction: Inappropriate therapies are the most frequent adverse event in patients with implantable cardioverter defibrillators (ICDs). Most ICDs offer a stability criterion to discriminate ventricular tachycardia (VT) from atrial fibrillation and an onset criterion to discriminate VT from sinus tachycardia. The efficacy and safety of these criteria, if used immediately after implantation, is unknown. Methods and Results: In a case control study, 87 patients in whom stability and onset criteria had been activated immediately after ICD implantation were matched to 87 patients in whom these criteria had not been activated. The groups were matched for known predictors of inappropriate therapies. With stability and onset criteria off, 24 patients (28%) received inappropriate therapies due to atrial fibrillation (n = 14) or sinus tachycardia (n = 11); with stability and onset on, only 11 patients (13%) were treated by the ICD due to atrial fibrillation (n = 5) or sinus tachycardia (n = 7) (log rank: P = 0.029). Five patients suffered inappropriate therapies despite the fact that onset (n = 4) or stability (n = 1) criteria were not fulfilled once tachycardias continued for a prespecified duration. Only one patient experienced a failure to detect VT due to the onset criterion; none because of stability. Conclusion: The immediate use of stability and onset criteria after ICD implantation reduces inappropriate therapies due to atrial fibrillation and sinus tachycardia. Because of the potential for underdetection of VT, this approach should be limited to tachycardia rates hemodynamically tolerated by the patient.