bluuebunny/crossref_metadata_2025_split huggingface dataset:
Prevention of Sudden Cardiac Death After a First Myocardial Infarction by Pharmacologic or Surgical Antiadrenergic Interventions
Authors: SCHWARTZ PETER J. , MOTOLESE MARIO , POLLAVINI GIORGIO , LOTTO ANTONIO , RUBERTI UGO , TRAZZI RINALDO , BARTORELLI CESARE , ZANCHETTI ALBERTO , GROUP THE ITALIAN SUDDEN DEATH PREVENTION 
Published: May 2007

Antiadrenergic Interventions and Prevention of Sudden Death after MI. Introduction: Growing evidence points to sympathetic hyperactivity as one critical trigger for life‐threatening arrhythmias among postmyocardial infarction patients. Methods and Results: We have evaluated, in a placebo‐controlled multicenter study, the efficacy of a β‐adrenergic blocking agent (oxprenolol 160 mg) and of a selective left cardiac sympathetic denervation in preventing sudden death in patients with a first and anterior myocardial infarction. Two patient groups were studied. The high‐risk group included 144 patients who survived a myocardial infarction complicated by either ventricular tachycardia or fibrillation. The relatively low‐risk group included 869 patients whose myocardial infarction did not have these complications; they were allocated only to placebo or oxprenolol. Randomization took place 30 days postmyocardial infarction; mean follow‐up was 22 months. In the high‐risk group the sudden cardiac death (crude rate) in the placebo subgroup was indeed high (21.3%), and was strikingly reduced to 2.7% and to 3.6% by oxprenolol and by left cardiac sympathetic denervation, respectively (P < 0.05). In the low‐risk group the sudden cardiac death (crude rate) in the placebo subgroup was 5.2% and was still reduced by oxprenolol to 1.6% (P < 0.05). The results for total mortality were quite similar to those for sudden death iu both groups. Conclusion: This study, unique for the populations studied and for one of the treatments used, demonstrates that pharmacologic and surgical antiadrenergic interventions significantly reduce sudden cardiac death in postmyocardial infarction patients at high and at low risk. With due consideration to the relatively small size of the high‐risk group, it seems reasonable to suggest that left cardiac sympathetic denervation may be considered as a possible alternative for high‐risk patients with contraindications to beta blockers. (J Cardiovasc Electrophysiol, Vol 3, pp. 2–16, February 1992)
The Effects of Unilateral Stellate Ganglion Blockade on Human Cardiac Function During Rest and Exercise
Authors: GARDNER MARTIN J. , KIMBER SHANE , JOHNSTONE DAVID E. , SHUKLA ROMESH C. , HORACEK B. MILAN , FORBES CHERYL , ARMOUR J. ANDREW 
Published: May 2007

Unilateral Stellate Block. Introduction: Left sided stellate ganglion predominance has been proposed as a mechanism responsible for lethal ventricular arrhythmias, due to hetaerae nouns ventricular repolarization. To determine the cardiovascular effects of such asymmetric sympathetic ganglion innervations in man, studies were performed in 15 patients undergoing unilateral stellate ganglion blockade for the management of chronic arm pain. Methods and Results: Standard 12‐lead ECGs, systemic blood pressure, body surface potential mapping, and radionuclide angiography were performed during rest and graded exercise before and after blockade. Successful unilateral blockade was accomplished in 13 of the patients, 11 of whom had right‐sided blockade and two left‐sided blockade. No significant changes due to blockade of stellate ganglia, including QT intervals, were detected during rest or graded exercise in standard ECGs. No cardiac rhythm disturbances occurred in these states, Body surface potential maps and arterial blood pressure were similar during resting supine and upright positions, as well as immediately after exercise before and after blockade. Unilateral ganglion blockade did not modify resting or exercise cardiac ejection fractions. Conclusion: Unilateral stellate blockade in man does not induce untoward cardiovascular effects during rest or exercise.
Activation Mapping of Reentry Around an Anatomical Barrier in the Canine Atrium:
Authors: BOYDEN PENELOPE A. , GRAZIANO JOSEPH N. 
Published: May 2007

d‐Sotalol and Atrial Reentry. Introduction: In the chronically instrumented animal and the isolated blood perfused heart, atrial reentry via a fixed path around an anatomical obstacle has been described and is terminated by the Class III antiarrhythmic agent, d‐sotalol. The precise mechanism by which d‐sotalol terminates this arrhythmia is not known. Methods and Results: In the present study, right atrial (RA) activation sequences in the isolated, coronary artery perfused canine heart during episodes of sustained flutter (n = 7) and drug administration were determined. A fixed array of bipolar electrodes was used to record endocardial electrograms from 96 sites on the RA simultaneously. Maps of all control flutters showed that the rhythm was due to persistent circus movement of the impulse around the tricuspid valve ring. D‐sotalol was effective in terminating atrial reentry in this model. In all episodes, block of the excitatory impulse in a specific region of the reentrant circuit accompanied these terminations. However, the events preceding the occurrence of block of the impulse were not similar. Two different modes of termination are described. Conclusion: The Class III antiarrhythmic agent d‐sotalol can terminate atrial reentry in several ways. In one mode, complete conduction block of he reentering impulse within the fixed path occurs to terminate the rhythm. In the other mode, interruption of the original reentrant circuit occurs when there is failure of a lateral boundary. Often in this latter case, interruption of the original circuit is by an extra impulse that is secondary to a change in the path of the impulse. In both modes cycle length oscillations are observed.
Inducibility of Atrial Fibrillation Before and After Radiofrequency Catheter Ablation of Accessory Atrioventricular Connections
Authors: KALBFLEISCH STEVEN J. , El‐ATASSI RAFEL , CALKINS HUGH , LANGBERG JONATHAN J. , MORADY FRED 
Published: May 2007

Inducibility of Atrial Fibrillation. Introduction: The purpose of this study was to evaluate the inducihility of atrial fibrillation in patients with an accessory atriovcentricular connection (AAVC) and to determine if the inducibility of atrial fibrillation is altered after successfulradiofrequency catheter ablation of the AAVC. Methods and Results: Thirty‐seven patients with an AAVC and 36 control patients wereprospectively evaluated using a standardized atrial pacing protocol. The high right atrium waspaced using a 25‐beat drive train, 1.5‐second intertrain pause, 10‐mA pulse amplitude, and 2‐msec pulse duration at cycle lengths of 250 to 100 msec, in 10‐msec decrements. Pacing wasperformed twice at each cycle length. Thirty patients with an AAVC underwent repeat atrialoverdrive pacing after successful radiofrequency ablation of the AAVC. Atrial fibrillation wasinduced in 26 (70%) patients with an AAVC and 22 (61 %) controls (P = NS). Atrial flutter wasinduced in 26 (70%) patients with an AAVC and 22 (61%) controls (P = NS). The cumulativepercentage of patients with atrial fibrillation/flutter induced at each pacing cycle length was thesame in each group. There was no difference in the duration of atrial fibrillation/flutterbetween control patients and patients with an AAVC. Among the 30 patients who underwentrepeat atrial overdrive pacing after radiofrequency ablation of an AAVC, there was no difference in the inducibility or duration of atrial fibrillation/atrial flutter after ablation compared tobaseline. Conclusion: These findings indicate that the vulnerability of the atrium to fibrillate inresponse to atrial pacing is independent of the presence of an AAVC.
Radiofrequency Catheter Ablation of AtypicalAtrioventricular Nodal Reentrant Tachycardia
Authors: STRTCKBERGER S. ADAM , KALBFLBISCH STEVEN J. , WILLIAMSON BRIAN , MAN K. CHING , VORPERIAN VICKEN , HUMMEL JOHN D. , LANGBERG JONATHAN J. , MORADY FRED 
Published: May 2007

Ablation of Atypical Atrioventricular Nodal Reentrant Tachycardia, Introduction: Published reports of radiofrequency ablation of atypical atrioventricular nodal reentranttacbycardia (AVNRT) have been limited. We present our experience in 10 consecutive patientswith atypical AVNRT wbo underwent radiofrequency ablation of the “slow” AV nodal pathway. Methods and Resttlts: there were 9 females and 1 male; their mean age was 44 ± 19 years (± SD), the mean AVNRT cycle length and ventriculoatrial (VA) interval at the His positionduring AVNRT were 340 ± 50 msec and 200 ± 70 msec, respectively. the slow pathway wassuccessfully ablated in all patients with a mean of 10 ± 7 radiofrequency energy applications inthe posteroseptal right atritim near the coronary sinus os. The mean procedure duration was 100 ± 35 minutes. There were no complications. In 4 patients, target sites were identified during sinus rhythm by mapping for possible slow pathway potentials, In the other 6 patients, target sites were identified by mapping retrograde atrial activation during AVNRT or ventricularpacing, The VA times at successful target sites were a mean of 45 ± 30 msec less tban the VAtime at the His cathetcr during AVNRT, There were no differences in success rate, number ofradiofrequency energy applications, or procedure duration between patients in whom mappingwas guided by possible slow pathway potentials or by retrograde atrial activation, During 6 ± 3 months of followup, 1 patient bad a recurrence of atypical AVNRT and underwent a secondablation procedure, which was successful. Conclusion: Radiofrequency ablation of atypical AVNRT can be safely and effectivelyaccomplisbed when target sites are identified based either on possible slow pathway potentialsduring sinus rbytbm or retrograde atrial activation times during tachycardia.
A Quantitative Measurement of Spatial Orderin Ventricular Fibrillation
Authors: BAYLY PHILIP V. , JOHNSON ERIC E. , WOLF PATRICK D. , GREENSIDB HENRY S. , SMITH WILLIAM M. , IDEKER RAYMOND E. 
Published: May 2007

Quantifying Spatial Order in Fibrillation. Introduction: The degree of organization in ventricular fibrillation (V F) is not known. As an objective measurement of spatial order, spatial correlation functions and their characteristic lengths were estimated from epicardial electrograms of pigs in VF. Methods and Results: VF was induced by premature stimulation in five pigs, EIectroj;raniswere simultaneously recorded with a 22 × 23 array of unipolar electrodes spaced 1.12 mmapart, Data were obtained by sampling the signals at 2000 Hz for 20 minutes immediately afterthe initiation of VF. Correlations between all pairs of signals were computed at various times.Correlation lengths were estimated from the decay of average correlation as a function of electrode separation. The correlation length of the VF in pigs was found to be approximately 4 to 10 mM. varying as fihrillation progressed. The degree of correlation decreased in the first 4 seconds after fibrillation then increased over the next minute. Conclusion: The correlation length is much smaller than the scale of the heart, suggestingthat many independent regions of activity exist on the epicardium at any one time. On theother hand, the correlation length is 4 to 10 times the interelectrode spacing, indicating thatsome coherence is present. These results imply that the heart behaves during VF as a highdimensional, but not random, system involving many spatial degrees of freedom, which mayexplain the lack of convergence of fractal dimension estimates reported in the literature.Changes in the correlation length also suggest that VF reorganizes slightly in the first minuteafter an initial breakdown in structure.
Endocardial Mapping of Reentry Around an Anatomical Barrier in the Canine Right Atrium:
Authors: PINTO JUDITH M.B. , GRAZIANO JOSEPH N. , BOYDEN PENELOPE A. 
Published: May 2007

Flecainide and Atrial Reentry. Introduction: Flecainide is effective in terminating stable atrial flutter in the conscious dog with a Y‐shaped right atrial lesion. In this model, flutter is due to circus movement of the impulse around a fixed anatomical barrier. Methods and Results: To investigate the mechanism of flecainide‐induced termination of this type of reentry, we determined the pattern of endocardial activation of the right and left atria before and during administration of flecainide by recording simultaneously from 192 electrode pairs in the isolated blood perfused heart. At least five consecutive flutter beats were analyzed before and during flecainide for each of eight termination episodes in five hearts. In all, flecainide increased flutter cycle length (164 ± 24 msec) by 89% to 309 ± 77 msec (P < 0.05) before termination. Atrial refractory period and conduction time during paced beats were also increased by flecainide. In flve episodes, termination was due to conduction block of the impulse at critical sites within the reentrant circuit (mode 1). Cycle length oscillations (± 30 msec) at sites proximal to site of block preceded termination in three of these episodes. In three other episodes, interruption of the original circuit occurred when there was failure of a lateral boundary, giving rise to an impulse that reset the original circuit (mode 2). In these episodes, long‐short cycle length oscillations led to return reexcitation by the impulse within the primary path and suhsequent termination. Conclusion: In summary, similar to our previous findings with the Class III agent, d‐sotalol, two different modes of termination of atrial reentry were observed with flecainide.
Rate‐Related and Autonomic Effects on Atrioventricular Conduction Assessed Through Beat‐to‐Beat PR Interval and Cycle Length Variability
Authors: LEFFLER CHRISTOPHER T. , SAUL J. PHILIP , COHEN RICHARD J. 
Published: May 2007

Atrioventricular Conduction Variability. Introduction: Atrioventricular AV) conduction time varies on a beat‐by‐beat basis in response to the influences of cardiac efferent autonomic activity and rate‐dependent electrical recovery processes. The goals of this study were to distinguish these effects on AV conduction time and to compare the variability in sinoatrial and AV nodal function. Methods and Results: The PR interval on the surface ECG served as an index of AV conduction time in this study of 14 adult human subjects undergoing a random interval breathing protocol. P and R waves were located by a template‐matching algorithm. Spectral analysis allowed frequency‐domain comparisons between PR and RR interval variability. Spectra of PR and RR intervals had similar power distributions, although the power of the RR interval spectra was much greater. Autonomic blockade with atropine plus propranolol reduced the power of both spectra. Standing significantly decreased the spectral power from 0.15 to 0.5 Hz for PR and RR spectra, and introduced a peak near 0.1 Hz in the mean PR and RR spectra, although the latter finding was significant only for the RR interval spectra. Propranolol had no significant effects on the PR and RR interval spectra. Linear regression analysis allowed quantification of the autonomic and recovery effects on AV conduction and showed which effect predominated. Simple linear regression confirmed in adults a previous finding in children that conduction time may be either positively or negatively correlated with cycle length. By multiple regression and transfer function analysis, the inverse relation seen in some subjects was attributed to the effect of recovery from the preceding cycle. With the preceding recovery period accounted for, the conduction time and cycle length of the current beat were positively correlated, presumably due to the parallel autonomic effects on the sinoatrial and AV nodes. The magnitude of the recovery effect predicted by the regression analysis was similar to published values. Conclusion: A noninvasive evaluation of the surface ECG can be used to compare variability in AV conduction time and cycle length and characterize the effects of autonomic efferent activity and rate‐related recovery on AV nodal function.
Ultrastructural Observations in the Myocardium Beyond the Region of Acute Coagulation Necrosis Following Radiofrequency Catheter Ablation
Authors: NATH SUNIL , REDICK JAN A. , WHAYNE JAMES G. , HAINES DAVID E. 
Published: May 2007

Ultrastructural Findings After RF Ablation. Introduction: We hypothesized that myocardial injury following radiofrequency (KF) catheter ablation may extend beyond the region of acute coagulation necrosis as defined by histochemical staining. Methods and Results: Five RF lesions were created in vivo in the left ventricle of two dogs using a 4‐inm tipped ablation electrode in which RF power was adjusted to maintain an electrode‐tissue interface temperature of 85°C for 60 seconds. The lesions were bisected; one half of the lesions were stained with nitroblue tetrazolium (NBT) and the other half processed for electron microscopy. Three zones of interest were identified extending 0–3 mm, 3–6 mm, and > 6 mm from the visible pathologic lesion border. The degree of Ultrastructural injury to the myocardium was scored for each zone. Electron microscopy demonstrated the presence of significant abnormalities of the plasma membrane, mitochondria, sarcomeres, sarcoplasmic reticuluni, and gap junctions of myocytes, as well as damage to the microvasculature extending up to 6 mm beyond the pathologic lesion edge. The plasma membrane and gap junctions of myocytes and the microvasculalure appeared particularly sensitive to thermal injury, whereas the intercalated discs were relatively thermally resistant. Conclusion: RF catheter ablation results in Ultrastructural damage to the myocardium extending up to 6 mm beyond the acute pathologic RF lesion border as denned by NBT histochemical staining.
Heart Rate and Heart Rate Variability in Normal Young Adults
Authors: COUMEL PHILIPPE , MAISON‐BLANCHE PIERRE , CATULI DIDIER 
Published: May 2007

Heart Rate and Heart Rate Variability. Introduction: The relationships between heart rate (HR) and HR variability (HRV) are not simple. Because both depend on the autonomic nervous system (ANS), they are not independent variables. Technically, the quantification of HRV is influenced by the duration of the cardiac cycles. The complexity of these relationships does not justify ignoring HK when studying HRV, as frequently occurs. Methods and Results: Using spectral and nonspectral methods, the HR and various normalized and non‐normalized indices of HRV were studied in 24‐hour recordings of a homogeneous cohort of seventeen 20‐year‐old healthy males. The HR‐HRV relationships were appraised by analyzing the same data in two different ways. The 24 mean hourly values provide consistent information on the circadian behavior of the indices, while the average 24‐hour individual data show a wide spectrum of normality. Combined approaches allow assessment of the direct impact of RR interval on HRV evaluation. The correlations between HR and normalized indices of HRV arc weaker in 24‐hour individual data than in pooled hourly data of the same individuals. These correlations are close to 1 in the latter case, which does not mean that measuring HRV is simply another method of evaluating HR, but that normal physiology supposes a harmonious behavior of the various indices. When considered individually without normalization, the specific indices of vagal modulation (high‐frequency band of the spectrum, short‐term HR oscillations of the nonspectral analysis) consistently increase at night and diminish during the day. However, the low‐frequency power, which supposedly reflects sympathetic influences, also increases at night, whereas more logically the longer HR oscillations would predominate during the day. Moreover, the selective analysis of HR oscillations during HR acceleration or decrease indicates that their behavior differs accordingly. Conclusion: We recommend that closer attention be paid to the complex relationships between HR and HRV. The strong correlations found in healthy subjects may reflect either the physiological harmony of ANS functions or simple redundancy. Their tendency to deteriorate in diseased hearts suggests that redundancy is not the cause and that abnormalities of ANS functions are not demonstrated by HRV analysis alone.
Trans venous‐Subcutaneous Defibrillation Leads:
Authors: BLOCK MICHAEL , HAMMEL DIETER , BÖCKER DIRK , BORGGREFE MARTIN , BUDDE THOMAS , ISBRUCH FRANK , SCHELD HANS H. , BREITHARDT GUNTER 
Published: May 2007

Effect of Transvenous Electrode Polarity on DFT. Introduction: The defibrillation threshold (DFT) of a transvenous‐subcutaneous electrode configuration is sometimes unacceptably high. To obtain a DFT with a sufficient safety margin, the defibrillation field can be modified by repositioning the electrodes or more easily by a change of electrode polarity. In a prospective randomized cross‐over study, the effect of transvenous electrode polarity on DFT was evaluated. Methods and Results: In 21 patients receiving transvenous‐subcutaneous defibrillation leads, the DFT was determined intraoperatively for two electrode configurations. Two monophasic defibrillation pulses were delivered in sequential mode between either the right ventricular (RV) electrode as common cathode and the superior vena cava (SVC) and subcutaneous electrodes as anodes (configuration I) or the SVC electrode as common cathode and the RV and subcutaneous electrodes as anodes (configuration II). In each patient, both electrode configurations were used alternately with declining energies (25, 15, 10, 5, 2 J) until failure of defibrillation occurred. The DFT did not differ between both configurations (18.3 ± 8.2 J vs 18.9 ± 8.9 J; P = 0.72). Eleven patients had the same DFT with both electrode configurations, 5 patients a lower DFT with the RV electrode as cathode, and 5 patients a lower DFT with the SVC as cathode. Four patients had a sufficiently low DFT (≤ 25 J) with only 1 of the 2 configurations. Conclusion: A change of electrode polarity of transvenous‐subcutaneous defibrillation electrodes may result in effective defibrillation if the first electrode polarity tested fails to defibrillate. In general, neither the RV electrode nor the SVC electrode is superior if used as a common cathode in combination with a subcutaneous anodal chest patch.