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Biomedical subjects

R Lazzara

Publications and source records attributed to R Lazzara.

At least 55 records · Page 3Linked to original sources
PubMed1997

Critical atrial site for ablation of pacing-induced atrial fibrillation in the normal dog heart.

INTRODUCTION: Radiofrequency catheter ablation (RFA) has been used recently to treat atrial fibrillation (AF). The purpose of this study was to investigate a new approach to preventing AF by RFA. METHODS AND RESULTS: In open chest, anesthetized dogs, AF (lasting > 30 sec) was induced after burst stimulation, and electrophysiologic parameters were recorded before and after RFA. In group 1 (9 dogs) we performed selective and combined slow and fast pathway RFA, whereas in group 2 (11 dogs) RFA was applied as a linear lesion at the mid-atrial septum between the inferior vena cava and the fossa ovalis. After ablation, the Wenckebach cycle length was significantly prolonged only in group 1 (194 +/- 23 vs 282 +/- 35 msec, P = 0.002), whereas the interval between the stimulus (S) artifact applied at the high right atrium to the His bundle (H) (SH interval) prolonged to the same extent in both groups (162 +/- 14 vs 146 +/- 45 msec, P = NS); group 1 due to an A-H prolongation whereas in group 2 it was due to an intra-atrial conduction delay. In group 1 AF still remained inducible, although with a longer mean R-R interval (215 +/- 16 vs 433 +/- 88 msec, P < 0.05). No instance of complete AV block developed. In group 2, sustained AF was noninducible in 10 dogs and its duration was markedly shorter in the remaining one (8 sec). Gross anatomy and histology did not reveal any damage inside of Koch's triangle, and particularly to the compact AV node. CONCLUSION: These findings suggest that RFA at the mid-atrial septum prevents AF in the normal dog heart. This approach might also be successful in those clinical settings in which the atrial septum plays a critical role in the maintenance of sustained AF.

Animals↗
PubMed1997

Early afterdepolarizations produced by d,l-sotalol and clofilium.

INTRODUCTION: The roles for L-type calcium current and Na-Ca exchange in early afterdepolarizations (EADs) attending d,l-sotalol and clofilium were examined in canine Purkinje fibers and in enzymatically dispersed myocytes from canine subepicardium. METHODS AND RESULTS: Spontaneous EADs were compared to EAD formation potentiated by stimulation of Na-Ca exchange and facilitation of ICa-L (Bay K8644). Bay K8644 (10(-8) M) and stimulation of Na-Ca exchange potentiated bradycardia-dependent EADs. Stimulation of Na-Ca exchange in Purkinje fibers pretreated with d,l-sotalol (10(-5) M) and clofilium (10(-7) M) induced EADs at takeoff potentials negative (-63 +/- 4 and -62 +/- 4 mV, respectively) to EADs potentiated by Bay K8644 (10(-8) M) (-33 +/- 2 and -34 +/- 2 mV, respectively, P < 0.05), or EADs induced by Bay K8644 alone (10(-6) M) (-31 +/- 5 mV). In myocytes, Bay K8644 (10(-8) M) potentiated EADs in d,l-sotalol- (10(-6) to 10(-4) M) or clofilium-treated (10(-9) to 10(-7) M) cells at reduced potentials (-10 +/- 3 and -10 +/- 4 mV, respectively) compared to EADs elicited by clofilium or d,l-sotalol alone (-25 +/- 3 and -24 +/- 3 mV, respectively), or stimulation of Na-Ca exchange in the presence of d,l-sotalol or clofilium (-26 +/- 4 and -26 +/- 4 mV, respectively). Spontaneous EADs or EADs elicited by stimulation of Na-Ca exchange coincident with drug treatment were suppressed by increasing Ca02+ but were not suppressed by nifedipine (10(-7) M). CONCLUSION: EADs elicited by d,l-sotalol and clofilium in canine Purkinje tissue and epicardial myocytes are dependent upon Na-Ca exchange rather than ICa-L "window current."

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1997

Class III electrophysiologic actions of imidazole-substituted diheterabicyclononanes in canine myocardium.

The electrophysiologic effects of the imidazole-substituted diheterabicyclo[3.3.1]nonane compounds GLG-V-13 and KMC-IV-84 were evaluated in canine ventricular tissues using intracellular and extracellular recordings. The drugs produced a concentration-dependent prolongation of action potential duration at 90% of repolarization in Purkinje (338 +/- 26 to 611 +/- 43 msec, 10 mg/l GLG-V-13; 328 +/- 17 to 468 +/- 18 msec, 10 mg/l KMC-IV-84), in right ventricular subendocardium (260 +/- 18 to 335 +/- 18 msec, 10 mg/l GLG-V-13; 221 +/- 9 to 264 +/- 13 msec, 10 mg/l KMC-IV-84) and in left ventricular epicardium (195 +/- 13 to 256 +/- 18 msec, 10 mg/l GLG-V-13; 203 +/- 11 to 273 +/- 26 msec, 10 mg/l KMC-IV-84) without altering resting membrane potential, action potential amplitude, overshoot potential, Vmax, conduction velocity or Purkinje fiber automaticity. Prolongation of the effective refractory period was proportional to the change in action potential duration at 90% of repolarization. Prolongation of action potential duration at 90% of repolarization was maximal at paced cycle lengths exceeding 1000 msec and was minimal at a paced cycle length of 250 msec (Purkinje: 266 +/- 20 vs. 6 +/- 8 msec, GLG-V-13; 178 +/- 12 vs. 10 +/- 10 msec, KMC-IV-84. Right ventricular subendocardium: 70 +/- 12 vs. 10 +/- 2 msec, GLG-V-13; 60 +/- 8 vs. 19 +/- 6 msec. Left ventricular epicardium: 67 +/- 13 vs. 10 +/- 5 msec, GLG-V-13; 68 +/- 12 vs. 16 +/- 8 msec, KMC-IV-84). An increase in K+(o) to 12 mM reduced action potential prolongation by GLG-V-13 and KMC-IV-84 in left ventricular epicardium. The results demonstrate selective class III electrophysiologic properties for imidazole-substituted diheterabicyclo[3.3.1]nonane compounds.

Action Potentials↗
PubMed1996

Multicenter comparison of truncated biphasic shocks and standard damped sine wave monophasic shocks for transthoracic ventricular defibrillation. Transthoracic Investigators.

BACKGROUND: The most important factor for improving out-of-hospital ventricular fibrillation survival rates is early defibrillation. This can be achieved if small, lightweight, inexpensive automatic external defibrillators are widely disseminated. Because automatic external defibrillator size and cost are directly affected by defibrillation waveform shape and because of the favorable experience with truncated biphasic waveforms in implantable cardioverter-defibrillators, we compared the efficacy of a truncated biphasic waveform with that of a standard damped sine monophasic waveform for transthoracic defibrillation. METHODS AND RESULTS: The principal goal of this multicenter, prospective, randomized, blinded study was to compare the first-shock transthoracic defibrillation efficacy of a 130-J truncated biphasic waveform with that of a standard 200-J monophasic damped sine wave pulse using anterior thoracic pads in the course of implantable cardioverter-defibrillator testing. Pad-pad ECGs were also examined after transthoracic defibrillation. After the elimination of data for 24 patients who did not meet all protocol criteria, the results from 294 patients were analyzed. The 130-J truncated biphasic pulse and the 200-J damped sine wave monophasic pulse resulted in first-shock efficacy rates of 86% and 86%, respectively (P = .97). ST-segment levels measured 10 seconds after the shock in 151 patients in sinus rhythm were -0.26 +/- 1.58 and -1.86 +/- 1.93 mm for the 130- and 200-J shocks, respectively (P < .0001). CONCLUSIONS: We found that 130-J biphasic truncated transthoracic shocks defibrillate as well as the 200-J monophasic damped sine wave shocks that are traditionally used in standard transthoracic defibrillators and result in fewer ECG abnormalities after the shock.

Adolescent↗
PubMed1996

Multiple mechanisms in the long-QT syndrome. Current knowledge, gaps, and future directions. The SADS Foundation Task Force on LQTS.

The congenital long-QT syndrome (LQTS) is characterized by prolonged QT intervals, QT interval lability, and polymorphic ventricular tachycardia. The manifestations of the disease vary, with a high incidence of sudden death in some affected families but not in others. Mutations causing LQTS have been identified in three genes, each encoding a cardiac ion channel. In families linked to chromosome 3, mutations in SCN5A, the gene encoding the human cardiac sodium channel, cause the disease, Mutations in the human ether-à-go-go-related gene (HERG), which encodes a delayed-rectifier potassium channel, cause the disease in families linked to chromosome 7. Among affected individuals in families linked to chromosome 11, mutations have been identified in KVLQT1, a newly cloned gene that appears to encode a potassium channel. The SCN5A mutations result in defective sodium channel inactivation, whereas HERG mutations result in decreased outward potassium current. Either mutation would decrease net outward current during repolarization and would thereby account for prolonged QT intervals on the surface ECG. Preliminary data suggest that the clinical presentation in LQTS may be determined in part by the gene affected and possibly even by the specific mutation. The identification of disease genes in LQTS not only represents a major milestone in understanding the mechanisms underlying this disease but also presents new opportunities for combined research at the molecular, cellular, and clinical levels to understand issues such as adrenergic regulation of cardiac electrophysiology and mechanisms of susceptibility to arrhythmias in LQTS and other settings.

Cardiology↗
PubMed1996

Para-Hisian pacing. A new method for differentiating retrograde conduction over an accessory AV pathway from conduction over the AV node.

BACKGROUND: Differentiation between ventriculoatrial (VA) conduction over an accessory AV pathway (AP) and the AV node (AVN) may be difficult, especially in patients with a septal AP. METHODS AND RESULTS: A new pacing method, para-Hisian pacing, was tested in 149 patients with AP and 53 patients without AP who had AV nodal reentrant tachycardia (AVNRT). Ventricular pacing was performed adjacent to the His bundle and proximal right bundle branch (HB-RB), initially at high output to capture both RV and HB-RB. The output was then decreased to lose HB-RB capture. The change in timing and sequence of retrograde atrial activation between HB-RB capture and noncapture was examined. Loss of HB-RB capture without change in stimulus-atrial (S-A) interval or atrial activation sequence indicated exclusive retrograde AP conduction. An increase in S-A interval without change in His bundle-atrial interval or atrial activation sequence indicated exclusive retrograde AVN conduction. A change in atrial activation sequence indicated the presence of both retrograde AP and AVN conduction. Para-Hisian pacing correctly identified retrograde AP conduction in 132 of 147 AP patients, including all septal and right free wall APs. Retrograde AVN conduction masked AP conduction in 9 of 34 patients with a left free wall AP and 6 of 9 patients with the permanent form of junctional reciprocating tachycardia. Para-Hisian pacing correctly excluded AP conduction in all 53 patients with AVNRT. CONCLUSIONS: Para-Hisian pacing reliably identifies retrograde conduction over septal and right free wall APs, but AVN conduction may mask APs located far from the pacing site or with a long retrograde conduction time.

Adolescent↗
PubMed1996

From first class to third class: recent upheaval in antiarrhythmic therapy--lessons from clinical trials.

In recent years, the results of large randomized and controlled trials of antiarrhythmic agents for primary and secondary prevention of ventricular tachycardia and ventricular fibrillation have changed perceptions of the actions of antiarrhythmic agents regarding both efficacy and risk. The premature termination of the CAST trials of primary prevention in postinfarct patients highlighted the proarrhythmic risk and inefficacy of the sodium channel blockers (class I action), encainide, flecainide, and moricizine, in patients at relatively low risk for death in the long term. The excess mortality with therapy was attributed to proarrhythmia due to facilitation of reentry, especially during acute ischemia. About the same time, European trials with amiodarone, a complex agent with antiadrenergic action and powerful action to prolong refractoriness (class III action), indicated enhanced survival after infarction with amiodarone but not with agents with class I action. Recent verbal reports of larger and placebo-controlled trials (EMIAT and CAM-IAT) confirm a significant reduction in arrhythmia mortality, possibly with a favorable trend in total mortality. While an older trial with dl-sotalol (class III and beta-blocking actions) showed a trend toward improved survival after infarction, a recent trial with d-sotalol in patients with recent infarction or remote infarction and heart failure was prematurely terminated because of excess mortality attributed to proarrhythmia (torsades de pointes), indicating the importance of beta-blocking properties of a class III agent. A secondary prevention trial (ESVEM) in patients surviving an episode of VT or VF showed significant superiority of dl-sotalol compared to an array of agents that block sodium channels with respect to both efficacy and tolerance. Occurrence rates of arrhythmias treated with drugs tested for efficacy either by suppression of inducible arrhythmias or by suppression of spontaneous ectopy were higher and equivalent for both testing methods. A secondary prevention trial of amiodarone and multiple agents that block sodium channels in survivors of cardiac arrest (CASCADE) showed a significant increased efficacy of amiodarone but poorer long-term tolerance compared with the other agents. Comparative analysis of the results of the various trials suggests that class III action coupled with antiadrenergic action is more efficacious in both primary and secondary prevention of life-threatening ventricular arrhythmias and that lethal proarrhythmias may be the predominant effect in attempts at primary prevention in low-risk populations due to class I or so-called pure class III action.

Adrenergic beta-Antagonists↗
PubMed1996

Role of the tricuspid annulus and the eustachian valve/ridge on atrial flutter. Relevance to catheter ablation of the septal isthmus and a new technique for rapid identification of ablation success.

BACKGROUND: Typical atrial flutter (AFL) results from right atrial reentry by propagation through an isthmus between the inferior vena cava (IVC) and tricuspid annulus (TA). We postulated that the eustachian valve and ridge (EVR) forms a line of conduction block between the IVC and coronary sinus (CS) ostium and forms a second isthmus (septal isthmus) between the TA and CS ostium. METHODS AND RESULTS: Endocardial mapping in 30 patients with AFL demonstrated atrial activation around the TA in the counter-clockwise direction (left anterior oblique projection). Double atrial potentials were recorded along the EVR in all patients during AFL. Pacing either side of the EVR during sinus rhythm also produced double potentials, which indicated fixed anatomic block across EVR. Entrainment pacing at the septal isthmus and multiple sites around the TA produced a delta return interval < or = 8 ms in 14 of 15 patients tested. Catheter ablation eliminated AFL in all patients by ablation of the septal isthmus in 26 patients and the posterior isthmus in 4. AFL recurred in 2 of 12 patients (mean follow-up, 33.9 +/- 16.3 months) in whom ablation success was defined by the inability to reinduce AFL, compared with none of 18 patients (mean follow-up, 10.3 +/- 8.3 months) in whom success required formation of a complete line of conduction block between the TA and the EVR, identified by CS pacing that produced atrial activation around the TA only in the counterclockwise direction and by pacing the posterior TA with only clockwise atrial activation. CONCLUSIONS: (1) The EVR forms a line of fixed conduction block between the IVC and the CS; (2) the EVR and the TA provide boundaries for the AFL reentrant circuit; and (3) verification of a complete line of block between the TA and the EVR is a more reliable criterion for long-term ablation success.

Adult↗
PubMed1996

Novel 3,7-diheterabicyclo[3.3.1]nonanes that possess predominant class III antiarrhythmic activity in 1-4 day post infarction dog models: X-ray diffraction analysis of 3-[4-(1H-imidazol-1-yl)benzoyl]-7-isopropyl-3,7-diazabicyclo[3.3.1]nona ne dihydroperchlorate.

Several 3,7-diheterabicyclo[3.3.1]nonanes (DHBCNs) were prepared and screened in the Harris dog model for their ability to abolish pace-induced and sustained ventricular tachycardia (SVT) or prevent induction of ventricular tachycardia. In addition, an electrophysiological examination was made in the infarcted hearts of each animal to determine if more than one class activity was present. The examples exhibited predominately class III antiarrhythmic activity via a prolongation of the ventricular effective refractory period (VERP) in the models, although there may well be an underlying class Ib action present as exemplified by the ability of several of the agents to slow conduction in the myocardial infarcted dog hearts. 3-[4-(1H-Imidazol-1-yl)benzoyl]-7-isopropyl-3,7-diazabicyclo[3.3.1]nonan e dihydroperchlorate displayed powerful class III activity in the model systems while several other DHBCNs exhibited various degrees of class III action. An X-ray diffraction analysis revealed that this compound has a 3,7-diazabicyclo[3.3.1]nonane bicyclic unit in a chair-chair conformation.

Animals↗
PubMed1996

Retrospective multicenter analysis of 3i endosseous dental implants placed over a five-year period.

Osseointegrated dental implants have now become an accepted form of treatment for patients with a fully or partially missing dentition. The purpose of this study was to evaluate the performance of 3i threaded and cylindrical implants. During a 5-year period, a total of 1969 3i endosseous implants were placed at 6 centers in the United States and 2 elsewhere in the edentulous and partially edentulous jaws of 653 consecutive patients ranging in age from 18 to 82 years. Of the total number of implants placed, 1341 were commercially pure titanium threaded implants and 628 were titanium plasma-sprayed implants with a cylindrical configuration. A total of 28 patients with 110 implants were lost to follow-up. Implants in these patients were considered neither a success nor a failure. Success was predicated on the osseointegration of each and every implant followed in this analysis rather than the persistence of prosthetic function. Confirmed bone anchorage was considered essential for success. A total of 625 patients with 1871 implants remain in the study with a follow-up period ranging from 6 to 60 months. A total of 93 implants (5.0% of the total implants followed) were considered as failures. A mean implant survival rate was 95.0% for both the threaded and the cylindrical implant was calculated. The success rate of threaded implants was 97.0% in the mandible and 93.8% in the maxilla. The success rate for the 3.3-mm cylindrical implants was 96.0% in the mandible and 95.5% in the maxilla, and the success rate of 4.0-mm-diameter cylindrical implants was 95% in the mandible and 92.0% in the maxilla. Causes of failure consisted of loss of osseointegration (2.3%), crestal bone loss requiring periodontal therapy after the first year of function (1.7%) had mechanical problems associated with the prosthesis (0.9%). This retrospective analysis of the 3i endosseous implant system is comparable to previous reports on other implant systems in terms of implant survival and prosthesis stability. It is demonstrated that 3i implants are predictable and can provide lasting osseointegration leading to improvement of oral function if the recommended surgical and restorative protocol is followed.

Adolescent↗
PubMed1996

Electrophysiological and inotropic characterization of a novel class III antiarrhythmic agent, GLG-V-13, in the mammalian heart.

GLG-V-13, a novel 3,7-diheterabicyclo(3.3.1)nonane, was examined both in vivo and in vitro to characterize its electrophysiological, hemodynamic, and inotropic properties. In anesthetized guinea pigs, GLG-V-13 [0.5-500 micrograms/kg intravenously (i.v.), n = 6] lengthened the epicardial monophasic action potential (MAP) duration, the atrioventricular (AV) conduction time and the RR interval in a dose-dependent manner. At the highest dose, these variables were increased by 30, 13, and 23%, respectively. No significant effects were noted on QRS duration or blood pressure (BP). In rabbit atrial and papillary muscle preparations, GLG-V-13 (0.32-3.2 mg/L) did not exert a negative inotropic action and in isolated rabbit cardiomyocytes the agent blocked the rapidly activating delayed rectifier K+ current (IKr, EC50 = 48 micrograms/L). In 10 intact anesthetized mongrel dogs, the left ventricular (LV) endocardial MAP was measured during atrial pacing before and after administration of GLG-V-13 (3 and 6 mg/kg i.v.). As compared with the drug-free state, the agent induced a significant prolongation of the MAP at all pacing frequencies (2.0-4.5 Hz). In 15 anesthetized dogs studied 1-4 days after two-stage ligation of the left anterior descending coronary artery (LAD), the antiarrhythmic/proarrhythmic potential of GLG-V-13 was compared with that of lidocaine. ECG, His bundle, LV (IZepi), and composite and normal zone composite electrograms were recorded. Programmed electrical stimulation (PES) and burst pacing (4.0-7.0 Hz) were delivered to the right ventricular outflow tract. In the drug-free state, sustained monomorphic ventricular tachycardia (SMVT) was inducible in 6 dogs (6 of 15). After lidocaine, SMVT was induced in 7 other dogs (13 of 15). GLG-V-13 prevented induction of SMVT in 5 of 6 dogs; a proarrhythmic action was noted in 1 dog only. GLG-V-13 slowed the heart rate (HR), increased the AH and the HV intervals, prolonged the paced (2.5 Hz) QT interval, and increased the ventricular effective refractory period (VERP). These effects were associated with 2:1 block of late potentials in the IZepi electrograms, a phenomenon also observed during rapid atrial pacing (2.5-3.5 Hz), suggestive of a marked prolongation of refractoriness in the ischemically damaged myocardium. In light of the recent Cardiac Arrhythmia Suppression Trial (CAST) study, the antiarrhythmic efficacy, together with the low proarrhythmic potential and lack of cardiodepressant properties of GLG-V-13, may merit further investigation of this novel class III antiarrhythmic agent.

Animals↗
PubMed1996

Mechanisms and management of congenital and acquired long QT syndromes.

The long QT syndromes can be divided into congenital and acquired forms. Early afterdepolarizations have been identified as triggering mechanisms for both congenital and acquired QT syndromes but reentry may play a role in the perpetuation of the ventricular tachycardia, torsade de pointes. Studies of the ionic mechanisms of early afterdepolarizations have implicated L-type Ca2+ current, persisting Na+ current, and Na+:Ca2+ exchange current related to Ca2+ loading. Different ionic mechanisms may be operative in early afterdepolarizations occuring at different levels of membrane potential in the setting of prolonged repolarization by blocking K+ currents or maintaining non-inactivating Ca2+ or Na+ currents or in early afterdepolarizations due to adrenergic stimulation. In the congenital long QT syndromes, two mutations have recently been discovered in the genes SCN5A and HERG which encode respectively the Na+ channel and a K+ channel conducting the current IKr. It is postulated that the SCN5A mutation leads to a problem with inactivation of Na+ current. In the case of the HERG mutation, the K+ current appears to be diminished. In the case of the acquired long QT syndromes, the therapeutic challenge is to maintain the prolonged repolarization but to interrupt the arrhythmogenic cascade. Current therapies for torsades de pointes include speeding of the heart rate, which enhances K+ current, and Ca2+ blockers or Mg, also a Ca2+ blocker. In the congenital long QT syndromes, therapy in the past has been directed toward reducting adrenergic influence either by betablockade or left cardiac sympathectomy. Recent discoveries open other possibilities such as Na+ channel blockers and methods to increase IKr such as elevation of extracellular K+.

Adrenergic beta-Antagonists↗
PubMed1995

Comparison of in vivo tissue temperature profile and lesion geometry for radiofrequency ablation with a saline-irrigated electrode versus temperature control in a canine thigh muscle preparation.

BACKGROUND: It is thought that only a thin layer of tissue adjacent to the electrode is heated directly by electrical current (resistive heating) during radiofrequency ablation. Most of the thermal injury is thought to result from conduction of heat from the surface layer. The purpose of this study was to determine whether lesion depth could be increased by producing direct resistive heating deeper in the tissue with higher radiofrequency power, allowed by cooling the ablation electrode with saline irrigation to prevent the rise in impedance that occurs when the electrode-tissue interface temperature reaches 100 degrees C. METHODS AND RESULTS: In 11 anesthetized dogs, the thigh muscle was exposed and bathed with heparinized canine blood (36 degrees C to 37 degrees C). A 7F catheter, with a central lumen, a 5-mm tip electrode with six irrigation holes, and an internal thermistor, was positioned perpendicular to the thigh muscle and held at a constant contact weight of 10 g. Radiofrequency current was delivered to 145 sites (1) at high constant voltage (66 V) without irrigation (CV group, n = 31), (2) at variable voltage (20 to 66 V) to maintain tip-electrode temperature at 80 degrees C to 90 degrees C without irrigation (temperature-control group, n = 39), and (3) at high CV (66 V) with saline irrigation through the catheter lumen and ablation electrode at 20 mL/min (CV irrigation group, n = 75). Radiofrequency current was applied for 60 seconds but was terminated immediately in the event of an impedance rise > or = 10 omega. Tip-electrode temperature and tissue temperature at depths of 3.5 and 7.0 mm were measured in all three groups (n = 145). In 33 CV irrigation group applications, temperature was also measured with a separate probe at the center (n = 18) or edge (n = 15) of the electrode-tissue interface. In all 31 CV group applications, radiofrequency energy delivery was terminated prematurely (at 11.6 +/- 4.8 seconds) owing to an impedance rise associated with an electrode temperature of 98.8 +/- 2.1 degrees C. All 39 temperature-control applications were delivered for 60 seconds without an impedance rise, but voltage had to be reduced to 38.4 +/- 6.1 V to avoid temperatures > 90 degrees C (mean tip-electrode temperature, 84.5 +/- 1.4 degrees C). In CV irrigation applications, the tip-electrode temperature was not > 48 degrees C (mean, 38.4 +/- 5.1 degrees C) and the electrode-tissue interface temperature was not > 80 degrees C (mean, 69.4 +/- 5.7 degrees C). An abrupt impedance rise with an audible pop and without coagulum occurred in 6 of 75 CV irrigation group applications at 30 to 51 seconds, probably owing to release of steam from below the surface. In the CV and temperature-control group applications, the temperatures at depths of 3.5 (62.1 +/- 15.1 degrees C and 67.9 +/- 7.5 degrees C) and 7.0 mm (40.3 +/- 5.3 degrees C and 48.3 +/- 4.8 degrees C) were always lower than the electrode temperature. Conversely, in CV irrigation group applications, electrode and electrode-tissue interface temperatures were consistently exceeded by the tissue temperature at depths of 3.5 mm (94.7 +/- 9.1 degrees C) and occasionally 7.0 mm (65.1 +/- 9.7 degrees C). Lesion dimensions were smallest in CV group applications (depth, 4.7 +/- 0.6 mm; maximal diameter, 9.8 +/- 0.8 mm; volume, 135 +/- 33 mm3), intermediate in temperature-control group applications (depth, 6.1 +/- 0.5 mm; maximal diameter, 11.3 +/- 0.9 mm; volume, 275 +/- 55 mm3), and largest in CV irrigation group applications (depth, 9.9 +/- 1.1 mm; maximal diameter, 14.3 +/- 1.5 mm; volume, 700 +/- 217 mm3; P < .01, respectively). CONCLUSIONS: Saline irrigation maintains a low electrode-tissue interface temperature during radiofrequency application at high power, which prevents an impedance rise and produces deeper and larger lesions. A higher temperature in the tissue (3.5 mm deep) than at the electrode-tissue interface indicates that direct resistive heating occurred deeper

Animals↗
PubMed1995

Heart rate variability during specific sleep stages. A comparison of healthy subjects with patients after myocardial infarction.

BACKGROUND: Heart rate variability (HRV) is typically higher during nighttime. This evidence supports the concept that overall, sleep is a condition during which vagal activity is dominant. Myocardial infarction (MI) results in a loss in the overall nocturnal HRV increase. However, the characteristics of HRV during specific sleep stages in normal subjects and, more importantly, after MI, are unknown. This study describes HRV during sleep stages in normal subjects and in patients with a recent MI. METHODS AND RESULTS: HRV was measured from 5 minutes of continuous ECG recording in 8 subjects with no clinical evidence of coronary artery disease (age, 47 +/- 4 years) and in 8 patients with a recent MI (age, 51 +/- 2 years; NS versus control subjects) in the awake state, non-rapid eye movement (REM), and REM sleep. In normal subjects, the low- to high-frequency ratio (LF/HF) derived from power spectral analysis of HRV decreased significantly from the awake state to non-REM sleep (from 4 +/- 1.4 to 1.22 +/- 0.33, P < .01). During REM sleep, the LF/HF increased to 3 +/- 0.74 (P < .01 versus non-REM, NS versus awake). In post-MI patients, the LF/HF showed an opposite trend toward an increase from 2.4 +/- 0.7 to 5.11 +/- 1.4 (NS, P < .01 versus the control subjects). REM sleep produced a further increase in the LF/HF up to 8.9 +/- 1.6 (P < .01 versus awake and versus REM in control subjects). CONCLUSIONS: Myocardial infarction causes a loss in the capability of the vagus to physiologically activate during sleep. This results in a condition of relative sympathetic dominance even in a situation such as sleep, normally described as a condition of vagal dominance and, consequently, low risk for lethal events. The evidence that the sleep-related vagal activation is lost after MI may provide new insights to understanding the nocturnal occurrence of sudden death.

Electrocardiography↗