Pulmonary vein isolation during atrial fibrillation: insight into the mechanism of pulmonary vein firing.
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Atrial Fibrillation↗
Biomedical subjects
Ralph Lazzara
Publications and source records attributed to Ralph Lazzara.
Heterogeneous regional endocardial repolarization is associated with increased risk for ischemia-dependent ventricular fibrillation after myocardial infarction.
UNLABELLED: Repolarization Heterogeneity and Sudden Death Risk. INTRODUCTION: The aim of this study was to investigate whether the characteristics of endocardial ventricular repolarization are associated with differential risk for sudden death. Prolonged surface QT interval is associated with increased arrhythmic risk after myocardial infarction (MI), but the underlying mechanism of QT prolongation and its relation to lethal arrhythmias are unclear. METHODS AND RESULTS: Ventricular fibrillation (VF) risk was assessed in 12 dogs 1 month after anterior MI during an exercise test coupled with brief circumflex coronary occlusion. Susceptible dogs (n = 5) developed VF during the brief ischemic episode, whereas resistant dogs did not (n = 7). Surface QT interval was measured at rest. Endocardial electroanatomic catheter maps of left ventricular repolarization were obtained in four unique regions identified by echocardiography and compared between groups. Compared to resistant dogs, susceptible dogs were characterized by prolonged surface QT intervals (240 +/- 10 msec vs 222 +/- 7 msec, P = 0.04). In addition, they had lower baroreflex sensitivity (9.7 +/- 1.5 msec/mmHg vs 28 +/- 9.8 msec/mmHg, P < 0.01) and a tachycardic response to acute ischemia suggesting higher propensity for stronger sympathetic reflexes. Surface QT interval prolongation in susceptible dogs was due to a marked heterogeneity of endocardial left ventricular repolarization (239 +/- 42 msec, basal anterior wall vs 197 +/- 35, lateral wall; P < 0.001). Resistant animals had no regional differences in endocardial repolarization. CONCLUSION: Sympathetic activation following MI not only produces adverse structural remodeling but also contributes to adverse electrophysiologic remodeling resulting in heterogeneous ventricular repolarization and in a myocardial substrate conducive to lethal reentrant arrhythmias.
Animals↗
Endovascular stimulation of autonomic neural elements in the superior vena cava using a flexible loop catheter.
It has been previously shown that parasympathetic nerve stimulation (PNS) can be achieved via basket electrode catheters (BEC) positioned in the superior vena cava (SVC). Since questions have been raised regarding formation of thrombi between and/or on the splines of the BECs, we investigated the use of a flexible loop "Lasso" catheter (LC) to achieve autonomic nerve stimulation in the SVC without clot formation. In 5 dogs, anesthetized with Na-pentobarbital, standard ECG leads II and aVR, blood pressure and right atrial electrograms were continuously monitored. The LC is a 7-French catheter at the end of which is a circular ring, 25 mm in diameter, equipped with ten 1-mm electrodes. The circular loop is made of a flexible, shape retaining, covered metal, which can be straightened in order to be inserted transvenously. The catheter was inserted through a sheath in the external jugular vein and positioned in the SVC. Stimulation was performed sequentially across each of the five bipolar pairs of electrodes, and consisted of square wave stimuli, each 0.1 msec duration, frequency 20 Hz at voltages from 1-40 V. The average voltage required to produce a 50% decrease in heart rate was 15 +/- 7 V, compared to 22 +/- 12 V with the standard BEC and 10 +/- 5 V with a modified BEC. We did not observe any thrombus formation at the end of a four-hour period during which the catheter was stabilized in the SVC. PNS can be achieved safely and effectively by the LC in the SVC in dogs.
Animals↗
Coronary sinus-ventricular accessory connections producing posteroseptal and left posterior accessory pathways: incidence and electrophysiological identification.
BACKGROUND: The coronary sinus (CS) has a myocardial coat (CSMC) with extensive connections to the left and right atria. We postulated that some posteroseptal and left posterior accessory pathways (CSAPs) result from connections between a cuff of CSMC extending along the middle cardiac vein (MCV) or posterior coronary vein (PCV) and the ventricle. The purpose of the present study was to use CS angiography and mapping to define and determine the incidence of CSAPs and determine the relationship to CS anatomy. METHODS AND RESULTS: CSAP was defined by accessory pathway (AP) potential or earliest activation in the MCV or PCV and late activation at anular endocardial sites. A CSAP was identified in 171 of 480 patients undergoing ablation of a posteroseptal or left posterior AP. CS angiography revealed a CS diverticulum in 36 (21%) and fusiform or bulbous enlargement of the small cardiac vein, MCV, or CS in 15 (9%) patients. The remaining 120 (70%) patients had an angiographically normal CS. A CSMC extension potential (CSE), like an AP potential, was recorded in the MCV in 98 (82%), in the PCV in 13 (11%), in both the MCV and PCV in 6 (5%), and in the CS in 3 (2%) of 120 patients. CSMC potentials were recorded between the timing of atrial and CSE potentials. CONCLUSIONS: CSAPs result from a connection between a CSMC extension (along the MCV or PCV) and the ventricle. The CS is angiographically normal in most patients.
Arrhythmias, Cardiac↗
Biphasic versus monophasic shock waveform for conversion of atrial fibrillation: the results of an international randomized, double-blind multicenter trial.
OBJECTIVES: This study compared a biphasic waveform with a conventional monophasic waveform for cardioversion of atrial fibrillation (AF). BACKGROUND: Biphasic shock waveforms have been demonstrated to be superior to monophasic shocks for termination of ventricular fibrillation, but data regarding biphasic shocks for conversion of AF are still emerging. METHODS: In an international, multicenter, randomized, double-blind clinical trial, we compared the effectiveness of damped sine wave monophasic versus impedance-compensated truncated exponential biphasic shocks for the cardioversion of AF. Patients received up to five shocks, as necessary for conversion: 100 J, 150 J, 200 J, a fourth shock at maximum output for the initial waveform (200 J biphasic, 360 J monophasic) and a final cross-over shock at maximum output of the alternate waveform. RESULTS: Analysis included 107 monophasic and 96 biphasic patients. The success rate was higher for biphasic than for monophasic shocks at each of the three shared energy levels (100 J: 60% vs. 22%, p < 0.0001; 150 J: 77% vs. 44%, p < 0.0001; 200 J: 90% vs. 53%, p < 0.0001). Through four shocks, at a maximum of 200 J, biphasic performance was similar to monophasic performance at 360 J (91% vs. 85%, p = 0.29). Biphasic patients required fewer shocks (1.7 +/- 1.0 vs. 2.8 +/- 1.2, p < 0.0001) and lower total energy delivered (217 +/- 176 J vs. 548 +/- 331 J, p < 0.0001). The biphasic shock waveform was also associated with a lower frequency of dermal injury (17% vs. 41%, p < 0.0001). CONCLUSIONS: For the cardioversion of AF, a biphasic shock waveform has greater efficacy, requires fewer shocks and lower delivered energy, and results in less dermal injury than a monophasic shock waveform.
Adult↗
Endovascular stimulation within the left pulmonary artery to induce slowing of heart rate and paroxysmal atrial fibrillation.
OBJECTIVE: In recent years there have been many reports dealing with basic models for sustained atrial fibrillation (AF), however few animal models exist for paroxysmal AF which closely simulate that seen clinically. METHODS: In 12 dogs, anesthetized with sodium pentobarbital, a right thoracotomy was performed. We stabilized a basket electrode catheter within the left pulmonary artery (LPA) through a purse string suture in the right ventricle. Electrode catheters were sutured to multiple atrial sites including the four pulmonary veins and the right and left atrial appendages, along Bachman's bundle and the coronary sinus. RESULTS: Continuous pulses of electrical stimulation (20 Hz square wave stimuli, each 0.1 ms in duration, voltage range 1-40 V) across adjacent splines of the five arms of the basket induced slow heart rates (at lower voltages) and then initiated atrial premature depolarizations (APDs), atrial tachycardia (AT) and AF (at higher voltages). To avoid possible direct activation of atrial myocardium, we also applied a train (50-100 ms duration) of high frequency stimuli (200 Hz) coupled to each atrial paced beat so that the train fell within the atrial refractory period. Stimulation in the LPA at an average of 14+/-7 V induced heart rate slowing, APDs were seen followed by AT/AF at a voltage of 20+/-6 V, P=0.002. Stimulation in the LPA resulted in APDs arising from a variety of sites including the left pulmonary veins (superior or inferior) and the left atrial appendage. After beta-blockade (intravenous esmolol or propranolol, 1 mg/kg) the voltage threshold for induction of AF rose from 14+/-7 to 25+/-10 V, P=0.02. Upon the addition of intravenous atropine (1-2 mg) the arrhythmic response (AF) to stimulation was completely abolished. Atrial pacing threshold was unchanged after autonomic blockade. Local application of radiofrequency energy (average number=3+/-2) across the metallic splines of the basket catheter in the LPA (70-80 V for 60 s) caused abolition of both the slowing and the arrhythmic response to LPA stimulation. CONCLUSION: These data suggest that stimulation of autonomic nerves in the LPA causes slowing of the heart rate followed by paroxysmal APD/AT/AF simulating the spontaneously occurring paroxysmal AF syndrome, associated with bradycardia, reported in patients.
Acute Disease↗
The cure of AV nodal reentrant tachycardia: the missing link between good and perfect.
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Animals↗
The elusive extracellular AV nodal potential: studies from the canine heart, ex vivo.
Various forms of extracellular recordings from the AV node (AVN) have been reported. However, lack of consistent validation have precluded the use of such recordings in experimental and clinical studies. In 14 Langendorff perfused dog hearts, the triangle of Koch (TOK) was exposed and an octapolar electrode catheter (2 mm rings, 2 mm spacing) was inserted under the endocardium so that the bipolar pairs recorded electrograms from the apex to the base of the TOK. All recording were filtered between 0.05 and 250 Hz, except for a His bundle (Hb) recording (30-250 Hz) made from another bipolar electrode catheter placed in the aortic root. Transmembrane action potentials (AP) were recorded close to the sites of extracellular electrograms. Pin electrodes at the periphery of the bath were arranged to register two ECG leads from the volume conductor. During recovery of electrical activity 11 of 14 preparations developed a junctional rhythm that initially manifested only an AV nodal extracellular and corresponding intracellular AV nodal potentials followed gradually by conduction to the Hb and ventricles but no retrograde atrial activation; 3 preparations initially produced Hb rhythms based on extracellular and transmembrane AP recordings from the AVN and Hb. The amplitude and duration of the AVN extracellular potentials (average: 97 +/- 26 microV and 92 +/- 25 msec, respectively) during AVN rhythms, significantly differed from those during atrial pacing (262 +/- 185 microV and 78 +/- 26 msec, p < 0.05). Histologic sections of the sites underlying the electrodes recording AVN potentials showed AVN tissue throughout. We conclude that extracellular AV nodal potentials are independent waveforms with specific qualitative and quantitative characteristics that distinguish them from adjacent atrial, transitional, Hb or ventricular potentials.
Action Potentials↗
Analysis of troponin I levels after spontaneous implantable cardioverter defibrillator shocks.
INTRODUCTION: Serum cardiac troponin I (cTnI) is a sensitive and specific marker for myocardial injury. Myocardial ischemia and/or injury can be a trigger for ventricular arrhythmias. The aim of this study was to assess the frequency and significance of elevated serum cTnI levels after spontaneous implantable cardioverter defibrillator (ICD) shocks. METHODS AND RESULTS: Serial cTnI measurements and ECGs were performed in 35 patients with transvenous ICDs who were admitted after spontaneous ICD shocks. Elevated cTnI levels were found in 18 patients (51%). Acute coronary syndrome was diagnosed in 5 (22%) of 23 patients with known coronary artery disease. After excluding the patients with acute coronary syndrome, elevated cTnI levels were present in 13 (43%) of 30 patients: 18% of patients with < or =3 shocks and 58% of patients with >3 shocks. Patients with elevated cTnI levels received a higher number of shocks (16+/-18 vs 5+/-7; P < 0.05) and had higher total delivered energies (475+/-538 J vs 128+/-184 J; P < 0.05) compared with patients with normal cTnI. Patients with acute coronary syndrome had higher peak cTnI levels (18+/-16 ng/mL) compared with patients with elevated cTnI without acute coronary syndrome (3.8+/-4.3 ng/mL; P < 0.01). CONCLUSION: Serum cTnI rises occur in the majority of patients after multiple (>3) spontaneous ICD discharges but are due to acute coronary syndrome only 14% of the time (22% of the time in patients with known coronary artery disease).
Aged↗
Spontaneous adverse event reports of serious ventricular arrhythmias, QT prolongation, syncope, and sudden death in patients treated with cisapride.
CONTEXT: Adverse cardiac events, typically long QT syndrome, have been reported in patients treated with the gastrointestinal prokinetic agent cisapride. OBJECTIVE: To analyze cases of cisapride-associated long QT syndrome and ascertain the degree of confidence in the diagnosis of long QT syndrome and the presence of risk factors. DESIGN: Review of all cases reported to the manufacturer, health authorities, or in the medical literature as of October 1999. METHODS: Before review, specific definitions and a classification scheme were agreed upon. Each case was classified by confidence in the long QT syndrome diagnosis and the presence of recognized risk factors (cofactors) or other medical conditions that were listed as contraindications in the June 1998 United States labeling (labeled conditions). RESULTS: Of 574 cases reviewed, 391 cases of long QT syndrome or isolated QT prolongation were confirmed. Most of these were classified as long QT syndrome with high (145, 37%) or medium (92, 23.5%) confidence in the diagnosis. Recognized cofactors were present in 262 (67%) cases. The proportion of cases with recognized cofactors rose with confidence in the diagnosis (P < 0.001) from 42.2% in the low-confidence group to 68.5% and 82.1% in the medium- and high-confidence groups, respectively. Conversely, the proportion of cases with other labeled conditions decreased with confidence in the diagnosis, from 33.3% for low confidence to 13% and 8.3% for medium and high confidence, respectively. Analysis of cases and prescribing data showed reporting rates decreased in studied months in 1999 compared with the average study period. CONCLUSION: In most cases with high or medium confidence in the diagnosis of cisapride-associated long QT syndrome, recognized cofactors for long QT syndrome were present. The risk of cisapride-related long QT syndrome may be minimized by avoiding cofactors.
Arrhythmias, Cardiac↗
Magnetism and cardiac arrhythmias.
Low-level electromagnetic fields (EMFs) have been used to treat various neurologic disorders. In the present study, we applied micro Gauss (microG) levels of EMFs either to the vagosympathetic nerve trunks, dissected in the neck, or across the chest in anesthetized dogs. Based on theoretical and empiric grounds, we compared EMFs (2.87 microG at 0.043 Hz) delivered to the vagosympathetic trunks in an experimental set (n = 5) with a sham control group (n = 6). Over a period of 2 to 3 hours, heart rate decreased after an initial 5-minute EMF exposure. The maximal heart rate changes in the experimental versus control groups was 29% versus 12% (P = 0.03). The voltage applied to the autonomic nerves required to induce atrioventricular (AV) conduction block decreased by 60% in the experimental group versus a 5% increase in the control group (P = 0.005). This effect also lasted 2 to 3 hours. Another EMF setting (amplitude 0.34 microG, frequency 2 kHz) applied for 5 minutes to the vagosympathetic trunks was associated with a significant increase in the occurrence of atrial premature depolarizations (APDs), atrial tachycardia (AT), and atrial fibrillation (AF) in response to autonomic nerve stimulation compared with control states before EMF exposure. No atrial arrhythmias could be induced after propranolol and atropine, even at the highest voltage used to stimulate the autonomic nervous input to the heart (n = 11). Only 2 dogs showed no response to this EMF application. In 3 dogs in whom atrial pacing (cycle length = 250 ms) and autonomic nerve stimulation induced AF, an EMF (2.87 microG at 0.043 Hz) delivered for 35 minutes across the chest suppressed AF for up to 3 to 4 hours, after which the same protocol again induced AF. We conclude that in these preliminary experiments, specific low-level EMFs alter heart rate, AV conduction, and heart rhythm. These effects were mediated through the autonomic nervous system inputs to the heart based on adjunctive effect of autonomic nerve stimulation and the inhibitory action of autonomic blockers.
Animals↗
Sinus node dysfunction in a heart transplant patient secondary to severe sinus node artery obstruction--a case report.
A case of sinus node dysfunction is reported secondary to severe sinus node artery obstruction 3 years after orthotopic heart transplantation. The patient first presented with frequent dizzy spells and presyncopal episodes for 3 months and then recurrent syncope in the presence of an acute myocardial infarction. Coronary angiography showed a diffusely narrowed sinus node artery without any apparent collateral vessels. The sinus node artery had had only minimal distal disease 3 months previously. A dual chamber permanent pacemaker was implanted with significant improvement in clinical symptoms.
Arterial Occlusive Diseases↗