bluuebunny/crossref_metadata_2025 huggingface dataset:
Subcutaneous Lidocaine Affects Inducibility in Programmed Electrophysiologic Testing of Children
Authors: BUCKLES CANDACE S. , GILLETTE PAUL C. , BUCKLES DAVID S.
Published: May 2007

Subcutaneous Lidocaine Affects Inducibility. A prospective study of 99 patients undergoing invasive electrophysiologic testing was conducted to determine whether the administration of lidocaine for local anesthesia influenced the inducibility of arrhythmias. Of the 99 patients, 42 had inducible arrhythmias. Multiple stepwise discriminant analysis indicated that the most important factor influencing inducibility was lidocaine dosage per weight, with a calculated cutoff of 3.2 mg/kg. There were 26/54 (48%) of patients who had no inducible arrhythmias below the cutoff, compared with 31/45 (69%) above the cutoff (P < 0.04). Of the 21 patients who had dose/kg > 3.2 mg/kg and serum concentration above 1.4 μg/mL (therapeutic range 1‐5 μg/mL) 1 hour after administration, 18 had no inducible arrhythmias (86%). Younger, smaller patients were more affected (P < 0.0001). It is recommended that dose/kg and serum concentrations be recorded during electrophysiologic testing. If the dose/kg is > 3.2 mg/kg or the serum concentration is > 1.4 μg/mL, failure to induce may be suspect.
The Sympathetic Imbalance Hypothesis of QT Interval Prolongation
Authors: ABILDSKOV J.A.
Published: May 2007

Sympathetic Imbalance. The demonstration of QT interval prolongation after left stellate ganglion stimulation led to the successful trial of left cervicothoracic sympathectomy for the control of arrhythmias in long QT syndromes. Based on those findings, sympathetic imbalance with excessive left‐sided effects became widely regarded as the mechanism of QT prolongation and arrhythmias in the syndromes. Prolongation of the interval was attributed to regional reduction of repolarization durations with exposure of previously cancelled electrocardiographic effects and arrhythmias to nonuniform recovery of excitability permitting reentrant excitation. Subsequent findings have not, however, supported this hypothesis. It has been shown that QT prolongation following left stellate ganglion stimulation is transient and unlikely to account for the sustained prolongation in the syndromes. It has also been shown that QT prolongation is not unique for left stellate stimulation and also occurs transiently after right stellate stimulation or bolus injections of catecholamines. It remains possible that sympathetic imbalance in the form of deficient right‐sided sympathetic effects on the heart that experimentally results in prolonged repolarization and sustained QT interval prolongation is a mechanism in long QT syndromes. ECG mapping suggests prolongation of repolarization in the region normally innervated by the right stellate ganglion and a plausible mechanism of torsade de pointes based on regionally disparate recovery has been proposed.
Cardiac Electrophysiologic Effects of 9‐Deoxydoxorubicin
Authors: MOLINA‐VIAMONTE VICTOR , HAMRA MARY , ROSEN MICHAEL R.
Published: May 2007

Electrophysiology of 9‐Deoxydoxorubicin.
Introduction: The purpose of this investigation was to use standard microelectrode techniques to study the actions of the anthracycline antibiotic, 9‐deoxydoxorubicin (9‐DOD), on cellular electrophysiologic properties of canine Purkinje fibers and on ouabain‐induced ventricular tachycardia (VT) in intact dogs. Methods and Results: 9‐DOD, 1‐5 μM, suppressed delayed afterdepolarizations and prolonged repolarization and the effective refractory period in Purkinje fibers. It had no effect on maximum diastolic potential, V̇max of phase 0, or action potential overshoot through a 10 μM concentration. Although 9‐DOD did augment early afterdepolarizations (EAD) induced by cesium, it did not induce EAD. In six of eight intact dogs with ouabain‐induced VT, 9‐DOD, 0.32‐1.28 mg/m2 IV, brought conversion to sinus or junctional rhythm. In its cellular and intact animal antiarrhythmic actions, 9‐DOD is about 50 times more potent than the parent compound, doxorubicin. Like doxorubicin, it is highly selective for delayed afterdepolarization‐induced rhythms, suppressing these at concentrations lower than those required to reduce the rate of automatic rhythms. Moreover, it has a greater Class III action than doxorubicin and prolongs the duration of normal and calcium‐induced (slow response) action potentials. Hence, this subtle variation on the doxorubicin molecule adds greatly to the antiarrhythmic action of the drug. Conclusions: Although useful as an investigative tool, clinical development of 9‐DOD as an antiarrhythmic is not possible because the antitumor activity of the parent compound, which results in lipid peroxidation and cardiotoxicity, persists.
Catheter Ablation of the Atrial Origin of a Decrementally Conducting Atriofascicular Accessory Pathway by Radiofrequency Current
Authors: OKISHIGE KAORU , STRICKBERGER S. ADAM , WALSH EDWARD P. , SAUL J. PHILIP , FRIEDMAN PETER L.
Published: May 2007

Radiofrequency Ablation of Pseudo‐Mahaim Fibers. Introduction: A young woman with refractory recurrent supraventricular tachycardia was referred for catheter ablation. Methods and Results: Electrophysiologic studies revealed the mechanism of tachycardia to be atrioventricular (AV) reentry, utilizing a decrementally conducting atriofascicular accessory pathway as the anterograde limb of the circuit and the normal intraventricular conducting system as the retrograde limb. Pace mapping in the right atrium during sinus rhythm suggested an atrial origin of the accessory pathway several centimeters distant from the AV node. Multiple radiofrequency lesions at the distal insertion of the accessory pathway in or near the right bundle branch failed to abolish preexcitation. In contrast, radiofrequency current applied to the ventricular side of the anterolateral tricuspid ring, adjacent to the atrial origin of the accessory pathway, was successful in abolishing preexcitation and inducible supraventricular tachycardia without affecting AV nodal conduction. Conclusion: Radiofrequency ablation can provide curative therapy for intractable supraventricular tachycardia due to decrementally‐conducting atriofascicular accessory pathways. The risk of AV block in such patients as a consequence of the procedure should be quite low.
Suspension of Neural Pathways for Pain and Nociception
Authors: BERKLEY KAREN J.
Published: May 2007

Suspension of Neural Pathways for Pain and Nociception. This review traces the changing conceptualization of the biological mechanisms underlying pain sensation from the time of Descartes. The anatomical basis for the existence of a system dedicated to pain is discussed in the light of detailed neuroanatomical knowledge developed during the past quarter century. The adequacy of defining pain in terms of noxious stimulation is questioned. Instead, pain sensation might better be understood in the context of somatovisceral function, with its underlying neuroanatomical complexity and dynamic interactions between ascending and descending systems.
Opioids in Pain and Cardiovascular Responses: Overview of Common Features
Authors: CARR DANIEL B. , VERRIER RICHARD L.
Published: May 2007

Common Opioid Actions in Pain and Cardiovascular Stress Responses. This overview describes three parallel aspects of the architecture and function of opioid action in nociceptive and cardiovascular spheres. First, in both circumstances, opioid secretion and receptor activation are essentially dormant during basal conditions and assume physiological importance only during stress. Second, in either context, opioids produce their responses by activating complementary mechanisms centrally and in the periphery. Third, endorphins act as “neuromodulators” of either type of response through a typical cellular architecture in which they diminish underlying excitatory neurotransmission.
Responses to High‐Dose Narcotic “Anesthesia” During Cardiac Surgery
Authors: LOWENSTEIN EDWARD
Published: May 2007

Narcotics as Anesthetics. Production of profound analgesia (“narcotic anesthesia”) without hemodynamic deterioration is easily and reliably achieved in patients with compromised cardiovascular systems by intravenous administration of large doses of opioids. Even extremely high plasma levels of opioids alone often fail to prevent hypertensive responses to anesthetic and surgical stimulation. It has not been possible to define a blood level of the narcotic that is consistently associated with prevention of hemodynamic or hormonal responses. Since some of the interventions that are associated with hemodynamic and hormonal responses are probably not painful per se, the hemodynamic and hormonal responses may not represent inadequate “anesthesia,” as it is usually defined. Different narcotics have different systemic and neurally mediated effects upon muscle vascular resistance. Local infusion of morphine produces a decline in vascular resistance, whereas local infusion of sufentanil does not. Intravenous administration of morphine is associated with a transient neurally mediated, passive decline in muscle vascular resistance that appears to be due to central sympatholysis, and a persistent neurally mediated increase in muscle vascular resistance. Sufentanil actively dilates muscle vasculature by a neural mechanism. Since the latter may be blocked by local α1‐adrenergic blockade or by the combination of local H1 and H2 blockers, we interpret these data to indicate that a local histaminergic system in the blood vessel walls is activated by withdrawal of α1‐adrenergic activity, possibly related to an α2 agonist action of sufentanil at central nervous system receptors.
Integration of Perioperative Pain and Stress with Cardiovascular Responses in Infants: Opiate Blunting of Humoral and Hypertensive Stress Responses
Authors: HICKEY PAUL R.
Published: May 2007

Opiate Blunting of Perioperative Stress Responses in Infants. Integration of nociceptive pathways and cardiovascular control centers in the neonatal brain stem are quite well developed as demonstrated by marked hormonal, metabolic, and cardiovascular responses to painful and stressful stimulation. During surgical procedures, the hormonal and metabolic responses to pain are extreme in the neonate and may be deleterious. Increases in levels of β‐endorphins, catecholamines, growth hormone, cortisol, and glucagon in neonates during major surgical procedures are greater than those seen in adults. These increased levels produce a substantial catabolic drive intraoperatively and postoperatively characterized by increased levels of oxygen consumption, glucose, lactate, pyruvate, tissue glycogen, and protein metabolism that are poorly tolerated by the fragile neonate. In contrast to other anesthetic agents, these extreme hormonal and metabolic stress responses to surgically‐induced pain can be at least partially attenuated by high‐dose opiates. Such high‐dose opiates have additional benefits such as increases in the threshold for ventricular fibrillation, but opiates also produce marked respiratory depression requiring a period of mechanical ventilation. In addition, high‐dose opiates blunt pulmonary vascular reactivity and decrease pulmonary hypertensive crises in infants with pulmonary hypertension. Further understanding of the integration of pain and cardiovascular responses in the neonate is needed to further improve our abilities to control these problems.
From Cardiac Nociception to the Brain: The Unstable Character of Angina Pectoris
Authors: LOMBARDI FEDERICO , MALLIANI ALBERTO
Published: May 2007

Sympathetic Afferents and Cardiac Pain. We analyzed some particular aspects of the peripheral pathways likely to be involved in the mediation of cardiac pain. The functional characteristics and the reflex function of cardiac sympathetic afferent fibers are discussed in relation to the afferent code transmitting nociception. A modified version of the intensity theory based on the extreme excitation of a spatially restricted population of afferent sympathetic fibers is proposed as the most likely mechanism involved in the genesis of cardiac pain.
Plasticity of the Unconditional Response: Evidence Linking Pain and Cardiovascular Regulation?
Authors: RANDALL DAVID C.
Published: May 2007

Plasticity of Unconditional Response. Dogs were classically conditioned by presenting them with a 30‐second tone (the conditional stimulus) followed by 1/2‐second shock (the unconditional stimulus). Well‐trained animals respond to presentation of the conditional stimulus with increases in blood pressure and heart rate (the conditional response); the unconditional stimulus produces additional cardiovascular reactions (the unconditional response). In the present experiments, shock delivery increased heart rate < 20/min in six of 11 dogs. If the size of the heart rate increase following shock delivery is used as an index of the animal's perception of pain, the relatively small unconditional response in these six animals may indicate a blunting of their perception of the painful nature of the unconditional stimulus. Two additional dogs tested during the acquisition of the conditional cardiovascular response showed a diminution of the unconditional tachycardia as the conditional blood pressure response increased in magnitude. These data thereby tentatively support the concept that learned increases in blood pressure have an antinociceptive effect that, in man, may contribute to the development of hypertension.
Psychological Correlates of Anginal Symptom Reporting in Patients with Coronary Artery Disease
Authors: CARNEY ROBERT M. , FREEDLAND KENNETH E.
Published: May 2007

Psychological Correlates of Angina. This paper reviews the research literature on psychological factors that affect the perception of anginal symptoms among patients with coronary artery disease (CAD). Early research in this area established that variables such as anxiety, depression, and somatic preoccupation predict anginal complaints among community samples and patients with CAD. More recent research has focused on the effects of these variables, as well as personality traits, on symptom reporting during actual ischemic episodes. Despite strong evidence of an association between these psychological variables and anginal symptoms, the direction of causality has not been resolved. Furthermore, potentially important interactions between the identified psychological variables and situational or environmental factors remain to be investigated.
Torsades de Pointes
Authors: LEENHARDT ANTOINE , COUMEL PHILIPPE , SLAMA ROBERT
Published: May 2007

Torsades de Pointes. Torsades de pointes are typically characterized by an ECG pattern of polymorphous but organized electrical activity of ventricular origin that occurs in the setting of a long QT interval, long‐coupled bigeminy, and has specific precipitating causes and therapeutic responses. Torsades de pointes can result from congenital (adrenergic dependent) and acquired (pause dependent) factors and may have similar cardiac substrates with different precipitating events. (J Cardiovasc Electrophysiol, Vol. 3, pp. 281–292, June 1992)
Orthostatic Versus Electrophysiologic Testing in Unexplained Syncope in Children and Adolescents
Authors: ROSS BERTRAND A. , HUGHES SUSANNE , ANDERSON ELAINE , GILLETTE PAUL C.
Published: May 2007

Orthostatic vs EP Testing in Pediatric Unexplained Syncope. Introduction: Unexplained syncope in the pediatric age group is a common problem that often requires cardiac evaluation. This work‐up is expensive and frequently unrevealing. Electrophysiologic and, more recently, tilt table or orthostatic testing have been used in the evaluation of unexplained syncope.

Methods and Results: We undertook to compare the results of these two forms of evaluation in a group of 26 young patients less than 19 years of age with episodes of unexplained syncope. Sixteen of the 26 patients (62%) had an abnormal electrophysiologic study with the majority having either mild sinus node dysfunction or inducible atrial flutter. Four of the 26 patients (16%) were thought to have an abnormality found that was clinically significant (sustained ventricular tachycardia [2], nonsustained ventricular tachycardia/polymorphic premature ventricular contractions [1], and high‐degree atrioventricular block [1]). An abnormal response to orthostatic testing was found in 14 of 26 patients (56%) with 13 of 14 developing syncope at an average standing time of 6.5 minutes. Sixteen patients underwent treatment based on the study findings and follow‐up with an average time of 1.6 years is available on 13 of 16 patients who underwent treatment. Of the nine patients treated for neurally mediated syncope (fludrocortisone [7], beta blocker [1], theophylline [1]), all are asymptomatic. The four patients with an arrhythmic cause of syncope found by electrophysiologic testing are asymptomatic on treatment (antiarrhythmic drug [3], permanent pacing [1]).

Conclusion: Orthostatic testing has a higher positive yield than electrophysiologic testing in the evaluation of unexplained syncope in young patients. Orthostatic or tilt table testing should be considered early on in the cardiovascular evaluations of these patients. (J Cardiovasc Electrophysiol, Vol. 3, pp. 418–422, October 1992)
Autonomic Modulation of Cellular Repolarization and of the Electrocardiographic QT Interval
Authors: ROSEN MICHAEL R. , JECK CYNTHIA D. , STEINBERG SUSAN F.
Published: May 2007

Autonomic Modulation of Repolarization. The modulation of repolarization on ECG, the currents contributing to it in cardiac myocytes, and the effects of autonomic stimulation on repoiarization are all complex areas that not only influence the normal rhythm of the heart, but have important implications with respect to arrhythmias. The following is a brief review that stresses the role of autonomic modulation of repolarization, summarizing the extent of our information with respect to the normal heart and the dysrhythmic heart. Particular emphasis is placed on the long QT syndrome and its relationship to lethal arrhythmias. (J Cardiovasc Electrophysiol, Vol. 3, pp. 487–499. October 1992)
The Frequency‐Dependent Effects of Verapamil on Antegrade Refractory Periods and Conduction in the Atrioventricular Node in Man
Authors: CURTIS ANNE B. , ELLENBOGEN KENNETH , HARTON J. MARCUS , TRAUSS HAROLD C
Published: May 2007

Frequency‐Dependent Effects of Verapamil. Introduction: The purpose of this study was to examine the frequency‐dependent effects of verapamil on refractoriness and development of conduction block in the human atrioventricular (AV) node.

Methods and Results: To more closely simulate conditions thai would be found when the drug is used clinically, the drug was assessed in the absence of autonomic blockade. Antegrade refractory periods were determined in nine patients before and during the administration of verapamil by constant intravenous infusion. In addition, continuous recordings were made during 30‐second sequences of atrial pacing at a long cycle length alternating with sequences at shorter pacing cycle lengths. Mean verapamil levels were constant throughout the study and averaged 111.6 ± 70.7 ng/mL. In the majority of patients, refractoriness in the atrium prevented determination of the effective refractory period of the AV node in the control state. Therefore, although the effective refractory period of the AV node lengthened with decrease in pacing cycle length in the presence of verapamil, the relative contribution of the change in cycle length itself compared to the effect of verapamil could not be determined. A frequency‐ and time‐dependent change in A‐H interval was found with verapamil during atrial pacing. Kinetic analysis of drug effect on AV nodal function was possible in only three patients; in these three patients the mean time constant for onset of block was 2.9 seconds (range 1.9–4.0 sec). In one patient at a pacing cycle length that did not result in second‐degree AV block, transient periods of alternation between short and long A‐H intervals occurred in the presence of verapamil.

Conclusion: Verapamil causes frequency‐dependent block of conduction through the AV node. Since changes in autonomic tone will vary from patient to patient, the actual magnitude of the effects of verapamil will vary as well. This may account for some of the interpatient variability seen with clinical use of this drug, despite comparable blood levels. (J Cardiovasc Electrophysiol, Vol. 3, pp. 21–33, February 1992)
Alterations in Repolarization of Cardiac Purkinje Fibers Recovering from Ischemic‐like Conditions:
Authors: Ph.D. GEORGE J. ROZANSKI. , WITT RICHARD C.
Published: May 2007

Abnormal Repolarization. Introduction: Triggered activity initiated from delayed after‐depolarizations has been proposed as a possible cause of arrhythmias during reperfusion of ischemic myocardium. However, the potential for abnormal repolarization and early afterdepolarizations (EADs) to develop under similar conditions has not been fully explored.

Methods and Results: Repolarization of the cell membrane during recovery from ischemic‐like conditions was analyzed from transmembrane recordings in isolated rabbit Purkinje fibers paced at different basic cycle lengths. Preparations were exposed to conditions of hypoxia (defined as oxygen tension < 30 mmHg, high potassium, and zero substrate) plus lactic acidosis (pH 6.7) for 45 minutes followed by recovery in normal Tyrode's solution. Compared to control, action potentials during recovery at basic cycle length of 3,000 msec (n = 11) were characterized by a: (1) −7.2 ± 2.1 mV shift in plateau potential (P < 0.01); (2) 126.1 ± 63.6 msec increase in plateau duration (P < 0.05); and (3) 0.29 ± 0.07 V/sec slowing of the maximum rate of terminal repolarization (phase 3; P < 0.01). These changes were larger when 10 to 20 μM amiloride was added to the hypoxic, acidotic lest solution hut were smaller when tissues were conditioned with hypoxia alone (zero lactate, pH 7.4). Following hypoxia plus acidosis, with or without amiloride, repolarization at long basic cycle lengths was often accompanied by EADs predominantly generated from potentials positive to −40 mV. These afterpotentials were blocked by Ca2+ channel antagonists and exhibited an activation threshold of −26.3 ± l.8 mV (n = 7).

Conclusion: These data are consistent with the hypothesis that the combined negative voltage shift in the plateau and increase in its duration lead to the genesis of low membrane potential EADs by allowing reactivation of Ca2+ channels. Moreover, these results suggest that bradycardia‐dependent EADs in Purkinje tissue may underlie arrhythmias in the intact heart during reperfusion of ischemic myocardium by mechanisms that are related in part to the acidosis established during the preceding ischemic conditions.
Radiofrequency Current Catheter Ablation for Control of Supraventricular Arrhythmias
Authors: GÜRSOY SINAN , SCHLÜTER MICHAEL , KUCK KARL‐HEINZ
Published: May 2007

Radiofrequency Catheter Ablation in SVT. With the advent of radiofrequency energy, catheter ablation techniques have become an accepted form of treatment for a variety of Supraventricular arrhythmias. The ablation of the atrioventricular (AV) node was performed first and is now widely used in patients with refractory atrial fibrillation or flutter. Ablation has also replaced surgery in patients with preexcitation syndromes, and as the complication rate in experienced centers is low, it has become the first line of treatment in these institutions. The results of catheter ablation in AV nodal reentrant tachycardia are excellent as well, although there is still debate about whether “slow” pathway ablation is superior to “fast” pathway ablation. Radiofrequency current ablation has also contributed to a better understanding of the pathophysiology of AV nodal reentrant tachycardia, as it has provided evidence for atrial participation in the reentrant circuit. Experience with atrial tachycardias and tachycardias due to Mahaim fibers remains limited. The ideal source of energy for specific arrhythmias is still unknown and improvement in catheter technology is needed.
Complexities of Junctional Tachycardias
Authors: PERRY JAMES C. , CARSON ARTHUR
Published: May 2007

Complexities of functional Tachycardias. The atrioventricular junction is a compact area in which most of the known electrophysiologic substrates and mechanisms play a role in the genesis and maintenance of tachyarrhythmias. The purpose of this review is to summarize the data on normal atrioventricular junction anatomy and electrophysiologic function and correlate that information with surface electrocardiographic recordings, intracardiac electrophysiologic data, and interventional data from surgical and catheter techniques. Models of tachycardia mechanisms are proposed for typical and atypical atrioventricular nodal reentrant tachycardia, permanent Junctional reciprocating tachycardia, and orthodromic supraventricular tachycardias utilizing “intermediate septal” accessory connections.
Idiopathic Ventricular Tachycardia and Fibrillation
Authors: BELHASSEN BERNARD , VISKIN SAMI
Published: May 2007

Idiopathic Ventricular Tachycardia and Fibrillation. Important data have recently been added to our understanding of sustained ventricular tachyarrhythmias occurring in the absence of demonstrable heart disease. Idiopathic ventricular tachycardia (VT) is usually of monomorphic configuration and can be classified according to its site of origin as either right monomorphic (70% of all idiopathic VTs) or left monomorphic VT. Several physiopathological types of monomorphic VT can be presently individualized, according to their mode of presentation, their relationship to adrenergic stress, or their response to various drugs. The long‐term prognosis is usually good. Idiopathic polymorphic VT is a much rarer type of arrhythmia with a less favorable prognosis. Idiopathic ventricular fibrillation may represent an underestimated cause of sudden cardiac death in ostensibly healthy patients. A high incidence of inducibility of sustained polymorphic VT with programmed ventricular stimulation has been found by our group, but not by others. Long‐term prognosis on Class IA antiarrhythmic medications that are highly effective at electrophysiologic study appears excellentJfy Cardiovasc Electrophysiol, Vol. 4, pp. 356–368, June 1993).
Intracoronary Ethanol Ablation in Swine:
Authors: HAINES DAVID E. , VEROW ANTHONY F. , SINUSAS ALBERT J. , WHAYNE JAMES G. , DiMARCO JOHN P.
Published: May 2007

Intracoronary Ethanol Ablation. Introduction: Physical or chemical ablation of arrhythmogenic tissue has been shown to be an effective modality of arrhythmia therapy. Chemical ablation by intracoronary infusion of ethanol into a specific coronary artery bed has been demonstrated, but the characteristics and distribution of necrosis relative to the coronary blood supply have not been delineated.

Methods and Results: A total of 40 myocardial lesions were created in 21 pigs by infusion of 1.6 ± 0.6 ml of 50% ethanol and 50% iohexol contrast solution through a 2.7 French infusion catheter advanced into a branch of the left anterior descending or circumflex coronary artery. Prior to ethanol infusion, 5.3 ± 1.2 mCi technetium‐99m (Tc‐99m) methoxyisobutyl isonitrile (sestamibi) was infused into the coronary branch in order to delineate the perfusion bed. After completion of the lesions, each heart was removed, sliced transversely in 5‐mm slices, and stained with nitro blue tetrazolium in order to define the ablation bed. The slices were then imaged with a gamma camera and the area of Tc‐99m sestamibi uptake was defined as the perfusion bed. These respective areas were planimetered for each slice and compared. No difference was observed in hemodynamic parameters between preablation and postablation measures except mean arterial pressure, which fell from 122 ± 22 mmHg to 116 ± 24 mmHg (P = 0.02). Significant ventricular arrhythmias were observed after 60% of the ablations. The mean left ventricular ejection fraction fell from 55%± 9% to 45%± 15% after completion of all ablations. The areas of the ablation beds were related to the areas of the perfusion beds but the correlation was poor (r = 0.41, P = 0.0001). Generally, the ablation bed was smaller than the perfusion bed, but evidence of ethanol reflux was observed in 29% of the lesions resulting in injury beyond the targeted perfusion bed.

Conclusions: Intracoronary ethanol ablation is a promising technique for the treatment of arrhythmias. Significant arrhythmias and a decrease in left ventricular ejection fraction are associated with this technique. Lesions are generally produced within the distribution of the targeted coronary bed, but are also frequently associated with reflux to a second vascular distribution.
Relationship Between Different Recovery Curves Representing Rate‐Dependent AV Nodal Function in Rabbit Heart
Authors: BILLETTE JACQUES , AMELLAL FARID , ZHAO JIE , SHRIER ALVIN
Published: May 2007

Nodal Function and Recovery Measures. Introduction: The rate‐dependent changes in atrioventricular (AV) nodal conduction time show different characteristics depending upon whether the conduction times are plotted against the atrial interval (AA‐recovery curve) or His‐atrial interval (HA‐recovery curve). This study characterizes these differences in the context of controlled changes of nodal functional properties, determines their functional significance, and tests the hypothesis that they are related solely to the nodal conduction time of the last beat (last conduction time) before the premature beat.

Methods and Results; Premature nodal conduction times obtained in isolated rabbit heart preparations under various steady‐state and transient conditions were plotted as a function of the corresponding HA and AA intervals, as well as the AA interval corrected for the last conduction time. Under all conditions, the corrected AA‐recovery curve was indistinguishable in shape from the HA‐recovery curve, and as such reflected similar underlying nodal functional properties. Moreover, a selective increase in the last conduction time, induced in the absence of time‐dependent effects associated with the functional property of fatigue, shifted the AA‐recovery but not the HA‐recovery curve upward with respect to the control curve.

Conclusion: The last conduction time accounts entirely for differences between AA‐recovery and HA‐recovery curves that otherwise reflect the same underlying nodal functional state. Thus, a consistent assessment of rate‐dependent changes in nodal function can be achieved with either measure of recovery time.
The Influence of Myocardial Systolic Shortening on Action Potential Duration Following Changes in Left Ventricular End‐Diastolic Pressure
Authors: COULSHED DAVID S. , HAINSWORTH ROGER , COWAN J. CAMPBELL
Published: May 2007

APD and Systolic Shortening. Introduction: Contraction‐excitation feedback may he an important factor in arrhythmogenesis in patients with heart failure. We have previously demonstrated the contrasting effects of raising left ventricular end‐diastolic pressure on action potential duration in dog and guinea pig hearts. The current study was undertaken to assess whether these differing effects might reflect differences in the effect of varying left ventricular end‐diastolic pressure on systolic shortening in the two models.

Methods and Results: Two models were studied and compared. In open chest dog hearts and isolated guinea pig hearts, measurements of myocardial segment length were made while left ventricular end‐diastolic pressure was raised and lowered at constant left ventricular peak systolic pressure. Action potentials were also recorded while left ventricular end‐diastolic pressure was changed. The dog hearts were studied further in a manner aimed at reproducing the contraction pattern of the guinea pig hearts. In the in situ dog heart, elevation of left ventricular end‐diastolic pressure, and the consequent increase in end‐diastolic segment length, was accompanied by a marked increase in systolic shortening, such that minimum systolic segment length remained unchanged. Elevation of left ventricular end‐diastolic pressure was accompanied by a prolongation of action potential duration. In the in vitro guinea pig model, elevation of left ventricular end‐diastolic pressure was accompanied by more modest changes in systolic shortening, which were not sufficient to compensate for increased diastolic segment length. Consequently, minimum systolic segment length increased as the hearts dilated. Elevation of left ventricular end‐diastolic pressure was accompanied by a shortening of action potential duration. In a further series of experiments, the effects of increased left ventricular end‐diastolic pressure were studied in the dog model while allowing aortic pressure to rise, thereby restricting systolic shortening. Under these circumstances, the dog model was similar to the guinea pig model, with an increase in left ventricular end‐diastolic pressure causing a shortening of action potential duration.

Conclusion: Our results suggest that the effects of preload changes on action potential duration depend on accompanying changes in systolic shortening. This suggests a possible role for contraction‐excitation feedback in arrhythmogenesis in patients with regional wall‐motion abnormalities.
Electrical Proarrhythmia with Procainamide:
Authors: FIKSINSKI EDMUND , MARTIN DAVID , VENDITTI FERDINAND
Published: May 2007

ICD‐Drug Proarrhythmia. A 78‐year‐old man with a transvenous cardioverter defibrillator system developed frequent shocks during oral procainamide therapy. Electrophysiologic evaluation demonstrated failure to terminate ventricular tachycardia with maximal energy shocks, but consistent termination by low energy discharges. Procainamide had no effect upon the defibrillation threshold. The failure of therapy with disopyramide and mexiletine to reproduce this observation suggests either a previously unreported electrophysiologic effect of, or idiosyncratic response to, procainamide.
Genetics of the Long QT Syndrome
Authors: KEATING MARK
Published: May 2007

Long QT Syndrome. The application of molecular biology to human genetics has led to the development of a new field, human molecular genetics. This field has already had a dramatic impact on our understanding of cardiovascular disease and has helped improve diagnosis and treatment of these disorders. We have learned a great deal during the past decade about the long QT syndrome, familial hypertrophic cardiomyopathy, Duchenne muscular dystrophy, hypertension, and supravalvular aortic stenosis. In the coming decade, the pace of discovery will accelerate, offering new opportunities for the prediction and prevention of cardiovascular disease.
Power Spectral Analysis of Cardiovascular Variability in Patients at Risk for Sudden Cardiac Death
Authors: MALLIANI ALBERTO , LOMBARDI FEDERICO , PAGANI MASSIMO , CERUTTI SERGIO
Published: May 2007

Heart Rate Variability. The time series of successive heart periods present important variations around its mean value, determining the phenomenon of heart rate variability (HRV), assessed with both time and frequency domain approaches. A low standard deviation of the heart period (a time domain index of HRV) is a powerful prognostic indicator of sudden coronary death in patients recovering from acute myocardial infarction. Spectral analysis of HRV usually demonstrates two major components: indicated as LF (low frequency, ∼ 0.1 Hz) and HF (high frequency, ∼ 0.25 Hz). They are defined by center frequency and associated power, which is expressed in msec2 or normalized units. When assessed in normalized units, LF and HF provide quantitative indicators of neural control of the sinoatrial node. Numerous experimental and clinical studies have consistently indicated that the LF component is a marker of sympathetic modulation and HF a marker of vagal modulation; the LF/HF ratio is a synthetic index of sympathovagal balance. In the analysis of 24‐hour Holter recordings of normal subjects, a circadian rhythmicity of spectral markers of sympathetic and vagal modulation is clearly present, with a sympathetic predominance during the day and a vagal predominance during the night. In patients recovering from an acute myocardial infarction, spectral analysis of HRV revealed an increased sympathetic and decreased vagal activity during early convalescence, and a return to their normal balance by 6 to 12 months. A clear increase of LF was also evident in patients studied within a few hours of the onset of symptoms related to an acute myocardial infarction, independent of its location. Similarly, LF increased during transient myocardial ischemia. An increase in markers of sympathetic activity has also been observed prior to episodes of malignant arrhythmias. Spectral analysis of HRV could help in the understanding of the role of abnormal neural mechanisms in sudden coronary death, thus contributing to its prevention.
Monophasic Action Potentials:
Authors: YUAN SHIWEN , BLOMSTROM‐LUNDQVIST CARINA , OLSSON S. BERTIL
Published: May 2007

Monophasic Action Potentials. Monophaisc action potential (MAP) recordings reproduce the repolarization time course of intrucellular action potentials with high accuracy and provide precise information on the local activation time. With the advantage of in vivo application and the development of the safer and simpler contact catheter technique, MAP recording has become the method of choice for evaluating myocardial repolarization changes. This review aims to provide information on practical application of MAP recording in the clinical setting. MAPs can easily be recorded from the endocardium with the contact catheter technique in the electrophysiology laboratory and from the epicardium with electrode probes during open heart surgery. The technical aspects are described in detail. The rate dependence of myocardial excitability and repolarization and the effect of antiarrhythmic drugs on MAP duration and effective refractory period are thoroughly reviewed. The use of MAPs in detecting myocardial ischemia, in studying early afterdepolarization and triggered arrhythmias, in measuring dispersion of repolarization, in identifying intracardiac conduction and the development of the T wave, and in verifying the arrhythmogenic effect of mechanoelectric feedback are presented. Computerized automatic analysis of MAPs and the limitations of the MAP technique are also discussed.
Effects of Incremental Doses of Procainamide in Patients with Sustained Uniform Ventricular Tachycardia
Authors: GRIMM WOLFRAM , CHO JEONG‐GWAN , MARCHLINSKI FRANCIS E.
Published: May 2007

Procainamide in Patients with Uniform VT. Introduction: Although intravenously administered procainamide has been used extensively during electropharmacologic testing for more than II) years, there is little information available on the effects of incremental dosing of procainamide in patients with inducible, monomorphic ventricular tachycardia (VT).

Methods and Results: Twenty‐nine patients with coronary artery disease had sustained monomorphic VT reproducibly induced in the baseline, drug‐free state. Programmed stimulation was repeated 5 minutes after loading infusion (50 mg/min) of 7.5 and 15 mg/kg (all patients) and 22.5 mg/kg of procainamide (15 patients), while maintaining continuous infusion of 0.055, 0.11, and 0.165 mg/kg per minute after each increment in dose, respectively. Corresponding procainamide plasma concentrations were 5.6 ± 2, 10.5 ± 3, and 14.5 ± 3 mg/L before, and 4.7 ± 2, 9.6 ± 3, and 14.6 ± 4 4 mg/L after electrophysiologic study at each increment in dose of procainamide, respectively. Each incremental dose of procainamide resulted in significant prolongation of tachycardia cycle length and QRS duration during sinus rhythm and right ventricular pacing. Five (17%), 7 (24%), and 1 (7%) patients, respectively, had no inducible sustained VT following the incremental dosing of procainamide. Three of five patients who had no inducible VT at 7.5 mg/kg had VT induced again at a higher dose of procainamide. Four of 24 patients whose VT remained inducible at 7.5 mg/kg of procainamide had no VT induced at 15 mg/kg of procainamide. Twelve (41%), 15 (52%), and 6 (40%) patients, respectively, no longer had VT with baseline morphology induced following the incremental dosing of procainamide. VT with new morphology compared to baseline was induced in more than 40% of patients at one or more of the three different procainamide dosing regimens. The mean cycle length of VTs with new morphology was significantly shorter than the cycle length of tachycardias with baseline morphology at each particular dose of procainamide.

Conclusion: Similar serum procainamide concentrations before and after programmed stimulation can be achieved at the described dosing regimen. Although 7.5 and 15 mg/kg of procainamide are both effective in suppressing induction of all VT in 20% to 25% of patients, non‐inducibility at a particular dose of procainamide does not predict noninducibility at a respectively higher or lower dose. New morphologies of VT that are frequently faster than VTs with baseline morphology at a particular dose of procainamide can be induced in approximately half of the patients, and the clinical significance of these arrhythmias remains to be determined.
Supernormal Conduction in the Left Bundle Branch
Authors: ORETO GIUSEPPE , SMEETS JOEP L.R.M. , RODRIGUEZ LUZ‐MARIA , TIMMERMANS CARL , WELLENS HEIN J.J.
Published: May 2007

Supernormal Conduction. This report describes a patient with tachycardia‐dependent left bundle branch block (LBBB) and atrial extrasystoles, some of which were followed by an unexpectedly narrow QRS complex. His‐bundle recordings and premature atrial stimulation were performed to analyze the mechanism underlying the normalized intraventricular conduction of some of the early atrial impulses. The results suggested the presence of supernormal conduction in the left bundle branch (LBB), because(1) the HV interval was identical in LBBB complexes and in early narrow QRS complexes; (2) during single lest stimulation using different paced atrial cycle lengths, there was a well‐defined range of H1, H2, intervals resulting in normalization of intraventricular conduction; and (3) atrial pacing with a cycle length of 500 msec resulted in alternation between wide and narrow QRS complexes. These findings rule out alternative mechanisms that could explain the unexpectedly normal intraventricular conduction of early impulses.
Epinephrine‐Induced Ventricular Premature Complexes Due to Early Afterdepolarizations and Effects of Verapamil and Propranolol in a Patient with Congenital Long QT Syndrome
Authors: SHIMIZU WATARU , OHE TOHRU , KURITA TAKASHI , TOKUDA TAKAHIRO , SHIMOMURA KATSURO
Published: May 2007

Epinephrine‐Induced VPCs and EADs in Congenital LQTS. We report a patient with congenital long QT syndrome in whom early afterdcpolarizations (RAl)s) were demonstrated on monophasic action potential (MAP) recordings in the left ventricular mid‐base inferior wall. Epinephrine infusion at 5 fig/mm increased the amplitude of the EADs and the late component of the T(U) wave. Epinephrine also induced ventricular premature complexes (VPCs) with right hundle branch block morphology and left‐axis deviation that occurred from the peak of the EADs. Verapamil injection (5 nig) during continuous epinephrine infusion abolished all VPCs with a slight reduction in the amplitude of the EADs. Propranolol injection (5 mg) in addition to verapamil further reduced the amplitude of the EADs and the late component of the T(U) wave. These findings suggest that the epinephrinc‐induced VPCs were closely related to triggered rhythm arising from the EADs, and that both verapumil and propranoloi were effective for the suppression of VPCs and EADs.
QT Dispersion: Problems of Methodology and Clinical Significance
Authors: STATTERS DEBORAH J. , MALIK MAREK , WARD DAVID E. , CAMM A. JOHN
Published: May 2007

QT Dispersion. QT dispersion is defined as the difference in QT interval between the different leads of the surface 12‐lead ECG. This may provide an indirect measure of the underlying inhomogeneity of myocardial repolarization, which is believed to be important in arrhylhmogenesis. Methodology for determining QT dispersion varies significantly between studies, and the results of these studies need to be interpreted in light of the methodology used. Although QT dispersion is developing into an important research tool, as yet it has no established role in clinical practice. Once standardization of methodology is achieved a clinical role may emerge, particularly in the assessment of patients before and after intervention aimed at reduction of arrhythmia risk.
Radiofrequency Catheter Ablation in Unusual Mechanisms of Atrial Fibrillation:
Authors: HAÏSSAGUERRE MICHEL , MARCUS FRANK I. , FISCHER BRUNO , CLÉMENTY JACQUES
Published: May 2007

RF Catheter Ablation in AF. Introduction: The purpose of this study was to test the feasibility of radiofrequency (RF) catheter ablation of localized mechanisms of atrial fibrillation (AF).

Methods and Results: Three patients underwent RF catheter ablation for drug‐resistant atrial arrhythmias. The first two patients had either incessant atrial tachycardia or AF. In the first patient, the KCG pattern of AF was mimicked by a very rapid atrial focus, whereas in the second patient, AF was due to true degeneration of the atrial activity triggered by atrial tachycardia. In both patients, the ablation of atrial focus led to the clinical disappearance of AF. The third patient had frequent episodes of AF, which lasted several days or weeks, and two documented episodes of atrial flutter. Mapping during AF showed an irregular atrial rhythm in the atrial septum, particularly in the region surrounding the coronary sinus, whereas the entire lateral right atrial free wall exhibited a constantly organized rhythm. RF energy was applied between the tricuspid ring and both the inferior vena cava and the coronary sinus, resulting in inability to reinduceatrial flutter or sustained AF. A 6‐month follow‐up in this patient showed the disappearance of prolonged episodes of AF.

Conclusion: The observations indicate that AF may be linked to “focal” mechanisms that can be treated by RF catheter ablation.
Smaller Capacitors Improve the Biphasic Waveform
Authors: RIST KEVIN , TCHOU PATRICK J. , MOWREY KENT , KROLL MARK W. , BREWER JAMES E.
Published: May 2007

Capicitance for Biphasic Waveform. Introduction: Current implantable cardioverter defibrillators (ICDs) use relatively large capacitance values. Theoretical considerations suggest, however, that improved defibrillation energy requirements may he obtained with smaller capacitance values.

Methods and Results: We compared the energy requirement for defibrillation in a porcine model using a biphasic waveform generated from two capacitance values of 140 μF and 85 μ K. Phase 1 reversal of the shock waveform occurred at 65% tilt. Phase 2 pulse width was equal to phase 1. Shocks were delivered through epicardial patch electrodes after 10 seconds of induced ventricular fibrillation. The defibrillation threshold (DFT) was determined by a “down‐up” technique requiring three reversals of defibrillation success or failure. The DFT was defined as the average of the values obtained with all trials starting from the successful shock prior to the first failure to defibrillate to the last successful defibrillation. In eight experiments, the measured parameters at DFT were as follows. The average stored and delivered DFT energies for the 85 μF capacitor were 6.1 ± 2.1 and 6.0 ± 2.0 J, respectively, compared to 7.5 ± 1.3 and 7.4 ± 1.3 J for the 140 μF capacitor (P < 0.04). The phase 1 pulse widths were significantly shorter for the 85 μF capacitor (5.1 ± 0.8 msec vs 9.2 ± 1.3 msec) and the impedances were lower (54.4 ± 5.8 Ω vs 59.9 ± 6.3 Ω). The mean leading edge voltage was trending higher for the 85 μF capacitor, but this difference did not reach statistical significance (374± 63 V vs 326 ± 30 V; P =0.055).

Conclusion: Smaller capacitance values do result in lower energy requirements for the biphasic waveform, at a possibly higher leading edge voltage and a much shorter pulse width. Smaller capacitance values could represent a significant enhancement of well‐established benefits demonstrated with the biphasic waveform.