The electrophysiological effects of calcium channel blockade during standard hyperkalemic hypothermic cardioplegic arrest

The addition of calcium channel-blocking agents to a standard hyperkalemic hypothermic cardioplegic solution has been examined both experimentally and clinically. None of these studies, however, have investigated the effect of calcium blockade during cardioplegic arrest on the specialized cardiac conduction tissues and on the subsequent development of arrhythmias after arrest. The present study examined the effect of adding nifedipine to standard cardioplegic solution administered in a canine experimental preparation modeled on routine clinical techniques. The time to and duration of electrical arrest following the administration of cardioplegia and the functional electrophysiological variables before and after arrest were measured using a 32-channel data acquisition system. The addition of nifedipine shortened the time to electrical arrest and prolonged the duration of arrest compared with standard potassium cardioplegic solution alone, without a deleterious effect on conduction function immediately after arrest. The occurrence of low-amplitude electrical activity (LEA) in both atria and ventricles during arrest was significantly reduced by the addition of nifedipine, thereby suggesting a possible correlation between LEA and calcium-mediated conduction occurring under conditions of standard cardioplegic arrest.     

The effects of cardioplegic potassium concentration and myocardial temperature on electrical activity in the heart during elective cardioplegic arrest

A major objective of cardioplegic arrest for protection of the heart during cardiac operations is total electromechanical quiescence. Recent studies from our laboratory in which we used multiple bipolar intracardiac and unipolar intramural electrodes have detected the presence of electrical activity in the lower atrial septum, the atrioventricular node-His bundle complex, and in ventricular myocardium during elective cardioplegic arrest that cannot be detected on the limb-lead electrocardiogram. Moreover, this low-amplitude electrical activity is not associated with visible mechanical activity of the heart and occurs at ventricular septal temperatures previously thought to be adequate for myocardial protection. The present study was designed to determine the effect of cardioplegic solution potassium concentration and myocardial temperature on the occurrence and duration of low-amplitude electrical activity during elective cardioplegic arrest. Fifty adult mongrel dogs were subjected to two consecutive 20 minute periods of cardioplegic arrest. The animals were divided into six groups, depending upon the cardioplegic solution potassium concentration they received and on whether or not topical cooling techniques were employed. The probability of occurrence of low-amplitude electrical activity during the arrest interval was significantly decreased by application of topical hypothermic techniques and reinfusion of hyperkalemic, as compared to normokalemic, cardioplegic solution. These effects of hyperkalemic cardioplegic solution and myocardial hypothermia acted synergistically, but independently, to decrease the likelihood of low-amplitude electrical activity occurring during the period of cardioplegic arrest. Nevertheless, low-amplitude electrical activity did occur in all groups after each cardioplegic solution administration and was not detected by routine monitoring techniques. This suggests that low-amplitude electrical activity may represent a fundamental type of metabolic activity that can be recorded from the heart during arrest and may be responsible for the temporary depression in ventricular function that frequently follows a period of elective cardioplegic arrest.     

Decreased incidence of supraventricular arrhythmias achieved by selective atrial cooling during aortic valve replacement

Inadequate atrial hypothermia and subsequent ischemic injury have been recognized as the major causes of supraventricular arrhythmias (SVAs) and conduction defects following cold chemical cardioplegia. This study was designed to assess the effects of right atrial cooling (15 degrees-20 degrees C) during cardioplegic arrest upon the incidence of postoperative SVAs and conduction defects in 40 consecutive patients undergoing isolated aortic valve replacement. Atrial preservation was ensured by combining systemic (24 degrees C) and topical hypothermia with snared double caval cannulation during arrest. Myocardial temperatures in the right atrial septum and anterior wall of the right ventricle were recorded before and after each cardioplegic infusion and upon release of caval tapes. Postoperatively, the incidence of SVAs and conduction defects was assessed by continuous rhythm monitoring, bipolar atrial electrograms and, in ten patients, 24-h Holter recordings during the first postoperative day. With the venae cavae snared, temperatures in the right atrial septum were not significantly different from those measured simultaneously in the right ventricle. Release of caval tapes resulted in right atrial temperatures increasing to systemic temperature (from 17.1 +/- 2.9 degrees C to 25.9 +/- 5.6 degrees C [m +/- SD]; P less than 0.01). Atrial rewarming between cardioplegic infusions did not exceed 2.9 degrees +/- 3.2 degrees C. Postoperatively, four patients (10%) developed sustained atrial fibrillation. One additional patient had a single episode of paroxysmal atrial fibrillation and two patients experienced asymptomatic episodes of junctional rhythm.(ABSTRACT TRUNCATED AT 250 WORDS)     

Right atrial temperature and electrical activity during cardioplegic cardiac arrest

In 18 patients undergoing coronary artery bypass surgery the relation between right atrial temperature and right atrial electrical reactivation during cardioplegic cardiac arrest was studied. The administration of cardioplegic solution induced immediate ventricular and atrial arrest in all patients. No recurrence of ventricular activity was observed while right atrial activity subsequently recurred in 11 patients. Activity at the surface ECG was recorded only in one patient with right atrial reactivation. No right atrial electrical activity was found below 19 degrees C. The average atrial temperature was 21.5 degrees C while the average apex temperature was 15 degrees C. The study has confirmed previous observations that during cardioplegic cardiac arrest the right atrium is not as well protected as the ventricular tissue against rewarming. Monitoring of the right atrial electrical activity or right atrial temperature is essential to ensure atrial arrest during the entire period of cardioplegic cardiac arrest.     

Failure of standard cardioplegic techniques to protect the conducting system

To determine the site of persistent electrical activity during cardioplegic arrest, microelectrodes that were also capable of recording temperature were placed along the conducting system in dogs undergoing one hour of cardioplegic arrest. Electrical activity was highest in the atrioventricular (AV) junction area (AV node and proximal bundle of His), and the temperature in this area could not be lowered to the level of the temperature in the left ventricular apex by routine cardioplegic technique. Neither changing K+ concentration (16 to 20 mEq/L) nor adding procaine hydrochloride abolished the activity of the conducting system during cardioplegia, and only 2 of 15 dogs were in sinus rhythm 30 minutes after reperfusion. When the conducting system temperatures were lowered to less than 15 degrees C by right AV lavage with iced saline solution, electrical activity was abolished during arrest and all 4 of 4 animals were in sinus rhythm 30 minutes after reperfusion. This study localizes the site of persistent conducting system activity during cardioplegic arrest, confirms it can be abolished with local cooling, and establishes the relationship between conducting system activity during cardioplegia and the incidence of conduction block and junctional rhythm following reperfusion.     

Curative surgical treatment of atrioventricular junctional re-entrant tachycardia by perinodal dissection

The medical treatment of an atrioventricular junctional (AV-nodal) re-entrant tachycardia (AVJRT) is often ineffective due to failure of response or significant side effects. Recently, reports of curative surgical procedures using either dissection or cryocoagulation in the AV node area with preservation of normal AV conduction, have been published with excellent short term results in small series. The present paper describes our experience of surgical treatment using the dissection method in five patients. In all patients, AVJRT with short retrograde conduction intervals was diagnosed during the pre- and intraoperative electrophysiological studies. The earliest site of atrial activation during tachycardia was seen close to the triangle of Koch, antero-medially to the AV node. Elective open heart surgery was performed and after cold cardioplegic arrest, the right atrial endocardium was incised and the perinodal atrium carefully disconnected from the AV node. After surgery, a tachycardia could not be induced in any of the patients. In a follow-up period of 14-29 months, all patients have been free of symptoms without antiarrhythmic drugs. Early electrophysiological evaluation of patients with supraventricular tachycardia is advocated and in patients with medically refractory AVJRT, surgery is recommended.     

Monitoring the voltage of the myocardium during cardioplegia arrest

Electrical activity was monitored with specially designed plunge electrodes in 19 animals undergoing 3 h of cardioplegic arrest. Electrical activity was recorded on electromagnetic tape and intramyocardial voltage was monitored with an inline voltmeter. Haemodynamic function was assessed before bypass and following 3 h of ischaemia and 45 min of reperfusion. Intramyocardial voltage during normothermic fibrillation measured 2.4 +/- 0.4 mv. Infusion of cardioplegia initiated a complete electrical arrest in all animals and reduced intramyocardial voltage to 33 +/- 7 mu v. Small amplitude electrical activity was present in 9 of 19 animals. Intramyocardial voltage increased to 108 +/- 12 mu v with the onset of small amplitude electrical activity and spectral analysis of the wave form indicated that the fundamental frequency was in the range of 3.08 Hz. Small amplitude electrical activity during cardioplegic arrest was associated with significant post-arrest depression of left ventricular function. Our data confirms that the presence of small amplitude electrical activity impairs myocardial functional recovery and suggests that continuous intramyocardial voltage monitoring may be used to guide the administration of cardioplegia during cardioplegic arrest.     

Internal cardiac cooling improves atrial preservation: electrophysiological and biochemical assessment

This study was designed to determine if the improved hypothermia that can be achieved with cold perfusion of the right atrium is associated with improved atrial preservation. During 120 minutes of cardioplegic arrest, 7 dogs with occlusive caval cannulation underwent right atrial (RA) perfusion with cold blood and 7 dogs with a single atriocaval cannula served as controls. RA perfusion produced a lower atrial septal temperature than atriocaval cannulation, 96% less electrical activity during arrest, and a lesser prolongation of the A-H interval after reperfusion (40% versus 123%; p less than 0.01). At the end of arrest, compared with atriocaval cannulation, RA perfusion was associated with improved preservation of creatine phosphate (71 +/- 10% versus 40 +/- 7% of control; p less than 0.05) and a lower level of lactate in the RA wall (8 +/- 1 mumol/gm versus 15 +/- 2 mumol/gm; p less than 0.01). We conclude that improved hypothermia reduces electrical activity and anaerobic metabolism in the atrial myocardium during cardioplegic arrest and improves atrioventricular conduction following arrest.     

Persistent atrial activity during cardioplegic arrest: a possible factor in the etiology of postoperative supraventricular tachyarrhythmias

We assessed the relationship between the duration of atrial activity during the cross-clamp period and the postoperative occurrence of supraventricular tachyarrhythmias in 50 patients undergoing elective coronary bypass operation. The atrial electrical activity was monitored continuously by means of a bipolar atrial electrogram from the onset of cardioplegic administration until removal of the aortic cross-clamp. While ventricular arrest was induced promptly and maintained in all patients, sustained atrial activity was observed in 44 out of 50 patients during the cross-clamp period. In the postoperative period, supraventricular tachyarrhythmias developed in 15 patients (Group 1). Thirty-five patients (Group 2) were free from such tachyarrhythmias. There was no significant difference between the two groups with respect to cross-clamp time, bypass time, amount of cardioplegic solution used, or number of grafts per patient. The mean duration of atrial activity during cardioplegic arrest, however, was significantly longer in Group 1 than in Group 2 (46 +/- 4.7 minutes versus 22.6 +/- 4.0 minutes, respectively, p less than 0.001). None of the 6 patients in whom atrial activity was completely abolished experienced supraventricular tachyarrhythmias. The strong correlation observed between the duration of atrial activity during cardioplegic arrest and the incidence of postoperative supraventricular tachyarrhythmias suggests the possibility that these arrhythmias may be a manifestation of inadequate atrial protection during global myocardial ischemia.     

The effects of cardioplegic arrest on right atrial function

Atrial electrical and mechanical activity persists during cardioplegic arrest. It has been postulated that atrial ischemia may occur and cause deterioration in atrial function. This study was designed to assess the effect of cardioplegic arrest on right atrial function. Twenty-one pigs were placed on cardiopulmonary bypass (CPB), and the right atrium was isolated from the circulation by snaring both venae cavae and incising the coronary sinus. The tricuspid valve was closed through a small right ventriculotomy, and baseline atrial function was assessed using a compliant balloon in the atrium. Fourteen pigs underwent one hour of cardioplegic arrest (7 with cardioplegia alone [CCA group] and 7 with the addition of topical hypothermia [CCA + TH group]) followed by one hour of normothermic reperfusion. Seven other pigs were placed on CPB for the same period of time (CPB group). Atrial electrical and mechanical activity persisted at 45 beats per minute in the CCA group but was virtually abolished in the CCA + TH group. Cardioplegic arrest caused considerable deterioration in right atrial function (developed pressure, 18.9 +/- 0.8 [baseline] versus 14.1 +/- 0.7 mm Hg; p less than 0.05; first derivative of atrial pressure [dP/dt], 187 +/- 19 versus 134 +/- 25 mm Hg per second; p less than 0.05; 60 minutes of reperfusion and balloon volume of 20 ml). It was not affected by topical cooling. Right atrial developed pressure was maintained, but dP/dt was significantly reduced in the CPB group. This study suggests that cardioplegic arrest does not protect the atrium.     

Differential electrical activity of the atria during cardioplegic arrest in pigs

To elucidate the electrical interrelationship of the atria during cardioplegic arrest, simultaneous bipolar right atrial (RA) and left atrial (LA) electrograms and myocardial temperatures of all four chambers of the heart were recorded in 10 pigs during an hour of aortic clamping. Five pigs (Group 1) underwent single venous cannulation; in 5 others (Group 2), snared double caval cannulation, RA venting, and intracavitary RA irrigation with cold saline solution were employed. Myocardial protection was provided by systemic hypothermia (28 degrees C) and intermittent intraaortic administration of cold (4 degrees C) hyperkalemic (20 mEq/L) crystalloid cardioplegic solution. Single RA cannulation was associated with sustained RA activity during cardioplegic arrest and with the warmest mean myocardial temperatures. Electrical activity was infrequent in the left atrium, which was often silent while RA impulses continued to be observed. Four Group 1 pigs exhibited high-grade RA-LA block, whereas in 2 animals completely asynchronous RA-LA electrical activity occurred. Isolated LA activity was not encountered. The combined methods used in Group 2 pigs significantly reduced mean myocardial temperatures. Both RA and LA impulses were practically abolished, and their mean durations decreased 96% and 85%, respectively. It is concluded that the pattern of electrical activity differs in the two atria during cardioplegic arrest when a single venous cannula is employed. Intracavitary RA irrigation with cold saline solution in the presence of snared caval cannulas provides improved myocardial hypothermia and effectively eliminates both RA and LA activity in the course of cold crystalloid cardioplegia.     

Influence of atrial and ventricular temperature during cardiac arrest for open heart surgery on postoperative arrhythmias

Myocardial hypothermia during extracorporeal circulation is commonly created by perfusion of cool cardioplegic solution into the ascending aorta and burial of ice sludge in the pericardial sac. Measurement of temperature of the atrial and ventricular septums during animal experiment and operations for ASD and VSD showed: (1) The temperature was obviously higher in the atrial septum than ventricular. (2) The atrial and ventricular temperature exceeded 15 degrees C 5 minutes after cardioplegic perfusion. (3) Influence on postoperative heart rate and rhythm was obvious when ventricular temperature raised above 15 degrees C during cardiac arrest, especially when the temperature difference between the atrium and ventricule was above 3 degrees C. But this influence may be decreased by maintaining ventricular temperature below 15 degrees C and temperature gradient less than 3 degrees C with a combination of cardioplegic perfusion, ice sludge in pericardial sac plus constant lavage of intracardiac cavity with saline at 4 degrees C.     

Effect of high-volume cardioplegia on small-amplitude electrical activity during cardioplegia arrest

The effects of high-volume cardioplegia on the presence of small-amplitude electrical activity during cardioplegia arrest were investigated in 19 mongrel dogs. The animals were randomly assigned to receive either high-volume crystalloid cardioplegia (HV-plege) or crystalloid cardioplegia guided by continuous electrical monitoring (V-plege). Cardiac index, left ventricular stroke work index dp/dt, and myocardial oxygen consumption were measured before bypass and following 90 min ischemia and 45 min reperfusion. Biopsies were taken for measurement of adenosine triphosphate (ATP) and examination of myocardial ultrastructure. Nine animals received HV-plege, while the remaining 10 animals received cardioplegia guided by voltage criteria. Small-amplitude electrical potentials were recorded within 10-15 min after the infusion of cardioplegia in all animals receiving cardioplegia guided by voltage criteria. Electrical activity, however, was immediately abolished by reinfusion of cardioplegia. HV-plege reduced the incidence of small-amplitude electrical activity during cardioplegia arrest but did not prevent electrical activity. Left ventricular function and myocardial ultrastructure were better preserved when cardioplegia was guided by electrical monitoring. ATP decreased similarly in both groups following cardioplegic arrest, but myocardial oxygen consumption was significantly higher following the arrest in the V-plege group. Conclusions: HV-plege does not prevent small-amplitude electrical activity and may have adverse effects on myocardial metabolic and functional recovery.     

Computerized activation sequence mapping of the human atrial septum

To delineate the propagation of electrical activation in the atrial septum, atrial epicardial and atrial septal maps were recorded intraoperatively using a 156-channel computerized mapping system in 12 patients during sinus rhythm (n = 10), supraventricular tachycardia associated with septal pathways in Wolff-Parkinson-White syndrome (n = 3), atrioventricular (AV) node reentrant tachycardia (n = 4), and atrial flutter (n = 5). The epicardial and septal data were recorded simultaneously from 156 atrial electrodes, digitized, analyzed, and displayed as isochronous maps on a two-dimensional diagram of the atria. During sinus rhythm, the activation wave fronts propagated most rapidly along the large muscle bundles of the atrial septum. During supraventricular tachycardia associated with Wolff-Parkinson-White syndrome, the earliest site of retrograde atrial activation usually corresponded to the position of atrial insertion of the septal pathways. However, the earliest site of activation during orthodromic supraventricular tachycardia was different from that during ventricular pacing in 1 patient with a posterior septal accessory pathway localized by the epicardial mapping study. The data document the rationale for dividing the ventricular end of the accessory pathways (ie, the endocardial technique) rather than the atrial end (ie, the epicardial technique) in patients with Wolff-Parkinson-White syndrome. During AV node reentrant tachycardia, atrial activation data suggested that atrial tissue lying outside the confines of the anatomical AV node is a necessary link in this common arrhythmia. Thus, these atrial septal maps explain why surgical dissection, or properly positioned small cryolesions placed in the region of the AV node, can ablate AV node reentrant tachycardia without altering normal AV node function. The maps recorded during atrial flutter suggest the importance of the atrial septum as one limb of a macroreentrant circuit responsible for the arrhythmia, and imply that atrial flutter is amenable to control by surgical techniques. These studies demonstrate the details of normal atrial septal activation, the importance of the atrial septum in a variety of different atrial arrhythmias, and the basis of and potential for surgical ablation of the most common types of supraventricular arrhythmias.     

Surgical approach to anterior septal accessory pathways in 20 patients with the Wolff-Parkinson-White syndrome

Right anterior septal accessory pathways in the Wolff-Parkinson-White syndrome are generally defined by electrophysiological criteria, the most important being that earliest retrograde atrial activation during AV reciprocating tachycardia occurs at the anterior medial segment of the tricuspid annulus (His bundle catheter). The purpose of our study is to describe intraoperative mapping in 20 patients with anterior septal accessory pathways, and to assess if intraoperative mapping contributes to the operative approach. At surgery, all patients had identical early ventricular activation during pre-excitation at the infundibulum. However, two groups could be identified on the basis of retrograde atrial epicardial activation during AV reciprocating tachycardia or right ventricular pacing. Group 1 comprised 16 patients with earliest activation at the interatrial septum adjacent to the His bundle. Epicardial dissection failed to affect accessory pathway conduction. The accessory pathway was only ablated when a discrete endocardial approach to the atrial septum was used. Group 2 comprised 4 patients with early atrial activation "paraseptally" in the right coronary fossa. These accessory pathways were ablated by an epicardial approach without using cardiopulmonary bypass. We conclude that right anterior septal accessory pathways as defined by electrophysiological criteria can be divided into two groups on the basis of the atrial activation sequence: (1) right septal accessory pathways in the septal para-Hissian region and (2) right anterior 'paraseptal' accessory pathways. This classification is of practical importance because the latter can be ablated using an epicardial approach without the need for cardiopulmonary bypass or atriotomy.     

Oxygenated cardioplegia ameliorates the adverse effects of small amplitude electrical recording of activity on myocardial metabolic and functional recovery

Small amplitude electrical activity has been recorded from the myocardium during cardioplegic arrest in the absence of electromechanical activity. The presence of persistent electrical activity has been associated with impaired myocardial metabolic and functional recovery. To determine whether or not oxygenated cardioplegia would provide sufficient oxygen to support the increased metabolic activity associated with persistent electrical activity during cardioplegic arrest, we randomized 14 adult mongrel dogs to receive either non-oxygenated or oxygenated cardioplegia during 90 min of ischaemia. Cardiac index (CI), left ventricular stroke work index (LVSWI) and dp/dt were measured before bypass and after 90 min of ischaemia and 45 min of reperfusion. Myocardial oxygen consumption (MVO2) and lactate extraction were measured before and after bypass. Intramyocardial voltage was monitored during cardioplegic arrest, and MVO2 was measured during cardioplegia infusion. The onset of small amplitude electrical activity was associated with a rise in intramyocardial voltage and an increase in MVO2. CI, LVSWI and dp/dt were better preserved in those animals receiving oxygenated cardioplegia. MVO2 and lactate consumption following cardioplegia arrest were also higher in this group. Conclusions: (1) small amplitude electrical activity during cardioplegic arrest is associated with a rise in MVO2. (2) Oxygenated cardioplegia increases myocardial protection by providing oxygen for the increased metabolic activity associated with the presence of this small amplitude electrical activity.     

Electrophysiological Consequences of Hypothermic Hyperkalemic Elective Cardiac Arrest

A bstract While the development of pharmacological cardioplegic solutions for myocardial protection during cardiopulmonary bypass (CPB) have significantly lengthened the safe operating time for cardiac surgical procedures, the introduction of hypothermic hyperkalemic cardioplegia (CPG) has markedly increased the incidence of postoperative arrhythmias and conduction abnormalities. Using a customized modification of a computerized mapping system, we have developed a large animal porcine model of CPB that is exquisitely sensitive to the electrophysiological (EP) derangements imposed by ischemia and cardiac arrest. This model is able to measure spatial and temporal parameters of ventricular activation with high resolution, using an array of up to 84 epicardial electrodes that can be reproducibly placed on the surface of the heart utilizing known epicardial anatomical markers (e.g., coronary arteries). With this system we have measured the spectrum of clinically observed EP disturbances caused by CPG, from slowed intraventricular conduction to complete heart block. Compared to the control group of hypothermia alone, 2 hours of crystalloid CPG arrest had a significant slowing effect on ventricular activation (p < 0.05). CPG was accompanied, in each animal, by profound changes in the spatial distribution of ventricular activation and persistent slowing of ventricular activation. Traditional EP parameters of effective refractory period and pacing threshold were unchanged by CPG. Smaller temporal and spatial changes were observed in the control group, but were always reversed by 90 minutes of warm reperfusion. We conclude that CPG induces injury of the specialized conducting system and, to a lesser degree, the myocardium. This model will afford us the opportunity to test new methods of CPG to further improve myocardial preservation during CPB.     

The effect of augmented atrial hypothermia on atrial refractory period, conduction, and atrial flutter/fibrillation in the canine heart.

The purpose of this study was to test the assumption that the cause for postoperative atrial flutter/fibrillation after cardiopulmonary bypass is inadequate atrial myocardial protection. Dogs were subjected to cardioplegic arrest for 60 minutes without augmented atrial hypothermia (seven dogs, control group) or augmented atrial hypothermia with topical atrial cooling (seven dogs, study group). Twenty-five electrodes (15 on the right atrium and 10 on the left atrium) were fixed on the atria to measure effective refractory period and conduction time. Data were taken before bypass, immediately after bypass, and 2 hours after bypass. During cardioplegic arrest the mean temperatures measured in the atria were significantly lower (p less than 0.001) in the study group (13.5 degrees +/- 7.0 degrees C) than in the control group (23.7 degrees +/- 3.2 degrees C). There was no significant change in the mean effective refractory period after bypass in the control or study groups or in the prevalence of inducibility of atrial flutter/fibrillation by extrastimulation (3/7 dogs in the control group and 2/7 in the study group). During right atrial pacing, total conduction times were significantly longer (p less than 0.025 at cycle lengths of 300 and 350 msec) in the control group (74 +/- 5 msec and 75 +/- 7 msec, respectively) than in the study group (65 +/- 9 msec and 64 +/- 8 msec, respectively) immediately after bypass. Two hours after bypass, however, there were no significant differences under the same conditions between the two groups. There were no significant differences in conduction during left atrial pacing after bypass. Comparing those atria that were inducible with those not inducible demonstrated a significantly increased dispersion of effective refractory period (90 +/- 23 msec versus 74 +/- 18 msec, p less than 0.05) and increased conduction time in the inducible group. We concluded that augmented atrial hypothermia during cardioplegic arrest had no effect on the inducibility of fibrillation, had no effect on repolarization, and had only a small effect on conduction, which resolved within 2 hours after bypass. However, the study demonstrates that when the atria are inducible the substrates are an increased dispersion of refractoriness and a prolongation of conduction time.     

Sodium/hydrogen-exchanger inhibition during cardioplegic arrest and cardiopulmonary bypass: an experimental study

OBJECTIVE: We sought to determine whether pretreatment with a sodium/hydrogen-exchange inhibitor (EMD 96 785) improves myocardial performance and reduces myocardial edema after cardioplegic arrest and cardiopulmonary bypass. METHODS: Anesthetized dogs (n = 13) were instrumented with vascular catheters, myocardial ultrasonic crystals, and left ventricular micromanometers to measure preload recruitable stroke work, maximum rate of pressure rise (positive and negative), and left ventricular end-diastolic volume and pressure. Cardiac output was measured by means of thermodilution. Myocardial tissue water content was determined from sequential biopsy. After baseline measurements, hypothermic (28 degrees C) cardiopulmonary bypass was initiated. Cardioplegic arrest (4 degrees C Bretschneider crystalloid cardioplegic solution) was maintained for 2 hours, followed by reperfusion-rewarming and separation from cardiopulmonary bypass. Preload recruitable stroke work and myocardial tissue water content were measured at 30, 60, and 120 minutes after bypass. EMD 96 785 (3 mg/kg) was given 15 minutes before bypass, and 2 micromol was given in the cardioplegic solution. Control animals received the same volume of saline vehicle. Arterial-coronary sinus lactate difference was similar in both animals receiving EMD 96 785 and control animals, suggesting equivalent myocardial ischemia in each group. RESULTS: Myocardial tissue water content increased from baseline in both animals receiving EMD 96 785 and control animals with cardiopulmonary bypass and cardioplegic arrest but was statistically lower in animals receiving EMD 96 785 compared with control animals (range, 1.0%-1.5% lower in animals receiving EMD 96 785). Preload recruitable stroke work decreased from baseline (97 +/- 2 mm Hg) at 30 (59 +/- 6 mm Hg) and 60 (72 +/- 9 mm Hg) minutes after cardiopulmonary bypass and cardioplegic arrest in control animals; preload recruitable stroke work did not decrease from baseline (98 +/- 2 mm Hg) in animals receiving EMD 96 785 and was statistically greater at 30 (88 +/- 5 mm Hg) and 60 (99 +/- 4 mm Hg) minutes after bypass and arrest compared with control animals. CONCLUSIONS: Sodium/hydrogen-exchanger inhibition decreases myocardial edema immediately after cardiopulmonary bypass and cardioplegic arrest and improves preload recruitable stroke work. Sodium/hydrogen-exchange inhibition during cardiac procedures with cardiopulmonary bypass and cardioplegic arrest may be a useful adjunct to improve myocardial performance in the immediate postbypass or arrest period.     

The surgical treatment of atrial fibrillation. II. Intraoperative electrophysiologic mapping and description of the electrophysiologic basis of atrial flutter and atrial fibrillation

Computerized mapping of atrial fibrillation was performed in animals and man. To study atrial fibrillation in a systematic manner, we developed a clinically relevant experimental model of atrial fibrillation. Chronic mitral regurgitation was created surgically in 25 dogs without opening the pericardium. After several months of chronic mitral regurgitation, the atria became enlarged and sustained atrial fibrillation could be induced by standard programmed electrical stimulation techniques. Computerized isochronous activation maps of the atria were recorded during atrial fibrillation from 208 bipolar electrodes simultaneously. In a parallel study, human atrial fibrillation was mapped with a separate 160-channel intraoperative mapping system in patients with paroxysmal atrial fibrillation who were undergoing surgical correction of the Wolff-Parkinson-White syndrome. The canine activation sequence maps demonstrated a spectrum of rhythm abnormalities ranging from simple atrial flutter to complex atrial fibrillation. They also showed that macroreentrant circuits within the atrial myocardium were responsible for the entire spectrum of arrhythmias. Atrial reentry was also documented during human atrial fibrillation. All patients had nonuniform conduction around regions of bidirectional block in both atria resulting in multiple discrete wave fronts. In addition, six patients had a single reentrant circuit in the right atrium in which bidirectional block of the activation wave front occurred along the sulcus terminals between the venae cavae. The left atrium in all patients demonstrated multiple wave fronts and conduction block, but left atrial reentry could not be detected. Both the experimental study and the clinical study demonstrated that multiple wave fronts, nonuniform conduction, bidirectional block, and large (macroreentrant) reentrant circuits occur during atrial fibrillation. The presence of macroreentrant circuits and the absence of either microreentrant circuits or evidence of atrial automaticity suggests that atrial fibrillation should be amenable to surgical ablation.