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J L Cox

Publications and source records attributed to J L Cox.

At least 163 records · Page 9Linked to original sources
PubMed1991

Temporary external DDD pacing after cardiac operations.

Temporary atrial and ventricular pacing in the DVI, VVI, and AOO modes using atrioventricular sequential DVI devices is routinely used in cardiac operations. This study evaluated a new temporary external DDD pacemaker (Medtronic 5345 External Pulse Generator) capable of ten pacing modes. Thirty-nine devices have been applied to 38 adult patients (27 male, 11 female) after a variety of open heart procedures. Group 1 had atrial pacing wires placed 1.5 to 2.0 cm apart superiorly on the right atrium, group 2 had atrial wires placed 1.0 to 1.5 cm apart on the right atrial free wall, and group 3 had atrial wires placed on the right atrial free wall 0.8 cm apart, using a Silastic ring for fixation. Ventricular wires were placed on the free wall (group 1) or the diaphragmatic surface (groups 2 and 3) of the right ventricle. Postoperative atrial and ventricular sensing and pacing thresholds were obtained on return to the intensive care unit; analysis of variance demonstrated a significantly greater atrial sensing threshold in group 3. Four patients in group 1 permanently lost atrial sensing, 1 patient in group 2 intermittently lost atrial sensing at 24 hours with return at 36 hours postoperatively, and 1 patient in group 1 lost ventricular sensing capability. All other patients had adequate atrial and ventricular sensing capability documented until elective pacemaker removal (mean, 166 hours; range, 17 to 667.5 hours). Nineteen patients required some form of temporary pacing postoperatively; 11 patients demonstrated hemodynamic benefit from a pacing mode that is not available on the currently used DVI devices, and 7 of these required true DDD pacing capability. Six patients benefited from atrial pacing with adequate atrial sensing and simultaneous ventricular backup. Burst pacing with the device was used successfully to treat postoperative atrial flutter in 2 patients. We conclude that temporary external DDD pacing is feasible and effective in postoperative cardiac surgical patients. Atrial sensing is possible in most patients but electrode positioning is important for adequate thresholds. In some patients, hemodynamic as well as electrophysiologic improvement can be demonstrated with universal DDD pacing capability as compared with standard DVI pacing.

Adult↗
PubMed1991

Significant left ventricular contribution to right ventricular systolic function.

To examine the importance of systolic ventricular interdependence on right ventricular function, we used a unique electrically isolated right ventricular free wall preparation. Double-peaked waveforms for right ventricular pressure and pulmonary arterial blood flow occurred over a wide range of pacing intervals between the left and right ventricles. One component of the waveforms could be directly related to right ventricular free wall contraction, whereas the other component was directly related to left ventricular and septal contraction. For left ventricular pressure, the left ventricular component was significantly larger than the right ventricular free wall component (92.7 +/- 3.2 vs. 7.3 +/- 3.2% peak-to-peak value, P less than 0.01). For right ventricular pressure, the left ventricular and septal component was significantly greater than the right ventricular component (63.5 +/- 10.9 vs. 36.5 +/- 10.9% peak-to-peak value, P less than 0.05). Similarly, for pulmonary arterial blood flow, the left ventricular component was significantly greater than the right ventricular component. When right ventricular free wall pacing stopped in diastole, 68 +/- 4% of right ventricular systolic pressure and 80 +/- 4% of pulmonary flow were obtained in the subsequent beat. The results of this study indicate that left ventricular contraction is very important for right ventricular developed pressure and volume outflow.

Animals↗
PubMed1991

Spontaneous tachyarrhythmias after cholinergic suppression in the isolated perfused canine right atrium.

Atrial fibrillation occurs spontaneously after bradycardia induced by acetylcholine infusion or vagal stimulation. To determine the mechanism of initiation of this tachyarrhythmia, we infused acetylcholine (5 ml, 10(-3.5) M) into Krebs-Henseleit-perfused isolated canine right atria (n = 10). Unipolar electrograms were recorded from 250 sites simultaneously during control rhythms, pacing (cycle length = 300 msec) with and without acetylcholine, and recovery of spontaneous activity. Activation sequence maps were constructed from each recording. Stable spontaneous rhythm was present in all preparations during control conditions. Activation sequence maps, recorded during continuous pacing with and without acetylcholine, demonstrated no dromotropic changes due to the acetylcholine. Focal asynchronous recovery of spontaneous activity was initiated from different sites, resulting in bigeminal or trigeminal premature depolarizations in 41 of 73 cases after infusion of acetylcholine. A reentrant tachyarrhythmia was initiated in 24 of 41 cases by the closely coupled recovery beats (A1A2 = 100 +/- 37 msec; A2A3 = 97 +/- 27 msec). The reentry was initiated by interaction of the premature impulse with regions of functional block that were a result of the cholinergically induced dispersion of refractoriness. All the tachyarrhythmias terminated spontaneously, and stable spontaneous control rhythms returned. In conclusion, the data suggest that the premature depolarizations that initiate the reentrant tachyarrhythmia are caused by the asynchronous recovery of multiple right atrial pacemakers accompanied by variable entrance block at the later depolarizing sites.

Acetylcholine↗
PubMed1991

Influence of activation origin, lead number, and lead configuration on the noninvasive electrophysiologic detection of cardiac allograft rejection.

An improved method of cardiac allograft surveillance, less invasive than endomyocardial biopsy (EMB), is required as the scope of cardiac transplantation increases. The correlation between changes in telemetrically recorded intramyocardial electrograms and the degree of rejection was examined. The electrophysiological parameter assessed was the unipolar peak-to-peak amplitude (UPPA), defined as the magnitude of the first, fast negative deflection of the QRS complex in unipolar electrograms. A canine model of intrathoracic heterotopic cardiac transplantation was employed in which each graft was instrumented with four unipolar intramyocardial electrodes (two left ventricle [LV] and two right ventricle [RV]) connected to two telemetric pacemakers. Immunosuppression was begun at operation and continued for a variable period of time following the acquisition of control data (postoperative days 6-10). Graft status was monitored via biweekly EMB. Intramyocardial electrograms were recorded from each lead during sinus rhythm and 36 atrial and ventricular pacing protocols on a daily basis. The daily UPPA was calculated for each rhythm sequence and expressed as percent of control UPPA. EMBs were qualitatively graded and assigned a quantitative rejection score (0 = none; 3 = severe). Criteria for rejection were rejection score (RS) greater than or equal to 0.66 or daily UPPA less than 85% control. Eight animals were included for study and, in all animals, rejection was documented. A total of 30 EMBs were obtained; in 11 EMBs rejection was present by histological criteria. Analysis of grouped UPPA data from all four leads revealed a sensitivity and specificity of 91% and 84%, respectively, in the detection of rejection. Analysis of grouped sinus UPPA data from the two LV leads revealed a sensitivity of 94% and 91%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

The surgical treatment of atrial fibrillation. I. Summary of the current concepts of the mechanisms of atrial flutter and atrial fibrillation.

Atrial fibrillation is a common arrhythmia that is frequently resistant to medical therapy and has no satisfactory surgical therapy. The development of an effective surgical procedure to treat atrial fibrillation has been hampered by the paucity of clinically relevant information on the basic mechanisms responsible for the arrhythmia. This paper summarizes the current concepts of the electrophysiologic abnormalities in atrial flutter and fibrillation.

Animals↗
PubMed1991

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.

Adult↗
PubMed1991

The surgical treatment of atrial fibrillation. III. Development of a definitive surgical procedure.

On the basis of the known electrophysiologic mechanisms of atrial fibrillation, multiple surgical procedures were designed and tested in dogs to determine the feasibility of developing a surgical cure for human atrial fibrillation. These experimental studies culminated in a surgical approach that effectively creates an electrical maze in the atrium. The atrial incisions prevent atrial reentry and allow sinus impulses to activate the entire atrial myocardium, thereby preserving atrial transport function postoperatively. Since September 1987, this surgical procedure has been applied in seven patients, five with paroxysmal atrial fibrillation of 2 to 9 years' duration and two with chronic atrial fibrillation of 3 and 10 years' duration. All seven patients have been cured of atrial fibrillation and none is receiving any postoperative antiarrhythmic medications.

Adult↗
PubMed1991

Feasibility of closed heart discrete cryomodification of atrioventricular conduction. Electrophysiologic effects in the canine heart.

Discrete cryosurgical modification of atrioventricular conduction abolishes refractory atrioventricular node reentry tachycardia with preservation of antegrade atrioventricular nodal conduction. This procedure presently requires cardiopulmonary bypass. To modify atrioventricular conduction without cardiac surgery, we evaluated the electrophysiologic effects of cryolesions applied to the peri-nodal area in the closed heart in 16 dogs before operation, during cryothermic exposure, and at 1 hour and 3 hours after operation. The electrophysiologic effects were evaluated in 10 of the 16 dogs at 2 weeks postoperatively. The dogs were given general anesthetics, and a cryoprobe was introduced into the right atrial cavity through the right atrial appendage. Cryolesions (-60 degrees C) were placed at nine to eleven preselected points around the perinodal area guided by electrodes on the tip of the cryoprobe. Postoperatively, there were significant prolongations of the atrio-His interval, Wenckebach's point, effective refractory period, and functional refractory period of the atrioventricular node. Atrial echo beats were eliminated or decreased in frequency. There was also a significant increase in retrograde ventriculoatrial conduction time. In the long-term observation period the atrio-His intervals remained significantly prolonged in comparison with the preoperative values, the atrial echoes progressively decreased, and ventriculoatrial conduction was absent in five of seven animals. A serendipitous atrioventricular node reentry tachycardia that was inducible in one animal with dual atrioventricular node conduction pathways was successfully eliminated and was not inducible at 2 weeks postoperatively. Complete atrioventricular block occurred during attempts to produce greater atrio-His prolongation in three of the 16 animals and persisted in two for the 2-week period of observation. Closed heart intracardiac cryomodification of atrioventricular conduction is feasible, with the cryoprobe in normothermic blood, producing changes in atrioventricular conduction similar to the open cardiac procedure.

Animals↗
PubMed1990

Transmural ventricular activation during consecutive cycles of sustained ventricular tachycardia associated with coronary artery disease.

Although computerized mapping has enabled the intraoperative delineation of global ventricular activation from a single complex of ventricular tachycardia (VT), beat-to-beat reproducibility of isochronic maps has not been defined. To determine the reliability of single-beat analysis, epicardial and transmural ventricular electrograms during 6 consecutive VT cycles were analyzed in 10 patients during intraoperative mapping of sustained monomorphic VT. Bipolar electrograms were recorded simultaneously using sock and needle electrodes from up to 96 epicardial and 156 transmural sites. In each patient, at each electrode site, local activation time, electrogram duration and morphology were compared over 6 consecutive beats. A total of 9,816 electrograms were analyzed. For each patient, the isochronic activation map during VT was reproducible. Mean beat-to-beat variations in local epicardial and transmural activation times were only 1.7 +/- 1.7 and 2.04 +/- 1.9 ms, respectively (difference not significant). Moreover, electrogram duration did not vary significantly. Mean variations in epicardial and transmural electrogram durations were 2.1 +/- 1.8 and 1.4 +/- 1.9 ms, respectively (difference not significant). There were only 2 instances of 2:1 conduction failure; both occurred intramurally and adjacent to a site of VT origin. Thus, transmural ventricular activation during sustained monomorphic VT is reproducible regardless of electrode site or electrogram duration. These results demonstrate that analysis of a single beat of VT is a reliable and expedient method to delineate ventricular activation during intraoperative computerized mapping for the purpose of clinical decision-making in patients with sustained monomorphic VT.

Aged↗
PubMed1990

Effect of the right ventricular isolation procedure on ventricular vulnerability to fibrillation.

A certain critical mass of myocardium is believed to be necessary to initiate ventricular fibrillation. The right ventricular isolation procedure, employed clinically to confine ventricular tachyarrhythmias to the right ventricle, decreases the ventricular mass available for fibrillation by isolating the ventricles from each other. The effect of this procedure on ventricular fibrillation thresholds is unknown. Left and right ventricular fibrillation thresholds were measured before and after right ventricular isolation in 10 adult mongrel dogs utilizing a single 5 ms stimulus of increasing current strength applied to the epicardium during the vulnerable period. There were no significant differences in heart rate, aortic blood pressure, left atrial pressure, temperature, arterial blood gases or regional myocardial blood flow between the study periods. In 9 of the 10 dogs, the isolated right ventricle could not sustain ventricular fibrillation despite the utilization of stimulus strengths of up to 80 mA. In the 10th dog, the right ventricular fibrillation threshold increased 150%, from 20 to 50 mA. The left ventricular fibrillation threshold markedly increased in every dog, with an average increase from 23 +/- 2 to 40 +/- 4 mA (p less than 0.0005). To determine whether time, cardiopulmonary bypass or the right ventricular incision could cause similar changes in ventricular fibrillation threshold, five different dogs underwent the entire experimental protocol except for incomplete isolation of the right ventricle. There were no significant changes in ventricular fibrillation thresholds in these dogs. Thus, in the canine model, right ventricular isolation can prevent the occurrence of sustained fibrillation in the isolated right ventricle and can significantly increase the left ventricular fibrillation threshold.

Animals↗
PubMed1990

Expression and induction by beta-adrenergic agonists of the cystatin S gene in submandibular glands of developing rats.

Repeated administration of the beta-adrenergic agonist isoprenaline (isoproterenol, IPR), which produces hypertrophic/hyperplastic enlargements of rat submandibular and parotid glands, induces synthesis of a secretory protein shown to be a cysteine proteinase inhibitor, rat cystatin S. In the current study, Northern blot and hybridizations in situ were carried out to establish the developmental and beta-adrenergic regulation of the expression of the cystatin S gene. Cystatin S mRNA was not detected in submandibular glands of 20-day-old fetuses, nor in the glands of newborn or 10-day-old rats. However, steady-state levels of cystatin S mRNA increased between 21 and 28 days, reaching a conspicuously high concentration at 28 days; cystatin S mRNA then declined rapidly to a barely detectable level in glands of 32-day-old rats. IPR administration for 4 days induced high levels of cystatin S mRNA in submandibular glands of developing and adult rats. In both prepubertal and mature animals, induction of cystatin S mRNA in submandibular glands was more pronounced in female than in male animals. Hybridizations in situ revealed cystatin S mRNA only in acinar but not in duct cells of the submandibular gland. Developmentally, expression of the cystatin S gene coincided with acinar cell differentiation. These data suggest a complex neural, hormonal and developmental regulation of salivary cystatin genes.

Adrenergic beta-Agonists↗
PubMed1990

Left ventricular pressure effects on right ventricular pressure and volume outflow.

Massive destruction of the right ventricular free wall has been shown to cause only mild hemodynamic alterations. Further, the derivative of right ventricular (RV) pressure (P) is broad or double peaked, with one peak occurring coincidentally with peak left ventricular (LV) dP/dt. Both observations suggest a direct LV assistance to RV function. Since the ventricles contract nearly simultaneously, the relative contribution of LV to RV pump function has been difficult to determine. This LV assistance was quantified in six canine experiments using a unique electrically isolated RV preparation. While on total cardiopulmonary bypass, the RV free wall was electrically isolated from the remainder of the heart. This preparation allowed for wide variations in the timing interval between RV and LV contractions. Double-peaked waveforms for RVP and pulmonary flow (RVF) occurred over a wide range (0 to 300 ms) of pacing intervals between the RV and LV. One derivative peak always followed RV contraction for RVP and RVF (r = 0.971 +/- .011, P less than 0.01: r = 0.972 +/- .012, p less than 0.01; respectively). The second derivative peak was unrelated to the RA-RV pacing interval (r = 0.297 +/- .191, P greater than 0.5 RVP; 4 = 0.237 +/- .278, P greater than 0.5 RVF), but corresponded to the maximal LVP rise. Additionally, the magnitude of the two derivative peaks was similar when the ventricles contracted synchronously. When RV contraction preceded or followed LV contraction, the derivative peak associated with LV contraction was significantly greater (P less than 0.05, range 2.1 +/- 0.6 to 6.7 +/- 1.6 for RVP; P less than 0.05 range 1.9 +/- 0.4 to 6.7 +/- 1.5 for RVF) than the derivative associated with RV contraction. These data demonstrate a normally present, large LV assistance to RV contraction and may help to explain the RV response to myocardial infarction.

Animals↗
PubMed1990

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.

Adolescent↗
PubMed1990

Computerized potential distribution mapping: a new intraoperative mapping technique for ventricular tachycardia surgery.

This study evaluated potential distribution mapping as a method for localizing the site of origin of ventricular tachycardia (VT). In contrast to conventional activation time maps, potential distribution maps require less editing and thus can be more automated and rapidly processed for interpretation of multiple beats of VT. As a series of potential distribution maps during VT is required for detailed analysis, an on-line computerized system was designed to display potential distribution maps sequentially at 1-ms intervals as a color movie. Potential distribution maps and activation time maps were constructed from 182 epicardial and endocardial unipolar electrodes during 12 episodes of reproducible monomorphic VT in 9 dogs four to six days after experimental myocardial infarction (mean cycle length, 162 +/- 21 ms). At the onset of each depolarization during VT, a potential minimum abruptly developed on the surviving epicardium and another on the surviving endocardium of the left ventricle, both immediately adjacent to the subendocardial infarct. These two minima on the initial potential distribution maps corresponded to the sites of earliest epicardial and endocardial activation breakthrough recorded on the activation time maps. These two minima subsequently expanded or moved into the adjacent area and coincided with the spread of activation fronts on the epicardial and endocardial surfaces. Thus, the rapid display of sequential, computerized potential distribution maps of multiple beats of VT provides a dynamic means of identifying the site of origin of VT, and therefore should facilitate intraoperative mapping.

Action Potentials↗
PubMed1990

Hemodynamic importance of systolic ventricular interaction, augmented right atrial contractility and atrioventricular synchrony in acute right ventricular dysfunction.

To delineate the determinants of right ventricular performance with acute right ventricular dysfunction, surgical electrical isolation of the right ventricular free wall was produced in 13 dogs. During atrioventricular (AV) pacing, hemodynamic and wall motion measurements were normal. When not paced, the right ventricular free wall became asystolic, resulting in a depressed and bifid right ventricular systolic pressure (33 +/- 5 to 18 +/- 4 mm Hg) and decreased left ventricular systolic pressure (100 +/- 18 to 80 +/- 18 mm Hg) and stroke volume (14 +/- 4 to 10.3 +/- 3.5 ml) (all p less than 0.05). Ultrasound demonstrated right ventricular free wall dyskinesia, increased right ventricular end-diastolic size (155 +/- 13% of control), but decreased left ventricular size (69 +/- 11% of control) (both p less than 0.05). Right atrial pressure increased (5.8 +/- 2.5 to 7.6 +/- 2.8 mm Hg, p less than 0.05) with an augmented A wave and blunted Y descent, indicating pandiastolic right ventricular dysfunction. The septum demonstrated reversed curvature in diastole and bulged paradoxically into the right ventricle during early systole, generating the initial peak of right ventricular pressure and reducing its volume. Later, posterior septal motion coincided with maximal left ventricular pressure and the second peak of the right ventricular waveform. Left ventricular pacing alone led to further decreases in right ventricular systolic pressure and size, left ventricular systolic pressure and stroke volume. The previously augmented A wave was replaced by a prominent V wave. Therefore, when contractility of its free wall is acutely depressed, right ventricular performance is dependent on left ventricular-septal contractile contributions transmitted by the septum.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Early application of topical 15% idoxuridine in dimethyl sulfoxide shortens the course of herpes simplex labialis: a multicenter placebo-controlled trial.

In a double-blind, randomized, patient-initiated treatment study at five medical centers, 301 immunocompetent patients experiencing a recurrence of herpes labialis were treated with topical 15% idoxuridine (IDU) in dimethyl sulfoxide (DMSO), 80% DMSO control solution, or 2% DMSO control solution. IDU did not prevent the development of lesions but significantly accelerated lesion resolution in comparison with the combined control groups. For the total population, the mean duration of pain was reduced by 1.3 days (35%, P = .01) and the mean healing time to loss of crust by 1.7 days (21%, P = .004). Analysis of subpopulations revealed that the beneficial activity of the treatment was concentrated among the patients who began treatment in the prodrome or erythema lesion stage. For these patients, the mean duration of pain was reduced by 1.8 days (42%, P = .08) and the mean healing time to loss of crust by 3.3 days (38%, P less than .001). If only patients with classic herpes lesions (vesicle, ulcer, or crust formation) were considered, there was a greater drug effect on the duration of pain (reduction by 2.6 days, 49%; P = .03) and the mean healing time to normal skin was significantly shortened (reduction by 2.3 days, 23%; P = .004). Adverse reactions to the medication were minimal.

Administration, Topical↗