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Biomedical subjects

M E Cain

Publications and source records attributed to M E Cain.

71 records · Page 4Linked to original sources

Cryosurgical treatment of atrioventricular node reentrant tachycardia.

Paroxysmal supraventricular tachycardia most commonly arises from reentry within the atrioventricular (AV) node. Although ablation of the His bundle has gained popularity for treating patients with AV node reentrant tachycardia refractory to medical therapy, undesirable sequelae include complete heart block and the necessity for a permanent pacemaker. To obviate this limitation, we have developed a discrete cryosurgical procedure that interrupts the reentrant circuit responsible for AV node reentrant tachycardia without blocking AV conduction. After first characterizing the salutary effects of this approach in experimental animals, we performed this procedure in eight patients with AV node reentrant tachycardia. Preoperative, intraoperative, and postoperative electrophysiologic studies were performed in each patient. Under conditions of normothermic cardiopulmonary bypass and during atrial pacing at a constant rate with continuous monitoring of AV conduction, nine separate 3 mm cryolesions (-60 degrees C for 2 min) were placed at predetermined sites around the triangle of Koch in the lower right atrial septum. Postoperatively, each patient had a single AV node conduction curve. No patient had AV node reentrant tachycardia induced or has experienced AV node reentrant tachycardia clinically during a follow-up of up to 5 years. The cryosurgical procedure had no detrimental effects on the AH or HV interval or on the paced cycle length at which AV node Wenckebach occurred. Based on these results, this curative operation offers promise for patients with AV node reentrant tachycardia that is refractory to medical treatment.

Adolescent↗

Improved selection of patients for programmed ventricular stimulation by frequency analysis of signal-averaged electrocardiograms.

Improved selection of patients with suspected sustained ventricular tachycardia (VT) for programmed ventricular stimulation is needed. To determine if frequency analysis detects patients in whom sustained VT might be induced, we first obtained fast-Fourier transforms (FFT) of signal-averaged electrocardiograms (ECGs) from 20 patients with spontaneous sustained VT (group 1) and compared them with the results of programmed ventricular stimulation with single and double extrastimuli during two cycle lengths and burst pacing from two right ventricular sites. The FFT data were expressed as an area ratio that quantified the relative contributions of 20 to 50 Hz frequencies in the terminal QRS and ST segment. A logistic regression with inducibility as the dependent variable was used to help define area ratio values greater than 20 as abnormal. Sustained monomorphic VT was induced in 18 patients, each with an area ratio value greater than 20. Sustained VT was not induced in two patients, each with an area ratio value less than 20. FFT data were then compared prospectively with the results of programmed stimulation in 38 patients (group II) with nonsustained VT (12 patients) or syncope (26 patients) referred for electrophysiologic study. In none of the 26 patients in group II with normal FFT values was VT inducible. Sustained monomorphic VT was induced in five of 12 patients with abnormal FFT values. Thus, the results of FFT analysis correctly predicted the results of programmed ventricular stimulation in 88% of patients studied and in 82% of patients in group II with syncope or nonsustained VT. Moreover, all five patients in group II in whom sustained VT was induced were identified correctly.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Simultaneous computer mapping to facilitate intraoperative localization of accessory pathways in patients with Wolff-Parkinson-White syndrome.

Sixteen patients with the Wolff-Parkinson-White syndrome underwent simultaneous intraoperative computer mapping from multiple sites before surgical division of the accessory pathways. A 16-bipolar electrode band was positioned around the atrioventricular groove. Ventricular epicardial electrograms from single beats were recorded simultaneously during atrial pacing, resulting in maximal preexcitation, and atrial electrograms were recorded during orthodromic supraventricular tachycardia. Four-level transmural plunge needle electrodes were used concomitantly in 3 patients. Electrograms were processed separately using a guarded signal conditioner that isolates, amplifies, filters and analog-to-digitally converts synchronously at 2 kHz with 12-bit accuracy. Digital data were transmitted by fiber optics to a high-density digital recorder and processed with a computer having rapid interactive graphics. Results in the 16 patients revealed 20 distinct Kent bundles. Two patients had only nonsustained supraventricular tachycardia induced intraoperatively and 1 patient manifested intermittent anterograde ventricular preexcitation. Multiple pathways were identified in 4 patients. This simultaneous multiple electrode mapping procedure facilitates intraoperative mapping by requiring only a single beat for analysis of anterograde and retrograde activation times, decreases cardiac manipulation during mapping and obviates the need for cardiopulmonary bypass, and permits analysis of transmural activation patterns. This approach decreases markedly the time required for mapping and permits accurate study of nonsustained arrhythmias as well as rapid identification of multiple accessory pathways.

Adolescent↗

Quantification of differences in frequency content of signal-averaged electrocardiograms in patients with compared to those without sustained ventricular tachycardia.

To quantify differences in the frequency content of signal-averaged electrocardiograms between patients with and without sustained ventricular tachycardia (VT), the energy spectra of the terminal QRS and ST segments of signal-averaged orthogonal ECGs were computed in 3 groups of patients by squaring the magnitude of the fast-Fourier transformed data. The terminal 40 ms of the QRS complex and ST segment were analyzed as a single unit to enhance frequency resolution. Group I comprised 23 patients with documented, remote myocardial infarction who had manifested subsequent episodes of sustained VT; group II comprised 53 patients with previous, remote infarction without subsequent sustained VT; and group III comprised 11 normal subjects. The terminal QRS and ST segments from patients with sustained VT contained a 10- to 100-fold greater proportion of components in the 20- to 50-Hz range compared with corresponding electrocardiographic segments in patients without VT. There were no significant differences in the peak frequencies among patient groups. However, the relative contribution of the magnitudes of these peak frequencies to the overall maximum magnitude of the spectral plot differed significantly (p less than 0.0001). No frequencies above 50 Hz contributed substantially to the energy spectra of the terminal QRS and ST segments in any group. Thus, differences in the energy spectra do not result from differences in the frequencies of components, but are attributable instead to differences in the amplitudes of components within a relatively narrow range of frequencies. The quantitative approach developed should provide objective indexes for assessing effects of antiarrhythmic interventions on abnormalities recognizable by frequency-domain analysis and improve noninvasive definition of risk for development of sustained VT.

Adult↗

Effects of infarction, procainamide, coupling interval, and cycle length on refractoriness of extrastimuli.

The effects of prematurity, cycle length, site of stimulation, and procainamide on ventricular refractoriness following an extrastimulus (S2) were assessed in 10 dogs with and 10 dogs without infarction. Extrastimuli were introduced at preselected coupling intervals (S1-S2) from normal right and left ventricular sites and from left ventricular sites of infarction during drive cycle lengths (S1-S1) of 350 and 250 ms. At each S1-S2 interval, the effective refractory period of S2 was determined by introducing a second extrastimulus (S3). At all stimulation sites, cycle lengths, and before and during infusion of procainamide (mean concn 18.6 +/- 3.5 micrograms/ml), shortening (greater than 10 ms change) in refractoriness was most marked over a narrow range of closely coupled S1-S2 intervals. Regardless of stimulation site, the effective refractory period of S2 was less during a cycle length of 250 ms compared with a cycle length of 350 ms. In dogs without infarction, the effective refractory periods of S2 from left ventricular sites tended to be longer than from right ventricular sites, particularly during procainamide administration. The refractory period of S2 at sites of infarction did not differ consistently from those at normal sites. Finally, at all stimulation sites and cycle lengths, procainamide prolonged refractoriness of S2 at each S1-S2 interval and blunted the total shortening in refractoriness in response to S2.

Animals↗

Experience with 118 consecutive patients undergoing operation for the Wolff-Parkinson-White syndrome.

Between July 1, 1980, and April 1, 1985, 118 patients underwent operation for correction of the Wolff-Parkinson-White syndrome. There were 72 male and 46 female patients with ages ranging from 9 months to 70 years (mean 28 +/- 6 years). The major indications for operation were medical refractoriness or drug intolerance (60%) and previous cardiac arrest (14%). Associated abnormalities included Ebstein's anomaly (12%), other arrhythmias (34%), coronary artery disease (6%), cardiomyopathy (6%), and congenital heart disease other than Ebstein's anomaly (22%). Two patients had undergone operations for Wolff-Parkinson-White syndrome previously at other institutions. Twenty percent of patients had multiple (two to four) accessory pathways, a total of 149 pathways being present in the 118 patients. Distribution of the accessory pathways was as follows: 58% left free wall, 24% posterior septal, 13% right free wall, and 5% anterior septal. The surgical technique employed previously for the Wolff-Parkinson-White syndrome and for the first 10 patients in the present series was modified in August, 1981, to include 2.5 power optical magnification, exclusive use of the endocardial approach under cardioplegic arrest, wider margins of surgical dissection, sharp dissection of the involved valve anulus, division of only the ventricular insertion of the accessory pathway, and internal identification of the ventricular epicardial peel in all regions of dissection. Of the 149 accessory pathways present, 148 were successfully divided in the 118 patients and, by means of the above modifications, 137 of 137 accessory pathways have been divided successfully in the last 108 patients in the series. The surgical results in these patients document an increase in the success rate for division of accessory pathways from 86% to 99.3%, a decrease in the reoperation rate from approximately 15% to 0%, and a decrease in the incidence of permanent complete heart block from 10.5% to 0.8%. The mortality was 5.0% in the entire series, but only one death occurred following elective operation in the absence of associated cardiac abnormalities (0.8%). Using the present surgical technique, these results suggest that surgical therapy is a conservative alternative to a lifetime of medical therapy in young, otherwise healthy patients with the Wolff-Parkinson-White syndrome.

Adolescent↗

Fast-Fourier transform analysis of signal-averaged electrocardiograms for identification of patients prone to sustained ventricular tachycardia.

Electrocardiograms obtained from patients during arrhythmia-free intervals do not identify those prone to sustained ventricular tachycardia (VT) despite the occult delayed activation that is presumably present. To determine whether frequency-domain analysis facilitates detection of this hallmark of predisposition to VT, fast-Fourier transform analysis (FFTA) procedures were developed and tested with a computer-generated mathematical model. The FFTA approach developed allows inherent limitations of high-gain amplification and a priori filtering used commonly for time-domain analysis to be avoided. After demonstrating that FFTA detected low-amplitude oscillatory waveforms in signal-averaged recordings in the frequency domain, the procedure was applied to signal-averaged X, Y, and Z lead recordings from the following three groups of patients: group I, patients with prior myocardial infarction and episodic sustained VT (n = 16); group II, patients with prior myocardial infarction without overt sustained VT (n = 35); and group III, normal control subjects (n = 10). Results of FFTA demonstrated significant (p less than .0001) differences in the decibel drop at 40 Hz and the area under the curve from the fundamental frequency to the frequency at which the spectral amplitude was decreased by 60 dB for both the terminal 40 msec of the QRS and ST segment in patients in group I compared with those in groups II and III, in whom results were similar. Results were independent of QRS duration (r = .2), left ventricular ejection fraction (r = .19), and complexity of spontaneous ventricular ectopy. Thus, patients known to manifest sustained VT also exhibited relatively greater high-frequency content in arrhythmia-free intervals in the terminal QRS and ST segment than those without VT (88%, 15%, and 0% in groups I through III, respectively). FFTA offers promise for the noninvasive detection of patients at risk for the development of sustained VT.

Aged↗

Changes in ventricular refractoriness after an extrastimulus: effects of prematurity, cycle length and procainamide.

This study was performed to determine the ability of extrastimuli to change ventricular refractoriness. We prospectively evaluated the effects of stimulus prematurity and paced cycle length (PCL) in 30 patients and the effect of procainamide in 8 patients on changes in the ventricular effective refractory period (ERP) after a right ventricular extrastimulus (S2). An S2 was introduced at preselected coupling intervals at a PCL (S1-S1) of 600 and 400 ms. At each S1-S2 interval, a second extrastimulus (S3) was introduced in 5-ms decrements and the ERP of S2 measured. The decrease in the ERP after an S2 was directly related to prematurity and most of the shortening occurred over a narrow range of S1-S2 intervals. At a PCL of 600 ms, the ERP of S2 at S1-S2 intervals less than or equal to 400 ms was significantly shorter than the ERP of S1 (maximal shortening 23%). At a PCL of 400 ms, the ERP of S2 at S1-S2 intervals less than or equal to 350 ms was significantly shorter than the ERP of S1 (maximal shortening 25%). The ERP of S2 at the shortest S1-S2 interval was greater with a PCL of 600 ms than with 400 ms (200 +/- 31 versus 180 +/- 26 ms, p less than 0.001). However, the total shortening in ERP (ERPS1 - ERPS2 at shortest S1-S2 interval) was similar at both PCLs (55 +/- 14 versus 59 +/- 13 ms). Procainamide significantly prolonged the ERP of S2 at each S1-S2 interval.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Ventricular activation during ventricular endocardial pacing. II. Role of pace-mapping to localize origin of ventricular tachycardia.

Intraoperative pace-mapping has been proposed as a method of identifying the origin of ventricular tachycardia; however, both epicardial activation and electrocardiographic configuration have limitations in localizing the origin of ventricular tachycardia. Because most ventricular tachycardias associated with ischemic heart disease appear to arise near the endocardium, this study evaluated the ability of bipolar catheter endocardial pacing at or near the endocardial site of origin of spontaneous ventricular tachycardia to mimic the QRS configuration of the spontaneous tachycardia. Twelve patients were studied who had ventricular tachycardia whose origin was determined with catheter endocardial mapping. Three patients had ventricular tachycardia with two distinct configurations. The electrocardiogram of ventricular tachycardia was compared with the electrocardiogram produced by pacing at the site of origin (10 patients) and at multiple (two to nine) additional sites in 8 patients. It was observed that (1) pacing at the known site of origin of ventricular tachycardia produced an electrocardiogram and activation sequence similar to those produced by the ventricular tachycardia; (2) pacing at sites in close proximity to the site of origin of ventricular tachycardia produced either a similar or a grossly different electrocardiographic pattern from that during ventricular tachycardia. It is concluded that catheter endocardial pace-mapping (1) is a corroborative method of identifying the origin of ventricular tachycardia; (2) may be useful in patients with noninducible ventricular tachycardia or rapid ventricular tachycardia who cannot undergo catheter or intraoperative mapping; and (3) is neither easier, more accurate nor quicker than direct localization by mapping during ventricular tachycardia.

Adult↗

Termination of ventricular tachycardia. Evaluation of a new pacing method.

Ventricular extrastimuli or rapid ventricular pacing used to terminate ventricular tachycardia (VT) may be ineffective or may accelerate VT. Therefore, a new method to facilitate termination of VT and decrease the incidence of acceleration was evaluated. The new method utilized rapid ventricular pacing at cycle length 10 to 100 ms shorter than VT cycle length with the introduction of 1 or 2 ventricular extrastimuli. The efficacy of this combination method in terminating VT was assessed in 25 patients in whom ventricular extrastimuli and rapid ventricular pacing at cycle lengths and coupling intervals comparable with those used in the new method were unsuccessful. This combination method successfully terminated VT in 21 of 25 patients with cycle lengths of 230 to 400 ms. VT was terminated in 6 of 8 patients receiving drugs in whom VT could not be terminated by 1 to 2 ventricular extrastimuli or rapid ventricular pacing; in 6 of 8 patients unresponsive to ventricular extrastimuli and in whom rapid ventricular pacing produced acceleration of VT; and in 9 of 9 patients in whom antiarrhythmic agents made VT unresponsive to ventricular extrastimuli or rapid ventricular pacing. A combination of rapid pacing and extrastimuli can terminate VT unresponsive to ventricular extrastimuli or rapid ventricular pacing alone and may avoid acceleration of VT using rapid ventricular pacing at very short cycle lengths for termination.

Adult↗

Termination of ventricular tachycardia: role of tachycardia cycle length.

The mode of termination of ventricular tachycardia (VT) and its relation to tachycardia cycle length was evaluated in 139 patients. Tachycardia was terminated by programmed stimulation in 110 patients (79%) and cardioversion was required in 29 patients (21%). Single, double, and triple ventricular extrastimuli terminated the tachycardia in 23 of 85 (27%), 39 of 62 (63%), and 7 of 16 patients (44%), respectively. In all patients requiring 1 extrastimulus, in 35 patients (90%) requiring 2 extrastimuli, and in 6 patients (86%) requiring 3 extrastimuli, the tachycardia cycle length exceeded 300 ms. Rapid ventricular pacing terminated tachycardia in 41 of 54 patients (76%). In 21 (51%) of these patients the tachycardia cycle length exceeded 300 ms. However, rapid ventricular pacing caused acceleration of the arrhythmia in 19 patients (35%). The ability of procainamide to modify the termination of VT was studied in 23 patients. In 7 of these patients (30%) procainamide increased the tachycardia cycle length by 49 +/- 42 ms (p less than 0.01) and did not modify the mode of termination. In 6 patients (26%) procainamide increased cycle length by 142 +/- 108 ms (p less than 0.01), but termination was more difficult. In 10 patients (44%) procainamide increased the cycle length by 138 +/- 110 ms (p less than 0.001) and termination was easier. We conclude that termination of VT by timed extrastimuli requires a tachycardia cycle length longer than 300 ms. Rapid pacing or cardioversion is usually required when the cycle length is less than 300 ms. Although procainamide slows tachycardia, it can unpredictably make termination more difficult in 1 of 4 patients.

Adolescent↗

Termination of ventricular tachycardia with ventricular stimulation: salutary effect of increased current strength.

The effect of increased stimulus current strength on the right ventricular effective refractory period during sustained ventricular tachycardia and on the ability of single premature right ventricular stimuli to terminate ventricular tachycardia was evaluated. Studies were performed during 53 episodes of sustained ventricular tachycardia in 25 patients. Forty-four of 53 episodes were slowed by pharmacologic therapy. Current intensities of twice diastolic threshold, 5 mA and 10 mA were used. Increasing current from twice diastolic threshold (1.52 +/- 0.66 mA) to 5 mA (32 episodes) shortened the mean ventricular effective refractory period from 213 +/- 50 to 188 +/- 43 msec (p less than 0.001); and from twice diastolic threshold (1.53 +/- 0.60 mA) to 10 mA (42 episodes), from 206 +/- 55 to 176 +/- 50 msec (p less than 0.001). There was a direct correlation between cycle length of ventricular tachycardia and the ventricular effective refractory period measured at twice diastolic threshold (r = 0.77, p less than 0.001). However, the cycle length of ventricular tachycardia and the amount of shortening of ventricular effective refractory period as current was increased were not significantly correlated (r = 0.40). Eleven episodes of ventricular tachycardia (21%) that could not be terminated by ventricular stimulation at twice diastolic threshold were terminated when increased current strength was used. The ability to terminate ventricular tachycardia was associated with a decrease in ventricular effective refractory period and long tachycardia cycle length. The mean cycle length of the 11 episodes terminated was 455 +/- 50 msec, compared with 381 +/- 63 msec in the 42 episodes not terminated at increased current.

Adult↗

Anatomic and electrophysiologic correlates of ventricular tachycardia requiring left ventricular stimulation.

In 108 patients with reproducible initiation of ventricular tachycardia by programmed ventricular stimulation, the ventricular tachycardia was initiated only by left ventricular stimulation in 12 (11 percent). Programmed ventricular stimulation included single and double extrastimuli extrastimuli at three cycle lengths and bursts of rapid pacing to cycle lengths of 250 ms. Clinical, electrocardiographic, angiographic, hemodynamic and electrophysiologic data were available in 74 of 96 patients with ventricular tachycardia initiated by right ventricular stimulation (Group A) and in all 12 patients with ventricular tachycardia initiated only by left ventricular stimulation (Group B). there were no significant differences between Groups A and B in clinical characteristics, hemodynamics or presence and site of infarction or aneurysm. Comparison of electrophysiologic variables revealed no significant differences between Groups A and B mean A-H interval (92 +/- 22 versus 89 +/- 15 ms, respectively), H-V interval (59 +/- 15 versus 59 +/- 15 ms) or right ventricular (241 +/- 38 versus 260 +/- 40 ms) or left ventricular (232 +/- 28 versus 251 +/- 42 ms) effective refractory period. Ventricular tachycardia with right bundle branch block and superior axis was more prevalent in Group B (92 percent versus 31 percent, p less than 0.001) but was observed in 32 patients in Group A. It is concluded that 11 percent of patients with clinically documented sustained ventricular tachycardia will require left ventricular programmed stimulation to reproducibly initiate the tachycardia. No clinical, anatomic, electrocardiographic or electrophysiologic features can predict whether left ventricular programmed stimulation will be required. Because initiation of ventricular tachycardia by programmed ventricular stimulation has important prognostic and therapeutic implications in such patients, stimulation should be performed from the left ventricle when the tachycardia is not initiated by stimulation from the right ventricle.

Adolescent↗

Potential arrhythmogenic electrophysiological derangements in canine Purkinje fibers induced by lysophosphoglycerides.

We have recently detected accumulation of lysophosphoglycerides, catabolites of phospholipids, in ischemic myocardium early after coronary occlusion. In the present study we delineated effects of selected concentrations of albumin-bound lysophosphatidyl choline (LPC) comparable to those accompanying ischemia in vivo on action potentials of isolated canine Purkinje fibers. Lysophosphoglycerides induced concentration-dependent (0.75-3.0 mM) decreases in resting membrane potential, overshoot of phase 0, maximal velocity of upstroke (Vmax) of phase 0, and action potential duration. The highest concentrations (2.0-3.0 mM) induced fractionation of the action potential into several components, unresponsiveness to external stimulation, and enhanced automaticity at normal and reduced membrane potentials. LPC induced a rightward shift in the membrane response curve, a 40-fold prolongation of conduction time, and an increase in the ratio of effective refractory period to action potential duration such that the effective refractory period persisted beyond action potential duration, resulting in postrepolarization refractoriness. These electrophysiological alterations were entirely reversible after 70 minutes of perfusion without LPC, with the exception of a persistent depression in the Vmax of phase 0. Lysophosphatidyl ethanolamine (LPE) elicited alterations in action potentials indentical to those elicited by LPC. Furthermore, LPC (3.0 mM) induced comparable alterations in action potentials recorded from isolated rabbit papillary muscles. Since lysophospholipids accumulate early after myocardial ischemia, and since concentrations equivalent to those occurring in vivo induce electrophysiological alterations resembling those seen in ischemic myocardium in vivo, lysophosphoglycerides may be of major importance as biochemical mediators of malignant dysrhythmia induced by ischemia.

Action Potentials↗