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Biomedical subjects

W G Stevenson

Publications and source records attributed to W G Stevenson.

At least 145 records · Page 8Linked to original sources

Limitations of bipolar and unipolar conditioning stimuli for inhibition in the human heart.

Noncapturing, conditioning electrical stimuli (Sc) delivered within the ventricular refractory period can prolong refractoriness and prevent later stimuli from eliciting a propagated response (inhibition). The purpose of this study was to further define the spatial effects of Sc, to determine if the effects of Sc can be enhanced by the use of unipolar as opposed to bipolar stimulation, and to evaluate the effect of Sc on the physiologic spread of excitation during atrioventricular reentry tachycardia. In 23 patients the right ventricular refractory period was determined before and after the introduction of bipolar, unipolar cathodal, and unipolar anodal noncapturing Sc with pulse widths of 2 or 9 msec and strengths of twice diastolic threshold and 10 MA. Pacing and conditioning stimuli were delivered at the same site and at sites separated by 3 mm. During ventricular pacing both bipolar and unipolar Sc prolonged the ventricular refractory period by greater than or equal to 10 msec in 22 of 23 patients when both Sc and pacing stimuli were delivered to the same site. However, when Sc was delivered 3 mm away from the pacing stimuli, the ventricular refractory period increased by greater than or equal to 10 msec in only 1 of 17 patients who received bipolar Sc and in none of 13 patients who received unipolar Sc. In seven patients bipolar conditioning stimuli were delivered as close as possible to the atrial insertion of an accessory atrioventricular connection during circus movement tachycardia with a well-localized accessory pathway. Sc did not terminate or slow tachycardia in any patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Effect of spatial separation of stimulation sites on ventricular refractoriness during programmed electrical stimulation.

To determine if electrical stimulation during the basic ventricular drive train introduces local effects that influence ventricular refractoriness during endocardial stimulation in humans, 10 patients were studied. With a hexapolar catheter with 3 mm interelectrode distances positioned at the right ventricular apex, the ventricular functional and effective refractory periods were determined for unipolar cathodal stimuli of 2 and 5 times diastolic threshold. Stimulation was performed with both the scanning extrastimulus (S2) and basic ventricular drive stimuli (S1) delivered to the same site and to sites separated by 6 mm. The functional refractory period was not changed by delivering the basic drive and extrastimuli to the same as opposed to separate sites (273.5 +/- 16 vs 273.5 +/- 19 msec during stimulation at 2 times threshold and 270 +/- 16 vs 270 +/- 18 msec at 5 times threshold; p = NS). The longest S1-S2 interval at which S2 failed to capture (effective refractory period) was longer by 5.5 +/- 8.2 msec at twice threshold (0.05 less than p less than 0.10) and 5.5 +/- 3.5 msec at 5 times threshold stimulation (p less than 0.01) when the basic drive and extrastimuli were delivered to separate sites. This is consistent with later activation of the extrastimulus sites during the basic drive when the stimulation sites were separate. Thus, with this method of endocardial programmed electrical stimulation, separation of the stimulation sites for the basic drive and extrastimuli does not affect ventricular refractoriness determined by the extrastimulus technique.

Adult↗

Poor survival of patients with idiopathic cardiomyopathy considered too well for transplantation.

Although the success of cardiac transplantation has encouraged earlier referral of potential candidates, those with mild symptoms of heart failure are frequently considered "too well" for transplantation. Outcome was investigated for 28 patients with non-ischemic dilated cardiomyopathy and ejection fraction of 25 percent or less who were denied transplantation due to lack of severe symptoms. One-year survival without transplantation was 46 percent. Low stroke volume and history of ventricular arrhythmias were independent predictors of early mortality. High risk, defined as either stroke volume of 40 ml or less or history of ventricular arrhythmia, identified 13 of 14 patients who did not survive one year and only one of 12 one-year survivors (p less than 0.001). Low stroke volume predicted hemodynamic failure (p less than 0.05) whereas arrhythmic history predicted sudden death (p less than 0.001). Clinical status improved in only six patients, all of whom had symptom duration of seven or less months at initial evaluation (p less than 0.001). Thus, patients referred to transplantation for dilated cardiomyopathy with an ejection fraction of 25 percent or less have a poor prognosis even if symptoms are mild. Patients with high hemodynamic risk may require early transplantation, whereas those with high arrhythmia risk may require other aggressive therapy in order to avoid transplantation until symptoms become severe.

Cardiomyopathy, Dilated↗

Enhancement of conduction in an accessory pathway by local noncaptured stimuli.

Subthreshold stimuli have been reported to prolong the refractory period of myocardial tissue. This report presents the first case of reproducible acceleration of a reentrant tachycardia by apparently subthreshold stimuli delivered to the os of the coronary sinus during the atrial refractory period in a child with incessant orthodromic tachycardia utilizing a posteroseptal pathway. Mechanisms by which these stimuli could influence the tachycardia circuit are proposed, and the potential usefulness of this finding for mapping tachyarrhythmias is discussed.

Cardiac Pacing, Artificial↗

Contribution of the anode to ventricular excitation during bipolar programmed electrical stimulation.

Anodal excitation may contribute to the initiation of ventricular arrhythmias during bipolar pacing in the canine ventricle. To determine if anodal excitation occurs during bipolar programmed ventricular stimulation in humans, ventricular electrograms adjacent to the anode and cathode were recorded using a specially designed hexapolar electrode catheter in 10 patients. Single extrastimuli were delivered during ventricular pacing at stimulus strengths slightly above the late diastolic threshold and at 2 to 5 times late diastolic threshold. Evidence of anodal excitation was observed in 18 of the 52 combinations (35%) of stimulus strengths and electrode configurations tested, and occurred in 9 of the 10 patients; it consisted of earliest ventricular activation adjacent to the anode (8 patients) or simultaneous activation at the anode and cathode (3 patients). This occurred either with premature stimuli (3 patients) or during the basic drive and extrastimuli (6 patients). Comparison of local activation times during unipolar pacing supported an anodal contribution to excitation during bipolar pacing and suggested that inhomogenous conduction delays were not responsible for these findings. Thus, anodal excitation occurs frequently during bipolar programmed stimulation and produces marked changes in local myocardial activation, which may potentially influence the initiation of ventricular arrhythmias.

Adult↗

Electrophysiologic characteristics of ventricular tachycardia or fibrillation in relation to age of myocardial infarction.

Evaluation of ventricular myocardium after the onset of acute myocardial infarction (AMI) suggests that the substrate for ventricular arrhythmias changes as the substrate for ventricular arrhythmias changes as the AMI heals. To determine if the ability of programmed stimulation to initiate ventricular tachycardia (VT) varies according to the interval between AMI and electrophysiologic testing, the clinical and electrophysiologic data of 42 patients with spontaneous sustained VT and 12 patients with ventricular fibrillation (VF) more than 3 days after a single AMI were analyzed. For patients with VT, there were no significant differences in the incidence of initiation of sustained monomorphic VT among those evaluated 1 to 3 weeks (100%), 3 to 8 weeks (75%), 2 to 6 months (100%), 6 to 18 months (80%) or more than 18 months (81%) after AMI, and the mean number of extrastimuli required for initiation did not differ among the groups. Patients evaluated more than 4 weeks after the initial episode of VT had a lower incidence of inducible VT than those studied earlier (14 of 21 [71%] vs 21 of 21 [100%], p less than 0.05), although this appeared to be a result of earlier termination of the stimulation protocol owing to initiation of polymorphic arrhythmias in those studied later. The 14 patients evaluated within 8 weeks of AMI had significantly faster VT rates (mean cycle length 269 +/- 45 ms) than the 28 patients studied later (320 +/- 75 ms, p less than 0.01), possibly because of more out-of-hospital presentations of VT in patients studied later.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Can potentially significant polymorphic ventricular arrhythmias initiated by programmed stimulation be distinguished from those that are nonspecific?

Polymorphic ventricular arrhythmias (PVAs) initiated by programmed electrical stimulation may be a nonspecific response or evidence of ventricular electrical instability. To determine if PVAs initiated in patients with spontaneous sustained ventricular tachycardia or fibrillation differ from those which are clearly a nonspecific response in structurally normal hearts, the initiation, characteristics, and relationship to ventricular repolarization of PVAs greater than five beats in duration were evaluated in 32 patients without structural heart disease and in 36 patients with spontaneous sustained ventricular arrhythmias more than 9 days after myocardial infarction. Patients received one to four extrastimuli during sinus rhythm and right ventricular pacing. In a comparison with patients who completed the same steps (defined by the basic drive cycle length and number of extrastimuli) in the stimulation protocol, there was no difference in the cumulative risk of initiation of a PVA between the patients with and those without heart disease at any step. This risk was 51% vs 38% for patients who received two or fewer extrastimuli at four basic cycle lengths (p = NS). PVAs were initiated by the same mean number of extrastimuli (2.3 +/- 0.5 vs 2.6 +/- 0.9 p NS) with the same degree of prematurity in both groups. Forty-four percent of the PVAs in the myocardial infarction group had a cycle length greater than 250 msec or a coupling interval of the first tachycardia beat to its initiating stimulus greater than 320 msec as opposed to only one (6%) in the group without heart disease (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Effects of early reperfusion in acute myocardial infarction on arrhythmias induced by programmed stimulation: a prospective, randomized study.

This study compares inducibility of ventricular tachyarrhythmias by programmed electrical stimulation of the heart in patients with myocardial infarction with and without reperfusion after streptokinase therapy. Sixty-two consecutive patients admitted with an acute myocardial infarction were randomized to either combined intravenous and intracoronary streptokinase (streptokinase group) or to standard coronary care unit treatment (control group). Thirty-six of the 62 patients (21 patients from the streptokinase and 15 from the control group) with a first myocardial infarction were studied by programmed ventricular stimulation after a mean of 26 +/- 14 days. No patient had a history of antiarrhythmic drug use or documentation of a ventricular arrhythmia before the initial admission. A sustained ventricular arrhythmia was induced in 10 (48%) of the 21 patients randomized to streptokinase therapy and in all 15 (100%) control patients (p less than 0.001). Sustained monomorphic ventricular tachycardia was induced in 6 (29%) and 10 (67%) patients, respectively (p less than 0.05). To terminate an induced arrhythmia, direct current countershock was required in 33% of patients in the streptokinase group and 73% of patients in the control group (p less than 0.02). Seventeen of the 21 patients treated with streptokinase and no control patient had evidence of early reperfusion 200 +/- 70 minutes after the onset of pain. In comparison with patients without early reperfusion, patients in the reperfused group had a lower maximal serum creatine kinase value (p less than 0.01), a shorter time to peak creatine kinase value (p less than 0.001) and a higher angiographic left ventricular ejection fraction (62 versus 45%, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Comparison of bipolar and unipolar programmed electrical stimulation for the initiation of ventricular arrhythmias: significance of anodal excitation during bipolar stimulation.

To determine if anodal excitation during bipolar stimulation facilitates the initiation of sustained monomorphic ventricular tachycardia, nonsustained polymorphic ventricular tachycardia, or repetitive ventricular responses, both bipolar and cathodal unipolar programmed ventricular stimulation with one to three extrastimuli delivered during ventricular pacing at two rates from the right ventricular apex were performed in 28 patients evaluated for spontaneous sustained ventricular tachycardia or ventricular fibrillation (11 patients), nonsustained tachycardia (eight patients), or syncope (nine patients). In 25 patients a hexapolar pacing catheter was used to record local endocardial activation times adjacent to the cathode and anode and ventricular excitation during bipolar stimulation was defined as predominantly anodal, cathodal, or simultaneous at both anode and cathode. When bipolar and unipolar stimulation were compared there was no difference in the incidence of initiating sustained monomorphic ventricular tachycardia (57% vs 57%), nonsustained polymorphic ventricular tachycardia (14% vs 14%), or repetitive ventricular responses (21% vs 21%), although the response to bipolar vs unipolar stimulation was not concordant in every patient. Evidence of anodal excitation was observed in 11 (44%) patients but did not indicate increased risk of initiation of any ventricular arrhythmia, despite the fact that it was associated with shortening of the ventricular effective refractory period by 5.2 +/- 8.7 msec (p less than .05) during bipolar as opposed to unipolar stimulation. We conclude that unipolar and bipolar stimulation produce a similar incidence of initiation of arrhythmia, despite the frequent occurrence of anodal excitation during bipolar stimulation. Thus, the risk of initiation of nonspecific ventricular arrhythmias during programmed stimulation is unlikely to be reduced by the use of unipolar stimulation.

Adolescent↗

Torsades de pointes due to n-acetylprocainamide.

A 66-year-old female with chronic renal failure received five doses of procainamide and developed marked QT interval prolongation and recurrent episodes of torsades de pointes, which were temporally related to high serum n-acetylprocainamide (NAPA) levels and not to procainamide levels. Repeated hemodialysis was effective in lowering NAPA levels. Torsades de pointes is a potential hazard of NAPA accumulation during procainamide administration to patients with renal insufficiency.

Acecainide↗

Clinical, angiographic, and electrophysiologic findings in patients with aborted sudden death as compared with patients with sustained ventricular tachycardia after myocardial infarction.

After the acute phase of myocardial infarction, patients who develop sustained ventricular arrhythmias present with either sudden death or ventricular tachycardia (VT). Although current evidence suggests that VT frequently precedes ventricular fibrillation (VF) in patients presenting with sudden death, the factors resulting in rapid deterioration of VT to VF have not been delineated in humans. To determine whether left ventricular function, coronary anatomy, or electrophysiologic characteristics could differentiate patients with sudden death from those with VT without sudden death, we compared results of cardiac angiography and programmed electrical stimulation in 42 patients referred for evaluation of sustained VT or surviving "aborted" sudden death for more than 9 days after myocardial infarction. By univariate analysis there were no differences between patients with sudden death and those with VT in age, time from myocardial infarction to VT or sudden death, ejection fraction (0.31 +/- 0.12 vs 0.29 +/- 0.09), or the number of patients with a major area of contracting myocardium supplied by an artery with a 50% or greater or a 70% or greater stenosis (84% vs 64% and 68% vs 41%). Thirty-six percent of patients with sudden death but no patient with VT had two separate areas of infarction. During programmed electrical stimulation, a sustained ventricular arrhythmia was initiated in 100% of patients with VT and 73% of patients with sudden death and rapidly produced syncope in 67% of patients with sudden death but in only 5% of those with VT. This difference was due to the more frequent initiation of rapid polymorphic VT or VF (27% of patients) and to the shorter VT cycle length (242 +/- 31 vs 319 +/- 69 msec) when monomorphic VT was induced in the group with sudden death. No difference was found in the number of extrastimuli required for initiation of a sustained ventricular arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Cardiac involvement in myotonic muscular dystrophy (Steinert's disease): a prospective study of 25 patients.

The presence, degree and frequency of disorders of cardiac conduction and rhythm and of regional or global myocardial dystrophy or myotonia have not previously been studied prospectively and systematically in the same population of patients with myotonic dystrophy. Accordingly, 25 adults with classic Steinert's disease underwent electrocardiography, 24-hour ambulatory electrocardiography, vectorcardiography, chest x-rays, echocardiography, electrophysiologic studies, and technetium-99m angiography. Clinically important cardiac manifestations of myotonic dystrophy reside in specialized tissues rather than in myocardium. Involvement is relatively specific, primarily assigned to the His-Purkinje system. The cardiac muscle disorder takes the form of dystrophy rather than myotonia, and is not selective, appearing with approximately equal distribution in all 4 chambers. Myocardial dystrophy seldom results in clinically overt ventricular failure, but may be responsible for atrial and ventricular arrhythmias. Since myotonic dystrophy is genetically transmitted, a primary biochemical defect has been proposed with complete expression of the gene toward striated muscle tissue, whether skeletal or cardiac. Specialized cardiac tissue and myocardium have close, if not identical, embryologic origins, so it is not surprising that the genetic marker affects both. Cardiac involvement is therefore an integral part of myotonic dystrophy, targeting particularly the infranodal conduction system, to a lesser extent the sinus node, and still less specifically, the myocardium.

Adult↗

A new type of ventriculo-atrial gap phenomenon in man.

A new type of ventriculo-atrial (V-A) gap phenomenon was observed in a patient who underwent a cardiac electrophysiology study and had complete antegrade infranodal A-V block but intact V-A conduction. During ventricular extrastimulus testing, a split retrograde His potential emerged from the ventricular electrogram. As the prematurity of the extrastimulus was increased, the later of the two retrograde His deflections disappeared suddenly at a critical coupling interval and V-A conduction was interrupted. More premature extrastimuli resulted in progressive delay in the His-Purkinje system and delayed appearance of the earlier retrograde His deflection. As a result of this delay, conduction through the His bundle eventually resumed, the second (split) retrograde His reappeared and conduction to the atria resumed. Thus, the initial site of block during the V-A gap phenomenon in this patient was located in the His bundle, with proximal delay occurring in the distal His-Purkinje system. The results indicate that the classic mechanism of gap phenomenon is operative. To our knowledge, this type of V-A gap phenomenon has not been previously described in man.

Aged↗

Control of sudden recurrent arrhythmic deaths: role of amiodarone.

Patients resuscitated after out-of-hospital cardiac arrest have electrical instability of the myocardium, with 30% to 40% propensity for recurrent arrest in the first year. About 85% to 90% of such patients have complex ventricular ectopy and runs of ventricular tachycardia; in 70% to 80%, ventricular tachycardia or fibrillation are inducible by programmed electrical stimulation. The attempt to control recurrent cardiac arrest using these parameters and conventional antiarrhythmic drugs has yielded conflicting or variable results. Amiodarone was therefore studied in 40 consecutive patients (with previous cardiac arrests) in whom conventional antiarrhythmic therapy had proved ineffective or was not tolerated. The mean ejection fraction of the group was 0.29 +/- 0.12. At a mean follow-up of 16 months (range 5 to 40 months) six patients had died, three from heart failure, one from liver failure (not drug induced), and two from sudden (presumably arrhythmic) death. Late occurrences of arrhythmia were found in two patients (complicated by digitalis intoxication in one). Ambulatory ECG recordings showed that amiodarone had a potent suppressant effect on ventricular ectopy and runs of VT, but electrophysiologic studies demonstrated that it did not inhibit inducible VT/VF in greater than 65% despite an excellent clinical outcome. Limiting adverse reaction was seen in only one patient; other relatively minor side effects occurred in 10% to 15% of patients receiving maintenance therapy. Our data provide further evidence for the effectiveness of amiodarone in life-threatening ventricular arrhythmias, with a potential for the prolongation of survival in patients resuscitated after out-of-hospital cardiac arrests.

Amiodarone↗

An unusual mechanism of initiation of circus movement tachycardia in a patient with concealed Wolff-Parkinson-White syndrome.

Infranodal conduction delay is an uncommon mechanism of initiation of circus movement tachycardia in the Wolff-Parkinson-White syndrome. A patient with a concealed left free wall atrioventricular accessory pathway who underwent electrophysiological study is presented. During atrial extrastimulus testing, a pattern of alternating bundle branch block was observed and was most marked after the administration of intravenous procainamide. Conversion from right bundle branch block to left bundle branch block was reproducibly associated with the initiation of circus movement tachycardia utilizing the normal conducting system antegradely and the accessory pathway retrogradely. Initiation of tachycardia was critically related to the increase in the HV interval associated with left bundle branch block. Of interest, conduction in the right bundle branch became progressively slower as the prematurity of the atrial extrastimulus increased, whereas conduction time through the left bundle branch remained fixed prior to block. Implications of these findings are discussed. To our knowledge, this is the first report of alternating bundle branch block during atrial extrastimulus testing as a mode of initiation of circus movement tachycardia in the Wolff-Parkinson-White syndrome.

Adult↗