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Biomedical subjects

W G Stevenson

Publications and source records attributed to W G Stevenson.

At least 127 records · Page 7Linked to original sources
PubMed1990

Selecting therapy for sustained ventricular tachycardias: importance of the sensitivity and specificity of programmed electrical stimulation for predicting arrhythmia recurrences.

Antiarrhythmic therapy for prevention of sustained ventricular tachycardia is commonly guided by programmed electrical stimulation, and the persistent ability to initiate ventricular tachycardia during drug therapy often leads to the use of nonpharmacologic therapies such as surgery. Prior studies suggest that programmed stimulation has a high sensitivity but a lower specificity for predicting recurrences of ventricular tachycardia during drug therapy. We constructed a model to evaluate the impact of various programmed stimulation specificities and sensitivities on total mortality when patients with inducible ventricular tachycardia during drug therapy proceed to arrhythmia surgery. Assumptions for this model included an 11.5% surgical mortality, a 13% risk of arrhythmia recurrence for surgery survivors, and that 33% of ventricular tachycardia recurrences are fatal. In this model the relative impact of test sensitivity and specificity on total population mortality depended on the pretest probability that drug therapy would be effective. When this probability was high, variations in test sensitivity had relatively little impact on mortality, but a low specificity increased mortality by increasing the number of false positive patients treated surgically who then suffered the surgical mortality. When the probability of effective drug therapy was low, varying test specificity had relatively little impact on mortality, but a low sensitivity increased mortality by increasing the number of patients with a false negative test who suffered fatal arrhythmia recurrences. If the specificity of programmed stimulation is low and the probability that drug therapy will be effective is high, the total population mortality can exceed the mortality expected from drug therapy alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed1990

Facioscapulohumeral muscular dystrophy: evidence for selective, genetic electrophysiologic cardiac involvement.

Facioscapulohumeral muscular dystrophy is an autosomal dominant disorder with an incidence of 3 to 10 cases per million. The only type of cardiac involvement ascribed to this neuromuscular disorder is a unique form of heart disease--permanent atrial paralysis. However, reported cases of facioscapulohumeral muscular dystrophy probably represented instead what is now recognized as phenotypically similar Emery-Dreifuss dystrophy. Cardiac involvement, therefore, has not been convincingly reported in facioscapulohumeral muscular dystrophy, but because of the clinical similarity of that disorder to Emery-Dreifuss dystrophy and its genetic variants, a prospective investigation of the electrophysiologic properties of the atria and atrioventricular (AV) node and infranodal conduction was undertaken in 30 rigorously documented cases of facioscapulohumeral muscular dystrophy. All patients had a 12 lead surface electrocardiogram (ECG), 22 had a 24 h ambulatory ECG, 15 patients had two-dimensional echocardiographic/Doppler studies and 10 patients underwent 12 intracardiac electrophysiologic investigations. Left atrial, right atrial or biatrial P wave abnormalities were present in 60% of the surface ECGs. Evidence of abnormal AV node or infranodal conduction was present on intracardiac electrophysiologic study or surface ECG in 27% of patients. Atrial flutter or fibrillation was induced by single atrial extra stimuli in 10 of the 12 intracardiac electrophysiologic studies. Sinus node function was abnormal in three patients. This investigation provides the first secure evidence of cardiac involvement in facioscapulohumeral muscular dystrophy. The involvement is represented by relatively high susceptibility to induced atrial flutter or fibrillation during electrophysiologic study, together with less frequent evidence of abnormal sinus node function and abnormal AV node or infranodal conduction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Effects of filtering on right ventricular electrograms recorded from endocardial catheters in humans.

Criteria for identifying electrically abnormal myocardium based on analysis of electrogram, amplitude, duration, and morphology have recently been proposed as an aid to catheter mapping in humans. Electrogram characteristics are likely to be influenced by analog filtering and the distance between recording electrodes. These parameters can be varied and differ among electrophysiology laboratories. To determine the magnitude of the effect of low pass and high pass filtering and interelectrode distance on human bipolar right ventricular electrograms eight patients were studied. The signal from a single bipolar electrode pair was recorded simultaneously on five channels with variable filtering. As the high pass filter frequency increased above 10 Hz, the electrogram duration and amplitude decreased. The decrease in amplitude was described by a monoexponential function with a 30% decrease in amplitude at a filter setting of 30 Hz and a 69% decrease at a filter setting of 100 Hz. As the low pass filter frequency decreased from 2,500 to 250 Hz, electrogram characteristics were not significantly altered. Low pas filtering at 100 Hz decreased electrogram amplitude slightly. Neither high nor low pass filter settings or interelectrode distance affected electrogram timing. However, filtering could markedly alter electrogram morphology, introducing the possibility for errors in visual assessment of electrograms. Electrogram duration increased linearly with increasing distance between recording electrodes. The effects of filtering on electrograms were similar regardless of interelectrode spacing. Thus, varying the high pass filter setting over a range that is used clinically (from 1 to 100 Hz) can substantially alter electrogram duration, amplitude, and morphology. Low pass filtering at 250 Hz and above had no effect on these electrograms although it is possible that alterations would be observed in signals from areas of slow conduction that we did not study.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Linking: a mechanism of intermittent preexcitation in the Wolff-Parkinson-White syndrome.

Intermittent preexcitation in the Wolff-Parkinson-White syndrome has been equated with a long accessory pathway refractory period and long R-R interval between preexcited beats in atrial fibrillation and therefore a low risk for sudden death. A case of Wolff-Parkinson-White syndrome in which preexcitation became intermittent following procainamide infusion, with only moderate prolongation of the accessory pathway refractory period but marked prolongation of the shortest preexcited R-R interval in atrial fibrillation, is described. Programmed ventricular and atrial stimulation demonstrated that intermittent preexcitation was caused by concealed conduction producing a linking phenomenon, facilitated by the antiarrhythmic drug. Linking due to concealed retrograde penetration of a propagated impulse into the accessory pathway may contribute to the disparity between accessory pathway refractory period and shortest preexcited R-R interval in atrial fibrillation in some patients and may be a confounding factor in the interpretation of noninvasive tests of accessory pathway conduction.

Adolescent↗
PubMed1990

Frequency-dependent effects of quinidine on the ventricular action potential and QRS duration in humans.

We studied the frequency-dependent effects of quinidine on the right ventricular action potential and QRS duration in 10 patients (nine men and one woman; mean age, 57 +/- 14 years) undergoing electrophysiologic studies for clinical indications. The right ventricular monophasic action potential, electrocardiographic, and conventional intracardiac electrical signals from various sites were recorded at different pacing cycle lengths from 30 seconds to 1 minute before and after a 10-mg/kg i.v. quinidine infusion. We used the extrastimulus technique to determine the effects of quinidine on ventricular refractory periods at different pacing cycle lengths and on the abrupt changes of the action potential duration. The action potential duration progressively decreased as the ventricular pacing rate increased at baseline and after quinidine infusion. Quinidine significantly increased the action potential duration from that of control by 25 msec (p less than 0.02) at the relatively slow pacing cycle lengths of 600, 500, and 400 msec. Quinidine's effect on the action potential duration was attenuated at the pacing cycle length of 350 msec and became negligible at 300 msec. In contrast, quinidine progressively lengthened the QRS duration as the pacing rate increased (20, 18, 37, 46, and 34 msec at pacing cycle lengths of 600, 500, 400, 350, and 300 msec, respectively; p less than 0.05). There were no rate-dependent changes in the QRS duration during the control period. The relation between the ventricular refractory periods and the action potential duration at different pacing cycle lengths was also determined before and after quinidine infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1990

Noninvasive identification of patients at risk for ventricular tachycardia with the signal-averaged electrocardiogram.

The signal-averaged electrocardiogram (SAE) is a noninvasive means of detecting cardiac late potentials. Late potentials in patients with coronary artery disease indicate a high risk for the development of ventricular tachycardia. Although the usefulness of the SAE for directing therapy has not yet been clearly established, the test appears to be useful in the stratification of arrhythmia risk in select groups of high-risk patients. As critical care nurses frequently care for these patients, they need to be familiar with tools such as the SAE that may be used in high-risk patient assessment. This article describes the physiologic basis underlying the use of the SAE, the SAE technique, implications for nursing practice, and clinical applications of the SAE.

Arrhythmias, Cardiac↗
PubMed1989

The spectrum of death after myocardial infarction: a necropsy study.

To determine the relative frequency of the causes of death in the acute (less than 24 hours), early (24 hours to 3 weeks), and chronic (greater than 3 weeks) phases of myocardial infarction, data from all autopsies performed at a university hospital during a 56-month period were reviewed. Autopsies were performed in 56% of in-hospital deaths and 27% of patients dead on arrival in the emergency room (out-of-hospital deaths). In 271 cases of suspected cardiac death, a myocardial infarction of any age was identified. Death had occurred in the acute phase of a first infarction in 19 patients and was most frequently due to pump failure (37%) followed by cardiac rupture (26%) and arrhythmias (21%). Death had occurred 24 hours to 3 weeks after a first infarction in 80 patients and was most frequently due to pump failure (44%), rupture (27%), and arrhythmias (16%). Recurrent acute infarction was found in 32% of patients whose deaths were due to arrhythmias or pump failure and in 19% of those whose deaths were due to rupture. Death had occurred greater than 3 weeks after a first infarction in 172 patients. In 132 (77%) of these patients death was due to a complication of a new acute or recent infarction. Myocardial rupture was a less frequent cause of death in patients with recurrent infarction (8%) than in those dying in the acute or early phase after their first infarction (27%, p = 0.0009). A primary arrhythmia in the absence of recurrent infarction or ischemia accounted for only 14% of out-of-hospital deaths late after an infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

Is the adaptation of right ventricular refractoriness to an abrupt increase in heart rate impaired in chronic heart failure?

Chronic heart failure is associated with a high risk of ventricular arrhythmias and sudden death, although the mechanisms leading to these arrhythmias are not fully understood. To determine if the adaptation of ventricular refractoriness to an abrupt increase in heart rate is impaired in heart failure, electrophysiologic findings in 11 patients with structurally normal hearts (group I) were compared to findings in 28 patients with chronic heart failure (mean left ventricular ejection fraction 0.23 +/- 0.05). Heart failure was due to coronary artery disease in 14 patients (group II) and to idiopathic dilated cardiomyopathy in 14 patients (group III). The effective refractory period at the right ventricular apex was measured during unipolar cathodal pacing at twice diastolic threshold following a 12-beat ventricular drive at a cycle length of 600 msec. The pacing cycle length was then decreased to 400 msec for one, two, and three beats and the refractory period was determined for each beat at the faster rate. For each beat the mean refractory periods of group II and III patients were similar and were significantly longer than those of group I patients (p less than 0.01). The refractory period progressively shortened at the 400 msec cycle length and the percent decrease for each beat was similar among all three groups (p greater than 0.10). In the group II and III patients there was no correlation of the refractory period or change in refractory period with the pulmonary artery, right atrial, and pulmonary capillary wedge pressures.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Fractionated endocardial electrograms are associated with slow conduction in humans: evidence from pace-mapping.

Fractionated ventricular electrograms recorded during catheter mapping may arise from areas of asynchronous depolarization associated with slow conduction, the substrate for reentrant ventricular tachycardia, but can also be a nonspecific abnormality or even artifact. To determine whether fractionated sinus rhythm electrograms are associated with slow conduction in humans, the results of endocardial catheter mapping and pacing at 133 endocardial sites in 13 patients were analyzed. Eleven patients had sustained monomorphic ventricular tachycardia and two patients had old myocardial infarction without ventricular tachycardia. Functional evidence of slow conduction at the recording site was assessed by pacing at that site and measuring the interval between the stimulus artifact (S) and the onset of the QRS complex in the 12 lead electrocardiogram (ECG). During pacing at 89 of 90 sites without fractionated sinus rhythm electrograms, the S-QRS interval was less than 40 ms, a value consistent with rapid propagation of the stimulated wave front away from the pacing site. During pacing at 21 (49%) of 43 sites with fractionated sinus rhythm electrograms, the S-QRS interval was greater than 40 ms (range 40 to 140), consistent with slow conduction at the pacing site (p less than 0.001 versus nonfractionated sites). In 9 of the 11 patients with ventricular tachycardia analysis of the paced QRS configuration, electrograms during induced ventricular tachycardia or programmed stimulation during tachycardia suggested that a site with a long S-QRS interval during pacing was located at or near a ventricular tachycardia circuit. Therefore, fractionated sinus rhythm electrograms are often associated with slow conduction, which may be the substrate for reentrant ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Programmed electrical stimulation at potential ventricular reentry circuit sites. Comparison of observations in humans with predictions from computer simulations.

The purpose of this study was to define specific types of resetting responses to programmed electrical stimulation during human ventricular tachycardia and to use computer simulations of reentry circuits to assess the possible mechanisms and pacing site location relative to the reentry circuit for each type of response. The effects of scanning single stimuli at 35 left ventricular endocardial sites during sustained monomorphic ventricular tachycardia in 12 patients were studied. In considering alterations in QRS configuration and the delay between the stimulus and the advanced QRS, we identified three types of resetting responses to scanning stimuli consistent with stimulation at sites in or near the reentry circuit at 12 abnormal endocardial sites in eight patients. Type 1: all capturing stimuli were followed after a delay by early QRS complexes that had the same configuration as the tachycardia complexes. Type 2: late stimuli reset tachycardia as in type 1 but early stimuli reset the tachycardia after altering the QRS configuration. Type 3: late stimuli reset tachycardia as in type 1, but early stimuli advanced tachycardia with a short stimulus to QRS delay without altering the QRS configuration. In the simulations, premature depolarization of sites in the circuit produced orthodromic and antidromic wavefronts. The orthodromic wavefront propagated through the circuit and exited the circuit at the same site as did the previous tachycardia wavefronts and advanced the tachycardia without altering the configuration of the advanced QRS. The antidromic wavefront of relatively late stimuli was confined within or near the circuit by collision with the orthodromic wavefront of the preceding tachycardia beat and failed to alter ventricular activation distant from the circuit. Therefore, the QRS configuration after the stimulus was unchanged. A type 1 response occurred when all capturing stimuli produced this effect. However, with increasing stimulus prematurity, the antidromic wavefront propagated farther before colliding with an orthodromic wavefront, and under some conditions, it exited the circuit from a site other than the original circuit "exit," and altered the ventricular activation sequence distant from the circuit and, therefore, the QRS configuration, producing a type 2 pattern. The type 3 pattern occurred when the antidromic wavefront of early premature beats captured the original circuit exit. The effect of a stimulus was dependent on the stimulus prematurity, the relative conduction times from the stimulation site to the potential sites of "exit" from the circuit, and the timing of the excitable gap at the stimulation site.(ABSTRACT TRUNCATED AT 400 WORDS)

Cardiac Pacing, Artificial↗
PubMed1989

Diverse mechanisms of unexpected cardiac arrest in advanced heart failure.

To define the mechanisms of unexpected cardiac arrest in advanced heart failure, we reviewed the causes of cardiac arrest as established from electrocardiographic monitoring and from clinical and autopsy data in patients hospitalized for cardiac transplantation evaluation and management of advanced heart failure (mean left ventricular ejection fraction, 0.18 +/- 0.08) who were stable while on vasodilator and diuretic therapy such that hospital discharge to home was anticipated. Twenty-one cardiac arrests occurred in 20 of 216 (9%) such patients during a 4-year period. Heart failure was due to coronary artery disease with prior myocardial infarction in 13 patients and nonischemic cardiomyopathy in seven patients. The rhythm at the time of arrest was severe bradycardia or electromechanical dissociation (BA/EMD) in 13 (62%) patients. The precipitating cause of the BA/EMD arrest was coronary artery thrombosis or embolism in two patients, pulmonary embolism in one patient, hyperkalemia in two patients, and unexplained hypoglycemia in one patient. In seven of 13 (54%) patients, a precipitating cause of the bradycardia arrest could not be established. Only eight of 21 (38%) arrests were due to ventricular tachycardia or fibrillation (VT/VF), and all occurred in patients with prior myocardial infarction (p = 0.02 vs. BA/EMD arrests). Two VT/VF arrests were due to acute or recent infarction, and one patient had hyperkalemia. The patients who suffered a BA/EMD arrest were similar to those who had a VT/VF arrest in age, ventricular arrhythmia history, ventricular function, and serum potassium levels. Serum sodium levels were lower in patients with BA/EMD arrests (129 +/- 3 vs. 133 +/- 4 meq/l, p = 0.025).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Complicated atherosclerotic lesions: a potential cause of ischemic ventricular arrhythmias in cardiac arrest survivors who do not have inducible ventricular tachycardia?

Sudden cardiac death that is not due to acute myocardial infarction may be due to primary ventricular tachycardia or to an arrhythmia secondary to a transient episode of ischemia. The purpose of this study was to determine if the incidence of complicated coronary lesions, which may be a cause of unstable ischemic syndromes, is increased in survivors of an aborted sudden death, especially those without ventricular tachycardia inducible by programmed ventricular stimulation. Nineteen consecutive survivors of an aborted sudden death not due to an acute infarction who underwent coronary angiography and programmed ventricular stimulation within 3 weeks of the event were matched for age, sex, previous infarction, and severity of coronary artery disease with 38 control patients with stable coronary artery disease. There was no difference in the incidence of complicated coronary lesions between the total group of sudden death victims and controls (47% vs 42%). However, 6 of the 11 (64%) sudden death patients who did not have inducible ventricular tachycardia had a complicated lesion as compared to only two of the eight (25%) patients with inducible ventricular tachycardia (p = 0.10). Angiograms identified a complicated lesion or functioning myocardium supplied only by collateral vessels as possible sources of transient ischemia in 73% of noninducible sudden death patients and in 25% of inducible sudden death patients (p = 0.04). Thus coronary angiography in cardiac arrest survivors who do not have inducible ventricular tachycardia often suggests a possible mechanism of transient ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1988

Inducible ventricular arrhythmias and sudden death during vasodilator therapy of severe heart failure.

Sudden death is common in patients with severe heart failure, but antiarrhythmic drug therapy has potential risks as well as benefits. Programmed electrical stimulation may offer a means of identifying lower risk patients who are less likely to benefit from antiarrhythmic therapy and who could potentially be spared the risk of adverse drug effects. Therefore 72 consecutive patients referred for management of severe heart failure (left ventricular ejection fraction 0.18 +/- 0.06) were studied. The mean age was 47 +/- 12 years; 45 (61%) patients had idiopathic dilated cardiomyopathy and 24 (33%) had coronary artery disease. Fifty-eight (82%) patients had nonsustained ventricular tachycardia. Following adjustment of vasodilators and diuretics, programmed stimulation was performed from the right ventricular apex with one, two, and three extrastimuli. Sustained ventricular tachycardia was initiated in nine (13%) patients and all received chronic antiarrhythmic drug therapy. During follow-up of 176 +/- 187 days, 1 of 13 patients treated for inducible ventricular tachycardia and 13 of 63 noninducible patients died suddenly (p = 0.20). The actuarial risk of sudden death in the noninducible patients was 13% at 6 weeks and 30% at 6 months. The only independent predictors of sudden death were pulmonary artery systolic pressure greater than 55% mm Hg and a pulmonary capillary wedge pressure with vasodilator therapy greater than 16 mm Hg. Of the 63 noninducible patients, 11 (17%) received long-term antiarrhythmic agents due to atrial fibrillation or referring physician preference, and antiarrhythmic therapy was not associated with a lower risk of sudden death in these patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Resetting of ventricular tachycardia: implications for localizing the area of slow conduction.

Analysis of local endocardial electrograms recorded during reentrant ventricular tachycardia does not provide direct information as to the participation of the recording site in the tachycardia circuit. To determine if programmed electrical stimulation at the recording site can assist in localizing areas of slow conduction that are participating in the tachycardia circuit, seven patients with sustained monomorphic ventricular tachycardia were studied. The cardiac cycle was scanned with single stimuli delivered during ventricular tachycardia at multiple endocardial sites. In four patients, an endocardial site was identified at which stimuli advanced the tachycardia with marked conduction delay and without alteration of the ventricular activation sequence, as indicated by a lack of change in the configuration of the QRS complex and endocardial electrograms distant from the stimulation site. This finding was seen only during stimulation at sites displaying abnormal electrograms and is consistent with premature depolarization of an area of slow conduction within the tachycardia focus by stimuli delivered at or near that area. Attempted endocardial catheter ablation at or adjacent to these sites in three patients was followed by persistent noninducibility of ventricular tachycardia in one patient, marked modification of the configuration and cycle length of inducible tachycardia in one patient and transient noninducibility of tachycardia in one patient. Programmed electrical stimulation during ventricular tachycardia at sites with abnormal electrograms may provide information about the proximity of the stimulation site to the tachycardia circuit.

Aged↗