Endocardial and epicardial recordings. Correlation of twelve-lead electrocardiograms at the site of origin of ventricular tachycardia.
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Bundle of His↗
Biomedical subjects
M E Josephson
Publications and source records attributed to M E Josephson.
A quantitative evaluation of refractoriness within a reentrant circuit during ventricular tachycardia. Relation to termination.
Programmed ventricular stimuli introduced during sustained monomorphic ventricular tachycardia frequently reset the tachycardia, resulting in a less than fully compensatory pause. A resetting response curve is generated when the set of return cycles is evaluated as the function of the coupling intervals of the extrastimuli delivered during the ventricular tachycardia. If the stimulated wave front encounters tissue within the tachycardia circuit that is not fully recovered, interval-dependent conduction changes should occur producing an increasing resetting response pattern. We quantified the magnitude of this interval-dependent conduction slowing in 17 morphologically distinct ventricular tachycardias. The slope of the increasing limb of the resetting response curve was determined by linear regression analysis and ranged from -0.30 to -1.14 (mean +/- SD, 0.70 +/- 0.25). Seven of the 17 ventricular tachycardias (41%) terminated during introduction of ventricular extrastimuli. The slope of the resetting response pattern in those ventricular tachycardias that terminated were significantly steeper than in those that did not terminate (-0.85 +/- 0.15 versus -0.61 +/- 0.21, respectively, p = 0.025). Six of the seven ventricular tachycardias terminated with programmed ventricular stimuli had a slope steeper than -0.75, whereas only one of 10 ventricular tachycardias that did not terminate exceeded this value. In conclusion, the slope of the increasing portion of the resetting response curve correlates with ability to terminate uniform sustained ventricular tachycardia by timed extrastimuli. This slope is the quantification of the magnitude of interval-dependent conduction slowing. Additionally, tissue within the reentrant circuit displaying greater degrees of interval-dependent conduction slowing may also have relatively longer effective refractory periods.
Cardiac Pacing, Artificial↗
Current status of antitachycardia devices.
With the limitations of currently available modalities for treating clinically important tachycardias, the role of implanted antitachycardia devices will continue to expand. The challenge of the future will not only involve continued technological advances but the socioeconomic impact of this efficacious but expensive mode of therapy in an era of increasing financial restraints. Further studies to definitively prove the efficacy of more widespread use of antitachycardia device therapy will be needed.
Cardiac Pacing, Artificial↗
Differential diagnosis of supraventricular tachycardia.
We firmly believe that a systematic approach to the 12-lead ECG can provide information that can diagnose the difference between ventricular and supraventricular tachycardia, and in many instances diagnose the mechanism and site of origin of the supraventricular tachycardia. The mechanism of supraventricular tachycardia is able to be diagnosed in more than 80% of narrow complex tachycardias, and one should be able to distinguish supraventricular from ventricular tachycardia in more than 90% of tachycardias. In the presence of aberration, the mechanism of supraventricular tachycardias is more difficult to define unless retrograde P waves are seen. In such instances the morphology of the P wave (if seen), the effect of oscillation of cycle length on the RP interval, and response to vagal maneuvers may be useful in distinguishing mechanisms for ventricular tachycardia.
Bundle-Branch Block↗
Antiarrhythmic agents and the danger of proarrhythmic events.
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Anti-Arrhythmia Agents↗
Procainamide-induced slowing of ventricular tachycardia with insights from analysis of resetting response patterns.
To investigate the mechanism of slowing of the rate of ventricular tachycardias (VTs) by procainamide, resetting response patterns were characterized in 24 VTs in 22 patients. All patients had coronary artery disease and inducible sustained VT during procainamide therapy. Only tachycardias with the same surface QRS morphology before and after procainamide were studied: all were slowed by procainamide. The mean cycle length was 292 +/- 61 ms before and 374 +/- 61 ms after procainamide (p less than 0.05). The mean effective refractory period, measured at the right ventricle, was 241 +/- 21 ms before and 261 +/- 24 ms after procainamide (p less than 0.05). During procainamide therapy, single and double extrastimuli were delivered during VT and resetting response patterns identified. Patterns were characterized as flat, increasing or flat plus increasing. Resetting was seen in 17 (71%) of these VTs and resetting response patterns were identified in 16 (94%) of these. The resetting response pattern was flat in 7, flat plus increasing in 5 and increasing in 4. The finding of some flat portion at the end of resetting response patterns in 12 VTs after procainamide indicates that the reentrant impulse conducts through fully recovered tissue within the circuit. It suggests that procainamide slowed these VTs by slowing conduction velocity in fully recovered tissue due to sodium channel blockade and not by prolongation of action potentials and refractory periods.
Cardiac Pacing, Artificial↗
Sinus mapping in patients with cardiac arrest and coronary disease--results and correlation with outcome.
Electrophysiological testing and left ventricular endocardial mapping in sinus rhythm were performed in 61 patients with coronary artery disease who presented with cardiac arrest in an attempt to relate the results of these studies to clinical outcome. Forty-one patients (67%) had inducible sustained arrhythmias (18 uniform ventricular tachycardia, 23 polymorphic ventricular tachycardia/ventricular fibrillation) and 20 had no inducible arrhythmia. Patients with inducible arrhythmia had 45% abnormal and 6% fractionated electrograms versus 31% and 0% for those without inducible arrhythmia (P greater than 0.05 for both comparisons). Sixteen of 59 patients (27%) with adequate follow-up had arrhythmia recurrence (11/39 [31%] with inducible arrhythmia and 5/20 [25%] without inducible arrhythmia) over a mean follow-up period of 27 months. Of five patients without inducible arrhythmia who experienced recurrence, two did so despite the anti-ischemic therapy. In the 20 patients without inducible arrhythmia, the 15 who remained arrhythmia-free had a mean of 78 +/- 22% normal sites versus 46 +/- 24% normal sites in those with recurrence (P greater than 0.05). We conclude that in patients with coronary artery disease and cardiac arrest: 1) patients without inducible arrhythmia have less marked endocardial electrical abnormality than those with inducible arrhythmia, 2) those patients who have marked endocardial abnormality despite the lack of inducible arrhythmia are at risk for clinical recurrence which suggests that these abnormalities may represent an anatomic substrate for arrhythmia which cannot be identified by programmed stimulation. These patients are candidates for AICD implantation and 3) patients with relatively normal endocardial electrograms do well with anti-ischemic therapy alone.
Aged↗
Fusion with the prolonged first postpacing interval in pacing of ventricular tachycardia.
In cases of recurrent sustained ventricular tachycardia (VT), constant fusion and progressive fusion in the surface electrogram were observed during overdrive pacing of VT. However, following cessation of pacing, the return cycle of VT (stimulus to the first nonpaced QRS) was longer than the VT cycle length. This phenomenon can be explained by orthodromic capture of the exit site of the VT current with a conduction time (stimulus to QRS) exceeding the VT cycle length. This site can therefore be activated during entrainment of VT during the mid-to-terminal portion of the paced QRS complex, resulting in constant fusion.
Cardiac Pacing, Artificial↗
Predicting ventricular tachycardia cycle length after procainamide by assessing cycle length-dependent changes in paced QRS duration.
To determine if paced cycle length-dependent changes in the QRS duration correlate with the change in ventricular tachycardia (VT) cycle length after procainamide, we measured the QRS duration during sinus rhythm and during right ventricular pacing before and after procainamide (mean concentration, 9.9 micrograms/ml) in 18 patients with morphologically identical VT induced at both study periods. Pacing was performed at 600 msec or the longest cycle length that allowed for uninterrupted capture and at a cycle length that was within 50 msec of the VT cycle length observed during the control study (mean, 313 +/- 51 msec). After procainamide, the VT cycle length increased from 285 +/- 62 to 368 +/- 70 msec (percent change, 30 +/- 13%). The QRS duration during sinus rhythm increased from 125 +/- 25 to 145 +/- 29 msec (percent change, 16%). The QRS duration at both paced cycle lengths was the same in the baseline state (191 +/- 26 msec). However, the change in QRS duration after procainamide at the shorter paced cycle length compared to a 39 +/- 13 msec (18%) increase at the longer paced cycle, p less than 0.001. There was a significant correlation between the percent change in QRS duration at the shorter paced cycle length and the percent change in VT cycle length (r = 0.84, p less than 0.001) with the relation expressed by the regression equation: percent change in VT cycle length = -2.8 + 1.16 x percent change in QRS duration.(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
The human atrial strength-interval relation. Influence of cycle length and procainamide.
We defined the atrial strength-interval relation in 23 patients at cycle lengths of 600, 450, and 300 msec before and after procainamide. The atrial diastolic threshold was similar at cycle lengths of 600 and 450 msec, but the threshold at 300 msec was significantly higher than that determined at 600 and 450 msec both before and after procainamide. Procainamide significantly increased the diastolic threshold only at a cycle length of 300 msec. The strength-interval relation was nonlinear, showing progressively decreasing decrements in the measured refractory period as the stimulating current was increased. Progressive decreases in the drive cycle length from 600 to 450 to 300 msec caused similar decreases in refractory periods. The shape of the curves was similar at cycle lengths of 600 and 450 msex. However, at low current strengths, the slope of the curve determined at 300 msex was significantly more vertical than the slopes of the curves at the longer drive cycle lengths. Procainamide caused similar increases in apparent refractory periods at each paced cycle length. Procainamide did not alter the shape of the curves at any paced cycle length. These observations confirm the importance of stimulation frequency on atrial excitability. They suggest that the effects of procainamide on the effective refractory period of the atrium are not cycle length dependent, although the drug effects on threshold are dependent on the drive cycle length.
Adult↗
Surgical decisions in the management of sudden cardiac death and malignant ventricular arrhythmias. Subendocardial resection, the automatic internal defibrillator, or both.
Subendocardial resection and implantation of an automatic implantable cardioverter/defibrillator are the current preferred treatments for the management of drug-resistant malignant ventricular arrhythmias and sudden cardiac death. We reviewed retrospectively the case histories of 269 patients who had subendocardial resection and 77 patients who had defibrillator implantation to define clinical characteristics of each group and compare operative and long-term results. All patients treated by subendocardial resection had recurrent sustained ventricular tachycardia as a result of a myocardial infarction. From the standpoint of arrhythmia substrate and cardiac disease, patients receiving the defibrillator were a more heterogeneous group. Forty-eight (62%) had coronary artery disease, 28 (36%) cardiomyopathy, and one patient had a primary electrical abnormality. Among patients receiving the defibrillator, 55% had sustained ventricular tachycardia and 45% polymorphic ventricular tachycardia or ventricular fibrillation. Overall ventricular function was similar in the two groups. Operative mortality rate was better in the group having defibrillator implantation (3% versus 15%). Complications related to the defibrillator device or implantation occurred in 46 (60%) patients, with asymptomatic shocks occurring in 35 patients (45%). Since the defibrillator was not designed to prevent arrhythmias, the arrhythmia-free survival rate was much better in the group having subendocardial resection (95% versus 44% at 3 years). Fewer patients treated by subendocardial resection required antiarrhythmic medications (33% versus 66%). The actuarial survival rate was similar in the two groups (approximately 60% at 4 years), with heart failure the most common cause of death. Thus both subendocardial resection and defibrillator implantation are highly effective in preventing sudden cardiac death. The choice of procedure depends on (1) arrhythmia diagnosis, (2) cardiac disease, and (3) intangible factors.
Aged↗
Prognosis following sustained ventricular tachycardia occurring early after myocardial infarction.
Eighty-seven patients with sustained ventricular tachycardia (VT) between 3 and 90 days after acute myocardial infarction (AMI) were evaluated to define factors associated with a high risk of arrhythmia recurrence or death. Most patients had poor left ventricular function (mean ejection fraction 29 +/- 12%), multivessel coronary artery disease (71%) and inducible sustained VT with programmed stimulation (87%). During a mean follow-up of 26 months, 36 patients (41%) died and 21 patients had arrhythmia recurrence (with 19 sudden deaths). Factors independently associated with mortality included: (1) treatment before 1981 (p less than 0.01); (2) anterior AMI (p less than 0.05); (3) short time from AMI to first episode of VT (p less than 0.06); and (4) multivessel coronary artery disease (p less than 0.07). Factors independently associated with arrhythmia recurrence were: (1) medical treatment (as opposed to surgical) (p less than 0.01); (2) greater than or equal to 3 episodes of spontaneous VT (p = 0.01); (3) multivessel coronary disease (p less than 0.05); and (4) anterior AMI (p less than 0.07). Medically and surgically treated patients did not differ significantly in overall survival (49 vs 61%, respectively), although short-term (6 month) surgical survival improved from 31% during the first half of the study to 96% in the latter half (p less than 0.01). For patients with sustained VT early after AMI the risk of death and arrhythmia recurrence can be assessed based on clinical and angiographic characteristics; in addition, surgical treatment is associated with a lower incidence of arrhythmia recurrence than medical treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Electrocardiographic criteria for ventricular tachycardia in wide complex left bundle branch block morphology tachycardias.
Four electrocardiographic criteria for ventricular tachycardia (VT) were proposed and evaluated. These included (1) an R wave in V1 or V2 of greater than 30-ms duration; (2) any Q wave in V6; (3) a duration of greater than 60 ms from the onset of the QRS to the nadir of the S wave in V1 or V2 and (4) notching on the downstroke of the S wave in V1 or V2. The data showed that all 4 criteria had high predictive accuracy (96 to 100%) and specificity (94 to 100%). The relatively low sensitivities of the 4 criteria alone (30 to 64%) might limit their efficacy. Grouped criteria, however, could differentiate VT from supraventricular tachycardias with high sensitivity, specificity and predictive accuracy. The amount of tracings having either electrocardiographic criteria (1) or (2) or (3) or (4) was determined. The proposed combined criteria had a sensitivity of 100%, specificity of 89% and a predictive accuracy of 96%. Left axis deviation alone was of no value in distinguishing VT from supraventricular tachycardia. Characteristic patterns were present for left bundle branch block pattern VT associated with anterior and inferior myocardial infarction. In conclusion, the 12-lead electrocardiogram alone, when systematically analyzed, can be used to accurately diagnose the origin of wide complex tachycardias with left bundle branch block pattern. Attention to these criteria may lead to more rapid and effective therapy.
Bundle-Branch Block↗
Coupling intervals of ventricular extrastimuli causing resetting of sustained ventricular tachycardia secondary to coronary artery disease: relation to subsequent termination.
Single and double ventricular extrastimuli (VE) delivered during sustained, uniform ventricular tachycardia (VT) are able to reset or terminate the tachycardia. The relation between the coupling intervals of single and double VE resetting VT and those terminating it was examined in 80 uniform, morphologically distinct VT occurring in 52 patients. Of the 80 tachycardias receiving single VE, 41 were reset and 8 terminated. The corrected coupling interval of single VE first causing resetting was 0.81 +/- 0.08 compared with 0.66 +/- 0.06 for termination (p less than 0.001). Forty-two tachycardias received double VE with 33 being reset and 13 terminating. The corrected coupling interval of double VE at which resetting was first seen was 0.86 +/- 0.08 compared with 0.73 +/- 0.05 for termination (p less than 0.001). If the longest corrected coupling interval causing resetting was greater than or equal to 0.75, then 7 of 34 tachycardias terminated with single VE and 13 of 31 terminated with double VE compared with only 1 of 46 terminating with single VE and 0 of 10 with double VE if resetting was not observed by a corrected coupling interval of 0.75 (p less than 0.01 and p less than 0.02, respectively). If the longest corrected coupling interval at which resetting occurred was greater than or equal to 0.75, the predictive value for VT termination was 21% with single VE and 42% with double VE compared with only 2% with single VE and none with double VE if resetting was not observed by this corrected coupling interval.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiac Pacing, Artificial↗
Anterior left ventricular aneurysm: factors associated with the development of sustained ventricular tachycardia.
Fifty patients with anteroapical left ventricular aneurysm secondary to prior myocardial infarction underwent aneurysmectomy, at which time endocardial sinus rhythm mapping was performed. Forty patients had a history of recurrent sustained monomorphic ventricular tachycardia, and 10 had an aneurysm but no history of spontaneous sustained tachycardia. A comparison of the clinical, angiographic and sinus rhythm endocardial electrographic characteristics of these two groups revealed that the patients without spontaneous ventricular tachycardia had more severe coronary artery disease (2.6 +/- 0.5 versus 1.9 +/- 0.8 coronary arteries having greater than 70% stenosis; p less than 0.03), underwent surgery earlier after infarction (3 +/- 2 versus 46 +/- 53 months; p less than 0.03) and had less extensive wall motion abnormalities on contrast ventriculography (0 of 8 versus 13 of 35 patients assessed had an abnormally contracting ventriculographic segment length greater than 60%; p less than 0.04). During intraoperative programmed electrical stimulation, all 40 patients with and 4 of 10 without a history of spontaneous ventricular tachycardia had inducible tachycardia. The patients with inducible tachycardia had a larger area of endocardium from which abnormal electrograms (duration greater than 70 ms or amplitude less than 0.7 mV) were recorded (62 +/- 17 versus 45 +/- 20% of electrograms; p less than 0.03) as well as fractionated (duration greater than 90 ms, amplitude less than 0.3 mV) electrograms (20 +/- 14 versus 9 +/- 7% of electrograms; p less than 0.04) than did patients without inducible tachycardia, but there were no angiographic differences between groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiac Pacing, Artificial↗
Cycle length-dependent effects on normal and abnormal intraventricular electrograms: effect of procainamide.
The effect of procainamide (mean concentration 9.1 +/- 2.0 micrograms/ml) on cycle length-dependent changes in electrographic characteristics was determined in 10 patients with prior myocardial infarction. Intracardiac bipolar electrograms were recorded from an abnormal left ventricular site in the distribution of prior (greater than 6 month) myocardial infarction and from a normal right ventricular site. Pacing was performed for 15 beats from the right ventricular apex at cycle lengths of 600 (or 500), 400 and 300 ms. In the control state, the QRS width, the normal electrogram and in 9 of the 10 patients the abnormal electrogram did not change with decreasing cycle lengths. After procainamide the mean QRS width increased from 203 +/- 32 to 240 +/- 50 ms (+18%, p less than 0.01) at a paced cycle length of 600 (or 500) ms, from 198 +/- 34 to 245 +/- 59 ms (+24%, p less than 0.01) at a paced cycle length of 400 ms and from 197 +/- 36 to 258 +/- 67 ms (+31%, p less than 0.01) at a paced cycle length of 300 ms.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiac Pacing, Artificial↗
Cardiac cryolesions: factors affecting their size and a means of monitoring their formation.
Twenty-seven endocardial cryolesions were created in mongrel dogs and analyzed to determine the effects on cryolesion size of both the initial myocardial temperature (37 degrees C versus 12 degrees C) and the pressure within the nitrous oxide delivery line (tank pressure of more than 700 pounds per square inch [psi] versus tank pressure of less than 700 psi). In addition, local myocardial temperatures were monitored to determine their utility in the intraoperative determination of the extent of cryothermic cell death. Cryolesion volume was significantly affected by both the initial myocardial temperature (p less than 0.001) and the line pressure (p = 0.014). In a 37 degrees C myocardium, the mean lesion volume ranged from 0.501 +/- 0.183 cc at line pressures lower than 700 psi to 0.839 +/- 0.258 cc at line pressures greater than 700 psi. In a 12 degrees C myocardium, the mean volume was 1.151 +/- 0.436 cc at line pressures lower than 700 psi and 1.361 +/- 0.288 cc at line pressures higher than 700 psi. A myocardial temperature of 0 degrees C occurs at the edge of the area of cell death. When analyzing the range from -5 degrees to +5 degrees C, the probability of a point at or lower than 0 degrees C falling inside the cryolesion is 84.2%. Monitoring intramyocardial temperature will predict the border of a cryolesion.
Animals↗
Atrioventricular nodal supraventricular tachycardia with 2:1 block above the bundle of His.
A patient with narrow complex supraventricular tachycardia underwent electrophysiological study at which time a tachycardia was initiated which had 2:1 AV conduction, with block occurring above the His bundle. The modes of tachycardia initiation, as well as the responses to atrial and ventricular premature depolarizations during tachycardia, made a diagnosis of atrioventricular nodal reentry as the tachycardia mechanism. The unusual finding of 2:1 supra-His block suggests the presence of tissue situated between the tachycardia circuit and His bundle, and effectively excludes the possibility of a His-atrial bypass tract as the retrograde limb of the tachycardia circuit.
Adult↗