Demonstration of the mechanism of transient entrainment and interruption of ventricular tachycardia with rapid atrial pacing.

An unusual case is presented in which ventricular tachycardia at a rate of 141 beats/min was transiently entrained by rapid atrial pacing at rates of 150, 155 and 160 beats/min, and was interrupted by rapid atrial pacing at a rate of 165 beats/min. During each period of transient entrainment, constant ventricular fusion beats were present except for the last entrained beat, and progressive ventricular fusion (different fusion QRS complexes) was demonstrated when comparing QRS complex configurations during transient entrainment at each pacing rate. Interruption of the ventricular tachycardia was associated with localized conduction block to the right ventricular recording site, followed by activation of that site from a different direction and with a shorter conduction time by the subsequent pacing impulse. These data clearly distinguish transient entrainment of a tachycardia from overdrive suppression of a tachycardia, and strongly suggest that reentry was the underlying mechanism of the ventricular tachycardia.

Percutaneous transluminal coronary angioplasty after intracoronary streptokinase in evolving acute myocardial infarction.

To achieve optimal myocardial revascularization and prevent rethrombosis of the infarct-related coronary artery, percutaneous transluminal coronary angioplasty (PTCA) was attempted in 18 patients with evolving acute myocardial infarction (9 anterior and 9 inferior) after administration of intracoronary streptokinase. PTCA was attempted 338 +/- 151 minutes after the onset of symptoms. After thrombolytic therapy, 11 patients had a severe residual stenosis and 7 a persistent total occlusion of the infarct-related coronary artery. PTCA was successful in 13 of 18 patients: in 9 of 11 with coronary stenoses and in 4 of 7 with total coronary occlusions. PTCA reduced the severity of the coronary lesion from 91 +/- 2% to 27 +/- 7% (p less than 0.001), and the transstenotic pressure gradient from 38 +/- 5 to 6 +/- 2 mm Hg (p less than 0.01). One patient in cardiogenic shock died during urgent coronary surgery after unsuccessful PTCA. After PTCA, all patients received heparin and antiplatelet agents. One patient had reinfarction with reocclusion of the infarct-related artery 5 days after PTCA. The other 12 patients had an uneventful hospital course, and cardiac catheterization before hospital discharge (8 to 17 days) revealed reocclusion of the infarct-related coronary artery in 3 and persistent patency in 9. Persistent patency of the infarct-related artery was associated with preservation of left ventricular end-diastolic volume (initial 86 +/- 6 ml/m2, follow-up 91 +/- 6 ml/m2), and improvement in left ventricular ejection fraction in some patients.

Paroxysmal ventricular arrhythmias and familial sudden death associated with neural lesions in the heart.

A high school athlete with history of syncopal attacks died suddenly. Paroxysmal ventricular arrhythmias had been documented many times, as had at least one episode of ventricular fibrillation. A brother with similar history also had died suddenly and unexpectedly at about the same age. Except for the syncope and arrhythmias, they were both considered to be in good health. At postmortem examination, no significant extracardiac abnormalities were found, and the heart was normal on gross examination. The cardiac conduction system was the subject of special study. Focal inflammatory degeneration of small nerves and ganglia was found in various sites within the heart, including atrioventricular node, but were especially prominent in and around the sinus node. There was epicardial edema and thickening of the pericardium in that vicinity, but all of the pericardium elsewhere was normal. Some persistent fetal dispersion of the atrioventricular node was present. Ways are discussed in which these neural lesions may have contributed to the pathogenesis of paroxysmal arrhythmias and eventually sudden death. The possible etiology of the neural disease and the basis for its familial occurrence are considered.

Use of temporarily placed epicardial atrial wire electrodes for the diagnosis and treatment of cardiac arrhythmias following open-heart surgery.

We retrospectively assessed our experience with the use of bipolar atrial epicardial electrodes in 70 consecutive patients following open-heart surgery. These patients, representing 1 month's experience on one of our cardiac surgical services, are a random sample of our total experience with more than 6.000 patients in whom we have routinely placed such electrodes. The atrial wire electrodes were used diagnostically and/or therapeutically in 57 patients a total of 139 times. In only 13 patients were the atrial wires not used for any reason. Atrial electrograms were recorded 63 times in 34 patients, 41 times to establish a diagnosis of an arrhythmia and 22 times to confirm the diagnosis of an arrhythmia originally suspected from interpretation of a standard or monitor electrocardiogram (ECG). Atrial pacing was used to treat abnormalities of rhythm or conduction or both in 75 instances in 49 of the 70 patients. Because of their great utility in the diagnosis and treatment of arrhythmias, we conclude that routine placement of atrial wire electrodes at the time of operation is indicated regardless of the nature of the open-heart procedure or the preoperative rhythm.

A reappraisal of surgical intervention for acute myocardial infarction.

Eighty-three patients underwent coronary artery bypass during acute evolving myocardial infarction 6.8 +/- 2.8 hours after the onset of symptoms. Linear discriminant analysis of preoperative variables identified predictors of mortality with an accuracy of 84%. Significant predictors in decreasing order of importance were cardiogenic shock, age over 65 years, left ventricular ejection fraction less than or equal to 0.30, cardiac index less than or equal to 2.0 L/min/m2, and absent collateral flow. Time to reperfusion did not influence outcome nor did the infarct-related artery. Hospital mortality was 15.6% (13/83). Among 51 low-risk patients under 65 years of age without cardiogenic shock, there were three deaths (5.9%). Follow-up angiography was performed in 21 patients. The graft patency rate was 94%. Left ventricular ejection fraction improved from 0.39 +/- 0.10 to 0.49 +/- 0.11 (p less than 0.05). Left ventricular end-systolic volume decreased from 53.2 +/- 19.3 ml/m2 to 41.4 +/- 16.8 ml/m2 (p less than 0.05), and end-diastolic volume remained unchanged: 86.2 +/- 21.2 ml/m2 before operation and 78.7 +/- 24.0 ml/m2 after operation (no significant difference). Regional ejection fraction of the infarct area, determined by the centerline method, increased 0.23 +/- 0.15. In contrast, among 215 patients treated by nonsurgical reperfusion (intracoronary thrombolysis or angioplasty, or both), mortality was 13.5%. In this group, reperfusion was successful in 144 patients (67%) and 89 underwent follow-up angiography. Persistent patency of the infarct artery was demonstrated in 73 (82%). Ejection fraction increased from 0.45 +/- 0.10 to 0.50 +/- 0.15 (p less than 0.05). We conclude that preoperative variables enable identification of patients with evolving acute myocardial infarction in whom coronary artery bypass is associated with low operative mortality and improved ventricular performance.

Overdrive pacing for supraventricular tachycardia: a review of theoretical implications and therapeutic techniques.

Rapid atrial pacing for treatment of supraventricular arrhythmias has been demonstrated to be safe and effective. Virtually any supraventricular tachycardia with the exception of atrial fibrillation, Type II atrial flutter, and probably sinus tachycardia can be treated successfully with pacing techniques. The recognition of the advantages of cardiac pacing over drug therapy or DC cardioversion has resulted in its widespread use, especially after open-heart surgery. Although the response to overdrive pacing may not reliably identify the underlying mechanism of supraventricular tachycardia, the response of the arrhythmia to pacing (i.e., whether it is interruptable or noninterruptable), is most useful in the approach to management of the individual patient.

Transient entrainment and interruption of ventricular tachycardia.

The effects on spontaneously occurring ventricular tachycardia of rapidly pacing the right ventricle at rates faster than the rate of the ventricular tachycardia were studied during 10 episodes in seven patients. In three episodes, ventricular pacing interrupted the ventricular tachycardia at the initial pacing rate (111%, 114%, and 119% of the ventricular tachycardia rate, respectively). In seven episodes, the initial pacing rate failed to interrupt the ventricular tachycardia. In six of those seven episodes, the ventricular tachycardia was transiently entrained to the faster pacing rates. In one of those seven episodes, transient entrainment of the ventricular tachycardia could not be distinguished from over-drive suppression. In all seven episodes, the tachycardia was later interrupted by pacing at more rapid rates. The successful pacing rate ranged from 111-141% (mean 125%) of the spontaneous ventricular tachycardia rate. It is concluded that when utilizing rapid ventricular pacing to interrupt ventricular tachycardia, a critical pacing rate may be required before interruption is achieved. Pacing at rates slower than the critical rate but faster than the spontaneous ventricular tachycardia rate may only transiently entrain the ventricular tachycardia to the pacing rate without interrupting it. During the period of transient entrainment, fusion QRS complexes are likely to be present.

Noninvasive diagnosis and treatment of atrial flutter utilizing previously implanted dual chamber pacemaker.

Patients with previously implanted dual chamber pacemakers (PM) may develop atrial flutter (AFL). The Siemens-Pacesetter AFP and Genesis PM have the capability of noninvasively synchronizing to a standard external electrophysiology (EP) stimulator. Any arrhythmia termination or induction protocol may be used with a refractory period limitation of approximately 127 msec (472 ppm). The PM stimulation sequence is directly controlled by the APS Model 370EP Programmer which acts as an interface between the PM and EP stimulator. All testing is conducted with the PM functioning in a single chamber mode. The external EP stimulation is detected by the programmer and a 37 KHz coded radio frequency transmission is used to control the PM stimulation in a 1:1 fashion. Real-time intracardiac electrograms (IEG) can be recorded from either the atrial (A) or ventricular lead. The IEG can be used for: (1) hard-copy for diagnosis and cycle length determination; (2) monitoring during and after the procedure; and (3) a synchronization signal to the EP stimulator. Two patients presented with three episodes of AFL with A rates ranging from 220-290 bpm. An A-IEG was obtained in each case to document the exact rhythm and rate. Rapid A pacing from 300-340 ppm was accomplished using a standard external rapid A pacemaker in concert with the 370EP programmer and PM. In two episodes, the AFL accelerated to transient A fibrillation followed by spontaneous conversion to sinus rhythm (SR). In the other episode, the AFL converted directly to SR.(ABSTRACT TRUNCATED AT 250 WORDS)

Characterization of atrial fibrillation in man: studies following open heart surgery.

The nature of localized atrial activation during atrial fibrillation was characterized in 34 patients following open heart surgery. Bipolar atrial electrograms (AEG) recorded in each patient with atrial fibrillation exhibited a myriad of sizes, shapes, polarities, amplitudes, and beat-to-beat intervals. On the basis of the AEG morphology and the nature of its baseline, we have classified the recordings into four Types. Type I was characterized by discrete AEG complexes separated by an isoelectric baseline free of perturbation, Type II by discrete AEG complexes but with perturbations of the baseline between complexes, Type III by AEGs which failed to demonstrate either discrete complexes or isoelectric intervals, and Type IV in which AEGs of Type III alternated with periods characteristic of Type I and/or Type II. In 22 patients, the AEGs were recorded a second time, and in 11 of these patients the type of atrial fibrillation changed between the first and second recording period. An atrial flutter-fibrillation pattern in the ECG was associated with a relatively ordered atrial activation pattern and a relatively slow atrial rate. Human atrial fibrillation is not an electrophysiologically homogeneous process when compared among different patients or ad seriatim in the same patient.

Entrainment and interruption of atrial flutter with atrial pacing: studies in man following open heart surgery.

To examine the question of why the pacing rate and duration of atrial pacing are crucial factors in the successful interruption of atrial flutter, studies were performed on 30 patients in the period following open heart surgery. In each patient the diagnosis of atrial flutter was made using a pair of wire electrodes placed on the right atrial epicardium at the time of operation and brought out through the anterior chest wall. The same electrodes were used for atrial pacing. Pacing faster than the spontaneous rate of the atrial flutter which failed to interrupt the atrial flutter was associated with transient entrainment of the atrial flutter up to the atrial pacing rate. Atrial flutter was interrupted successfully when the atria were paced at a rate which was too fast for the atrial flutter to follow. This was heralded by the conversion of previously negative flutter waves to positive atrial complexes in ECG lead II. When pacing the atria at a constant rate, 2-22 seconds with a mean of 10 seconds were required to interrupt the atrial flutter.

Continuous rapid atrial pacing to control recurrent or sustained supraventricular tachycardias following open heart surgery.

A technique is described to control recurrent or sustained supraventricular tachycardia associated with rapid ventricular rates following open heart surgery. The technique utilizes a pair of temporarily implanted atrial epicardial wire electrodes to pace the heart. In one group of patients with recurrent atrial flutter and 2:1 A-V conduction, continuous rapid atrial pacing at 450 beats/min produced and sustained atrial fibrillation. The ventricular response rate immediately slowed when compared to that during atrial flutter, and if further slowing was required, it was easily accomplished by the administration of digitalis. Another group of patients with different arrhythmias (recurrent paroxysmal atrial tachycardia, sustained ectopic atrial tachycardia, or sinus rhythm with premature atrial beats which precipitated runs of atrial fibrillation) was treated with continuous rapid atrial pacing to produce 2:1 A-V block. In all instances, the continuous rapid atrial pacing suppressed the supraventricular tachycardia and maintained the ventricular response rate in a therapeutically desirable range. It was demonstrated that the technique is safe, effective, and reliable.

P waves during ectopic atrial rhythms in man: a study utilizing atrial pacing with fixed electrodes.

Threshold bipolar pacing was performed from one of 12 selected atrial sites with temporary implanted electrodes in 69 patients following open-heart surgery in order to study P wave polarity and morphology and the P-R interval during paced ectopic atrial rhythms. A negative P wave was recorded in lead I only with pacing the left atrium and only when pacing near the left pulmonary veins. A positive bifid P wave in V1 was recorded only with left atrial pacing and only when pacing was near the inferior pulmonary veins and coronary sinus. P wave polarity and morphology were otherwise of no use in localization of the origin of the impulse in these studies. The pacing stimulus to P wave interval was found to vary between 10 and 54 msec, making the duration of the P-R interval an unreliable indicator of the site of origin of the paced impulse. Although the relation of these paced rhythms to spontaneously occurring ectopic rhythms is unclear, the previously published criteria for localizing ectopic atrial rhythms are again demonstrated to be unreliable. P wave polarity and morphology and the P-R interval are of limited value in ascertaining the origin of ectopic atrial rhythms in man.