A Castellanos

Body surface detection of delayed depolarizations in patients with recurrent ventricular tachycardia and left ventricular aneurysm.

In eight patients with chronic ventricular tachycardia and left ventricular aneurysms, we detected delayed ECG wave forms after the QRS complex from the body surface using a high-resolution ECG recorder, amplification and signal averaging. Delayed wave-form activity (D wave) extended a mean of 70 msec beyond the termination of the QRS complex. This delayed activity frequently extended to the limit of the recording window, and may thus continue throughout much of diastole. Antiarrhythmic agents never abolished the delayed activity; however, it was abolished by aneurysmectomy in four patients. Ventricular tachycardia did not recur after surgery in the four patients during a mean follow-up of 1 year. The D wave was not found in eight control patients who had chronic recurrent ventricular tachycardia nor in 11 of 12 who had aneurysms alone. The surface D wave can be readily and reproducibly detected by high-resolution electrocardiography and appears to be specific for patients with left ventricular aneurysms who also have chronic recurrent ventricular tachycardia. This delayed wave-form activity has been noted during catheter and surgical endocardial and epicardial mapping. It may represent persistence of the cardiac impulse in islands of myocardium and may be a manifestation of the delayed and fractionated activity, noted by previous investigators.

Electrocardiographic antecedents of primary ventricular fibrillation. Value of the R-on-T phenomenon in myocardial infarction.

Primary ventricular fibrillation was seen in 20 of 450 consecutive patients (4-4%) admitted within 24 hours after the onset of acute myocardial infarction. Compared with patients without primary ventricular fibrillation they showed a lower mean age group and a higher incidence of anterior infarction. Warning ventricular arrhythmias preceded primary ventricular fibrillation in 58% of cases. However, warning arrhythmias were also present in 55% of patients without primary ventricular fibrillation. The following mechanisms of initiation of primary ventricular fibrillation were seen. 1) In one patient, it was initiated by supraventricular premature beats showing aberrant intraventricular conduction. 2) In 2 patients, ventricular tachycardia degenerated into primary ventricular fibrillation. 3) In 17 patients, it was initiated by a ventricular premature beat; in 10 of these, the premature beat showed early coupling (RR/QT less than 1--the R-on-T phenomenon). However, ventricular premature beats showing the R-on-T phenomenon were also observed in 49% of patients without primary ventricular fibrillation. In 7, primary ventricular fibrillation was initiated by a late-coupled ventricular premature beat (RR/QT greater than 1); in 2, the very late coupling resulted in a ventricular fusion beat. The study suggests that warning arrhythmias and the R-on-T phenomenon are poor predictors of primary ventricular fibrillation in acute myocardial infarction. The observation that 41% of primary ventricular fibrillation was initiated by a late-coupled ventricular premature beat suggests that ventricular vulnerability during acute myocardial infarction may extend throughout most of the cardiac cycle and is not necessarily confined to the QT interval.

Antiarrhythmic drug therapy in survivors of prehospital cardiac arrest: comparison of effects on chronic ventricular arrhythmias and recurrent cardiac arrest.

We studied the long-term effects of membrane-active antiarrhythmic agents on chronic ventricular arrhythmias in patients who have survived prehospital cardiac arrest. Among 16 patients treated with a dose-adjusted, plasma level-monitored antiarrhythmic regimen, eight have survived for longer than 12 months eight have had recurrent cardiac arrests (RCAs). Monthly Holter monitor tapes (HIM) recorded during the 4 months before the eight RCAs were compared with monthly HM tapes matched for time of entry duration of follow-up in the eight patients who did not have RCAs. Transient or persistent complex ventricular ectopic depolarizations (VEDs) have been recorded on 47 of the 63 monthly HM tapes (75%). The difference between VEDs in the RCA patients (mean 153 VEDs/hr, median 19 VEDs/hr) VEDs in the patients who have not had RCA (mean 122 VEDs/hr, median 8 VEDs/hr) was not significant (p ≥ 0.2); nor was there a predictable relationship between therapeutic plasma levels of antiarrhythmic agents the frequency complexity of chronic asymptomatic VEDs (therapeutic levels mean 104 VEDs/hr, median 6 VEDs/hr; subtherapeutic levels – mean 184 VEDs/hr, median 21 VEDs/hr). Differences were not significant (p ≥ 0.1). In contrast, all eight RCA patients had unstable plasma levels (21 of 31 determinations subtherapeutic) while six of the eight patients who have not had RCA had consistently therapeutic levels (p ≤ 0.01). Thus, adequate plasma levels of antiarrhythmic agents may protect against RCA, despite failure to suppress VEDs predictably. The apparent dissociation between predictable suppression of chronic VEDs protection against RCA suggests that clinical effectiveness of these agents may not be best measured by their effect on chronic VEDs.

Long-term survival after prehospital cardiac arrest: Analysis of outcome during an 8 year study

We analyzed long-term follow-up data accumulated during an 8 year study of survivors of prehospital cardiac arrest. All patients included in this study were primary entrants via community-based rescue systems; patients who were tertiary referrals (survivors of cardiac arrest from other hospitals) were not included in this analysis. In the group of 61 patients entering our study between 1975 and 1980, with a follow-up to 1983, there have been a total of 24 deaths (39%). Sixteen of the 24 deaths were the result of recurrent cardiac arrest; eight were nonsudden cardiac deaths or noncardiac deaths. The mean duration from entry to death in the nonsurvivors was 27.5 +/- 19.7 months, and the time from the index event to last follow-up in the long-term survivors was 59.9 +/- 19.4 months. Life table analysis demonstrated a 10% rate of recurrence of cardiac arrest in the first year, with a 5% per year rate in each of the subsequent 3 years. Left ventricular ejection fractions at entry were not significantly different between survivors (mean = 45.3 +/- 13.6%) and nonsurvivors (mean = 37.6 +/- 12.6%), and the severity of ejection fraction abnormality at entry did not correlate with time to death in the nonsurvivors. However, ejection fraction was significantly lower in patients who died from causes other than recurrent cardiac arrest than in those who died of cardiac arrest (24.5 +/- 9.1% vs 42.7 +/- 9.2%; p less than .002).(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanisms of spontaneous alternation between reciprocating tachycardia and atrial flutter-fibrillation in the Wolff-Parkinson-White syndrome.

In a group of 36 consecutive patients with the Wolff- Parkinson-White (WPW) syndrome undergoing electrophysiological studies because of paroxysms of reciprocating tachycardia (RT) and/or atrial flutter-fibrillation (AF), 7 patients (19%) had repeated episodes of spontaneous alternation between RT and AF. Electrophysiological studies demonstrated left-sided anomalous pathways (AP) in all 7 patients. Atrial vulnerability, as evidenced by the occurrence of repetitive atrial responses or a paroxysm of AF following a single atrial premature stimulus, was also noted in all. Invariably, spontaneous conversion of RT to AF (7 patients) was triggered by an atrial premature depolarization which resulted in atrial asynchrony during the atrial vulnerable phase. In contrast, spontaneous conversion of AF to RT (3 of the 7 patients) required the presence or the development of antegrade unidirectional block in the AP prior to the cessation of AF. The demonstration of atrial vulnerability in association with the phenomenon of spontaneous alternation between RT and AF provides further information pertaining to the understanding of the mechanisms of tachyarrhythmias in the WPW syndrome. It is suggested that the occurrence of this electrophysiological phenomenon may be more common than is generally appreciated, and optimal medical treatment should be directed toward controlling both RT and AF in this group of Wolff-Parkinson- White patients.

Relationship between plasma levels of procainamide, suppression of premature ventricular complexes and prevention of recurrent ventricular tachycardia.

We compared the relationship between plasma levels of procainamide and suppression or prevention of various forms of ventricular arrhythmias in 18 patients, six of whom had premature ventricular complexes (PVCs) during acute myocardial infarction (AMI), six of whom had PVCs in the setting of stable chronic ischemic heart disease (CIHD), and six of whom had recurrent symptomatic ventricular tachycardia (VT) with chronic PVCs between episodes of VT. The mean plasma level of procainamide required for 85% suppression of PVCs in the AMI patients was 5.0 ± 0.5, g/ml, while that required for the CIHD patients was 9.3 ± 0.7 gg/ml (p < 0.05). The mean plasma level required for prevention of spontaneous episodes of symptomatic sustained tachycardia in the VT group was 9.1 ± 3.4, g/ml, while the mean level required for 85% suppression of PVCs in the same patients was 14.9 ± 3.8, g/ml (p < 0.01). In the VT group, PVC frequency was decreased by a nmean of only 36% (range 11-63%) at plasma levels of procainamide sufficient to prevent spontaneous VT. The relationship between plasma levels of procainamide and PVC suppression appears to be different in AMI and CIHD patients; furthermore, a high degree of PVC suppression is not a necessary endpoint of antiarrhythmic therapy when attempting to protect patients against recurrent symptomatic VT.

Arrhythmias Related to Cardioversion

DC countershock abolished 92 of 101 episodes of atrial fibrillation in 86 patients, an incidence of 91 per cent. Supraventricular arrhythmias were not infrequent immediately after countershock. These were transient and did not complicate the procedure nor were they hazardous to the patient. On two occasions a slow atrioventricular nodal rhythm appeared followed by recurrence of atrial fibrillation a few hours later. Sinus node activity did not return in these patients. Ventricular tachycardia, fibrillation, or standstill did not occur in this series.The following arrhythmias were observed immediately after countershock but prior to the establishment of a regular sinus rhythm: atrioventricular dissociation, 12 times; passive atrioventricular nodal rhythm, five times; atrioventricular nodal tachycardia, five times; atrial flutter or tachycardia, four times.The conversion of fibrillation to flutter by countershock implies that the effect of the electric current was merely to shorten the length of the circulating wave, a phenomenon that can also be observed in the treatment of atrial fibrillation with quinidine.Disorders of rhythm, probably having a different mechanism, were also observed after countershock had established a regular sinus pacemaker. In the group not treated with quinidine prior to countershock (74 episodes) atrial extrasystoles were seen 26 times (35 per cent); atrioventricular nodal extrasystoles or escapes, 18 times (24.3 per cent); atrial flutter or tachycardia, six times (8.1 per cent); atrial fibrillation, eight times (18 per cent); atrioventricular nodal tachycardias, twice (2.6 per cent); and a bizarre, multifocal atrial arrhythmia, once (1.3 per cent). The arrhythmias considered to be responsible for the recurrence of atrial fibrillation and also the possible mechanisms involved were discussed.Pretreatment with quinidine was effective in reducing the incidence of arrhythmias occurringafter conversion (27 episodes), atrial extrasystoles six times (22 per cent), atrioventricular nodal extrasystoles or escapes six times (22 per cent); atrial flutter or tachycardia three times (11 per cent); atrial fibrillation once (3.7 per cent); and atrioventricular nodal tachycardia once (3.7 per cent).

Analysis of surgically-induced right bundle branch block pattern using intracardiac recording techniques.

SUMMARY Using intracardiac recording techniques, His bundle (H) and right ventricular apical (RVA) electrograms were recorded in 16 patients with a postoperative electrocardiographic pattern of right bundle branch block (RBBB). Their ages ranged from 5 to 12 years (mean 6.9 years) at surgery and the follow-up period was 1 to 7 years (mean 2.7 years). All were asymptomatic and in sinus rhythm at the time of study. The P-A interval was normal in all and the A-H, H-V, and V-RVA intervals were prolonged in one, one, and six patients, respectively. The V-RVA interval was normal (≤30 msec) in ten out of the 1I patients (91%) without associated left anterior hemiblock (LAH), indicating a physiologically intact main right bundle branch, and was abnormally lengthened (45–62 msec) in all five patients (100%) with associated LAH. These findings suggest that there are two subgroups of patients with surgically-induced RBBB pattern and the measurement of the V-RVA interval in conjunction with the H-V interval may be of ultimate importance in understanding the longterm prognostic implication of surgically-induced RBBB pattern with or without LAH.

Significance of complete right bundle-branch block with right axis deviation in absence of right ventricular hypertrophy.

Complete right bundle-branch block with right axis deviation was seen in nine patients who did not have right ventricular hypertrophy, pulmonary disease, or extensive lateral myocardial infarction. Four patients had chronic block and five had acute myocardial infarction. This pattern was attributed to a coexisting block in the right branch and in the inferior division of the left branch. It frequently alternated with other significant intraventricular conduction defects, namely, complete left bundle-branch block, complete right bundle-branch block, and complete right bundle-branch block with block in the superior division of the left branch. A type II Mobitz block, evolving from a prolonged, or normal, PR interval, appeared in eight patients. The latter was probably due to a simultaneous conduction disturbance in the right branch and in both divisions of the left branch (trifascicular bloch). All patients required intracardiac pacing. The prognosis was not good due to the extensive involvement of the conducting system.

Dynamic Behavior and Autonomic Regulation of Ectopic Atrial Pacemakers

BACKGROUND Heart rate (HR) variability reflects the neural regulation of normal pacemaker tissue, but the autonomic nervous regulation of abnormal atrial foci originating outside the sinus node has not been well characterized. We compared the HR variability of tachycardias originating from the ectopic foci and the sinus node. METHODS AND RESULTS R-R-interval variability was analyzed from 24-hour Holter recordings in 12 patients with incessant ectopic atrial tachycardia (average HR 107+/-14 bpm), 12 subjects with sinus tachycardia (average HR 106+/-9 bpm), and 24 age- and sex-matched subjects with normal sinus rhythm (average HR 72+/-8 bpm). Time- and frequency-domain HR variability measures, along with approximate entropy, short- and long-term correlation properties of R-R intervals (exponents alpha(1) and alpha(2)), and power-law scaling (exponent beta), were analyzed. Time- and frequency-domain measures of HR variability did not differ between subjects with ectopic and sinus tachycardia. Fractal scaling exponents and approximate entropy were similar in sinus tachycardia and normal sinus rhythm, but the short-term scaling exponent alpha(1) was significantly lower in ectopic atrial tachycardia (0.71+/-0.16) than in sinus tachycardia (1.16+/-0.13; P<0.001) or normal sinus rhythm (1.19+/-0.11; P<0.001). Abrupt prolongations in R-R intervals due to exit blocks from the ectopic foci or instability in beat-to-beat R-R dynamics were the major reasons for altered short-term HR behavior during ectopic tachycardias. CONCLUSIONS HR variability obtained by time- and frequency-domain methods does not differ between ectopic and sinus tachycardias, which suggests that abnormal atrial foci are under similar long-term autonomic regulation as normal pacemaker tissue. Short-term R-R-interval dynamics are altered toward more random behavior in ectopic tachycardia, which may result from a specific autonomic disturbance or an intrinsic abnormality of ectopic atrial pacemakers.