Episodes Of Nonsustained Ventricular Tachycardia Research Articles

Prediction of the location and time of spontaneous termination of reentrant ventricular tachycardia for radiofrequency catheter ablation therapy

Ventricular tachycardia caused by reentrant excitation can lead to cardiac arrest and sudden death. Drug treatment and surgical procedures have been used with limited effectiveness. Catheter ablation methods are more promising because they are less invasive than surgery. Although ablation has come to be highly effective in the treatment of supraventricular tachycardias, the overall success rate remains low for ventricular tachycardias, which may be due in part to an inaccurate localization of the reentrant pathway. The authors hypothesize that a site in the myocardium exists that is critical for the maintenance of reentry and that when ablated, will result in permanent cessation of the tachycardia. The authors also hypothesize that this is the same site where the reentrant impulse blocks during spontaneous termination of tachycardia. A series of experiments has been designed to determine if there are specific properties of extracellular electrograms recorded from reentrant circuits that would enable the circuits to be identified without activation maps and, more specifically, allow the site of block causing spontaneous termination to be localized. For quantitative analysis of electrograms, a paradigm is developed to characterize electrogram morphology using a canine infarct model. Changes in morphology (shape, size, and location of signal deflections) can be considered (1) motions of a coordinate system and/or (2) conformational changes of shape. To a first approximation, stationarity over short time segments is assumed so that the motions and conformations can be parameterized. These parameters were extracted for 50 cardiac cycles during an episode of nonsustained ventricular tachycardia, in which 196-bipolar electrode pairs were positioned in an array format across the epicardial surface of the heart. The results of these studies of changes in electrogram morphology suggest that during cycles 5 to 49 of ventricular tachycardia, in many electrograms near the circuit, the cycle length increases linearly, the amplitude increases, and the duration of activation decreases. During cycles 50 to 54, the cycle length increases much more markedly, the amplitude decreases, and the duration of activation increases. These observations suggest that cycle lengthening may be an important property of some spontaneous terminations, and moreover that other morphologic characteristics are affected differently at different stages of cycle lengthening. Further, all motion parameters tended to oscillate from cycle to cycle in either an alternans pattern or longer oscillation. The variations in morphology were typically only a few percent from cycle to cycle. Such variability would not be evident using only ruler-and-caliper measurements made by hand because of the lack of precision and the sheer volume of data. It is expected that this approach for characterization of electrogram morphology will be extremely useful clinically to (1) increase speed and accuracy of ablation site selection and (2) reduce multichannel electrogram recording complexity during ablation site selection

Comparison and frequency of ventricular arrhythmias after defibrillator implantation by thoracotomy versus nonthoracotomy approaches

Postoperative exacerbation of ventricular arrhythmias has been reported in some patients treated with thoracotomy implantable cardioverter-defibrillators (ICDs). This phenomenon, which may be related to epicardial patch electrodes, may be less frequent after nonthoracotomy ICD implantation. In this nonrandomized study, postoperative arrhythmias in thoracotomy approaches (n = 52) were compared with those in nonthoracotomy approaches (n = 59). Preoperatively, all patients were clinically stable receiving an antiarrhythmic regimen chosen by serial drug testing. Nine of 52 patients in the thoracotomy group developed sustained ventricular tachycardia postoperatively while receiving the same antiarrhythmic regimen chosen preoperatively, and 1 patient eventually died. Two additional patients developed frequent and prolonged episodes of nonsustained ventricular tachycardia requiring changes in the antiarrhythmic regimen. In the nonthoracotomy group, only 3 of 59 patients developed sustained ventricular tachycardia and 1 developed frequent nonsustained ventricular tachycardia. Thus, only 4 of 59 patients in the nonthoracotomy group developed clinically significant ventricular arrhythmia during the postoperative period compared with 11 of 52 patients in the thoracotomy group (p < 0.05). Surgical mortality was 6% in the thoracotomy group, and 0% in the nonthoracotomy group. In the remaining clinically stable patients, a marked (sevenfold) increase in asymptomatic ventricular arrhythmias was noted in 15 of 39 patients in the thoracotomy group, and in 3 of 55 patients in the nonthoracotomy group (p < 0.05). Thus, postoperative exacerbation of ventricular arrhythmia, sometimes noted with thoracotomy approaches, is very rare with nonthoracotomy approaches.

Effects of long-term oral magnesium chloride replacement in congestive heart failure secondary to coronary artery disease

Magnesium deficiency frequently develops in patients with congestive heart failure and may increase susceptibility to lethal arrhythmias and sudden death via multiple pathophysiologic mechanisms. The effects of peroral magnesium supplementation were investigated in a randomized, double-blind, crossover trial involving 21 patients with stable congestive heart failure secondary to coronary artery disease. All were receiving long-term loop diuretics, and had normal renal function, and low or normal serum magnesium concentrations. Subjects alternately received enteric-coated magnesium chloride (15.8 mmol magnesium per day) and placebo for 6 weeks. Magnesium therapy increased serum magnesium from 0.87 ± 0.07 to 0.92 ± 0.05 mmol/liter (p < 0.05), serum potassium from 4.0 ± 0.3 to 4.3 ± 0.4 mmol/liter (p < 0.01) and urinary magnesium excretion from 2.82 ± 0.96 to 4.74 ± 2.38 mmol/ 24 hours (p = 0.001). There was no significant change in heart rate or Doppler cardiac index, but mean arterial pressure decreased from 91 ± 10 to 87 ± 10 mm Hg (p < 0.05) and systemic vascular resistance from 1,698 ± 367 to 1,613 ± 331 dynes s cm −5 (p = 0.047). The frequency of isolated ventricular premature complexes was reduced by 23% (95% confidence interval [CI] 6 to 37%; p < 0.02), couplets by 52% (95% CI 30 to 65%; p < 0.001) and nonsustained ventricular tachycardia episodes by 24% (95% CI 15 to 49%; p < 0.01). Plasma epinephrine decreased from 447 ± 535 to 184 ± 106 pg/ml (p = 0.02), but there was no corresponding change in plasma norepinephrine or heart rate variability. Gastrointestinal adverse effects were reported by 6 patients, necessitating withdrawal in 2 cases. In conclusion, magnesium supplementation reduced the frequency of asymptomatic ventricular arrhythmias, possibly due to secondary changes in potassium homeostasis, and produced a minor degree of vasodilation.

The value of time and frequency domain, and spectral temporal mapping analysis of the signal-averaged electrocardiogram in identification of patients with hypertrophic cardiomyopathy at increased risk of sudden death.

Late potentials detected by the signal-averaged ECG (SAECG) identify post-infarction patients at risk from sustained ventricular tachycardia (VT) and sudden death. Hypertrophic cardiomyopathy (HCM) is also associated with increased risk of sudden death. In adults, episodes of non-sustained VT on ambulatory ECG monitoring are a marker of high risk patients. In children and adolescents, however, there is no reliable ECG marker, and clinical features have low predictive accuracy. The prognostic value of the SAECG in HCM has not been systematically evaluated. We examined the relation of detailed time domain, frequency domain, and spectral temporal mapping analysis of the SAECG and clinical and echocardiographic features, and the results of 48 h ambulatory ECG monitoring in 121 consecutive patients with HCM. Non-sustained VT on Holter monitoring was recorded in 27 (23%) patients. An abnormal time domain SAECG was present in three (11%) patients with VT vs three (3%) without VT (ns). Of the SAECG variables, reduced (below 150 microV) voltage of the initial 40 ms of the signal-averaged QRS complex was the best predictor for non-sustained VT (sensitivity: 95%; specificity: 74%: positive predictive accuracy: 64%; negative predictive accuracy: 97%). Nine patients (of whom eight were < or = 30 years of age) experienced catastrophic events: three died suddenly and six had been resuscitated from out-of-hospital ventricular fibrillation. None of them had an abnormal time domain SAECG. The frequency domain analysis and spectral temporal mapping of the SAECG did not improve the identification of patients with VT or patients with catastrophic events. In conclusion, alterations of the initial portion of the signal-averaged QRS complex identified patients with HCM and non-sustained VT, but the SAECG was not useful in identifying young patients who suffered cardiac arrest.

Spontaneous and inducible ventricular arrhythmias in a canine model of chronic heart failure: relation to haemodynamics and sympathoadrenergic activation.

The relationship between the incidence, frequency and complexity of spontaneous ventricular arrhythmias and the extent of haemodynamic compromise and sympathoadrenergic hyperactivity was evaluated in a canine model of chronic heart failure produced by multiple sequential intracoronary microembolizations. Ambulatory ECG Holter monitoring recorded during chronic heart failure in 18 dogs revealed spontaneous ventricular arrhythmias ranging from single ventricular premature beats (VPBs) to non-sustained episodes of ventricular tachycardia (VT). Single VPBs were present in 94% of dogs, couplets in 67%, triplets in 28% and spontaneous episodes of non-sustained VT in 33%. Dogs with > 28 VPBs.h-1 (n = 9) had a markedly higher plasma norepinephrine (PNE) concentration (1001 +/- 185 vs 561 +/- 31 pg.ml-1) (P < 0.03), and a higher pulmonary artery wedge pressure (PAWP) (18 +/- 2 vs 12 +/- 1 mmHg) (P < 0.03) than dogs with < or = 28 VPBs.h-1 (n = 9). Dogs that developed spontaneous episodes of VT also had significantly higher PNE levels (1119 +/- 247 pg.ml-1) compared to dogs that did not develop VT (612 +/- 64 pg.ml-1) (P < 0.02). Programmed ventricular stimulation performed in seven of 18 dogs resulted in the development of sustained monomorphic VT in three and ventricular fibrillation in three dogs each (43%, 43%). Dogs with inducible sustained monomorphic VT had a significantly higher number of ambient arrhythmias and higher PAWP compared to dogs that did not develop sustained VT. The observed complexity, frequency and incidence of spontaneous and inducible ventricular arrhythmias in this canine model are similar to those described in patients with chronic heart failure.

Influence of left ventricular hypertrophy and function on the occurrence of ventricular tachycardia in hypertrophic cardiomyopathy.

Sixty-nine patients with hypertrophic cardiomyopathy were studied by 2-dimensional and Doppler echocardiography and 72-hour Holter monitoring to examine the relation between the degree of left ventricular (LV) hypertrophy and dysfunction and the occurrence of ventricular tachycardia (VT). Episodes of nonsustained VT were detected in 20 patients (29%). Maximal wall thickness was not different between patients with (22 +/- 5 mm) and without (21 +/- 5 mm) VT. Total hypertrophy score, calculated as the sum of 10 segmental wall thicknesses, was also similar in both groups (157 +/- 22 and 153 +/- 32 mm, respectively; p = not significant). Furthermore, no significant differences were found between the 2 groups in LV end-diastolic dimension (41 +/- 7 vs 40 +/- 6 mm), fractional shortening (33 +/- 7 vs 34 +/- 10%) and left atrial size (40 +/- 10 vs 41 +/- 11 mm). An LV outflow tract gradient was detected in 25% of patients with and 35% without VT (p = not significant). One or more Doppler indexes of diastolic function were abnormal in 70% of patients, but no difference in any of these indexes was found between those with and without VT. In summary, the occurrence of VT in hypertrophic cardiomyopathy is not related to the degree of LV hypertrophy, outflow tract gradient or dysfunction. This finding suggests a dissociation between the arrhythmogenic substrate and echocardiographic features of the disease.

Significance of ventricular arrhythmias in systemic hypertension with left ventricular hypertrophy

Hypertensive patients with the electrocardiographic (ECG) pattern of left ventricular (LV) hypertrophy and strain are at increased risk of sudden death. It has been suggested that ventricular arrhythmias may be responsible. The prevalence and significance of ventricular arrhythmias was therefore studied in 90 hypertensive patients with LV hypertrophy and strain by undertaking 48-hour ambulatory ECG monitoring, ECG signal-averaging and programmed ventricular stimulation. Complex ventricular ectopic activity (Lown grade ≥3) was detected in 59 patients (66%). Eleven patients (12%) had episodes of nonsustained ventricular tachycardia. There were no sustained arrhythmias either on ambulatory ECG monitoring or induced by programmed ventricular stimulation. Only 1 patient had ventricular late potentials recorded by the signal-averaged electrocardiogram. Therefore, there was little to suggest an underlying arrhythmogenic substrate in these patients. In conclusion, whereas ventricular arrhythmias occur often in patients with LV hypertrophy associated with systemic hypertension, their significance, if any, remains to be established.

Exacerbation of ventricular arrhythmias during the postoperative period after implantation of an automatic defibrillator

The postoperative course of 68 consecutive patients treated with an implantable defibrillator during the period from 1982 through 1990 was studied. In 46 patients (group 1), no concomitant surgery was performed during the implantation. In 22 patients (group 2), concomitant surgery (coronary artery bypass [n = 12], valve replacement [n = 3] or arrhythmia surgery [n = 7]) was performed. All patients in group 1 were clinically stable before surgery, receiving an antiarrhythmic regimen chosen by serial drug testings. The same regimen was continued postoperatively.Eight of the 46 patients in group 1 whose condition had been stable in the hospital for 19 ± 25 days preoperatively developed multiple episodes of sustained ventricular tachycardia 4 ± 9 days after implantation while receiving the same antiarrhythmic regimen. Although the exacerbation was transient in some patients, six required different antiarrhythmic therapy and one eventually died. Two additional patients had frequent and prolonged episodes of nonsustained ventricular tachycardia that could trigger the defibrillator, requiring changes in the antiarrhythmic regimen. Another patient had progressive cardiac failure and died on day 5. A marked (sevenfold) increase in asymptomatic ventricular arrhythmias was noted in 42% of the remaining 35 patients.In group 2 (combined surgery), one patient developed refractory ventricular tachycardia 3 days postoperatively and died on that day. Three patients developed frequent nonsustained ventricular tachycardia postoperatively, requiring changes in the antiarrhythmic regimen. The overall surgical mortality rate was 4.4% (4.3% in group 1 and 4.5% in group 2) and was due to refractory ventricular tachycardia in two patients and cardiac failure in one.Thus, during the postoperative period after defibrillator implantation, exacerbation of ventricular arrhythmias was common. The exacerbation was clinically significant in many patients and included multiple episodes of sustained ventricular tachycardia (with eventual death in some patients) or frequent prolonged nonsustained ventricular tachycardia that could trigger the defibrillator. A sevenfold asymptomatic increase in ventricular ectopic activity was noted in 42% of the remaining clinically stable patients. The long-term effect of the exacerbation is unknown.

Case 31-1991

Presentation of CaseA 62-year-old man was admitted to the hospital because of two contrast-enhancing cerebral lesions and a right hemiparesis.There was a history of hypertension and of insulin-dependent diabetes mellitus. The patient was in a stable state of health in other respects until three months earlier, when repeated bouts of angina pectoris developed. Two days later he was admitted to another hospital, where evidence of an acute myocardial infarct was found. The patient's hospital course was complicated by second-degree and third-degree atrioventricular block and by episodes of nonsustained ventricular tachycardia; a temporary transvenous pacemaker and a central-venous-pressure catheter . . .

Effectiveness of glibenclamide on myocardial ischemic ventricular arrhythmias in non-insulin-dependent diabetes mellitus

Glibenclamide, a hypoglycemic sulfonylurea, is a blocker of the adenosine triphosphatase-modulated potassium ion channels. The opening of these channels in the myocardial cells, induced by acute myocardial hypoxia, can be responsible for ischemie ventricular arrhythmias. To evaluate the antiarrhythmic effects of this drug 19 non-insulin-dependent diabetic patients were selected. They had coronary artery disease and evidence on Holter monitoring of ventricular premature complexes or nonsustained ventricular tachycardia, or both, induced by transient myocardial ischemia. In all patients, 24-hour electrocardiographic monitoring was performed to evaluate the number and duration of myocardial ischemic events, the frequency of ventricular premature complexes and nonsustained ventricular tachycardia per minute of ischemia and the percentage of ventricular premature complexes versus total ischemic beats. Selected patients were classified in 2 groups: group A (9 patients) received metformin (placebo) and group B (10 patients) was treated with glibenclamide. On the fourteenth day patients underwent 24-hour control monitoring. Then a crossover between the 2 groups was made and a new Holter monitoring sequence was performed at the end of the second phase. Results indicate that glibenclamide significantly (p < 0.001) reduced both the frequency of ventricular premature complexes and the episodes of nonsustained ventricular tachycardia during transient myocardial ischemia, but did not change the number and duration of acute myocardial ischemic attacks and did not reduce the spontaneous ventricular arrhythmias. Thus, glibenclamide appears to have an antiarrhythmic effect in preventing ventricular arrhythmias induced by transient myocardial ischemia.

Amiodarone versus bretylium for suppression of reperfusion arrhythmias in dogs

Reperfusion arrhythmias are an important complication of interventions to limit infarct size. Recently, amiodarone has been shown to be rapidly effective in suppressing sustained, incessant ventricular tachycardia and ventricular fibrillation in this setting. This study evaluated the time course of arrhythmia suppression and comparative efficacy of amiodarone versus bretylium in a canine model of reperfusion arrhythmias. Of 23 dogs subjected to a Harris two-stage coronary artery ligation followed by release, 18 demonstrated clinically significant ventricular arrhythmias and received either intravenous amiodarone, 5 mg/kg (9 dogs), or intravenous bretylium, 5 mg/kg (9 dogs). Direct-current shocks for sustained ventricular tachycardia or ventricular fibrillation were administered as necessary. Amiodarone rapidly suppressed sustained ventricular tachycardia and ventricular fibrillation in this model with no dog in the amiodarone-treated group requiring cardioversion after completion of the 15-minute infusion versus 4 of 9 dogs in the bretylium-treated group ( p < 0.05). Amiodarone was more effective than bretylium in suppressing episodes of sustained ventricular tachycardia/ventricular fibrillation, episodes of nonsustained ventricular tachycardia, and premature ventricular complexes. The blood pressure and heart rate decreased more after amiodarone administration than after bretylium administration. We conclude that, in the canine reperfusion arrhythmia model, amiodarone is rapidly effective in suppressing ventricular arrhythmias and is more effective than bretylium.

Clinical and electrophysiological characteristics of ventricular tachycardia in children with normal hearts

Characteristics of 18 patients with clinical ventricular tachycardia (VT) and normal hearts documented by physical examination, echocardiography, and angiocardiography were analyzed. There were 13 males and 5 females, aged 1 to 16 years (mean ± SD, 9.7 ± 4.8 years). Six patients had hemodynamic instability during VT and the other 12 patients were hemodynamically stable. Two patients (11%) presented with sustained VT and 16 (89%) with episodes of nonsustained VT at varying intervals (3 of 16 with repetitive monomorphic VT). Among 14 patients on whom exercise tests were performed, seven had exercise-induced VT. During electrophysiologic studies, VT was induced in 16 of 18 (89%) (in 13 patients with morphology identical to clinical VT). VT was induced by programmed stimulation (single, double, and burst stimulation of the right atrium or right ventricular apex during sinus rhythm or during pacind for eight beats) in 5 of 18 (28%) patients; with isoproterenol, VT was aggravated spontaneously in 6 of 15 (40%) patients; and during stimulation VT was induced in 8 of 15 (53%) patients. Among patients whose VT was not induced during programmed stimulation, VT was induced with the addition of isoproterenol in 11 of 12 (92%). All 14 patients in follow-up are in stable condition, seven patients with medication and seven without medication. Pediatric patients with normal hearts and clinically detected VT usually have VT induced by programmed stimulation, either with or without isoproterenol stimulation.

Biobehavioral variables and mortality or cardiac arrest in the Cardiac Arrhythmia Pilot Study (CAPS)

The frequency of ventricular premature complexes and the degree of impairment of left ventricular ejection fraction are major predictors of cardiac mortality and sudden death in the year after acute myocardial infarction. Recent studies have implicated psychosocial factors, including depression, the interaction of social isolation and life stress, and type A-B behavior pattern, as predictors of cardiac events, controlling for known parameters of disease severity. However, results tend not to be consistent and are sometimes contradictory. The present investigation was designed to test the predictive association between biobehavioral factors and clinical cardiac events. This evaluation occurred in the context of a prospective clinical trial, the Cardiac Arrhythmia Pilot Study (CAPS). Five-hundred two patients were recruited with ≥10 ventricular premature complexes/hour or ≥5 episodes of nonsustained ventricular tachycardia, recorded 6 to 60 days after a myocardial infarction. Baseline behavioral studies, conducted in approximately 66% of patients, included psychosocial questionnaires of anxiety, depression, social desirability and support, and type A-B behavior pattern. In addition, blood pressure and pulse rate reactivity to a portable videogame was assessed. The primary outcome was scored on the basis of mortality or cardiac arrest. Results indicated that the type B behavior pattern, higher levels of depression and lower pulse rate reactivity to challenge were significant risk factors for death or cardiac arrest, after adjusting statistically for a set of known clinical predictors of disease severity. The implication of these results for future research relating behavioral factors to cardiac endpoints is discussed.

Circadian Influence in Cardiovascular Disease (Part 1)

This department will offer stylized clinical presentations of current cardiovascular issues. Questions raised as a case history evolves highlight key elements that are elaborated upon in the discussions which follow.

Signal-averaged electrocardiography in hypertrophic cardiomyopathy

A major goal in the management of patients with hypertrophic cardiomyopathy is the prediction of sudden death. To evaluate the high gain signal-averaged electrocardiogram (ECG) in this setting, 64 patients with hypertrophic cardiomyopathy and 50 age- and gender-matched control subjects were studied.An abnormal signal-averaged ECG was more common in patients than in control subjects: 13 (20%) of 64 patients with hypertrophic cardiomyopathy had abnormalities compared with 2 (4%) of the 50 control subjects (p < 0.001). There was a significant association between the presence of nonsustained ventricular tachycardia on 48 h ECG Holter monitoring and the presence of an abnormal signal-averaged ECG: 8 (47%) of the 17 patients with nonsustained ventricular tachycardia and 6 (86%) of 7 patients with more than three episodes of nonsustained ventricular tachycardia per 24 h had signal-averaged ECG abnormalities.There was no association between an abnormal signal-averaged ECG and a family history of premature sudden cardiac death, a history of syncope, symptomatic status, maximal left ventricular wall thickness, the presence of systolic anterior motion of the mitral valve or maximal rate of oxygen uptake on exercise. However, of four patients with a history of cardiac arrest, three had an abnormal signal-averaged ECG. Sensitivity was 50%; specificity was 93% and positive predictive accuracy was 77% for the signal-averaged ECG in detecting patients with electrical instability (defined as a history of cardiac arrest or the presence of nonsustained ventricular tachycardia, or both). In the young age group (≤25 years), the only patients with an abnormal signal-averaged ECG were two of the three with a history of cardiac arrest.It is concluded that the signal-averaged ECG may be a useful adjunct to the noninvasive assessment of patients with hypertrophic cardiomyopathy, particularly in the prediction of sudden death in the young age group, for whom no reliable prognostic marker currently exists.

Syncope in hypertrophic cardiomyopathy: Multivariate analysis of prognostic determinants

Twenty-nine consecutive patients with symptomatic hypertrophic cardiomyopathy and a mean age of 44.8 ± 12.2 years (range 21 to 63) underwent complex invasive and noninvasive testing to identify a risk profile for syncope. Clinical, morphologic, electrophysiologic and hemodynamic variables at rest and at a symptom-limited pacing rate were analyzed for a significant association with syncope. Exact stepwise logistic regression analysis identified three variables as significant independent predictors of syncope in hypertrophic cardiomyopathy: 1) age < 30 years (β = 4.803; p = 0.0007); 2) left ventricular end-diastolic volume index < 60 ml/m2 (β = 3.302; p = 0.006); and 3) nonsustained ventricular tachycardia on 72 h ambulatory electrocardiographic monitoring (β = 2.5909; p = 0.03). The combined occurrence of all three variables had a sensitivity and specificity of 100% in identifying eight patients with syncopal events.Thus, the risk for syncope in hypertrophic cardiomyopathy is high in young patients with the combination of low left ventricular filling volume and episodes of nonsustained ventricular tachycardia. This finding might also explain the mechanism of syncope in hypertrophic cardiomyopathy as low input-low output failure induced by a sudden increase in heart rate in the presence of a low filling volume.

Frequency and significance of cardiac rhythm disturbances in healthy elderly individuals

The authors examined the prevalence and significance of cardiac rhythm disturbances in healthy elderly individuals. They selected 26 men with active lifestyles, aged 70–81 years, after clinical, routine blood tests, chest radiographs, echocardiography, resting and exercise electrocardiograpy, and Gated cardiac blood imaging evaluations. The men were submitted to continuous electrocardiographic monitoring during their daily routine. The recording time ranged from 838 to 1,432 min (average = 1,307 ± 153 min). Clinical follow-up was done every six months. Sinus rhythm predominated in all subjects. The maximal, minimal, and average heart rate ranges (beats/min) were, respectively: during sleeping periods, 60–115 (85.8 ± 13.2), 42–80 (56.6 ± 8.7), 51–85 (64.0 ± 8.8); and during awake periods, 85–150 (118.4 ± 16.4), 50–85 (64.1 ± 9.1), 61–90 (75.3 ± 8.3). The longest sinus pauses were observed during sleep and ranged from 0.8 to 2.5 sec (1.25 ± 0.34 sec). Atrial ectopic beats were observed in 20 individuals (76.9%). They were frequent in four (15.4%) and repetitive in nine (34.6%) of them. Short-lasting episodes of paroxysmal atrial tachycardia and paroxysmal atrial flutter were observed in one case each. Ventricular ectopic beats were recorded in 20 individuals (76.9%). They were frequent in 6 (23%) and multiform in 13 (50%) of them. Couplets were observed in 5 cases (19.2%) and episodes of nonsustained ventricular tachycardia were present in 3 individuals (11.5%). No symptoms were referred by any individual during recording. No clinical signs of heart disease or symptoms were noticed during the average 40 ± 7.2 months of follow-up. In conclusion, in normal individuals older than 70 years, the sinus rhythm tends to be regular and ectopic beats are very common but do not cause symptoms nor modification of prognosis, even when they show high complexity.

Quantitative analysis of high-frequency components of signal-averaged QRS complex in chinese patients with acute myocardial infarction. A prospective study for prediction of ventricular tachycardia.

A prospective study was undertaken of the high-frequency components of the terminal portion of the QRS complex in 38 Chinese patients with acute myocardial infarction (AMI) (mean age 62 +/- 5.6 years) within the first week after the acute event (5.5 +/- 1.2 days). Another 44 normals served as controls (mean age 57 +/- 9.6 years). The electrocardiogram was averaged at a filter band pass of 80-300 Hz. The low voltage span (LVS) of the signals less than 40 microV in the terminal portion of QRS, the root-mean-square (RMS) voltage (V) of terminal 40 msec of the QRS complex, and the total duration of signal-averaged QRS vector complex were measured in both the normal subjects and patients. The LVS was abnormally prolonged in 16 of 38 patients (42%), and in only 16% of normals (p less than 0.05). The RMS-V was abnormal (less than 25 microV) in 29 of 38 patients (76%), and in only 20% of normals (p less than 0.0005), and the signal-averaged QRS vector complex was abnormal (greater than 120 msec) in 26 of 38 patients (68%), and only 9% of normals (p less than 0.005). There was no significant correlation between any of the signal-averaged parameters, the site of AMI and total creatine kinase (CK) or CK-MB values. The signal-averaged parameters also showed no relationship to either the cardiothoracic (C/T) ratio or the left ventricular ejection fraction, determined by the Tc-99 m pertechnetate first pass blood pool technique. Holter ECG monitoring was performed twice in all AMI patients, at 7 to 18 days after the acute event (12 days average) and 3 weeks after the first recording. There were only four episodes of non-sustained ventricular tachycardia (VT), all during the second monitoring period. Three episodes (10%) occurred in patients with positive late potentials (LPs), defined by an RMS-V less than 25 microV in the terminal portion of QRS vector; one episode (11%) occurred in patients with negative LPs (9 patients). Although the incidence of LPs is significantly higher in patients with an AMI than in normal controls, the LPs detected by body surface signal-averaged ECG did not predict the occurrence of in- and out-of-hospital VTs. Thus, after AMI, Chinese patients may not be as prone to develop VTs as are Caucasians. Furthermore, the appearance of LPs is independent of cardiac size and left ventricular ejection fraction.

Regional sympathetic denervation after myocardial infarction in humans detected noninvasively using I-123-metaiodobenzylguanidine

Transmural myocardial infarction in dogs produces denervation of sympathetic nerves in viable myocardium apical to the infarct that may be arrhythmogenic. It is unknown whether sympathetic denervation occurs in humans. The purpose of this study was to use iodine- 123-metaiodobenzylguanidine (MIBG), a radiolabeled guanethidine analog that is actively taken up by sympathetic nerve terminals, to image noninvasively the cardiac sympathetic nerves in patients with and without ventricular arrhythmias after myocardial infarction.Results showed that 10 of 12 patients with spontaneous ventricular tachyarrhythmias after myocardial infarction exhibited regions of thallium-201 uptake indicating viable perfused myocardium, with no MIBG uptake. Such a finding is consistent with sympathetic denervation. One patient had frequent episodes of nonsustained ventricular tachycardia induced at exercise testing that was eliminated by beta-adrenoceptor blockade. Eleven of the 12 patients had ventricular tachycardia induced at electrophysiologic study and metoprolol never prevented induction. Sympathetic denervation was also detected in two of seven postinfarction patients without ventricular arrhythmias. Normal control subjects had no regions lacking MIBG uptake.This study provides evidence that regional sympathetic denervation occurs in humans after myocardial infarction and can be detected noninvasively by comparing MIBG and thallium-201 images. Although the presence of sympathetic denervation may be related to the onset of spontaneous ventricular tachyarrhythmias in some patients, it does not appear to be related to sustained ventricular tachycardia induced at electrophysiologic study.

Left Ventricular Hypertrophy as a Factor in Arrhythmias and Sudden Death

Hypertensive patients with left ventricular hypertrophy (LVH) are predisposed to sudden cardiac death. Several studies have demonstrated that complex ventricular arrhythmias, including episodes of nonsustained ventricular tachycardia, occur commonly during ambulatory electrocardiographic monitoring of hypertensive patients with LVH. The prognostic significance of such arrhythmias is not known. In other forms of cardiac hypertrophy, however, such as hypertrophic cardiomyopathy, complex ventricular arrhythmias detected during ambulatory monitoring are predictive of subsequent sudden death and there is some evidence that appropriate antiarrhythmic drug therapy may reduce mortality.