Sleep-related breathing disorders are associated with ventricular arrhythmias in patients with an implantable cardioverter-defibrillator

STUDY OBJECTIVES: The aim of this study was to examine the influence of sleep-related breathing disorders (SBDs) on the occurrence of ventricular arrhythmias in patients with reduced left ventricular ejection fraction (LVEF), and life-threatening ventricular tachyarrhythmias treated with an implantable cardioverter-defibrillator. PATIENTS: Thirty-eight patients with LVEF of 36 +/- 13% (mean +/- SD) underwent a sleep study. When an apnea-hypopnea index (AHI) > 10/h occurred, SBD was diagnosed. MEASUREMENTS AND RESULTS: In patients with SBDs, ventricular arrhythmias (couplets, triplets, short runs) were recorded simultaneously by Holter ECG and differentiated in episodes with and without disordered breathing. An apnea-associated arrhythmia index (AI) was defined as the number of ventricular arrhythmias occurring simultaneous to disordered breathing. Accordingly, a nonapnea-associated arrhythmia index (NAI) was calculated as the number of ventricular arrhythmias during normal breathing. SBDs were diagnosed in 14 patients: Cheyne-Stokes respiration (CSR) [n = 8; AHI, 32.1 +/- 25.0/h], and obstructive sleep apnea (OSA) [n = 6; AHI, 34.1 +/- 14.6/h]. Four patients in the OSA group and four patients in the CSR group had ventricular arrhythmias during sleep, revealed by Holter ECG. In these eight patients, the AI was significantly higher than the NAI (20.9 +/- 18.8/h vs 4.9 +/- 3.3/h, respectively). CONCLUSIONS: These data show that ventricular arrhythmias occurred significantly more often in association with disordered breathing in patients at high risk for arrhythmias and reduced LVEF.     

Evaluation of antiarrhythmic drug effects with simultaneous analysis of single ventricular premature contractions, couplets and salvos.

To improve the clinical value of ambulatory Holter electrocardiographic (ECG) monitoring as a tool of antiarrhythmic therapy control, a new statistical model was developed. In a patient group at increased risk of sudden cardiac death, the spontaneous variability of ventricular arrhythmias was assessed, with simultaneous consideration of single ventricular premature complexes, couplets and salvos. The study included 100 patients who suffered from coronary heart disease or idiopathic dilated cardiomyopathy and for whom greater than 30 ventricular premature complexes/h and couplets had been demonstrated on the last Holter ECG before the study. Between 3 and 12 Holter recordings were made for each patient in a drug-free state; the mean follow-up period was 260 days (maximum 1,403). The mean hourly values of the ectopic events (EE) were assessed separately for ventricular premature complexes, couplets and salvos. The spontaneous variability (SV) was calculated for single ventricular premature complexes, couplets and salvos as SV = log (EEday 2 + 0.01/EEday 1 + 0.01) and linked in one, two and three dimensions. Compared with the consideration of only one type of arrhythmia (one-dimensional model), the simultaneous use of two or three types of arrhythmia (two- or three-dimensional model) resulted in considerably lower reduction and aggravation rates as sufficient proof of drug effects. With control intervals up to 1 week, the one-dimensional model yielded reduction rates for ventricular premature complexes, couplets and salvos of -63%, -90% and -95%, respectively. In contrast, with the three-dimensional model, the rates were -28%, -72% and -88%. The corresponding aggravation values were +370, +1,114% and +2,189% versus +38%, +256% and +747%.(ABSTRACT TRUNCATED AT 250 WORDS)     

Efficacy of amiodarone during long-term treatment of malignant ventricular arrhythmias in patients with chronic chagasic myocarditis

Oral amiodarone was administered to 24 patients with chronic chagasic myocarditis (CCM) and malignant ventricular arrhythmias. Control 24-hour Holter recordings revealed frequent ventricular premature beats (VPBs) (157 to 2572/hr; mean 714 ± 125), multiform VPBs, and countless numbers of ventricular couplets in all patients, R-on-T phenomenon in 17 patients, and ventricular tachycardia in 21 patients. Amiodarone caused total and persistent suppression of ventricular couplets and tachycardia and greater than 93% reduction of VPB number in 22 patients, during a follow-up of 26.6 months (range 2 to 55 months). In 1 patient, ventricular couplets and tachycardia persisted despite the fact that a 98.2% reduction of VPB number was achieved. This latter patient was the only one in the whole group who experienced sudden death. The maximal antiarrhythmic effect was attained gradually after 3 to 26 weeks (mean 7.4). In four patients in whom treatment was discontinued after 3 to 12 months, the antiarrhythmic protection lasted 4 to 9 weeks. In nine patients the dose of amiodarone was 600 to 800 mg/day. In 15 patients the dose had to be increased to 800 to 1000 mg/day. Despite the presence of congestive heart failure in seven patients and intraventricular block in 17 patients, no limiting side effects were observed. Amiodarone proved to be extremely effective and safe against the most malignant ventricular arrhythmias of CCM.     

Accuracy of the pacemaker event recorder versus Holter‐ECG to detect both symptomatic and asymptomatic ventricular arrhythmias

1 Background

Although new pacemakers can register cardiac rhythm, few studies were performed evaluating their accuracy in diagnosing ventricular arrhythmias (VA). This study aimed to assess the correlation and agreement between the pacemaker's monitor and the ambulatory Holter in detecting VA.

2 Methods and results

We studied 129 patients with pacemakers, mean age 68.6 ± 19.1 years, 54.8% female. Once Holter monitoring was connected, the pacemakers’ event counters were reset and clocks of both systems were synchronized to register electrocardiograms (ECG) simultaneously. Pacemakers were programmed to detect the lowest ventricular rate and lowest number of sequential beats allowed in their event monitors. After 72 hours, Holter and pacemakers records were analyzed. VA was defined in Holter and event monitor, respectively, as: isolated premature ventricular complexes: “PVC”; pairs: “couplets”; nonsustained ventricular tachycardia (NSVT): “triplets”—3 beats; “runs”—4–8 or > 8 beats, and high ventricular rates (“HVR”)—3–4 beats. Spearman correlations evaluated whether pacemaker and Holter identified the same parameters. Intraclass correlation coefficients (ICCs) and respective 95% confidence intervals were calculated to assess the concordance between methods. The agreement between both systems was low, except for “triplet” and three beats NSVT (ICC = 0.984). The correlation for more than 10 PVC/h was moderate (Kappa = 0.483). When the pacemaker was programmed to detect HVR sequences of three beats lower than 140 bpm (< 140/3), the correlation with NSVT was perfect (r = 1) and agreement was also quite high (ICC = 0.800).

3 Conclusions

Pacemakers' event monitors underestimate the occurrence of ventricular arrhythmias detected by Holter. Standardization of pacemakers’ algorithms is required before using this function for patients' clinical follow‐up.     

索他洛尔治疗心律失常的临床观察

通过探索不同剂量索他洛尔在门诊心律失常患者中的疗效、副作用和致心律失常作用,寻求索他洛尔治疗心律失常的合理剂量和安全性。选择门诊快速房性、室性心律失常患者 500例,男 276例、女 224例。均经 24h动态心电图检查,单形性室性早搏(简称室早)数≥2 000次(或≥100次 /h)或有成对室早、短阵室性心动过速及频发房性早搏、房性心动过速、心房扑动、心房颤动(简称房颤)。依次服用索他洛尔 40, 80, 120, 160mg/12h各两周,服药前及服药 3天后检查心电图测量QT、QTc间期、QTd。14天检查 24h动态心电图判定疗效。结果:索他洛尔对室性心律失常的总有效率 86. 8%,房性心律失常 59. 0%,对预防阵发性房颤发作效果较好(P<0. 05),而对持续性心房扑动、房颤以控制心室率较理想。对各种心率均有明显的减慢作用,第 2周末平均下降 13% ~20%,之后较为平稳,未继续下降。结论:索他洛尔最佳剂量 80~120mg/12h,副作用小,门诊应用较安全,起效时间 3 ~14天,持续用药可维持疗效,对房性及室性心律失常均有效。     

Effect of pharmacological wash-out in patients undergoing exercise testing after acute myocardial infarction

STUDY OBJECTIVES: Pharmacological therapy can reduce diagnostic and prognostic accuracy of exercise stress testing. However, the risk of withdrawing drugs early after myocardial infarction (MI) has not been established. We assessed safety and clinical implications of drug withdrawal in patients undergoing stress testing after uncomplicated MI. METHODS: A total of 362 MI patients underwent ECG Holter recording before and after withdrawing beta-blockers, calcium-antagonists and nitrates. QRS (QRS/h) and ventricular premature beats (VPB/h) count per hour, repetitive ventricular arrhythmias, ST segment changes and patient complaints were evaluated for reproducibility using kappa statistics and Bland-Altman method. RESULTS: No major complications occurred. Forty-three patients complained of >1 symptom on and 37 off therapy. QRS/h and VPB/h count were significantly (p<0.0001) higher off therapy but correlated with the corresponding values on therapy. A mean heart rate increase of 8 beats/min (agreement range -8 to +14 beats/min) and a five-fold increase in VPB/h (agreement range -141 to +151) were observed after withdrawing therapy. Repetitive ventricular arrhythmias and ST changes were also more frequent off therapy but intra-patient reproducibility was poor: kappa 0.12 (95% confidence interval (CI) -0.01 to 0.25) for arrhythmias, -0.02 (95% CI -0.46 to 0.39) for ST depression and -0.01 (95% CI -0.66 to 0.64) for ST elevation. CONCLUSIONS: The withdrawal of therapy is well tolerated soon after uncomplicated MI; however, a generic but not individual risk of ventricular arrhythmias and/or transient myocardial ischemia has to be taken into account.     

Recent myocardial infarction: incidence of the ventricular arrhythmias and correlations with some ecgraphic and hemodynamic parameters at rest and during exercise (author's transl)

To assess incidence of ventricular premature beats (VPB) and correlate ECGraphic and hemodynamic data of parameters at rest and during exercise, 176 oligo or asymptomatic patients (167 males and 9 females) with recent myocardial infarction (RMI) (20-60 days after AMI) underwent a maximal symptom limited exercise test in supine position during hemodynamic monitoring (Swan-Ganz cath. 7F placed in pulmonary artery) without medical therapy. During the following 24 hours the patients underwent a continuous ambulatory ECG. 71 patients (40%) had no VPB (class 0), 56 patients (32%) had less than 1 VPB/hour (class 1), 35 patients (20%) had less than 6 VPB/minute and less than 30 VPB/hour (class 2) and 14 patients (8%) had greater than 6 VPB/minute and greater than 30 VPB/hour (class 3). Patients with VPB were then divided into qualitative classes: class A: 57 patients (54%) with isolated and unifocal VPB; class B: 38 patients (36%) with polifocal, bigeminal and paired VPB; class C: 10 patients (10%) with R on T or consecutive beats (3 or more). 28% of the patients had complex VPB (class B and C). 20% of all the patients (36/176) had VPB during exercise, 8 patients had VPB only during exercise, increasing the percentage of arrhythmias from 60% to 64%. VPB were more frequent and complex in patients with inferior or anterior + inferior MI than in patients with anterior MI and patients aged more than 60. Patients with complex VPB had cardiac volume index higher (p less than 0.05) than patients without VPB or with isolated VPB. Patients of different classes showed work capacity of 75-80 watts with 75-80% of maximal theoretic heart rate. Infarct size (NQ) was not correlated with number of VPB. Arrhythmias were slightly more frequent in patients with exercise ST depression (66%) than in patients without exercise ST depression (57%) (NS). No significant difference was found between ST elevation at rest and during exercise and VPB. PWP was, on the average, normal at rest (10 mmHg in the different classes) and slightly pathological during exercise with no differences between patients without VPB (class 0 = 21.7 mmHg) and patients with VPB (class 1 = 22.4 mmHg, Class 2 = 24.4 mmHg, Class 3 = 20.8 mmHg). In conclusion: in oligo or asymptomatic patients with RMI: a) exercise slightly increased the sensitivity of continuous ambulatory ECG to reveal VPB b) poor correlations were found between VPB and ECGraphic and hemodynamic parameters both at rest and during exercise.     

Suppressive effect of nicorandil in ventricular arrhythmias after reperfusion therapy in patients with acute myocardial infarction

BACKGROUND: Nicorandil is reported to inhibit reperfusion arrhythmias in patients with acute myocardial infarction (AMI), but few studies have counted ventricular arrhythmias with Holter electrocardiograms in patients treated with nicorandil following AMI reperfusion. OBJECTIVES: In the present study, we examined the effects of nicorandil by investigating the occurrence of ventricular arrhythmia with Holter electrocardiogram monitoring after percutaneous coronary intervention with acute myocardial infarction. METHODS: Forty patients with AMI who underwent successful percutaneous coronary intervention (PCI) were enrolled and randomly assigned to nicorandil or placebo groups. Following PCI, nicorandil was infused intravenously at 6 mg/hr for 24 hr, with Holter electrocardiogram monitoring. Patients with 100 or more premature ventricular contractions (PVCs) over the 24-hour period were studied. The total number of PVCs, frequency of occurrence of ventricular tachycardia, and clinical characteristics were compared between the two groups. RESULTS: Fourteen patients in the nicorandil group and 12 patients in the placebo group exhibited 100 or more PVCs over the 24-hour period. Lesion characteristics and procedural factors did not differ between the two groups. Fewer PVCs were counted in the nicorandil group than in the placebo group(144.6 +/- 106.5 vs 286.8 +/- 159.1 beats/day, p = 0.012). The frequency of coupled PVCs was lower in the nicorandil group (6.9 +/- 6.9 vs 16.3 +/- 12.8 beats/day, p = 0.025). Although the frequency of ventricular tachycardia did not differ between the two groups, ventricular tachycardia duration was significantly shorter in the nicorandil group (3.73 +/- 2.30 vs 8.34 +/- 7.45 sec, p = 0.03). CONCLUSIONS: Our study indicates nicorandil inhibits ventricular arrhythmias following PCI for patients with AMI. Nicorandil treatment following PCI for AMI is convenient and may reduce the rate of cardiac events by inhibiting ventricular arrhythmias, thereby potentially improving the prognosis.     

Residual flow to the infarct zone against lethal ventricular tachyarrhythmias during the acute phase of myocardial infarction

BACKGROUND: The benefits of residual flow to the infarct zone have been demonstrated in acute myocardial infarction (AMI), but its relation to ventricular tachyarrhythmias remains uncertain. HYPOTHESIS: This study was undertaken to test the hypothesis that residual flow is an important determinant of lethal ventricular tachyarrhythmias (sustained ventricular tachycardia or ventricular fibrillation) during the acute phase of AMI. METHODS: We investigated the determinants of lethal ventricular tachyarrhythmias within 24 h after the onset of symptoms in 310 consecutive patients (256 men; age 57.4 +/- 11.5 years) with AMI undergoing primary angioplasty. Patients were divided into two groups: those with (Group 1, n = 40) and those without (Group 2, n = 270) lethal ventricular tachyarrhythmias. Residual flow was defined as the presence of anterograde flow (> or = Thrombolysis in Myocardial Infarction [TIMI] 2 flow) or good angiographic collaterals (> or = grade 2) on a preintervention angiogram. RESULTS: Univariate determinants of lethal ventricular tachyarrhythmias were cardiogenic shock, systolic blood pressure, peak level of creatine kinase, culprit artery, spontaneous reperfusion, and residual flow. In multivariate analysis, however, cardiogenic shock (odds ratio [OR] = 4.79, 95% confidence interval [CI] 1.63-14.11, p = 0.004), residual flow (OR = 0.34, 95% CI 0.14-0.81, p = 0.015), and the right coronary artery as the culprit artery (OR = 2.09,95% CI 1.03-4.22, p = 0.040) were independent determinants of these arrhythmias. In-hospital death occurred in 10 patients and was more common in Group 1 than in Group 2 (12.5% vs. 1.9%, respectively, p < 0.001). CONCLUSION: The absence of residual flow was associated with greater risk of lethal ventricular tachyarrhythmias during the acute phase of AMI, suggesting a protective role of residual flow against these arrhythmias in AMI.     

Rhythmic profiles of the late phase of acute myocardial infarction as a function of age]

OBJECTIVES: To evaluate the incidence of ventricular arrhythmias in the late phase of acute myocardial infarction (AMI) and to compare it with the following clinical parameters: age, sex, AMI localization, ventricular function (Killip classes), maximal creatinokinase (CK max) and the presence of sinus tachycardia. DESIGN: Prospective study, during a period of 31 months, of a non-selected group of patients with AMI. SETTING: Coronary Care Unit (UTIC-Arsénio Cordiero). PATIENTS: Non-selected group of 153 patients with acute myocardial infarction who survived the second week of disease. MATERIAL AND METHODS: 24-hour Holter ECG performed between the 4th and the 25th day of AMI. The patients were divided into two groups according to the hourly frequency of premature ventricular beats (PVB): less than 3 per hour (PVB less than 3/h) and 3 or more per hour (PVB greater than or equal to 3/h). RESULTS: PVB greater than or equal to 3/h occurred in 36 patients (24%). There was no differences in the occurrence of ventricular arrhythmias between sex, AMI localization, AMI size evaluated by CK max, and the presence of sinus tachycardia. Patients in Killip class III had more ventricular arrhythmias (67%) than patients in Killip class I (23%) (p less than 0.005), in Killip class II (18%) (p = 0.007), and in Killip IV (0%) (p = 0.017). In patients with serious left ventricular failure (classes III + IV) the ventricular arrhythmias were not significantly higher (40%) than in patients without serious left ventricular failure (classes I + II) (22%) (chi 2 = 2.5; p less than 0.25 NS). Patients with less than 41 years old had less PVB greater than or equal to 3/h (4%) than patients between ages 41-69 (24%) (p less than 0.05), and than patients over 70 years old (47%) (p = 0.00075). CONCLUSIONS: The majority of patients (76%) showed a low risk rithmic profile (PVB less than 3/h) in the late phase of AMI. Among all parameters the age of the patients was the one best related to the occurrence of ventricular arrhythmias. Sex, AMI localization, AMI size, and the presence of sinus tachycardia were not related to the presence of PVB. A slight tendency was found in patients with heart failure to have more PVB. On the other hand the elder group carried a statistically significant risk factor for a higher occurrence of ventricular premature beats.     

Efficacy of amiodarone during long-term treatment of potentially dangerous ventricular arrhythmias in patients with chronic stable ischemic heart disease

Amiodarone was administered orally to 30 patients with chronic stable coronary artery disease and severe ventricular arrhythmias. Control studies revealed frequent (more than 30/hr) ventricular premature beats (VPBs) (27 patients), bigeminy (21 patients), couplets (29 patients), R-on-T phenomenon (14 patients), ventricular tachycardia (16 patients), and ventricular fibrillation (1 patient). Two 24-hour Holter recordings and stress tests were performed before treatment, and an average of 3.6 per patient were done during treatment. Amiodarone caused suppression of all ventricular arrhythmias in 13 (43%) of the 30 patients and suppression of all complex forms and greater than 90% reduction of VPB number in 14 patients (47%) during a follow-up of 12.4 months. The mean dose was 590 mg/day in the 27 responders and 300 mg/day in the three nonresponders. A similar antiarrhythmic response was observed during stress testing. One of the 30 patients died due to massive pulmonary embolism and no arrhythmias were detected. In addition, amiodarone suppressed the occurrence of anginal pain and effort-induced ST changes in 9 of 10 patients and in 11 of 13 patients, respectively. The rate—pressure product and peak heart rate were significantly reduced in all patients. Our results suggest that amiodarone may be ideally suited for treatment of ventricular arrhythmias and for possible prevention of sudden death in patients with ischemic heart disease.     

High dose caffeine and ventricular arrhythmias.

The effect of high dose caffeine on ventricular arrhythmias was examined in 35 patients with recent myocardial infarctions. All patients received caffeine 450 mg or placebo on separate days using a randomized double-blind study design. Continuous Holter electrocardiographic recordings were performed for 8 h. Caffeine ingestion did not cause any increase in the frequency or complexity of ventricular ectopy with 19 of 35 patients experiencing ventricular arrhythmias after caffeine compared with 24 of 35 with placebo. Serious ventricular ectopic activity (including ventricular couplets and tachycardia) was similar on both study days. Moderately high doses of caffeine do not appear to increase ventricular arrhythmias in this patient population with ischemic heart disease.     

Noninvasive diagnosis of ventricular arrhythmias by means of ambulatory-ECG monitoring

Ambulatory ECG monitoring has enabled documentation of the type and frequency of ventricular arrhythmias and their relation to symptoms as well as prognosis. On 24-hour ambulatory ECG monitoring, ventricular premature beats (VPB) can be found in healthy subjects with a prevalence of 40 to 80% which is directly related to age. Complex ventricular arrhythmias are uncommon. The prevalence of VPB is higher in patients who have underlying structural heart disease; in those resuscitated from out of hospital sudden cardiac death, it is reported to be 100%. One of the most important concerns with regard to ventricular arrhythmias is the problem of spontaneous variability. There is, however, a higher degree of reproducibility on two consecutive days in patients with more than 300 VPB/hour and in patients who have experienced sustained ventricular tachycardia than in those with infrequent VPB. When ambulatory monitoring is repeated months up to one year after the initial investigation, reproducibility of arrhythmias is poor. The mechanism of sudden cardiac death has been shown to be ventricular tachycardia or ventricular fibrillation, both of which are associated with an antecedent increase in VPB. In patients with chronic coronary artery disease, idiopathic or hypertrophic cardiomyopathy, a relationship between the presence of ventricular arrhythmias and sudden cardiac death has been described but VPB are considered to be of independent prognostic value only in those with myocardial infarction. Ambulatory ECG monitoring is the preferred noninvasive method for drug evaluation in patients with frequent ventricular arrhythmias. In general, the available antiarrhythmic drugs are effective for suppression of ventricular arrhythmias in 45 to 80% of patients. As a side-effect dependent on the underlying condition, the incidence of proarrhythmic effects varies from 6 to 19%. Medical treatment may be effective in prolonging life in resuscitated patients. Limitations of ambulatory monitoring include low reliability in the presence of infrequent ventricular arrhythmias or marked spontaneous variability, low specificity with respect to prognosis, lack of standardized definition for treatment efficacy and problems of recognizing complex forms of ventricular arrhythmias.     

Ambulatory electrocardiographic correlates of ventricular inducibility during programmed electrical stimulation

To determine the relation between spontaneous and induced ventricular arrhythmias, ambulatory electrocardiographic (Holter) monitoring and programmed electrical stimulation were performed in 48 adult patients with suspected life-threatening ventricular arrhythmias. Nine had no inducible arrhythmia, 11 demonstrated 1 to 2 beats of intraventricular reentry, 19 exhibited non-sustained ventricular tachycardia and 9 exhibited sustained ventricular tachycardia during electrophysiologic studies. Patients without arrhythmia inducibility had a high incidence of multiformity (56%) and bigeminy (44%), but a low incidence of either couplets (11%) or spontaneous ventricular tachycardia (11%) on Holter monitoring. An increasing incidence of all "complex" ectopic features was found with increasing degrees of ventricular inducibility. In patients with inducible sustained ventricular tachycardia, multiformity was present in 100%, bigeminy and couplets in 89% and spontaneous ventricular tachycardia in 78%. Premature ventricular complex frequency, couplet frequency and the repetition index (the ratio of couplets to premature ventricular complexes) were also found to be directly correlated with the degree of ventricular inducibility. Three quantitative arrhythmia variables were identified which predicted ventricular tachycardia inducibility. Seven (78%) of 9 patients with a mean premature ventricular complex frequency of 100 or more/1,000 normal beats, 11 (85%) of 13 with a mean couplet frequency of 1 or more/1,000 normal beats and 19 (83%) of 23 with a mean repetition index value of 15 or more/1,000 premature ventricular complexes proved to have inducible ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of 24-hour Holter Monitoring with 14-day Novel Adhesive Patch Electrocardiographic Monitoring

Background

Cardiac arrhythmias are remarkably common and routinely go undiagnosed because they are often transient and asymptomatic. Effective diagnosis and treatment can substantially reduce the morbidity and mortality associated with cardiac arrhythmias. The Zio Patch (iRhythm Technologies, Inc, San Francisco, Calif) is a novel, single-lead electrocardiographic (ECG), lightweight, Food and Drug Administration–cleared, continuously recording ambulatory adhesive patch monitor suitable for detecting cardiac arrhythmias in patients referred for ambulatory ECG monitoring.

Methods

A total of 146 patients referred for evaluation of cardiac arrhythmia underwent simultaneous ambulatory ECG recording with a conventional 24-hour Holter monitor and a 14-day adhesive patch monitor. The primary outcome of the study was to compare the detection arrhythmia events over total wear time for both devices. Arrhythmia events were defined as detection of any 1 of 6 arrhythmias, including supraventricular tachycardia, atrial fibrillation/flutter, pause greater than 3 seconds, atrioventricular block, ventricular tachycardia, or polymorphic ventricular tachycardia/ventricular fibrillation. McNemar's tests were used to compare the matched pairs of data from the Holter and the adhesive patch monitor.

Results

Over the total wear time of both devices, the adhesive patch monitor detected 96 arrhythmia events compared with 61 arrhythmia events by the Holter monitor (P < .001).

Conclusions

Over the total wear time of both devices, the adhesive patch monitor detected more events than the Holter monitor. Prolonged duration monitoring for detection of arrhythmia events using single-lead, less-obtrusive, adhesive-patch monitoring platforms could replace conventional Holter monitoring in patients referred for ambulatory ECG monitoring.     

Ventricular arrhythmias are not a short-term reproducible phenomenon – why long recording monitoring is necessary

Background

The variability of ventricular arrhythmias (VA) among different days of the week is not well detected by one-day Holter monitoring.

Aims

To evaluate whether there are differences in VA distribution pattern during long recording period.

Methods

The EKG was recorded for 14 h per day during 7 days by Holter system in 34 consecutive pat ventricular couplets and non-sustained ventricular tachycardia (NSVT) recording from patients provided graphic data. We applied the Hurst method (H Coefficient) which evaluates whether a repetitive phenomenon is random or not. When the H is > 0.5 and < 1 means it is not random and implies a long-term memory effect. Considering the arrhythmic variability, the data were also analyzed by repetitive ANOVA comparing incidence of arrhythmias among the days.

Results

Isolated PVCs and ventricular couplets during 98 h recording provided graphic of the occurrence. A trend of increasing and decreasing of arrhythmias was observed which looks erratic. The H coefficient, however, was significantly > 0.5 for all patients. Repeated ANOVA showed statistic difference among days in 31 patients with isolated PVCs; in 26 with ventricular couplets and 19 with NSVT when analyzed per hour during week days (p < 0.05).

Conclusion

PVCs, ventricular couplets and NSVT are not a random phenomenon. Our data suggest the occurrence of ventricular arrhythmias had no similarity among the days, making unlikely that a single Holter recording for 24 h may capture this phenomenon.     

Arrhythmias in relation to transient ST elevations in Prinzmetal angina: induction by occlusion and reperfusion

To study the temporal relationship of occlusion and reperfusion we examined 16 patients (14 m, 2f) with variant angina for the occurrence and time course of arrhythmias with episodes of ST-elevation (n = 82). The patients underwent frequency-modulated ambulatory ECG recording, episodes of ST elevation were defined, and the arrhythmias were counted before, during and after each episode. In 10 patients (group A) no or only infrequent extrasystoles occurred. Of the other 6 patients (group B), one had a-v block II degree, 5 had frequent (greater than 2/min) ventricular or supraventricular premature beats, 3 with couplets or runs of VPB. Patients of group A and B did not differ in age, severity of fixed coronary stenoses and ventricular ejection fraction. There was a tendency towards a greater incidence of higher ST-elevations (greater than 2 mm) in group B (4 of 6 patients versus 2 of 10 in group A, p = 0.09). The relationship of arrhythmias and ST changes showed different patterns: the maximum of arrhythmias occurred during the episode in 3 patients, during and after the episode in 2 patients and only after the episode in 1 patient. Potentially dangerous arrhythmias are frequent in patients with variant angina and persist beyond the ST segment changes in one half of the affected patients.     

Effect of barucainide on left ventricular ejection fraction in patients with ventricular cardiac arrhythmias]

We studied the effect of barucainide, an investigational class lb antiarrhythmic drug, on ventricular arrhythmias and left-ventricular ejection fraction in 10 patients with frequent and complex ventricular arrhythmias (Lown grade 4a/4b). The study was conducted as a single-blind and placebo-controlled trial. With placebo, mean frequency of ventricular arrhythmias was 6238 VPB/24 h, 510 couplets/24 h, and 24 salvos/24 h. Mean left-ventricular ejection fraction was 37.6%, ranging from 18% to 58%. Therapy with barucainide (300-400 mg/day) resulted in a significant reduction of ventricular arrhythmias in 7 of 10 patients; in one patient barucainide had a clear proarrhythmic effect. Over all, left-ventricular ejection fraction (37.6% +/- 12% with placebo vs 36.1% +/- 11% with barucainide) was not significantly altered. In one patient, however, it was depressed by more than 5%; one patient complained of shortness of breath during exercise. None of the four patients with an initial ejection fraction below 35% showed a drop of ejection fraction during therapy with barucainide. The only main adverse effect was a small, but significant (p less than 0.005) rise of serum-kreatinine (1.13 +/- 0.26 vs 1.39 +/- 0.38 mg%) in all patients. We conclude that barucainide has a good antiarrhythmic effect and is usually well tolerated in patients with markedly depressed left-ventricular function. The mechanism causing the rise of serum-kreatinin, however, needs to be clarified in further studies.     

A new noninvasive index to predict sustained ventricular tachycardia and sudden death in the first year after myocardial infarction: based on signal-averaged electrocardiogram, radionuclide ejection fraction and Holter monitoring

A prospective study of the prognostic significance of the signal-averaged electrocardiogram (ECG), left ventricular function and 24 hour Holter ECG monitoring was performed in 102 patients (age 63 +/- 11 years) after myocardial infarction. The signal-averaged ECG (40 Hz high pass bidirectional filtering) was obtained 10 +/- 6 days after the acute myocardial infarction and all three tests were performed within 72 hours of each other. Ejection fraction was determined by radionuclide ventriculography. An abnormal signal-averaged ECG was seen in 44% of patients; abnormal ejection fraction (less than 40%) in 52% and high grade ectopic activity (greater than or equal to 10 ventricular premature depolarizations/h or couplets, or nonsustained ventricular tachycardia, or a combination of these) in 62%. During a 12 +/- 6 month follow-up period, 15 patients (14.7%) had an arrhythmic event defined as sustained ventricular tachycardia or sudden cardiac death, or both. The event rates were higher in patients with an abnormal versus a normal signal-averaged ECG (29 versus 3.5%, p = 0.003), an abnormal versus a normal ejection fraction (24 versus 6%, p = 0.001) and the presence versus the absence of high grade ectopic activity (23 versus 9%, p = 0.09). Patients with an abnormal signal-averaged ECG and an abnormal ejection fraction had a significantly higher (p = 0.0007) event rate than did patients in whom both the tests were normal (36 versus 0%; odds ratio 30.1).(ABSTRACT TRUNCATED AT 250 WORDS)     

Coronary revascularization: influence on ventricular arrhythmias

Myocardial ischemia may cause severe cardiac arrhythmias. In the present study, the influence of revascularization on ventricular arrhythmias was investigated. A total of 68 patients (61 male, 7 female; mean age 53 years) with coronary artery disease was divided into three groups: Group A (21 patients) underwent percutaneous transluminal coronary angioplasty (PTCA); Group B (37 patients) had coronary artery bypass grafting (CABG); and Group C were 10 patients who served as controls, who had simple coronary angiography. All patients had a Holter ECG on the day before angiography. PTCA patients and controls were restudied on the day after the procedure, while in Group B, Holter ECG was repeated three weeks after surgery. Groups A and B were again studied 18 months after the first Holter ECG. The PTCA group showed a slight reduction in complex arrhythmias immediately following PTCA, which increased again after 18 months; the CABG group, however, revealed a significant increase in complex arrhythmias three weeks after bypass surgery, but a decrease after 18 months. There was no significant change in the control group before or after angiography. Thus, successful revascularization has no influence on ventricular arrhythmias after 18 months.