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Ambulatory ECG (AECG) is very commonly employed in a variety of clinical contexts to detect cardiac arrhythmias and/or arrhythmia patterns which are not readily obtained from the standard ECG. Accurate and timely characterization of arrhythmias is crucial to direct therapies that can have an important impact on diagnosis, prognosis or patient symptom status. The rhythm information derived from the large variety of AECG recording systems can often lead to appropriate and patient-specific medical and interventional management. The details in this document provide background and framework from which to apply AECG techniques in clinical practice, as well as clinical research., (© 2017 International Society for Holter and Noninvasive Electrocardiology, Heart Rhythm Society, and Wiley Periodicals, Inc.)

Background: The aim of the study is to contrast the role of conventional ambulatory electrocardiographic monitoring (AEM) artifacts with a less emphasized problem with potentially more serious implications, that is, the failure to recognize, and therefore misinterpret, a genuine arrhythmia episode in the AEM recording., Methods: The study material included 500 Holter recordings and 500 recordings from the cardiac telemetry unit., Results: Electrocardiographic (ECG) artifacts were more common in telemetry recordings (5.6%) compared to Holter recordings (4%) for a total of 4.8%. There were 35 examples of misinterpretation of AEM recordings (3.5%). These were significantly more common in telemetry recordings (2.6%) compared to Holter recordings (0.9%). The most common ECG artifacts were examples of pseudo ventricular tachyarrhythmia (VT). The majority of misinterpretation (26 of 35 examples) were fast supraventricular tachyarrhythmias with aberrant QRS (including six examples of atrial flutter with periods of 1:1 atrioventricular conduction) that were misdiagnosed as ventricular VT. Other examples were misinterpretation of arrhythmic episodes consistent with sick sinus syndrome, pacemaker malfunction, and long QT syndrome. Only 5 of 48 examples of AEM artifacts resulted in management errors of commission or errors of omission compared to all 35 examples of misinterpretation., Conclusions: Compared to conventional artifacts in AEM, misinterpretation of nonartifactual arrhythmic episodes consistently resulted in management errors. Misinterpretation was significantly more common with telemetry recordings compared to Holter ECG. This highlights the need for more appropriate training of the entire clinical team in charge of the management of the cardiac telemetry unit., (© 2014 Wiley Periodicals, Inc.)

Electrolyte disorders can alter cardiac ionic currents kinetics and depending on the changes can promote proarrhythmic or antiarrhythmic effects. The present report reviews the mechanisms, electrophysiolgical (EP), electrocardiographic (ECG), and clinical consequences of electrolyte disorders. Potassium (K⁺) is the most abundent intracellular cation and hypokalemia is the most commont electrolyte abnormality encountered in clinical practice. The most significant ECG manifestation of hypokalemia is a prominent U wave. Several cardiac and non cardiac drugs are known to suppress the HERG K⁺ channel and hence the I(K), and especially in the presence of hypokalemia, can result in prolonged action potential duration and QT interval, QTU alternans, early afterdepolarizations, and torsade de pointes ventricular tachyarrythmia (TdP VT). Hyperkalemia affects up to 8% of hospitalized patients mainly in the setting of compromised renal function. The ECG manifestation of hyperkalemia depends on serum K⁺ level. At 5.5-7.0 mmol/L K⁺, tall peaked, narrow-based T waves are seen. At > 10.0 mmol/L K⁺, sinus arrest, marked intraventricular conduction delay, ventricular techycardia, and ventricular fibrillation can develop. Isolated abnormalities of extracellular calcium (Ca⁺⁺) produce clinically significant EP effects only when they are extreme in either direction. Hypocalcemia, frequently seen in the setting of chronic renal insufficiency, results in prolonged ST segment and QT interval while hypercalcemia, usually seen with hyperparathyroidism, results in shortening of both intervals. Although magnesium is the second most abudent intracellular cation, the significance of magnesium disorders are controversial partly because of the frequent association of other electrolyte abnormalities. However, IV magnesium by blocking the L-type Ca(⁺⁺) current can successfully terminate TdP VT without affecting the prolonged QT interval. Finally, despite the frequency of sodium abnormalities, particularly hyponatremia, its EP effects are rarely clinically significant.

The cardiovascular drug carvedilol is characterized by multiple pharmacological actions, which translate into a wide-spectrum therapeutic potential. Its major molecular targets are membrane adrenoceptors, ion channels, and reactive oxygen species. Carvedilol's favorable hemodynamic effects are due to the fact that the drug competitively blocks beta(1)-, beta(2)-, and alpha(1)- adrenoceptors. Several additional properties have been documented and may be clinically important, including antioxidant, antiproliferative/antiatherogenic, anti-ischemic, and antihypertrophic effects. The antiarrhythmic action of carvedilol may be related to a combination of its beta-blocking effects with its modulating effects on a variety of ion channels and currents. Several studies suggest that the drug may be useful in reducing cardiac death in high-risk patients with prior myocardial infarction and/or heart failure, as well as for primary and secondary prevention of atrial fibrillation. This article will review experimental data available on the electrophysiologic properties of carvedilol, with a focus on their clinical relevance.

Objectives: This study investigated prediction of arrhythmic events by the signal-averaged electrocardiogram (ECG) and programmed stimulation in patients with nonischemic dilated cardiomyopathy., Background: Risk stratification in patients with nonischemic dilated cardiomyopathy remains controversial., Methods: Eighty patients with nonischemic dilated cardiomyopathy and spontaneous nonsustained ventricular tachycardia underwent signal-averaged electrocardiography (both time-domain and spectral turbulence analysis) and programmed stimulation. All patients were followed up for a mean of 22 +/- 26 months., Results: Sustained monomorphic ventricular tachycardia was induced in 10 patients (13%), who all received amiodarone. The remaining 70 patients were followed up without antiarrhythmic therapy. Of the 80 patients, 15% had abnormal findings on the time-domain signal-averaged ECG, and 39% had abnormal findings on spectral turbulence analysis. Time-domain signal-averaged electrocardiography had a better predictive accuracy for induced ventricular tachycardia than spectral turbulence analysis (88% vs. 66%, p < 0.01). During follow-up, there were 9 arrhythmic events (5 sudden deaths, 4 spontaneous ventricular tachycardia/fibrillation) and 10 nonsudden cardiac deaths. Cox regression analysis showed that no variables predicted arrhythmic events or total cardiac deaths. The 2-year actuarial survival free of arrhythmic events was similar in patients with or without abnormal findings on the signal-averaged ECG or induced ventricular tachycardia., Conclusions: In patients with nonischemic dilated cardiomyopathy, 1) there is a strong correlation between abnormal findings on the time-domain signal-averaged ECG and induced ventricular tachycardia, but both findings are uncommon; and 2) normal findings on the signal-averaged ECG, as well as failure to induce ventricular tachycardia, do not imply a benign outcome.

The predictive accuracy of time-domain (TD) late potential analysis of the signal-averaged electrocardiogram in postmyocardial infarction (MI) is limited by the high incidence of false positives in inferior MI. However, frequency-domain spectral turbulence (ST) analysis suffers from a high incidence of false positives, especially in anterior MI. A prospective study was conducted of 262 patients with acute MI to investigate the hypothesis that combined TD and ST analyses of the signal-averaged electrocardiogram could improve its predictive accuracy for serious arrhythmic events in the post-MI period. Abnormal TD criteria were RMS40 less than 25 microV at 25 Hz plus RMS40 less than 16 microV at 40 Hz, and abnormal ST criteria were a turbulence score of 3 or 4. Seventeen patients had arrhythmic events during 10.5 +/- 2.4 months of follow-up evaluation (13 sudden cardiac death judged to be due to arrhythmia and 4 nonfatal sustained ventricular tachycardia). The total predictive accuracy of combined TD and ST (92%) was higher than TD (87%), whereas ST had the lowest total predictive accuracy of 78%. The negative predictive accuracy of all three analyses was high (96-97%). However, the positive predictive accuracy of TD (28%) was higher than ST (14%). Combined TD and ST significantly improved the positive predictive accuracy of the test to 35% in the total group and to 40% in patients with first anterior or inferior MI. The best results were obtained in patients with first anterior MI, where the positive predictive accuracy of combined analysis was 50%.

The prevalence of an abnormal signal-averaged electrocardiogram (ECG) and ventricular arrhythmias on 24 h ambulatory electrocardiography was evaluated in 118 patients 13 +/- 2 days after acute myocardial infarction. Group 1 (46 patients) underwent intravenous thrombolysis within 6 h of the onset of symptoms, whereas Group 2 (72 patients) did not. An abnormal signal-averaged ECG was seen in 15% of patients in Group 1 and 21% of those in Group 2 (difference not significant). The number of ventricular premature complexes/h was lower in Group 1 than in Group 2: 2.58 +/- 1.63 versus 7.91 +/- 10.75 (p less than 0.01). However, complex arrhythmias (greater than or equal to 10 ventricular premature complexes/h or ventricular tachycardia) were equally common in Groups 1 and 2 (20% versus 22%, respectively). Their prevalence was similar in patients with or without an abnormal signal-averaged ECG (29% versus 18%, respectively, in Group 1 and 27% versus 21%, respectively, in Group 2). Comparison between patients with (n = 26) or without (n = 20) angiographic patency of the infarct-related coronary artery after thrombolysis showed no significant difference in the prevalence of an abnormal signal-averaged ECG (8% versus 25%, respectively) and complex ventricular arrhythmias (19% versus 20%, respectively). These data suggest that thrombolysis does not affect the prevalence of complex ventricular arrhythmias and an abnormal signal-averaged ECG or their relation after acute myocardial infarction.

Ventricular arrhythmias during transient myocardial ischemia were studied in 60 patients with spontaneous angina and greater than or equal to 1 ischemic attack with ST-segment depression during 24-hour ambulatory electrocardiography. The patients were divided into 2 groups: group 1, 10 patients (17%) who developed ventricular arrhythmias during 26 of 92 (28%) ischemic attacks; and group 2, 50 patients who did not show this phenomenon. Daily ischemic attacks, total ischemic time and the proportion of symptomatic ischemic attacks were significantly greater (p less than 0.01) in group 1 versus group 2. In group 1 patients, ischemic attacks were found to have twice the duration in the presence of arrhythmias than in their absence (20.4 +/- 11.9 vs 9.1 +/- 8.4 minutes, p less than 0.01); arrhythmias were more common during symptomatic than during silent ischemic attacks (39 vs 13%, p less than 0.02). Arrhythmias occurred at the onset or peak of ST-segment depression (ischemia phase) in 6 cases (60%), during the resolution of ST-segment depression (recovery phase) in 2 cases (20%) and during both phases of ischemic attacks in the remaining 2 (20%). When compared to recovery phase arrhythmias, ischemia phase arrhythmias were characterized by a later onset time (173 +/- 144 vs 58 +/- 54 seconds, p less than 0.01) and a longer duration (105 +/- 107 vs 41 +/- 22 seconds, p less than 0.01). During the ischemia phase, 16 of 353 ventricular premature complexes initiated ventricular tachycardia, while during the recovery phase only 1 of 161 ventricular premature complexes resulted in ventricular tachycardia (4.5 vs 0.6%, p less than 0.02). Thus, ventricular arrhythmias may accompany spontaneous ischemic ST-segment depression, when the latter is recurrent, prolonged and symptomatic; arrhythmias are characterized by a greater frequency, duration and malignancy during the ischemia phase than during the recovery phase of ischemic attacks.

Forty-two patients with variant angina were studied by ambulatory ECG monitoring to determine the incidence and the characteristics of ventricular arrhythmias during ischemic attacks. Twenty-six patients had no ventricular arrhythmias in 633 ischemic attacks; 16 patients had ventricular arrhythmias in 116/586 ischemic attacks. The number of ischemic attacks per day and the magnitude of ST elevation were significantly (p less than 0.05) greater in patients with ventricular arrhythmias. Ventricular arrhythmias appeared at the onset or at the peak of ST elevation (first phase) in 17 ischemic attacks, during the resolution of ST elevation (second phase) in 43 attacks, during both the phases in 9 attacks. ST alternans appeared during 6 ischemic attacks with arrhythmias. Two episodes of ventricular fibrillation and 22 runs of ventricular tachycardia occurred during the first phase, 17 episodes of ventricular tachycardia were recorded during the second phase. Ventricular tachycardia of the second phase compared with ventricular tachycardias of the first phase were significantly (p less than 0.01) slower, uniform and initiated by a late premature beat. Incidence of arrhythmias of the second phase was strictly correlated with the duration of ischemic attacks. Nine patients who showed ventricular arrhythmias during the second phase of ischemic attacks were enrolled in a cross-over study to assess the antiarrhythmic effects of nifedipine (120 mg/day) and verapamil (480 mg/day). During treatment with nifedipine, the frequency of ischemic attacks declined by 85%, while the frequency of attacks with arrhythmias declined by 97% (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

The ST alternans was recorded during at least one ischemic attack with ST elevation in nine of 65 patients with variant angina. The magnitude and duration of ST elevation during ischemic attacks were significantly greater in patients with than in those without ST alternans. It always appeared during the occlusion phase and disappeared during the reperfusion phase of ischemic attacks. In patients with episodic ST alternans, the ischemic attacks showed a greater ST elevation and a longer duration in the presence of ST alternans than in its absence. The incidence of occlusion phase ventricular arrhythmias was greater in patients with than in those without ST alternans; the incidence of reperfusion phase ventricular arrhythmias was similar in the two groups. The ST alternans always preceded the onset of occlusion phase arrhythmias. Thus, in variant angina, ST alternans represents an index of the severity of ischemia and a precursor of ventricular arrhythmias.

The incidence and time course of complex ventricular arrhythmias and of the abnormal signal averaged electrocardiogram were studied prospectively in 90 patients in the first two months after acute myocardial infarction. Serial recordings of both 24 hour ambulatory and signal averaged electrocardiograms were obtained 0-5 days (phase 1), 6-30 days (phase 2), and 31-60 days (phase 3) after infarction. A total of 264 ambulatory electrocardiograms and 264 signal averaged electrocardiograms were available for analysis. Complex ventricular arrhythmias were seen in 31%, 17%, and 38% of patients during phases 1, 2, and 3 respectively, and abnormal signal averaged electrocardiogram in 13%, 24%, and 16%. The incidence of complex ventricular arrhythmias was not significantly different in patients with or without an abnormal signal averaged electrocardiogram in the entire study period nor in any of the three phases after infarction. During phase 2 when abnormal signal averaged electrocardiograms were most common complex ventricular arrhythmias were least common. This lack of correlation suggests that the abnormal signal averaged electrocardiogram and complex ventricular arrhythmias after infarction have different electrophysiological bases.

Serial recordings of the signal-averaged ECG and the 24-hour ambulatory ECG were obtained from 156 patients with acute myocardial infarction up to 5 days (phase 1), 6 to 30 days (phase 2), and 31 to 60 days (phase 3) after the infarction. Left ventricular ejection fraction by radionuclide ventriculography was also determined in phase 2. The signal-averaged ECG was abnormal during one or more of the three phases in 51 patients (31%). In 35 of these patients (69%) the recording changed category between normal and abnormal with the highest prevalence of abnormal recording occurring during phase 2. Eight patients had ventricular tachycardia/ventricular fibrillation in the first 48 hours after myocardial infarction. The signal-averaged ECG was abnormal in only one of these patients. Twelve patients had late arrhythmic events during the first year of follow-up (four sudden deaths and eight instances of documented ventricular tachycardia or ventricular fibrillation). Nine of the 12 patients had an abnormal signal-averaged ECG in phase 2 and four of these nine had a normal recording in phase 1. Five patients had a transient abnormal signal-averaged ECG in phase 1, whereas six patients had an abnormal recording only in phase 3. None of these 11 patients had an arrhythmic event. Stepwise logistic regression showed that an abnormal signal-averaged ECG in phase 2 has the most significant relation to late arrhythmic events. Both an abnormal signal-averaged ECG and a left ventricular ejection fraction less than 40%, but not complex ventricular arrhythmias, were independent significant risk factors for late arrhythmic events.(ABSTRACT TRUNCATED AT 250 WORDS)

In order to assess the efficacy and safety of oral indecainide in patients with serious ventricular arrhythmias we studied 11 patients with high-grade ventricular ectopy and ventricular tachycardia (VT) which were refractory to therapy with at least one standard antiarrhythmic drug. Spontaneous arrhythmias were quantitated by 24-h Holter monitor before and during therapy with indecainide. Spontaneous VT was sustained in 4 patients and nonsustained in 7. Ten patients underwent baseline electrophysiologic study (EPS) and VT was induced in 9. The mean ejection fraction was 25 +/- 14%. Indecainide was given orally at a dose of 211 +/- 118 mg/day. The frequency of ventricular premature beats (VPBs) was significantly (greater than 85%) decreased in 90% of patients, while ventricular couplets frequency decreased in 78%. Spontaneous VT was abolished in 5 of 11 (45%). Sustained VT was induced in 5 of 7 (71%) patients who underwent follow-up EPS. The QRS duration was significantly prolonged during therapy (0.13 +/- 0.04 s) compared to control (0.10 +/- 0.02 s). The PR, QTc, and JTc intervals were not significantly changed. Indecainide was well tolerated, but 2 patients died of ventricular tachyarrhythmias while receiving the drug. Indecainide suppressed VPBs in a high percentage of patients, but was much less successful in controlling VT. Caution is necessary when using this drug because of its potential for exacerbation of arrhythmia.