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Purpose: Heart rate variability is a commonly used measurement to evaluate functioning of autonomic nervous system, psychophysiological stress, and exercise intensity and recovery. HRV measurements contain artefacts such as extra, missed or misaligned beat detections, which can produce significant distortion on HRV parameters. In this paper, a robust automatic method for artefact detection from HRV time series is proposed. Methods: The proposed detection method is based on time-varying thresholds estimated from distribution of successive RR-interval differences combined with a novel beat classification scheme. The method is validated using simulated extra, missed and misaligned beat detections as well as real artefacts such as atrial and ventricular ectopic beats. Results: The sensitivity of the algorithm to detect simulated missed/extra beats was 100%. The sensitivity to detect real atrial and ventricular ectopic beats was 96.96%, the corresponding specificity being 99.94%. The mean error in HRV parameters after correction was <2% for missed and extra beats as well as for misaligned beats generated with large displacement factors. Misaligned beats with smallest displacement factor were the most difficult to detect and resulted in largest HRV parameter errors after correction, largest errors being <8%. Conclusions: The HRV artefact correction algorithm presented in this study provided comparable specificity and better sensitivity to detect ectopic beats as compared to state-of-the-art algorithms. The proposed algorithm detects abnormal beats with high accuracy, is relatively easy to implement, and secures reliable HRV analysis by reducing the effect of possible artefacts to tolerable level.

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METHODS: Atrial premature beats are frequently diagnosed during pregnancy, supraventricular tachycardia (atrial tachycardia, AV nodal reentrant tachycardia, circus movement tachycardia) less frequently. For acute therapy, electrical cardioversion with 50-100 J is indicated in all unstable patients. In stable supraventricular tachycardia, initial therapy includes vagal maneuvers to terminate breakthrough tachycardias. For short-term management, when vagal maneuvers fail, intravenous adenosine is the drug of first choice and may safely terminate the arrhythmia. For long-term therapy, beta-blocking agents with beta(1) selectivity are first-line drugs; class Ic agents or the class III drug sotalol represent effective and therapeutic alternatives. Ventricular premature beats are also frequently present during pregnancy and benign in most of the unstable patients; however, malignant ventricular tachyarrhythmias (sustained ventricular tachycardia, ventricular flutter, ventricular fibrillation) are less frequently observed. Electrical cardioversion is necessary in all patients with hemodynamically unstable situation and life-threatening ventricular tachyarrhythmias; in hemodynamically stable patients, initial therapy with ajmaline, procainamide or lidocaine is indicated. If prophylactic therapy is needed, beta-blocking agents with beta(1) selectivity are regarded as drugs of first choice. If this therapy proves ineffective, class Ic agents or sotalol can be considered. In patients with syncopal ventricular tachycardia, ventricular fibrillation, ventricular flutter or aborted sudden death, an implantable cardioverter-defibrillator is indicated. In patients with symptomatic bradycardia, a pacemaker can be implanted using echocardiography at any stage of pregnancy. CONCLUSIONS: The treatment of the pregnant patient with cardiac arrhythmias requires important modifications of the standard practice of arrhythmia management. The goal of therapy is to protect the patient and fetus through delivery, after which chronic or definitive therapy can be administered.

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The 24-hour periodicity of supraventricular (SVPB) and ventricular (VEB) extrasystoles in healthy elderly men (age 49-69 years) was studied at two altitudes during 24 h Holter ECG monitoring. At the low altitude (200 m, n = 26), SVPB were more frequent than VEB. The highest occurrence of SVPB was at 17:00 h, the lowest at 01:00 and 02:00 h (P<0.001). The highest occurrence of VEB was at 09:00 h, the lowest one at 04:00 h (P<0.001). At 1350 m (n=9) the incidence of both SVPB and VEB was approximately twofold higher compared to that at the low altitude (P<0.001). The highest occurrence of SVPB was at 13:00 h, the lowest at 06:00 h (P<0.001). VEB were the most frequent at 10:00 h and 13:00 h, while the lowest frequency was observed at 06:00 h (P<0.001). Our results indicate that the incidence of SVPB and VEB in healthy persons at the moderate altitude is twofold and its periodicity is shifted compared to the low altitude. The cause of increased occurrence of extrasystoles is probably due to beta-adrenergic activation of the heart at the higher altitude.

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PURPOSE: To evaluate the results of 24-h Holter monitoring performed on healthy U.S. Air Force aircrew with asymptomatic ectopy on resting electrocardiograms (ECG). METHODS: A historical review of the USAF Central ECG Library database was conducted on all Holter studies completed for evaluation of ECG ectopy between 1 Jan 86 and 31 Dec 97. Univariate and multivariate statistical analyses were performed to determine the association between ectopy and the aeromedical dispositions of aircrew evaluated for incidental ECG ectopy. RESULTS: During this period, 147,571 resting ECGs were submitted to the Aeromedical Consultation Service (ACS) for interpretation. The mean age of the subjects was 35 yr (range 19 to 57 yr). There were 480 24-h Holter studies performed for ECG ectopy. Of these, 49% had normal or normal variant findings; another 11% were found acceptable for flying after normal treadmill testing and echocardiography. ACS evaluation was required for the remaining 40% of subjects. Overall, 4% were permanently disqualified, and 17% were lost to follow-up. Excluding subjects lost to follow-up, 95% of aircrew were returned to flying status (with or without a waiver). CONCLUSIONS: When controlled for age, no significant difference of aeromedical outcome was seen when comparing supraventricular and ventricular ectopy. Of the subjects, 51% had abnormal Holter studies, but the vast majority were returned to flying. Results of this study provide information useful in further defining aircrew medical evaluation protocols for evaluation of asymptomatic ECG ectopy with Holter monitoring.

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Dado que por lo general la presencia de extrasístoles cardiacos fetales son considerados arritmias no asociadas a complicaciones, nos propusimos mostrar el resultado perinatal de 48 casos de fetos con extrasístoles cardiacos estudiados en nuestra unidad desde 1994 hasta 1999. El promedio de edad gestacional al momento del diagnóstico fue de 30.2 semanas, y al parto de 37.8 semanas. El peso promedio al nacimiento fue de 3050 g y el puntaje Apgar de 8.9 puntos a los 5 minutos. La gran mayoría de los extrasístoles fueron catalogadas como extrasístoles auriculares. En 7 casos observamos 11 complicaciones asociadas (desarrollo de arritmias más complejas, malformaciones cardiacas, muerte neonatal y malformaciones extracardiacas). En 4 casos se observó la concomitancia de administración de betamiméticos y presencia de arritmias cardiacas fetales. En la mayoría de los casos los extrasístoles desaparecieron espontáneamente, y en los casos sin complicaciones, el manejo obstétrico no fue influenciado por la presencia de la arritmia. Concluimos que aunque la presencia de extrasístoles cardiacos fetales está asociado a una baja morbilidad perinatal, no están exentos de asociarse a patologías de mayor complejidad. Lo anterior hace mandatorio la ejecución de una ecocardiografía en todo feto que presente una alteración del ritmo cardiaco, para determinar el tipo de arritmia, evaluar la presencia de complicaciones asociadas y así definir el manejo perinatal

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OBJECTIVES: To establish a score or arrhythmic pattern for the prediction of long-term cardiac deaths on patients who have survived to the first acute myocardial infarction. PATIENTS AND METHODS: We studied prospectively 200 patients that survived at a first myocardial infarction and in whom ambulatory ECG monitoring during 24 hours between days 7th and 18th (mean 12th) from the infarction was performed. The mean follow-up time was 51 +/- 18 months. The number and type of ventricular arrhythmias were analyzed and a score was measured, accordingly with Castellanos and Lown's classifications. An "arrhythmic pattern" or "total punctuation" was defined and compared among two groups: group 1 > 65 points and group 2 < 65 points. RESULTS: The differential characteristics of both groups were: age (60 +/- 9 versus 56 +/- 10 years old; p = 0.004); hypertension (63% versus 29%; p < 0.001); clinic stage II-III (23% versus 11%; p = 0.02); echocardiographic ejection fraction (45 +/- 11% versus 50 +/- 10%; p = 0.04); positive exercise testing (73% versus 56%; p = 0.01); arrhythmias on the exercise test (15% versus 25%; p = 0.006). The long-term cardiac mortality was 25% versus 6% (p = 0.01), with an incidence of sudden death of 11% versus 3% (p < 0.05). Specificity, sensibility, positive predictive value and negative predictive value (reference cut point of 100) were 94, 65, 71 and 91%, respectively. CONCLUSIONS: The use of a score of arrhythmic pattern may identify 2 groups of patients with different clinic profiles that probably justify a different long-term prognosis after a first acute myocardial infarction.

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The prognostic significance of ventricular premature beats (VPB) and their proper management are still a subject of controversy, particularly since during the last few years a number of publications have raised doubts as to the effectiveness and safety of antiarrhythmic drugs. An appropriate assessment of the VPB must consider: 1) electrocardiographic characteristics. 2) Associated symptoms. 3) Presence or absence of underlying disease, and 4) Ventricular function (VF). On this basis VPB may be classified as "Benign" (isolated; asymptomatic; mild or absent cardiopathy, and preserved VF); "Hazardous" (presence of complex VPB; with or without symptoms, and recognized organic heart disease), and "Malignant" (complex VPB and ventricular tachyarrhythmias; symptomatic cardiac disease, and compromised VF). Antiarrhythmic drugs are indicated for "Hazardous" and "Malignant" VPB. However, selection and efficacy must be documented by objective testing (Holter, stress, plasma levels). When utilized in well defined groups of patients, with reduction in the hourly number of VPB (more than 50-70%) and mainly of complex forms, there is clear benefit in terms of long-term survival, including coronary disease and congestive heart failure.

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The morphology of ventricular premature beats has been described as a marker for the presence or absence of myocardial disease. Furthermore, the premature beat has been reported to be a potential marker for a dilated and hypokinetic left ventricle. To verify this previously tested hypothesis, 37 healthy patients with ventricular premature beats on an electrocardiogram (ECG), Holter monitor ECG, or a stress test ECG were classified according to the ventricular premature beat morphology. Group 1 had ventricular premature beat QRS complexes with a smooth contour or with narrow (less than 40 msec) notching. Group 2 had ventricular premature beats with broad (greater than 40 msec) notching or shelves. All of these patients had normal or borderline normal ECGs and normal multiple-gated acquisition (MUGA) scans. Nine patients had type 1 ventricular premature beats, 20 patients had type II ventricular premature beats, and eight patients had both type I and type II ventricular premature beats. We conclude that the presence of group 2 ventricular premature beats is so frequent in patients with normal left ventricular ejection fractions that the use of this marker in identifying abnormal left ventricular function is suspect.

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Los autores hacen una revisión de las arritmias propias de la infancia, en cuanto a etiología, patogenia, interpretación de ECG, manifestaciones clínicas, bases del tratamiento y prevención

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The effects of exercise on the frequency of ventricular premature contraction (VPC) and the clinical implications thereof were studied in 95 patients. Patients with ischemic heart disease and severe congestive heart failure were excluded from the study. The patients were divided into 7 groups according to changes in the frequency of VPC during and after exercise. Clinical background, exercise parameters and the efficacy of antiarrhythmic drugs were compared among these 7 groups. Plasma catecholamine concentration was measured in 34 patients, with a group of 12 healthy subjects serving as controls. An increase in the frequency of VPC both during and after exercise was observed in 16 patients (Group II). In comparison with the other groups, this group was older, and exhibited a higher incidence of underlying heart disease, lower tolerance to exercise and more serious ventricular arrhythmias. Beta-blockers were the most effective treatment for this group. However, plasma catecholamine concentration was not significantly higher in this group than it was in the other groups or the healthy subjects. A decrease in the frequency of VPC during exercise and an increase after exercise was observed in 25 patients (Group DI). This group also exhibited a high incidence of underlying heart disease and serious ventricular arrhythmias. The daily frequency of VPC was highest in this group. Class I and IV antiarrhythmic drugs were the most effective treatment. Although plasma catecholamine concentration was not significantly different from that of the other groups or the group of healthy subjects, a shorter QT interval was observed after exercise as compared with the healthy subjects. In this group, therefore, the mechanism of VPC may be related to a disturbance in the rate-adaptation of the QT interval, causing nonuniformity in the refractory period of the ventricular muscle. A decrease in the frequency of VPC during and after exercise was observed in 26 patients (Group DD). As compared with the other groups, this group was younger, and exhibited a lower incidence of underlying heart disease and a higher tolerance to exercise. This group was thus regarded as comprising the less severe cases. Seventeen patients showed no change in the frequency of VPC during exercise and an increase after exercise (Group UI). This group had the second highest average age and exhibited the lowest daily frequency of VPC. The incidence of underlying heart disease and serious ventricular arrhythmias fell between that of Groups IL/DI and Group DD.(ABSTRACT TRUNCATED AT 400 WORDS)

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This paper presents four cases of pediatric extrasystole which did not fulfil the diagnostic criteria for parasystole. By calculating various ectopic intervals, we established the phase-response curve demonstrating that sinus electrotonic activities modulated the parasystolic focus in each case. Our results showed these cases to be modulated parasystole.

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An analyzer for ventricular premature contraction (VPC) arrhythmias was developed. At 60 times real time, the analyzer processes the Holter tape in which the long-term ambulatory electrocardiogram was recorded. Template matching algorithm using Pearson product-moment correlation coefficient is employed. A microprocessor controls the analyzer. Circuits for calculation of correlation coefficients were developed to support insufficient computing speed of the microprocessor. Evaluation study shows that the sensitivity for detecting the normal QRS complexes and the VPCs were 98.9% and 99.4%, and that the specificity for these were 97.5% and 98.4%. Algorithm for high-speed calculation of correlation coefficients is also considered.

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The decision of whether or not to treat a ventricular extrasystole depends in the first instance on the benign or severe nature of the disorder, and on whether there is subjacent cardiopathy. The results of 24-hour Holter monitoring, exercise tolerance tests and clinical and echographic examinations will define the pathological character of a ventricular extrasystole and will indicate any subjacent cardiopathy. Electrophysiological exploration with programmed stimulation should be reserved for so-called lethal cases of arrhythmia, such as attacks of sustained ventricular tachycardia. Ischemic cardiopathy is by far the most frequent cause of ventricular extrasystoles. The two major risks of sudden death after myocardial infarction are due to left ventricular dysfunction and repetitive and/or complex ventricular extrasystoles, as well as to attacks of ventricular tachycardia. Heart patients presenting these disorders must receive urgent treatment with antiarrhythmics. Isolated, monomorphic ventricular extrasystoles are also treated in heart patients at risk if their frequency is greater than 10 per hour, measured by 24-hour Holter monitoring. In the absence of subjacent cardiopathies, the therapeutic indications are much less well defined. Approximately five per cent of subjects in a normal population present ventricular extrasystoles, the frequency of which, however, rarely exceeds 100 per 24 hours. Repetitive phenomena are only seen in 10 per cent of cases. Attacks of ventricular tachycardia are almost never seen. Ventricular extrasystoles that develop in apparently normal hearts, but which do not fulfill the above criteria, can be considered abnormal. Nevertheless, there is no categorical proof that these ventricular extrasystoles represent any risk, notably of sudden death.(ABSTRACT TRUNCATED AT 250 WORDS)

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