Correlated bursts and the role of memory range

Inhomogeneous temporal processes in natural and social phenomena have been described by bursts that are rapidly occurring events within short time periods alternating with long periods of low activity. In addition to the analysis of heavy-tailed inter-event time distributions, higher-order correlations between inter-event times, called correlated bursts, have been studied only recently. As the possible mechanisms underlying such correlated bursts are far from being fully understood, we devise a simple model for correlated bursts by using a self-exciting point process with variable memory range. Here the probability that a new event occurs is determined by a memory function that is the sum of decaying memories of the past events. In order to incorporate the noise and/or limited memory capacity of systems, we apply two memory loss mechanisms, namely either fixed number or variable number of memories. By using theoretical analysis and numerical simulations we find that excessive amount of memory effect may lead to a Poissonian process, which implies that for memory effect there exists an intermediate range that will generate correlated bursts of magnitude comparable to empirical findings. Hence our results provide deeper understanding of how long-range memory affects correlated bursts.Comment: 9 pages, 7 figure

Clinical and Genetic Screening for Hypertrophic Cardiomyopathy in Paediatric Relatives: Changing Paradigms in Clinical Practice

Hypertrophic cardiomyopathy (HCM) is an important cause of morbidity and mortality in children. While the aetiology is heterogeneous, most cases are caused by variants in the genes encoding components of the cardiac sarcomere, which are inherited as an autosomal dominant trait. In recent years, there has been a paradigm shift in the role of clinical screening and predictive genetic testing in children with a first-degree relative with HCM, with the recognition that phenotypic expression can, and often does, manifest in young children and that familial disease in the paediatric age group may not be benign. The care of the child and family affected by HCM relies on a multidisciplinary team, with a key role for genomics. This review article summarises current evidence in clinical and genetic screening for hypertrophic cardiomyopathy in paediatric relatives and highlights aspects that remain to be resolved

751-5 Rapid Angiographic Progression of “Target” and “Non-target” Stenoses in Patients Awaiting Coronary Angioplasty

Coronary angioplasty (PTCA) is effective therapy for angina pectoris but coronary events occur after successful PTCA which may be caused by both restenosis and progression of mild pre-existing, “non-target”, stenoses. To compare the short-term evolution of “target”versus “non-target”stenoses in patients awaiting PTCA, we prospectively studied 161 consecutive stable angina patients (124 men and 37 women). After diagnostic angiography, “target”stenoses for PTCA and “non-target”lesions were identified. Patients were put on a routine waiting list and followed up regularly until repeat coronary arteriography (mean±SD: 7±3 months). which was performed immediately preceding angioplasty (138 patients) or soon after acute coronary events (23 patients) when these occurred. Stenosis diameters were measured using computerized arteriography. Progression was defined as 2:20% diameter reduction, new total occlusion, or development of “new” stenoses 2:30%. At study entry, diameters of target (n=207) and non-target (n=184) lesions were 68±9% and 38±9%, respectively (p < 0.001). Disease progression occurred in 33 patients (20%). in whom 18 target (9%) and 15 nontarget stenoses (8%) progressed and 7 new lesions (1 total occlusion) developed. Total occlusion developed in 15 of the 18(83%) target and in 6 of the 15 (40%) non-target stenoses; (p=0.03). During follow up, 3 patients (2%) had a myocardial infarction and 20 (12%) developed unstable angina. These events were associated with progression of target stenoses in 10 patients, of non-target stenoses in 7 patients, and with new lesions in one patient. In 5 patients events were not associated with stenosis progression.Thus a similar proportion of target and non-targetlesions progressed rapidly. Targetstenoses, however, were more likely to progress to total occlusion than non-targetlesions. Progression of non-targetstenoses may contribute to recurrence of angina and new coronary events after successful angioplasty and their role should be considered when developing strategies aimed at improving survival after angioplasty

The role of the electrocardiographic phenotype in risk stratification for sudden cardiac death in childhood hypertrophic cardiomyopathy.

Aims The 12-lead electrocardiogram (ECG) is routinely performed in children with hypertrophic cardiomyopathy (HCM). An ECG risk score has been suggested as a useful tool for risk stratification, but this has not been independently validated. This aim of this study was to describe the ECG phenotype of childhood HCM in a large, international, multi-centre cohort and investigate its role in risk prediction for arrhythmic events. Methods and results Data from 356 childhood HCM patients with a mean age of 10.1 years (±4.5) were collected from a retrospective, multi-centre international cohort. Three hundred and forty-seven (97.5%) patients had ECG abnormalities at baseline, most commonly repolarization abnormalities (n = 277, 77.8%); left ventricular hypertrophy (n = 240, 67.7%); abnormal QRS axis (n = 126, 35.4%); or QT prolongation (n = 131, 36.8%). Over a median follow-up of 3.9 years (interquartile range 2.0–7.7), 25 (7%) had an arrhythmic event, with an overall annual event rate of 1.38 (95% CI 0.93–2.04). No ECG variables were associated with 5-year arrhythmic event on univariable or multivariable analysis. The ECG risk score threshold of >5 had modest discriminatory ability [C-index 0.60 (95% CI 0.484–0.715)], with corresponding negative and positive predictive values of 96.7% and 6.7% Conclusion In a large, international, multi-centre cohort of childhood HCM, ECG abnormalities were common and varied. No ECG characteristic, either in isolation or combined in the previously described ECG risk score, was associated with 5-year sudden cardiac death risk. This suggests that the role of baseline ECG phenotype in improving risk stratification in childhood HCM is limited.post-print967 K

Response to Skinner: Risk stratification in hypertrophic cardiomyopathy: Time to think about the electrocardiogram

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