The presence of ESVEA, SVEC and runs of SVEC showed a significantly higher risk of all cause mortality (secondary endpoint) on univariate analysis (HR=2.12 95% CI, 1.30-3.47 p=0.003 HR=1.49 95% CI, 1.24-1.79 p<0.0001 and HR =1.12 95% CI, 1.03-1.21 p=0.006 respectively). Episodes of SVEC, as a continuous variable, also correlated with a significant increase in the primary endpoint of stroke or mortality on univariate analysis (HR=1.46 95% CI, 1.22-1.73 p<0.0001 for SVEC HR=1.13 95% CI, 1.05-1.21 p=0.0007 for runs of SVEC), whilst multivariate analyses was significant for SVEC only (HR 1.27 95% CI, 1.05-1.53 p=0.013 for SVEC HR=1.06 95% CI, 0.98-1.15 p=0.14 for runs of SVEC). Furthermore, subjects with ESVEA had significantly more hospital admissions for AF, from both univariate and age/sex adjusted Cox regression models (p=0.011 and p=0.035 respectively). The primary endpoint (a composite of thrombo-embolic stroke and death), was significantly higher in the ESVEA group on univariate analysis (p<0.0001), and remained significant in this group after adjustment of conventional risk factors: smoking, systolic blood pressure, diabetes mellitus, cholesterol, sex and age (Hazard ratio = 1.64 95 % confidence interval, 1.03-2.60 p=0.036). In the 678 subjects recruited, 99 had ESVEA, 70 had SVEC > 30/hour and 42 had runs of ≥ 20 SVEC (13 had both).Īt baseline, the ESVEA positive group were older (67.6 ± 6.3 years vs 63.9 ± 6.7 years p < 0.0001), had higher systolic and diastolic blood pressure, and higher N-terminal prohormone B-type natriuretic peptide levels from multivariable logistic regression analysis. Excessive supraventricular ectopic activity (ESVEA) was thereby defined as ≥ 30 SVEC per hour or any episodic runs of ≥ 20 SVEC. There were no previous definitions to determine the frequency of “excessive” supraventricular ectopy hence the investigators used an arbitrary cut-off value being the top 10th percentile for both frequency and length of the runs of SVEC. The observed arrhythmias were divided into isolated supraventricular ectopic complexes (SVEC) and runs of ≥ 3 SVEC. The enrolled subjects had 48 hour ambulatory Holtor monitoring whereby supraventricular arrhythmias were identified. The participants were followed up for up to 7 years (median of 6.3 years). The population sample consisted of 678 Caucasian subjects (41.4 % females) aged 55-75 years (mean 64.5 ± 6.8 years), and who otherwise had no previous history of stroke or heart disease. in their recent article entitled “ Excessive supraventricular ectopic activity and increased risk of atrial fibrillation and stroke” in Circulation 2010, had conducted a population based cohort study of Danish individuals from the Copenhagen Holtor study, evaluating the hypothesis that excessive supraventricular ectopy would predispose to a higher incidence of thrombo-embolic stroke, death and AF. Supraventricular ectopy can be a manifestation of hypertensive heart disease or other structural heart disease, resulting in left atrial enlargement and increased wall stress, that could be associated with subsequent development of AF.īinici et al. Electrophysiology studies have implicated that spontaneous atrial ectopic beats that originate in or near pulmonary veins adjacent to the left atrium, may initiate paroxysms of AF. The incidence of AF increases with age, affecting up to 5% in the elderly population. Atrial fibrillation (AF) is the commonest arrhythmia predisposing to thrombo-embolic stroke. The major subtypes of stroke are divided into thrombo-embolic, haemorrhagic and cryptogenic, with each having different predisposing risk factors and management strategies. Stroke is a significant cause of mortality and disabling morbidity.
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