The presence of a fragmented QRS complex (fQRS) in two contiguous leads of a standard 12-lead electrocardiogram (ECG) has been shown to be an indicator of myocardial scar in multiple different populations of cardiac patients. QRS fragmentation is also a predictor of adverse prognosis in acute myocardial infarction, coronary artery disease, and ischemic cardiomyopathy and a prognostic tool in structural heart diseases. An increased risk of sudden cardiac death associated with fQRS has been documented in patients with ischemic cardiomyopathy and hypertrophic cardiomyopathy. However, fQRS is also frequently observed in apparently healthy subjects. Thus, a more detailed classification of different QRS fragmentations is needed to identify the pathological fragmentation patterns and refine the role of fQRS as a risk marker of adverse cardiac events and sudden cardiac death. In most studies fQRS has been defined by the presence of an additional R wave (R′), or notching in the nadir of the S wave, or the presence of >1 R′ in two contiguous leads corresponding to a major coronary territory. However, this approach does not discriminate between minor and major fragmentations and the location of the fQRS is also neglected. In addition to this, the method is susceptible to large interobserver variability. We suppose that some fQRS subtypes result from conduction delays in the His-Purkinje system, which is a benign finding and thus can weaken the prognostic values of fQRS. The classification of fQRSs to subtypes with unambiguous definitions is needed to overcome the interobserver variability related issues and to separate fQRSs caused by myocardial scarring from benign normal variants. In this paper, we review the anatomic correlates of fQRS and the current knowledge of prognostic significance of fQRS. We also propose a detailed fQRS classification for research purposes which can later be simplified after the truly pathological morphologies have been identified. The research material of our study consist of 15,245 ECGs from the random general population and approximately six thousands (n = 6,241) ECGs from subjects with a known cardiac disease.

Original ArticleBackground-Prevalence and prognostic significance of abnormal P terminal force (PTF) in the general population are not known. The aim of this study was to assess the prevalence of abnormal PTF and to compare clinical outcomes of middleaged subjects with and without the PTF. Methods and Results-The presence of PTF was assessed in a cohort of 10 647 middle-aged subjects (mean age [SD], 44[8] years; 47.2% female). The subjects were followed 35 to 41 years, and data on mortality and hospitalizations were obtained from national registers. Primary outcomes were all-cause mortality, cardiac mortality, and arrhythmic death. Secondary outcomes were hospitalization because of congestive heart failure, coronary heart disease, new onset atrial fibrillation, and stroke. The Cox proportional hazards model was used to assess the risk for death (all-cause), and the Fine and Gray competing risks model was used for other outcomes. The prevalence of PTF 0.04 to 0.049, 0.05 to 0.059, and ≥0.06 mm•s were 4.8%, 1.5%, and 1.2%, respectively. Subjects presenting PTF ≥0.04 mm•s were at increased risk for death, cardiac death, and congestive heart failure, and subjects presenting PTF ≥0.06 mm•s were at increased risk for atrial fibrillation. However, after adjustment for potential confounding factors, an increased risk was observed only for death (hazard ratio, 1.76; 95% confidence interval, 1.45-2.12; P<0.001) and atrial fibrillation (hazard ratio, 1.91; 95% confidence interval, 1.34-2.73; P<0.001) in subjects presenting PTF ≥0.06 mm•s. Conclusions-PTF ≥0.04 mm•s is a relatively common finding in a 12-lead ECG of middle-aged subjects. PTF ≥0.06 mm•s is associated with increased risk for atrial fibrillation and death in the general population. (Circ Arrhythm Electrophysiol.

BackgroundDiabetes predisposes to sudden cardiac death (SCD). However, it is uncertain whether greater proportion of cardiac deaths are sudden among diabetes patients than other subjects. It is also unclear whether the risk of SCD is pronounced already early in the course of the disease. The relationship of impaired glucose tolerance (IGT) and SCD is scarcely documented.MethodsA general population cohort of 10594 middle-aged subjects (mean age 44 years, 52.6 % male, follow-up duration 35–41 years) was divided into diabetes patients (n = 82), subjects with IGT (n = 3806, plasma glucose ≥9.58 mmol/l in one-hour glucose tolerance test), and controls (n = 6706).ResultsDiabetes patients had an increased risk of SCD after adjustment confounders (hazard ratio 2.62, 95 % confidence interval 1.46–4.70, p = 0.001) but risk for non-sudden cardiac death was similarly increased and the proportion of SCD of cardiac deaths was not increased. The SCD risk persisted after exclusion of subjects with baseline cardiac disease or non-fatal cardiac events during the follow-up. Subjects with IGT were at increased risk for SCD (univariate hazard ratio 1.51; 95 % confidence interval 1.31–1.74; p < 0.001) and also for non-sudden cardiac deaths and non-fatal cardiac events but adjustments for other risk factors attenuated these effects.ConclusionsDiabetes was associated with increased risk of SCD but also the risk of non-sudden cardiac death was similarly increased. The proportion of cardiac deaths being sudden in subjects with diabetes was not increased. The higher SCD risk in diabetes patients was independent of known cardiac disease at baseline or occurrence of non-fatal cardiac event during the follow-up.