BackgroundRisk stratification of the early repolarization pattern (ERP) is needed to identify malignant early repolarization. J-point elevation with a horizontal ST segment was recently suggested as a malignant feature of the ERP. In this study, the prevalence of the ERP with a horizontal ST segment was examined among survivors of sudden cardiac arrest (SCA) without structural heart disease to evaluate the value of ST-segment morphology in risk stratification of the ERP.MethodsWe reviewed the data of 83 survivors of SCA who were admitted from August 2005 to August 2010. Among them, 25 subjects without structural heart disease were included. The control group comprised 60 healthy subjects who visited our health promotion center; all control subjects were matched for age, sex, and underlying disease (diabetes mellitus, hypertension). Early repolarization was defined as an elevation of the J point of at least 0.1 mV above the baseline in at least two continuous inferior or lateral leads that manifested as QRS slurring or notching. An ST-segment pattern of <0.1 mV within 100 ms after the J point was defined as a horizontal ST segment.ResultsThe SCA group included 17 men (64%) with a mean age of 49.7 ± 14.5 years. The corrected QTc was not significantly different between the SCA and control groups (432.7 ± 37.96 vs. 420.4 ± 26.3, respectively; p = 0.089). The prevalence of ERP was not statistically different between the SCA and control groups (5/25, 20% vs. 4/60, 6.7%, respectively; p = 0.116). The prevalence of early repolarization with a horizontal ST segment was more frequent in the SCA than in the control group (20% vs. 3.3%, respectively; p = 0.021). Four SCA subjects (16%) and one control subject (1.7%) had a J-point elevation of >2 mm (p = 0.025). Four SCA subjects (16%) and one (1.7%) control subject had an ERP in the inferior lead (p = 0.025).ConclusionThe prevalence of ERP with a horizontal ST segment was higher in patients with aborted SCA than in matched controls. This result suggests that ST morphology has value in the recognition of malignant early repolarization.
Protein S deficiency is one of the several risk factors for thrombophilia and can cause blood clotting disorders such as deep vein thrombosis and pulmonary embolism. A 54-year-old man was admitted with the complaint of dyspnea and was diagnosed with pulmonary embolism. The patient had very low level of free protein S, total protein S antigen, and protein S activity (type I protein S deficiency). In history taking, we found that his mother, 78 year old, had a history of same disease 10 years ago, and confirmed the pronounced low level of protein S. The patient's son also had very low level of protein S, however there had not been any history of pulmonary embolism yet. This case study suggests that asymptomatic persons with a family history of protein S deficiency and pulmonary embolism should be checked regularly for early detection of the disease, as protein S deficiency can be suspected.
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