Younghoon Kwon1, Stephen McHugh2, Kayvon Ghoreshi3, Genevieve R Lyons4, Yeilim Cho5, Kenneth C Bilchick6, Sula Mazimba7, Bradford B Worrall8, Nazem Akoum9, Lin Y Chen10, Elsayed Z Soliman11. 1. Department of Medicine, University of Virginia, United States; Department of Medicine, Division of Cardiology, University of Washington, 325 9th Ave., 2CT-69.1, Box 359748, Seattle, WA 98104, United States. Electronic address: yhkwon@uw.edu. 2. Department of Medicine, Temple University, United States. Electronic address: stephen.mchugh@tuhs.temple.edu. 3. Department of Medicine, University of Virginia, United States. Electronic address: ksg9re@virginia.edu. 4. Department of Public Health Sciences, Division of Biostatistics, University of Virginia, United States. Electronic address: grl2b@virginia.edu. 5. Department of Medicine, University of Virginia, United States. 6. Department of Medicine, University of Virginia, United States. Electronic address: KCB7F@hscmail.mcc.virginia.edu. 7. Department of Medicine, University of Virginia, United States. Electronic address: SM8SD@hscmail.mcc.virginia.edu. 8. Departments of Neurology and Public Health Sciences, University of Virginia, United States. Electronic address: bbw9r@virginia.edu. 9. Department of Medicine, Division of Cardiology, University of Washington, 325 9th Ave., 2CT-69.1, Box 359748, Seattle, WA 98104, United States. Electronic address: nakoum@uw.edu. 10. Department of Medicine, Cardiovascular Division, University of Minnesota, United States. Electronic address: chenx484@umn.edu. 11. The Epidemiological Cardiology Research Center, Department of Epidemiology and Prevention, Division of Public Health Sciences and Department of Medicine, Section on Cardiology, Wake Forest School of Medicine, Winston-Salem, NC, United States. Electronic address: esoliman@wakehealth.edu.
Abstract
BACKGROUND: P wave indices represent electrocardiographic marker of left atrial pathology. We hypothesized that P wave would be more abnormal in patients presenting with ischemic stroke than a comparable group without ischemic stroke. METHODS: We compared P wave terminal force in V1 (PTFV1) between patients admitted with ischemic stroke (case) and patients followed in cardiology clinic (control) at a single medical center. Using logistic regression models, we tested for an association between abnormal PTFV1 (> 4000 µV ms) and ischemic stroke. We also defined several optimal cut-off values of PTFV1 using a LOESS plot and estimated odds ratio of ischemic stroke when moving from one cut-point level to the next higher-level. RESULTS: A total of 297 patients (case 147, control 150) were included. PTFV1 was higher in patients with vs. those without ischemic stroke (median 4620 vs 3994 µV ms; p=0.006). PTFV1 was similar between cardioembolic/cryptogenic and other stroke subtypes. In multivariable analyses adjusting for sex, obesity, age, and hypertension, the association between abnormal PTFV1 and ischemic stroke ceased to be significant (OR 1.53 [0.95, 2.50], p=0.083). Increase to the next cutoff level of PTFV1 (900, 2000, 3000, 4000, 5000, and 6000 µV ms) was associated with 18% increase in odds of having ischemic stroke (vs. no ischemic stroke) (OR 1.18 [1.02, 1.36], p=0.026). CONCLUSION: Patients presenting with acute ischemic stroke are more likely to have abnormal PTFV1. These findings from a real-world clinical setting support the results of cohort studies that left atrial pathology manifested as abnormal PTFV1 is associated with ischemic stroke.
BACKGROUND: P wave indices represent electrocardiographic marker of left atrial pathology. We hypothesized that P wave would be more abnormal in patients presenting with ischemic stroke than a comparable group without ischemic stroke. METHODS: We compared P wave terminal force in V1 (PTFV1) between patients admitted with ischemic stroke (case) and patients followed in cardiology clinic (control) at a single medical center. Using logistic regression models, we tested for an association between abnormal PTFV1 (> 4000 µV ms) and ischemic stroke. We also defined several optimal cut-off values of PTFV1 using a LOESS plot and estimated odds ratio of ischemic stroke when moving from one cut-point level to the next higher-level. RESULTS: A total of 297 patients (case 147, control 150) were included. PTFV1 was higher in patients with vs. those without ischemic stroke (median 4620 vs 3994 µV ms; p=0.006). PTFV1 was similar between cardioembolic/cryptogenic and other stroke subtypes. In multivariable analyses adjusting for sex, obesity, age, and hypertension, the association between abnormal PTFV1 and ischemic stroke ceased to be significant (OR 1.53 [0.95, 2.50], p=0.083). Increase to the next cutoff level of PTFV1 (900, 2000, 3000, 4000, 5000, and 6000 µV ms) was associated with 18% increase in odds of having ischemic stroke (vs. no ischemic stroke) (OR 1.18 [1.02, 1.36], p=0.026). CONCLUSION:Patients presenting with acute ischemic stroke are more likely to have abnormal PTFV1. These findings from a real-world clinical setting support the results of cohort studies that left atrial pathology manifested as abnormal PTFV1 is associated with ischemic stroke.
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