Electrocardiographic Deep Terminal Negativity of the P Wave in V 1 and Risk of Sudden Cardiac Death: The Atherosclerosis Risk in Communities (ARIC) Study

Author:

Tereshchenko Larisa G.12,Henrikson Charles A.2,Sotoodehnia Nona3,Arking Dan E.4,Agarwal Sunil K.5,Siscovick David S.36,Post Wendy S.1,Solomon Scott D.7,Coresh Josef5,Josephson Mark E.8,Soliman Elsayed Z.9

Affiliation:

1. Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD

2. Knight Cardiovascular Institute, Oregon Health & Science University, Portland, OR

3. University of Washington, Seattle, WA

4. McKusick‐Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD

5. Department of Epidemiology, Internal Medicine and Welch Center for Prevention, Epidemiology, and Clinical Research, Johns Hopkins School of Public Health, Baltimore, MD

6. The New York Academy of Medicine, New York, NY

7. Brigham and Women's Hospital, Harvard Medical School, Boston, MA

8. Division of Cardiovascular Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA

9. Epidemiological Cardiology Research Center (EPICARE), Division of Public Health Sciences and Department of Medicine, Cardiology Section, Wake Forest School of Medicine, Winston Salem, NC

Abstract

Background Identifying individuals at risk for sudden cardiac death ( SCD ) is of critical importance. Electrocardiographic ( ECG ) deep terminal negativity of P wave in V 1 ( DTNPV 1), a marker of left atrial abnormality, has been associated with increased risk of all‐cause and cardiovascular mortality. We hypothesized that DTNPV 1 is associated with increased risk of sudden cardiac death ( SCD ). Methods and Results This analysis included 15 375 participants (54.1±5.8 years, 45% men, 73% whites) from the Atherosclerosis Risk in Communities ( ARIC ) study. DTNPV 1 was defined from the resting 12‐lead ECG as presence of biphasic P wave (positive/negative) in V 1 with the amplitude of the terminal negative phase >100 μV, or one small box on ECG scale. After a median of 14 years of follow‐up, 311 cases of SCD occurred. In unadjusted Cox regression, DTNPV 1 was associated with an 8‐fold increased risk of SCD ( HR 8.21; [95% CI 5.27 to 12.79]). Stratified by race and study center, and adjusted for age, sex, coronary heart disease ( CHD ), and ECG risk factors, as well as atrial fibrillation ( AF ), stroke, CHD , and heart failure ( HF ) as time‐updated variables, the risk of SCD associated with DTNPV 1 remained significant (2.49, [1.51–4.10]). DTNPV 1 improved reclassification: additional 3.4% of individuals were appropriately reclassified into a higher SCD risk group, as compared with traditional CHD risk factors alone. In fully adjusted models DTNPV 1 was associated with increased risk of non‐fatal events: AF (5.02[3.23–7.80]), CHD (2.24[1.43–3.53]), HF (1.90[1.19–3.04]), and trended towards increased risk of stroke (1.88[0.99–3.57]). Conclusion DTNPV 1 is predictive of SCD suggesting its potential utility in risk stratification in the general population.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

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