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Sudden cardiac death
Original article
Electrocardiographic and clinical predictors separating atherosclerotic sudden cardiac death from incident coronary heart disease
  1. Elsayed Z Soliman1,
  2. Ronald J Prineas1,
  3. L Douglas Case2,
  4. Gregory Russell2,
  5. Wayne Rosamond3,
  6. Thomas Rea4,
  7. Nona Sotoodehnia4,
  8. Wendy S Post5,6,
  9. David Siscovick4,
  10. Bruce M Psaty4,7,
  11. Gregory L Burke8
  1. 1Epidemiological Cardiology Center (EPICARE), Department of Epidemiology and Prevention, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA
  2. 2Department of Biostatistics, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA
  3. 3Department of Epidemiology, School of Public Health, University of North Carolina, Chapel Hill, North Carolina, USA
  4. 4Cardiovascular Health Research Unit, Departments of Medicine, Epidemiology, and Health Services, University of Washington, Seattle, Washington, USA
  5. 5Department of Medicine, Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
  6. 6Department of Epidemiology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland, USA
  7. 7Group Health Research Institute, Group Health Cooperative, Seattle, Washington, USA
  8. 8Division of Public Health Sciences, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA
  1. Correspondence to Elsayed Z Soliman, Epidemiological Cardiology Center (EPICARE), Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157-1063, USA; esoliman{at}wfubmc.edu

Abstract

Objective To identify specific ECG and clinical predictors that separate atherosclerotic sudden cardiac death (SCD) from incident coronary heart disease (CHD) (non-fatal events and non-sudden death) in the combined cohorts of the Atherosclerosis Risk in Communities study and the Cardiovascular Health Study.

Methods This analysis included 18 497 participants (58% females, 24% black individuals, mean age 58 years) who were initially free of clinical CHD. A competing risk analysis was conducted to examine the prognostic significance of baseline clinical characteristics and an extensive electronic database of ECG measurements for prediction of 229 cases of SCD as a first event versus 2297 incident CHD cases (2122 non-fatal events and 175 non-sudden death) that occurred during a median follow-up time of 13 years in the Cardiovascular Health Study and 14 years in the Atherosclerosis Risk in Communities study.

Results After adjusting for common CHD risk factors, a number of clinical characteristics and ECG measurements were independently predictive of SCD and CHD. However, the risk of SCD versus incident CHD was significantly different for race/ethnicity, hypertension, body mass index (BMI), heart rate, QTc, abnormally inverted T wave in any ECG lead group and level of ST elevation in V2. Black race/ethnicity (compared to non-black) was predictive of high SCD risk but less risk of incident CHD (p value for differences in the risk (HR) for SCD versus CHD <0.0001). Hypertension, increased heart rate, prolongation of QTc and abnormally inverted T wave were stronger predictors of high SCD risk compared to CHD (p value=0.0460, 0.0398, 0.0158 and 0.0265, respectively). BMI was not predictive of incident CHD but was predictive of high SCD risk in a quadratic fashion (p value=0.0220). On the other hand, elevated ST height as measured at the J point and that measured at 60 ms after the J point in V2 were not predictive of SCD but were predictive of high incident CHD risk (p value=0.0251 and 0.0155, respectively).

Conclusions SCD and CHD have many risk factors in common. Hypertension, race/ethnicity, BMI, heart rate, QTc, abnormally inverted T wave in any ECG lead group and level of ST elevation in V2 have the potential to separate between the risks of SCD and CHD. These results need to be validated in another cohort.

  • Sudden cardiac death
  • coronary heart disease
  • ECG
  • risk stratification
  • atherosclerosis, epidemiology

https://doi.org/10.1136/hrt.2010.215871

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    Footnotes

    • EZS and RJP contributed equally to this work.

    • Funding This work was supported by the Donald W. Reynolds Cardiovascular Clinical Research Center at the Johns Hopkins University School of Medicine. The Atherosclerosis Risk in Communities (ARIC) study is carried out as a collaborative study supported by National Heart, Lung, and Blood Institute contracts HHSN268201100005C, HHSN268201100006C, HHSN268201100007C, HHSN268201100008C, HHSN268201100009C, HHSN268201100010C, HHSN268201100011C and HHSN268201100012C. The Cardiovascular Heart Study is supported by contracts. This study was supported by contracts NHLBI N01-HC-85079 through N01-HC-85086, N01-HC-35129, N01-HC-15103, N01-HC-55222, N01-HC-75150, N01-HC-45133, U01-HL-080295, R01-HL-087652 and R01-HL-088456. The funding source had no involvement in the design, analysis and interpretation of the data presented in this paper.

    • Competing interests None.

    • Ethics approval The CHS and ARIC study protocols were approved by the institutional review board of each participating centre, and informed consent was obtained from each study participant.

    • Provenance and peer review Not commissioned; externally peer reviewed.