Methods

ARIC prospectively enrolled 15,792 community-dwelling men and women between 45 and 64 years of age. Four field centers across the United States (Washington County, Maryland; Forsyth County, North Carolina; Jackson, Mississippi; suburban Minneapolis, Minnesota) recruited participants between 1987 and 1989. Participants returned for 4 follow-up examinations (1990 to 1992, 1993 to 1995, 1996 to 1998, and 2011 to 2013) and continue to be followed via annual telephone calls. End points are ascertained from hospital discharges that include any cardiovascular diagnoses from hospitals in the study communities. The study was approved by the institutional review boards at all participating universities, and all participants provided written informed consent at enrollment.

The following analysis aimed to examine the association of the J wave detected on the routine ECG with adverse cardiovascular outcomes. All participants with good quality ECG data and follow-up data were included. Participants were excluded if they had evidence of major ventricular conduction abnormalities (e.g., complete left or right bundle branch blocks), pacemakers, Wolf–Parkinson–White Syndrome or QRS duration ≥120 ms, or if they reported a race other than black or white.

Digital 12-lead ECGs were obtained at baseline and at follow-up examinations using MAC PC ECG machines (Marquette Electronics, Milwaukee, Wisconsin). All ECGs were inspected for technical errors and adequate quality at the Epidemiology Coordinating and Research Center at the University of Alberta (Edmonton, Alberta, Canada) during the initial phases of the study and at the Epidemiological Cardiology Research Center at the Wake Forest School of Medicine (Winston-Salem, North Carolina) during later phases.

The J wave was detected at baseline (1987 to 1989) and during the first 3 study visits (1990 to 1992, 1993 to 1995, and 1996 to 1998) as a time-dependent variable. J waves were defined as notches or slurs in the descending slope of the terminal portion of the QRS complex and were detected using a fully automated method described by Wang et al. Other electrocardiographic variables used in this analysis were heart rate, left ventricular hypertrophy, and J-point elevation. Left ventricular hypertrophy was defined by Cornell’s voltage criteria. J-point elevation was defined as a J-point amplitude of ≥0.1 mV (1 mm) in any lead.

The primary outcome of this analysis was physician-adjudicated sudden cardiac death (SCD). In ARIC, fatal coronary heart disease (CHD) events that occurred before December 31, 2010 were reviewed. Death certificates, informant interviews, physician questionnaires, coroner reports, and hospital discharge summaries were reviewed to classify fatal CHD events as definite SCD, possible SCD, or non-SCD. SCD was defined as a sudden pulseless condition of cardiac origin in a previously stable individual. Details of potential cases were reviewed by physician adjudicators separately. Disagreement between reviewers was resolved by discussion. Cases of definite SCD were used in the present study. Secondary outcomes included CHD death and cardiovascular mortality. Cardiovascular mortality included the composite of fatal CHD, heart failure, and stroke events. Events occurring between the baseline examination and December 31, 2010 were included in this analysis.

Age, gender, and race were self-reported. Tobacco use was defined as current or former cigarette smoking. Diabetes was defined as a fasting glucose level ≥126 mg/dl (or nonfasting glucose ≥200 mg/dl), a self-reported physician diagnosis of diabetes, or the use of diabetes medications. Systolic blood pressure was obtained from each participant using sphygmomanometers to measure 3 readings in the upright position after 5 minutes of rest. The average of the last 2 blood pressure measurements was used. Antihypertensive medication use was self-reported. Body mass index was defined as the weight in kilograms divided by the square of the height in meters. Low-density lipoprotein cholesterol levels were calculated indirectly using cholesterol values assayed from baseline serum samples. Prevalent CHD was defined by self-reported history of physician-diagnosed myocardial infarction, coronary artery bypass surgery, coronary angioplasty, or electrocardiographic evidence of myocardial infarction.

Baseline characteristics for study participants were stratified by the presence of the J wave. Categorical variables were reported as frequency and percentage, whereas continuous variables were recorded as mean ± SD. Follow-up was defined as the time between the baseline visit until the outcome of interest, death, loss to follow-up, or end of follow-up (December 31, 2010). For J wave cases identified during subsequent study visits, follow-up time began at the time of J wave ascertainment. Cox regression was used to compute hazard ratios (HRs) and 95% CIs for the association between the J wave and each outcome. Multivariable models were constructed as follows: model 1 adjusted for age, gender, and race; model 2 adjusted for model 1 covariates plus smoking, diabetes, systolic blood pressure, body mass index, low-density lipoprotein cholesterol, antihypertensive medications, left ventricular hypertrophy, CHD, and heart rate. Subgroup analyses by race, gender, and J-point elevation were performed, and tests for interaction were examined using model 2. Statistical significance for all comparisons, including interactions, was defined as p <0.05. SAS, version 9.4 (SAS Inc, Cary, North Carolina) was used for all analyses.

Results

A total of 14,592 (mean age = 54 ± 5.8 years; 56% women; 26% black) participants were included. There were 278 participants (1.9%) who had evidence of a J wave. Of these, 126 (45%) were detected on follow-up study visits. Baseline characteristics are listed in Table 1 .

Over a median follow-up of 22 years, 4,376 participants (30%) died. Of these, 503 (11%) were attributed to SCD, 778 (18%) were CHD deaths, and 2,303 (53%) were due to cardiovascular disease. In a multivariable Cox regression model adjusted for demographics, cardiovascular risk factors, and potential confounders, the J wave was not associated with an increased risk of SCD, CHD death, or cardiovascular mortality ( Table 2 ). An interaction was detected for cardiovascular mortality by gender, with men have a stronger association than women ( Table 3 ). Interactions were not detected by race or J-point elevation ( Table 3 ).

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