Bringing Critical Race Praxis Into the Study of Electrophysiological Substrate of Sudden Cardiac Death: The ARIC Study

Figure 1. Flowchart of study cohort development. ARIC indicates Atherosclerosis Risk in Communities; GEH, global electrical heterogeneity.

Figure 2. Estimated adjusted marginal (least‐squares) means and 95% CIs of peak spatial ventricular gradient (SVG) magnitude (A), area SVG magnitude (B), sum absolute QRST integral (SAI QRST) (C), and Cornell voltage (D) for white and black participants. Model 1 was adjusted for age, sex, and study center. Model 2 was additionally adjusted for heart failure, coronary heart disease, stroke, diabetes mellitus, hypertension, current smoking and alcohol intake, work, sport, and leisure physical activity levels, levels of total cholesterol, high‐density lipoprotein, and triglycerides, body mass index, use of antihypertensive and antiarrhythmic medications, serum concentrations of sodium, potassium, calcium, magnesium, phosphorus, and uric acid, total protein and albumin, blood urea nitrogen, and chronic kidney disease stage classified by estimated glomerular filtration rate (calculated using the Chronic Kidney Disease–Epidemiology Collaboration equation), heart rate, QRS duration, Bazett‐corrected QT interval, Cornell voltage, education level, occupation category, income, and health insurance.

Figure 3. Incidence of sudden cardiac death (SCD) per 1000 person‐years in black (black triangles) and white (red quadrants) participants with and without hypertension (HTN) and coronary heart disease (CHD), and by body mass index (BMI) subgroups. Black lines correspond to 95% CI bounds.

Figure 4. Adjusted Cox proportional relative hazard ratio and competing sudden cardiac death risk relative sub–hazard risk ratio with 95% CI for black compared with white participants, with hazard ratio/sub–hazard ratio for white participants equal 1.0. Models 1 (green diamond) and models 2 (orange triangle) for the QRS‐T angle and spatial ventricular gradient (SVG) magnitude are shown. Black lines correspond to 95% CI bounds. Model 1 was adjusted for age, sex, study center, prevalent heart failure (HF), coronary heart disease (CHD), stroke, diabetes mellitus, hypertension, levels of total cholesterol, high‐density lipoprotein, and triglycerides, body mass index, use of antihypertensive and antiarrhythmic medications, serum concentrations of sodium, potassium, calcium, magnesium, phosphorus, and uric acid, total protein and albumin, blood urea nitrogen, chronic kidney disease stage classified by estimated glomerular filtration rate (calculated using the Chronic Kidney Disease–Epidemiology Collaboration equation), smoking and alcohol intake, work, sport, and leisure physical activity levels, education level, occupation category, income, and health insurance. Time‐updated model 2 included…

Figure 5. Race‐stratified adjusted (models 1 and 2, as described in Figure 4 legend) Cox proportional hazard ratio and 95% CI of sudden cardiac death for QRS‐T angle and spatial ventricular gradient (SVG) magnitude in white (hollow rectangle) and black (black oval) individuals. Black lines correspond to 95% CI bounds.

Figure 6. Adjusted (models 1 and 2, as described in Figure 4 legend) competing risk sub–hazard ratio and 95% CI of sudden cardiac death for QRS‐T angle and spatial ventricular gradient (SVG) magnitude in white (hollow rectangle) and black (black oval) individuals. Black lines correspond to 95% CI bounds.

Figure 7. Adjusted (model 1, as described in Figure 4 legend) risk of sudden cardiac death associated with area and peak QRS‐T angle in black and white participants. Restricted cubic spline with 95% CI shows a change in the hazard ratio (y axis) in response to QRS‐T angle change (x axis). The 50th percentile of QRS‐T angle is selected as a reference. Knots of peak QRS‐T angle in white participants are at 10° to 28° to 44° to 118°, and in black participants are at 11° to 31° to 53° to 149°. Knots of area QRS‐T angle in white participants are at 22° to 48° to 69° to 112°, and in black participants are at 21° to 48° to 69° to 118°.

Figure 8. Adjusted (model 1, as described in Figure 4 legend) risk of sudden cardiac death associated with area and peak QRS‐T angle in black participants with and without hypertension. Restricted cubic spline with 95% CI shows a change in the hazard ratio (y axis) in response to QRS‐T angle change (x axis). The 50th percentile of QRS‐T angle is selected as reference. Knots of peak QRS‐T angle are at 10° to 29° to 45° to 120°. Knots of area QRS‐T angle in black participants with hypertension are at 21° to 50° to 72° to 130°, and in hypertension‐free black participants are at 20° to 46° to 66° to 103°.

Figure 9. The 2‐by‐2 interactions for area QRS‐T angle. Adjusted (model 2, as described in Figure 4 legend) Cox proportional hazard ratio and 95% CI of sudden cardiac death in white (red) and black (black) individuals with (diamonds) and without (quadrants) hypertension (HTN). Circles indicate body mass index (BMI) subgroups. Black lines correspond to 95% CI bounds.

Figure 10. The 2‐by‐2 interactions for voltage‐based ECG metrics (sum absolute QRST integral [SAI QRST], peak spatial ventricular gradient [SVG] magnitude, and Cornell voltage). Adjusted Cox proportional hazard ratio and 95% CI of sudden cardiac death in white (red) and black (black) individuals with (diamonds) and without (quadrants) coronary heart disease (CHD) (Cox model 1). Circles indicate body mass index (BMI) subgroups (Cox model 2). Black lines correspond to 95% CI bounds. Models as described in Figure 4 legend.