What is the clinical evidence from this study?

Study design: Cohort. Population: Asymptomatic volunteers free from clinical coronary heart disease (n=1083). Intervention: Exercise-induced ST-segment abnormalities vs. Normal exercise ECG. Primary outcome: Coronary events (angina pectoris, myocardial infarction, or coronary death) (RR 2.70 (code 11:1); RR 2.73 (code 11:5), p=0.0005 (code 11:1); 0.04 (code 11:5)).

November 25, 2002Open Access

Role of Nondiagnostic Exercise-Induced ST-Segment Abnormalities in Predicting Future Coronary Events in Asymptomatic Volunteers

Key Result

Classic ischemic ST-segment exercise response (RR 2.70) and intensification of minor preexercise ST depression to ≥1 mm (RR 2.73) independently predicted future coronary events.

Study Design

Type

Cohort (n=1,083)

Structured PICO

Do nondiagnostic exercise-induced ST-segment abnormalities predict future coronary events in asymptomatic volunteers?

Population

1083 asymptomatic volunteers from the Baltimore Longitudinal Study of Aging who were free from clinical coronary heart disease

Intervention

Maximal treadmill exercise test with ST-segment changes stratified by Minnesota code criteria (11:1, 11:2, 11:4, 11:5)

Comparator

Subjects with normal exercise ECG (n=611)

Outcome

Coronary events (angina pectoris, myocardial infarction, or coronary death)composite

In asymptomatic individuals, classic ischemic ST-segment exercise response and intensification of minor preexercise ST-segment depression to ≥1 mm independently predict future coronary events, whereas nondiagnostic changes (<1 mm or slowly rising) do not.

Main Result

Effect estimate: RR 2.70 (code 11:1); RR 2.73 (code 11:5)

p-value: p=0.0005 (code 11:1); 0.04 (code 11:5)

Abstract

Background— Whether exercise-induced ST-segment depression <1 mm is an independent predictor of future coronary events (CEs) in asymptomatic subjects is unknown. Methods and Results— We performed maximal treadmill exercise tests on 1083 volunteers from the Baltimore Longitudinal Study of Aging who were free from clinical coronary heart disease. Exercise ST-segment changes were stratified by Minnesota code criteria: 11:1 (n=213), flat or downsloping ST depression ≥1 mm; 11:2 (n=66), flat or downsloping ST depression ≥0.5 mm and <1 mm; 11:4 (n=124), ST-J depression ≥1 mm with slowly rising ST segments; and 11:5 (n=69), minor ST depression (<0.5 mm) before exercise that worsened to flat or downsloping ST depression ≥1 mm during or after exercise. Risk of CE was compared with subjects with normal exercise ECG (n=611). Over a mean follow-up of 7.9 years, 76 subjects developed CEs (angina pectoris, myocardial infarction, or coronary death). On univariate analysis, age (relative risk RR=1.07/year, P <0.0001), male sex (RR=1.98, P =0.009), plasma cholesterol (RR=1.02/mg per dL, P <0.0001), hypertension (RR=2.23, P =0.002), duration of exercise (RR=0.71/min, P =0.0001), and systolic blood pressure at peak effort (RR=1.02/mm Hg, P =0.002) were associated with CE. By Cox proportional hazards analysis, age (RR=1.06/year, P <0.0001), male sex (RR=2.76, P =0.0002), plasma cholesterol (RR=1.02 per 1 mg/dL, P <0.0001), duration of exercise (RR=0.87/min, P =0.004), and ST-segment changes coded as either 11:1 (RR=2.70, P =0.0005) or 11:5 (RR=2.73, P =0.04) were independent predictors of CE. Conclusions— Both a classic ischemic ST-segment exercise response and intensification of minor preexercise ST-segment depression to levels ≥1 mm independently predicted future CE in this asymptomatic population. Neither slowly rising ST depression nor horizontal ST depression <1 mm was prognostic.