Fig 1.
Patient flow diagram depicting the derivation of the study cohort.
Fig 2.
Examples of aVR elevation during stress electrocardiography with (A) and without (B) ST depression in lead V5. Note the subtle ST depression in tracing B does not meet criteria for ST depression on stress electrocardiography (defined as ≥1mm horizontal or down-sloping depression of the ST segment ≥80ms after the J-point for 3 consecutive beats).
Table 1.
Clinical characteristics of the study cohort stratified by presence or absence of ≥1mm aVR elevation.
Table 2.
Exercise and electrocardiographic findings stratified by presence or absence of ≥1mm aVR elevation.
Fig 3.
Prevalence of ischemia on SPECT myocardial perfusion imaging by the presence or absence of ≥1mm ST-depression in all leads and ≥1mm elevation in lead aVR.
There was a significant difference in prevalence by presence of absence of aVR elevation, but no significant difference by ST-depression within each aVR subgroup.
Fig 4.
Lead aVR results in those with and without ST-depression and rates of early revascularization.
In those without ST-depression, the rate of early revascularization was significantly higher in those with aVR elevation (p<0.001). In those with ST-depression, the subgroup with aVR elevation had a higher rate that was non-significant (p = 0.18) possibly due to reduced power from low numbers with ST-depression.
Fig 5.
Kaplan-Meier survival analysis for freedom from cardiac events stratified by ≥1mm of aVR elevation.
The presence or absence of ≥1mm elevation in lead aVR did not increase the risk of the composite outcome of cardiac death, nonfatal myocardial infarction, or late revascularization over a median 4.0 years of follow-up (p = 0.94).
Table 3.
Total incidence of cardiac events and annualized event rates stratified by presence or absence of ≥1mm aVR elevation in the 561 subjects with follow-up available.
Table 4.
Multivariable Cox proportional hazards analysis for total cardiac events.