Full Spectrum of Avr ST-Segment Changes in AMI

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Full Spectrum of Avr ST-Segment Changes in AMI

Abstract and Introduction

Abstract


Aims ST-elevation in lead aVR is known to be associated with a worse prognosis in patients with acute ST elevation myocardial infarction (MI) but the significance of ST depression in lead aVR has been unclear. Infarction of the inferior apex of the left ventricle may not be appreciated on the standard 12-lead electrocardiogram (ECG) except by observing ST depression in lead aVR which is reciprocal to lead V7. We therefore determined the prognostic value of the full spectrum of aVR ST changes in patients presenting with acute ST elevation MI.
Methods and results Lead aVR ST level was measured on randomization and 60 min ECGs in 15 315 patients with normal conduction from the HERO-2 trial. The outcome measure was 30-day mortality. aVR ST elevation ≥1 mm was associated with higher 30-day mortality for both inferior (22.5% for ≥1.5 mm and 13.2% for 1 mm) and anterior (23.5% for ≥1.5 mm and 11.5% for 1 mm) infarction. In contrast, deeper aVR ST depression (0, 0.5, 1, and ≥1.5 mm) was associated with higher mortality for anterior infarction (9.8, 13.2, 12.8, and 16.8%, respectively, trend P-value <0.0001) but not for inferior infarction. The resolution of aVR ST depression and ST elevation 60 min after fibrinolysis was associated with lower mortality.
Conclusion There is a U-shaped relationship between 30-day mortality and aVR ST level in patients presenting with anterior but not inferior ST elevation MI.

Introduction


The lead positions of a standard 12-lead ECG were standardized long before the current understanding of ST elevation acute myocardial infarction (AMI). Unavoidably parts of the heart are under-represented by the 12 surface ECG leads. The lead vector of aVR is orientated approximately from the cardiac apex to the outflow tract of the right ventricle. Directionally, lead aVR is as much reciprocal to V5 (facing the anteroapical region) as it is to V7 (facing the inferior-apical region). Transmural infarction in the basal interventricular septum may produce ST elevation in aVR when the injury current dipole has a component in the direction of the lead vector of aVR. At the same time, this injury current dipole induces ST depression in left lateral chest leads V5–V7 and in leads I and II because these leads are reciprocal to aVR, in that their lead vectors have components in a direction opposite to that of aVR. Likewise, a transmural apical infarction can produce aVR ST depression. Since V7 ST level recording changes from the inferior cardiac apex is not available on the standard 12-lead ECG, ST changes in the often neglected lead aVR are particularly relevant.

From the HERO-2 cohort, we recently reported that lead aVR ST elevation, as defined dichotomously, portended higher 30-day mortality particularly with inferior AMI. Patients with aVR ST elevation had lower summed ST elevation and higher summed ST depression from the other 11 ECG leads compared with patients without aVR ST elevation. The increased mortality risk associated with aVR ST elevation was unchanged after adjustment for summed ST elevation, indicating that aVR ST elevation adds to the prognostic importance of ST elevation in other leads, but was decreased after adjustment for summed ST depression, reflecting the directionally reciprocal relationship between lead aVR and the apical leads.

The unique non-anterior and non-inferior direction of lead aVR means that the prognostic implications of ST deviations (elevation or depression) could be different depending on the infarct location. In particular, aVR ST depression can be reflective of ST elevation in V7 that the standard 12-lead ECG fails to capture. The current study, therefore, investigated the prognostic relevance of the full spectrum of aVR ST changes (from elevation to depression) in anterior and in inferior AMI using a neutral ST level reference, adjusted to ST changes in the other 11 leads.

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