The relationship between initial ST-segment deviation and final QRS complex changes related to the posterolateral wall in acute inferior myocardial infarction.

摘要

OBJECTIVES: The aim of this study was to assess the relationship between initial ST-segment deviation and final QRS complex changes related to the posterolateral left ventricular wall in patients with acute inferior myocardial infarction receiving reperfusion therapy. The secondary aim was to determine if this relationship is stronger for patients who present early in the ischemia/infarction process in comparison with patients who present late. METHODS: The ST-segment depression in the leads V(1), V2, and -V6 were measured in the electrocardiograph (ECG) just before initiation of myocardial reperfusion. These leads were chosen because they represent the posterolateral wall in the Selvester score. In addition, the Anderson-Wilkins acuteness score was calculated in the admission ECG. Selvester criteria related to the posterolateral wall were identified in the ECG performed before hospital discharge to assess final infarct size. RESULTS: Fifty-six patients were included in this study. No significant relationship was found between the sum of initial ST-segment depression in the leads V(1), V(2), and -V(6), and final infarct size in the posterolateral left ventricular wall for the total study population (r = 0.19, P = .16). Patients were subgrouped by Anderson-Wilkins acuteness score of less than 3 vs 3 or more. In those with a low acuteness score, the amount of ST-segment depression had no relationship with final infarct size (r = -0.16, P = .41). However, the correlation was statistically significant for those with a high acuteness score (r = 0.42, P = .04). CONCLUSION: The initial ST-segment depression in leads V(1), V(2), and -V(6) can predict ECG-estimated amount of infarction in the posterolateral left ventricular wall in patients with acute inferior myocardial infarction receiving reperfusion therapy, but only in those who present early in the ischemia/infarction process.