Kimiaki Nagase

Significance of spontaneous normalization of negative T waves in infarct-related leads during healing of anterior wall acute myocardial infarction.

This study was conducted to elucidate the significance of spontaneous normalization of negative T waves in infarct-related leads during the chronic phase of anterior wall acute myocardial infarction. Results of this study indicate that patients with spontaneous normalization of negative T waves in infarct-related leads between 1 and 6 months after anterior wall acute myocardial infarction have smaller infarct size, decreased left ventricular dysfunction, and greater improvement in left ventricular wall motion in the infarct area, suggesting that T-wave normalization represents functional recovery of viable myocardium in the infarct area.

Relation of QT dispersion to infarct size and left ventricular wall motion in anterior wall acute myocardial infarction

Previous studies have shown that QT dispersion increases during acute myocardial infarction (AMI). However, the relation of QT dispersion to infarct size and left ventricular (LV) function in AMI has not yet been fully clarified. Accordingly, this study was conducted to elucidate this relation at 1 month after anterior wall AMI. We examined 94 patients with first anterior wall AMI (< or = 6 hours) who underwent coronary arteriography at admission, 1 month, and 6 months after AMI, and left ventriculography at 1 and 6 months after AMI. Mean QT dispersion on the chronic phase (about 1 month after AMI) electrocardiogram was 79 +/- 33 ms. There were no significant correlations between QT dispersion and peak creatine phosphokinase levels, LV ejection fraction, and regional wall motion in the infarct region at 1 month after AMI (r = 0.06, p = 0.57; r = 0.11, p = 0.29; r = -0.05, p = 0.63, respectively). In conclusion, the findings of this study suggest that QT dispersion on the resting electrocardiogram at 1 month after anterior wall AMI is unrelated to infarct size estimated by the peak creatine phosphokinase level and the degree of LV dysfunction.

Significance of Negative U Waves in the Precordial Leads During Anterior Wall Acute Myocardial Infarction

This study was conducted to clarify the clinical significance of negative U waves in the precordial leads during anterior wall acute myocardial infarction (AMI). In all, 141 patients with first anterior wall AMI (< or = 6 hours) were classified into 2 groups according to the presence (group A, n = 31) or absence (group B, n = 110) of negative U waves in the precordial leads on the admission electrocardiogram (ECG). The number of leads showing ST elevation > or = 1 mm on the admission ECG was smaller in group A than in group B (5.2 +/- 1.3 vs 6.2 +/- 1.7, p < 0.01). Emergent coronary arteriography revealed that group A had a higher incidence of good collateral circulation than group B (39% vs 19%, p < 0.05). Peak creatine kinase activity was lower in group A than in group B (1,708 +/- 1,271 vs 2,735 +/- 1,865 IU/L, p < 0.01). The number of abnormal Q waves on the predischarge ECG was smaller in group A (2.0 +/- 1.5 vs 3.4 +/- 2.0, p < 0.01). Group A had a greater left ventricular ejection fraction and better regional wall motion in the anterobasal, anterolateral, and apical regions in the chronic phase than group B. In conclusion, patients with anterior wall AMI having negative U waves in the precordial leads on admission had a relatively smaller mass of necrotic myocardium than those without the waves. Therefore, negative U waves during anterior wall AMI may be a useful marker for identifying patients with smaller infarction partly due to better collateral circulation.

Emergent coronary angiographic findings of patients with ST depression in the inferior or lateral leads, or both, during anterior wall acute myocardial infarction

In conclusion, the present study indicates that there are several distinctive differences in emergent coronary angiographic findings according to the presence or absence of ST depression in the inferior or lateral leads, or both, and location of the leads showing ST depression on admission electrocardiograms in patients with anterior AMI. The coronary angiographic features of patients with this ECG finding greatly support a poor prognosis. In patients with anterior AMI, analysis of ST depression on an admission electrocardiogram should be routinely performed because it is useful in predicting coronary anatomy, the extent of infarction, and its prognosis.

Spontaneous Normalization of Negative T Waves in Infarct-Related Leads Reflects Improvement in Left Ventricular Wall Motion even in Patients with Persistent Abnormal Q Waves after Anterior Wall Acute Myocardial Infarction

This study aimed to clarify whether spontaneous T-wave normalization (TWN) in infarct-related leads reflects improvement in left ventricular (LV) wall motion even in patients with persistent abnormal Q waves after acute myocardial infarction (AMI). Eighty-five patients were classified into the following 3 groups: patients with Q-wave regression (group A, n = 21), those with persistent abnormal Q waves and TWN (group B, n = 36), and those with persistent abnormal Q waves and absence of TWN (group C, n = 28). Groups A and B had greater improvement in LV ejection fraction and regional wall motion between 1 and 6 months after AMI than group C. In conclusion, spontaneous TWN in the healing stage of anterior AMI reflects functional recovery of viable myocardium in the infarct region even in patients with persistent abnormal Q waves.

Relation between negative U waves in precordial leads on the admission electrocardiogram and time course of left ventricular wall motion in anterior wall acute myocardial infarction

This study indicates that patients with anterior wall acute myocardial infarction showing negative U waves in the precordial leads on the admission electrocardiogram have greater improvement in left ventricular wall motion in the infarct region between 1 and 6 months after acute myocardial infarction. This suggests that these patients have a larger amount of stunned myocardium in the infarct region.