Objectives The aim of this study was to assess whether ultrasound attenuation and plaque rupture as detected by intravascular ultrasound (IVUS) are associated with the incidence of no-reflow ...phenomenon after percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI). Background No-reflow phenomenon is associated with worse long-term outcomes after STEMI. Therefore, reliable and feasible intravascular imaging techniques are needed to identify patient subgroups that would be at high risk for no-reflow phenomenon. Methods One hundred seventy consecutive patients with STEMI who underwent PCI within 12 h after symptom onset were enrolled. The IVUS interrogation was performed before PCI. Results No-reflow phenomenon occurred in 30 patients (18%), who had a higher incidence of no ST-segment resolution (50% vs. 9%; p < 0.001), a higher peak creatine kinase level (4,090 IU/l vs. 2,823 IU/l; p < 0.001), and a lower left ventricular ejection fraction in the chronic phase (51% vs. 59%; p < 0.01). Multivariate logistic regression analysis revealed that ultrasound attenuation with a longitudinal length of ≥5 mm, plaque rupture, and reperfusion time correlated with no-reflow phenomenon (all p < 0.05). In patients with both ultrasound attenuation ≥5 mm and plaque rupture, the incidence of no-reflow phenomenon was 88%, and the risk of decreased coronary reflow was higher than that predicted by either factor alone (p = 0.004 for interaction). Conclusions In patients with STEMI, a longer ultrasound attenuation and plaque rupture on IVUS are associated with an increased incidence of no-reflow phenomenon, suggesting that this subset of patients might be at high risk for distal embolism.
Impact of Plaque Rupture on Infarct Size in ST-Segment Elevation Anterior Acute Myocardial Infarction Ikuyoshi Kusama, Kiyoshi Hibi, Masami Kosuge, Naoki Nozawa, Hiroyuki Ozaki, Hideto Yano, ...Shinnichi Sumita, Kengo Tsukahara, Jun Okuda, Toshiaki Ebina, Satoshi Umemura, Kazuo Kimura Coronary plaque disruption followed by thrombus formation is the most frequent cause of acute coronary syndromes. Several studies have found that plaque disruption can be associated with either plaque rupture or plaque erosion. The present study demonstrates that plaque rupture at culprit lesions is significantly associated with morphologic characteristics of vulnerable lesions as well as with larger infarcts and a higher incidence of no-reflow phenomenon. The findings suggest that plaque embolism contributes to the progression of myocardial damage in patients with anterior acute myocardial infarction.
Negative T waves in precordial leads are often seen in patients with acute coronary syndrome (ACS), but also occur in those with acute pulmonary embolism (APE). However, little attention has been ...given to differences in negative T waves between patients with these 2 diseases. The present study examines the value of electrocardiograms for discriminating between 40 patients with APE and 87 patients with ACS who had negative T waves in the precordial leads (V1 to V4 ) on the admission electrocardiogram. In 77 patients (89%) with ACS, the culprit lesion was confirmed angiographically to be located in the left anterior descending coronary artery. Pulmonary P waves, S1 S2 S3 pattern, S1 Q3 T3 pattern, low voltage, and clockwise rotation were specific for APE, but sensitivities of these findings were very low. In patients with APE, negative T waves were commonly present in leads II, III, aVF, V1 , and V2 , but were less frequent in leads I, aVL, and V3 to V6 (p <0.05). Negative T waves in leads III and V1 were observed in only 1% of patients with ACS compared with 88% of patients with APE (p <0.001). The sensitivity, specificity, positive predictive value, and negative predictive value of this finding for the diagnosis of APE were 88%, 99%, 97%, and 95%, respectively. In conclusion, the presence of negative T waves in both leads III and V1 allows APE to be differentiated simply but accurately from ACS in patients with negative T waves in the precordial leads.
Objectives We sought to assess whether hyperinsulinemia is associated with percentage lipid and coronary plaque burden in nondiabetic patients with acute coronary syndromes (ACS). Background ...Hyperinsulinemia carries an increased risk of cardiovascular disease even in pre-diabetic patients, but the precise mechanisms of its effects remain unclear. Methods Nonculprit coronary lesions associated with mild-to-moderate stenosis in 82 nondiabetic patients with ACS were examined by integrated backscatter intravascular ultrasound (IB-IVUS), using a 40-MHz intravascular catheter. Conventional IVUS and IB-IVUS measurements from the worst 10-mm segment (1-mm intervals) were calculated. All patients underwent a 75-g oral glucose tolerance test (OGTT) to calculate the area under the insulin concentration-time curve (AUC insulin) from 0 to 120 min. Results Patients in the high tertile of AUC insulin had a significantly greater percentage lipid area and absolute lipid volume than did patients in the intermediate and low tertiles (tertile 3 vs. tertile 2 vs. tertile 1; 37.6 ± 16.6% vs. 25.8 ± 11.9% vs. 27.5 ± 14.7%, p < 0.01 by analysis of variance ANOVA, and 29.9 ± 22.6 mm3 vs. 15.3 ± 12.6 mm3 vs. 17.7 ± 12.7 mm3 , p < 0.01 by ANOVA, respectively) and a smaller percentage fibrosis area (55.0 ± 11.5% vs. 61.7 ± 9.4% vs. 60.7 ± 9.4%, p = 0.03 by ANOVA). Multiple regression analysis showed that the high tertile of AUC insulin was independently associated with an increased percentage lipid area (p < 0.05). On conventional IVUS analysis, external elastic membrane cross-sectional area was significantly increased with greater plaque volume in patients in the high tertile of AUC insulin (both p < 0.05 by ANOVA). Conclusions Hyperinsulinemia is associated with an increased lipid content and a greater plaque volume of nonculprit intermediate lesions in nondiabetic patients with ACS, suggesting that plaque vulnerability is increased in this subgroup of patients.
PDF
