Abstract 2255: Plaque With Calcified Nodule in the Culprit Lesion is Prone to Develop a Smaller Myocardial Infarction Size
Introduction: Coronary artery calcification is associated with plaque disruption of culprit lesion in the patient with acute myocardial infarction (MI). However, the impact of calcification in the culprit lesion of acute MI is unclear.
Hypothesis: We hypothesized that the existence of coronary artery calcification in the culprit lesion may cause different clinical outcome compared with none of that in patients with acute MI.
Methods: We studied 130 consecutive patients (107 men, 62.9+/−10.3 years) within 24 hours after MI onset in whom both angioscopy and intravascular ultrasound (IVUS) were performed immediately before and after percutaneous coronary intervention (PCI). Culprit lesion of infarct related artery was classified into plaque with calcified nodule (group C) or that without calcified nodule (group N) observed with the use of IVUS. Calcified nodule was defined as a bright echogenic signal accompanied by acoustic shadow with an arc of more than 10 degree in the coronary artery wall. We also assessed the morphological characteristics and vessel remodeling of the culprit lesion before PCI using by angioscopy and IVUS. We compared the clinical features between group C and group N.
Results: There were 60 patients in group C and 70 in group N. Group C had higher prevalence of non-ST-segment elevation MI (NSTEMI) on admission (18% vs. 6%; p=0.0248) and non-Q-wave MI (NQMI) at 1 month after onset (45% vs. 25%; p=0.0084) in comparison with group N. The incidence of vividly yellow color plaque (13% vs. 26%; p=0.0022), that of positive remodeling (22% vs. 44%; p=0.0022) and that of ruptured plaque (42% vs. 89%; p<0.0001) were lower in group C than in group N. Superimposed thrombus covering the surface of the stent after stenting was less frequent in group C than in group N (50% vs. 79%; p=0.0019). The locations of the culprit lesion were similar between the 2 groups.
Conclusions: Calcified nodule of coronary artery serve to limit the spread of vulnerability and thrombogenicity in the culprit lesion of acute MI, resulting in more frequent NSTEMI and NQMI.