Jong Goo Seo

Predictors of Recovery of Left Ventricular Systolic Dysfunction after Acute Myocardial Infarction: From the Korean Acute Myocardial Infarction Registry and Korean Myocardial Infarction Registry

Background and Objectives We investigated the predictors of the recovery of depressed left ventricular ejection fraction (LVEF) in patients with moderate or severe left ventricular (LV) systolic dysfunction after acute myocardial infarction (MI). Subjects and Methods We analyzed 1307 patients, who had moderately or severely depressed LVEF (<45%) on echocardiography soon after acute MI and who underwent a follow-up echocardiography, among 27369 patients from the Korea Working Group on the Myocardial Infarction Registry. Patients were categorized into two groups according to recovery of LVEF: group I with consistently depressed LVEF (<45%) at the follow-up echocardiography and group II with a recovery of LVEF (≥45%). Results Recovery of LV systolic dysfunction was observed in 51% of the subjects (group II, n=663; ΔLVEF, 16.2±9.3%), whereas there was no recovery in the remaining subjects (group I, n=644; ΔLVEF, 0.6±7.1%). In the multivariate analysis, independent predictors of recovery of depressed LVEF were as follows {odds ratio (OR) [95% confidence interval (CI)]}: moderate systolic dysfunction {LVEF ≥30% and <45%; 1.73 (1.12-2.67)}, Killip class I-II {1.52 (1.06-2.18)}, no need for diuretics {1.59 (1.19-2.12)}, non-ST-segment elevation MI {1.55 (1.12-2.16)}, lower peak troponin I level {<24 ng/mL, median value; 1.55 (1.16-2.07)}, single-vessel disease {1.53 (1.13-2.06)}, and non-left anterior descending (LAD) culprit lesion {1.50 (1.09-2.06)}. In addition, the use of statin was independently associated with a recovery of LV systolic dysfunction {OR (95% CI), 1.46 (1.07-2.00)}. Conclusion Future contractile recovery of LV systolic dysfunction following acute MI was significantly related with less severe heart failure at the time of presentation, a smaller extent of myonecrosis, or non-LAD culprit lesions rather than LAD lesions.

Rosuvastatin treatment improves arterial stiffness with lowering blood pressure in healthy hypercholesterolemic patients

☆ We presented our study in part as abstracts in the A 2013, San Francisco, CA, USA, on March 10, 2013. ☆☆ All authors take responsibility for all aspects of the re of the data presented and their discussed interpretation. ⁎ Corresponding author at: Cardiology Division, Dep Gachon University Gil Hospitial, 1198 Guwol-dong, Na Republic of Korea. Tel.: +82 32 460 3054; fax: +82 32 46 E-mail address: shhan@gilhospital.com (S.H. Han).

The role of insulin resistance and metabolic risk factors on culprit coronary plaque

BACKGROUND Detailed relationships between insulin resistance (IR) and vulnerable plaque are not clear, therefore, we sought the role of IR and metabolic risk factors on culprit coronary plaque. METHODS Plaque components at a region of interest (ROI, 10mm) were analyzed by virtual histology intravascular ultrasound. IR was defined as quantitative insulin sensitivity check index (QUICKI) ≤ 0.33. Seven metabolic risk factors (5 risk factors for metabolic syndrome defined by ATP III, history of smoking, and hsCRP) for IR were determined. RESULTS The data for 150 (males 104) patients were analyzed. Patients with IR (n = 69) had greater necrotic core (NC) at the ROI (21.2 ± 15.8mm(3) vs 15.7 ± 11.9 mm(3), p = 0.02) than in patients without IR (n = 81). The NC at the ROI was correlated with QUICKI (r = -0.16, p = 0.05), HbA1c (r = 0.24, p < 0.01), body mass index (r = 0.17, p = 0.04), presence of diabetes mellitus (r = 0.29, p < 0.001), hsCRP (r = 0.17, p = 0.04) and the numbers of risk factors for IR (r = 0.41, p < 0.001). The multivariate analysis revealed that the numbers of risk factors for IR was an independent factor for the NC at the ROI (beta coefficient = 0.44, p = 0.003), but QUICKI was not (beta coefficient = -0.01, p = 0.94). CONCLUSIONS Instead of a single measurement of IR index or each metabolic risk factor, clustering of risk factors for IR plays an important role on plaque vulnerability. CONDENSED ABSTRACT We investigated the role of insulin resistance (IR) on culprit coronary plaque. Patients with IR had a greater amount of necrotic core in culprit coronary lesions than in patients without IR. Rather than a single measurement of IR index or each metabolic risk factor, clustering of metabolic risk factors for IR plays an important role in plaque vulnerability in patients with coronary artery disease. Our study demonstrates the role of IR on culprit coronary plaque and highlights the importance of the clustering of metabolic risk factors for IR in vulnerable plaque pathogenesis.

TCT-115 Hybrid endovascular repair for aortic arch pathology: intermediate outcomes and complications

nos: 115-132