Soo Young Jang

Clinical, angiographic, and intravascular ultrasound predictors of early stent thrombosis in patients with acute myocardial infarction.

Risk factors reported for early stent thrombosis (EST) included acute coronary syndrome, suboptimal antiplatelet therapy, procedural factors such as residual dissection and underexpansion of stents, and smaller final lumen area and inflow/outflow disease (residual stenosis or dissection) by intravascular ultrasound (IVUS) [1–4]. However, the predictors of EST including all variables such as baseline characteristics, laboratory data, angiographic and IVUS findings in patients with acute myocardial infarction (AMI) are still not well known. From January 2007 to December 2009, we identified 418 consecutive patients with a first AMI who underwent pre-percutaneous coronary intervention (PCI) IVUS within 24 h from symptom onset, were stented successfully, and had post-PCI IVUS imaging. EST included acute (b24 h) and subacute ST (1 to 30 days) after stent implantation. Cardiac-specific troponin I (cTnI) levels were measured by a paramagnetic particle, chemiluminescent immunoenzymatic assay (Beckman, Coulter Inc., Fullerton, California). No-reflow was defined as postPCI TIMI grade 0, 1, or 2 flow. Tissue prolapse was defined as tissue extrusion through the stent strut at post-PCI. The baseline characteristics, angiographic and IVUS findings are summarized in Table 1. EST occurred in 16 patients (3.8%). Glycoprotein IIb/IIIa inhibitor was used more frequently in patients with EST compared with those without EST. Pre-PCI peak creatine kinase-MB and cTnI were significantly higher in patients with EST compared with those without EST. Pre-PCI TIMI flow grade was significantly lower in patients with EST compared with those without EST. More stents were deployed in patients with EST compared with those without EST. Noreflow during or after PCI was developed more frequently in EST group than in non-EST group (87.5% vs. 12.2%, p b 0.001). Plaque burden at the minimum lumen site was significantly greater in patients with EST compared with those without EST. Pre-PCI plaque rupture and IVUSdetected thrombuswere observedmore frequently in patients with EST compared with those without EST. Post-stenting tissue prolapse was observed more frequently in patients with EST compared with those without EST (68.8% vs. 32.6%, p= 0.003). Independent predictors of EST are summarized in Table 2. Multivariate analysis showed that noreflow, pre-PCI peak cTnI, and tissue prolapse were the independent predictors of EST. No-reflow can occur easily in lesions with various kinds of vulnerable plaque including plaque rupture and thrombus and this no-reflow is associated with microvascular damage which is likely to slow the epicardial coronary blood flow and to stagnate blood flow which may accelerate local thrombus formation [5]. The mechanism underlying the association between pre-PCI peak cTnI level and EST is not clear, although cTnI is associated with high thrombus grade with promoted thrombus formation in patients with AMI, who already have heightened systemic and intracoronary platelet reactivity, thrombin generation, and inflammation. Tissue prolapse may represent a source for thrombus accumulation in an environment that already has a high potential for thrombogenesis. Impaired arterial healing and ST have been associated with the prolapse of the necrotic core between stent struts. This is especially relevant in the setting of AMI, because such patients already have an increased risk for this devastating event [6]. In conclusion, the incidence of EST after stenting of infarct-related arteries was 3.8%. No-reflow, pre-PCI peak cTnI and tissue prolapse were associated with the development of EST after stent implantation in patients with AMI.

The Association of Socioeconomic Status with Three-Year Clinical Outcomes in Patients with Acute Myocardial Infarction Who Underwent Percutaneous Coronary Intervention

The aim of this study was to evaluate whether the clinical outcomes were associated with socioeconomic status (SES) in patients with acute myocardial infarction (AMI) who underwent percutaneous coronary intervention (PCI). The author analyzed 2,358 patients (64.9 ± 12.3 yr old, 71.5% male) hospitalized with AMI between November 2005 and June 2010. SES was measured by the self-reported education (years of schooling), the residential address (social deprivation index), and the national health insurance status (medical aid beneficiaries). Sequential multivariable modeling assessed the relationship of SES factors with 3-yr major adverse cardiovascular events (MACEs) and mortality after the adjustment for demographic and clinical factors. During the 3-yr follow-up, 630 (26.7%) MACEs and 322 (13.7%) all-cause deaths occurred in 2,358 patients. In multivariate Cox proportional hazards regression modeling, the only lower education of SES variables was associated with MACEs (hazard ratio [HR], 1.41; 95% confidence interval [CI], 1.04-1.91) and mortality (HR, 1.93; 95% CI, 1.16-3.20) in the patients with AMI who underwent PCI. The study results indicate that the lower education is a significant associated factor to increased poor clinical outcomes in patients with AMI who underwent PCI. Graphical Abstract

Relation between renal function and neointimal tissue characteristics after drug-eluting stent implantation: Virtual histology-intravascular ultrasound analysis

BACKGROUND Few data are available about neointimal tissue characteristics after drug-eluting stent (DES) implantation in patients with decreased renal function. We used virtual histology-intravascular ultrasound (VH-IVUS) to assess the neointimal tissue characteristics according to the baseline renal function. METHODS We compared neointimal tissue components between patients with chronic kidney disease (CKD) [n=19, estimated creatinine clearance (CrCl) <60mL/min] and those without CKD (n=229). The region of interest was placed between the luminal border and the inner border of the stent struts and tissue components were reported as percentages of neointimal volume. RESULTS Mean follow-up durations between DES implantation and follow-up VH-IVUS study were 12.0±4.1 months in the CKD group and 11.4±5.6 months in the non-CKD group (p=0.519). At follow-up, neointima volume was significantly greater (72±47mm(3) vs. 47±26 mm(3), p<0.001) and %neointima necrotic core (NC) volume was significantly greater (25.0±11.4% vs. 17.9±10.2%, p=0.012) in the CKD group compared with the non-CKD group. There was negative correlation between CrCl and neointima volume (r=-0.250, p<0.001), however, there was no significant correlation between CrCl and %neointima NC volume (r=-0.034, p=0.591). The only independent predictor of follow-up %neointima NC volume ≥10% was neointima volume (odds ratio 1.025, 95% confidence interval 1.013-1.036, p<0.001). CONCLUSIONS Renal function was associated with in-stent neointimal growth, but it was not associated with neointima NC formation. Instead, the amount of neointima was associated with more neoatherosclerosis in patients who underwent DES implantation.

Clinical impact of early intervention in octogenarians with non-ST-elevation myocardial infarction

myocardial infarction☆ Zhe Hao Piao , Myung Ho Jeong ⁎, Li Jin , Da Wei Qian , Soo Young Jang , Jae Yeong Cho , Hae Chang Jeong , Ki Hong Lee , Keun-Ho Park , Doo Sun Sim , Kye Hun Kim , Young Joon Hong , Hyung Wook Park , Ju Han Kim , Youngkeun Ahn , Jeong Gwan Cho , Sang Hyung Kim , Jong Chun Park , Young Jo Kim , Myeong Chan Cho , Chong Jin Kim , Hyo Soo Kim f and Other Korea Acute Myocardial Infarction Registry (KAMIR) Investigator a Chonnam National University Hospital, Gwangju, Republic of Korea b Jilin Central Hospital, Jilin, China c Yeungnam University Hospital, Daegu, Republic of Korea d Chungbuk National University Hospital, Cheongju, Republic of Korea e Kyung Hee University Hospital, Seoul, Republic of Korea f Seoul National University Hospital, Seoul, Republic of Korea

Predictors of recurrent sudden cardiac death in patients associated with coronary vasospasm

Even though coronary heart disease is the leading cause of sudden cardiac death (SCD), there is increasing evidence that SCD can be developed in the absence of organic heart disease. Coronary vasospasm or primary electrical disorder may play an important role in these circumstances. In aborted SCD patients associated with coronary vasospasm, medical treatment is recommended as the first line therapy. However, some patients experience recurrent SCD events despite medical treatment. Furthermore, although coronary vasospasm can cause life threatening arrhythmia, some patients did not have any ischemic symptoms before the index event. Therefore, coronary vasospasm itself might not be the sole cause of SCD event. We hypothesized that primary electrical abnormalities might be one of the important causes in recurrent SCD. A total of 68 aborted SCD patients who have angiographically proven coronary vasospasmwere analyzed. Patients were divided into 2 groups according to the presence of recurrent SCD episode (group 1, patients with recurrent events, n = 13; group 2, patients without recurrent events, n = 55). Coronary vasospasm was defined when coronary angiographic finding showed no significant obstructive coronary artery stenosis (stenosis b 50%) and either spontaneous coronary spasm or ergonovine induced vasospasm. Primary electrical disorders including Brugada syndrome, arrhythmogenic right ventricular dysplasia (ARVD), long QT syndrome (LQTS), and early repolarization syndrome were analyzed by two electrophysiologists blinded to clinical outcomes at the time of and after the index SCD event during 3.9 years median follow-up based on standard electrocardiographic diagnostic criteria [1–4]. The electrocardiographic diagnosis of early repolarization should have J point elevation≥0.1 mV in at least 2 inferior or lateral leads. These ECG findings were divided into notched or slurred type. ST segment patterns after the J point elevation were classified as concave/rapidly ascending (as N0.1 mVelevation of ST segment within 100 ms after the J point or a persistently elevated ST segment of N0.1 mV throughout the ST segment) or horizontal/ descending (≤0.1 mV elevation of the ST segment within 100 ms after the J point) [4]. The methods of unpaired t test, chi-square test, Kaplan–Meier estimation and Cox proportional hazards regression analysis were used (SPSS for window 18.0). Group 1 patients were younger (46.7 ± 10.2 vs. 52.5 ± 9.6 years old, p = 0.050). There were no differences in laboratory results and concomitant medications. Analysis of angiographic findings showed that the prevalence of coronary spasm was 57.4% in left anterior descending artery, 52.9% in right coronary artery, and 20.6% in left circumflex artery. Among the patients with right coronary artery vasospasm, diffuse type spasmwasmore common in the group 1 than the group 2 (50.0% vs. 5.3%, p = 0.017). Primary electrical abnormalities were found in 40 (58.8%) patients: Brugada type ECG in 5 (7.4%), ARVD in 3 (4.4%), LQTS in 2 (2.9%) and early repolarization in 33 (48.5%) patients. Two patients had both Brugada type 1 ECG and early repolarization, whereas one patient had both LQTS and early repolarization at a different time point of ECG follow-up. Group 1 had higher prevalence of Brugada type ECG (23.1% vs. 3.6%, p = 0.045), LQTS (15.4% vs. 0%, p = 0.034) than group 2. Among early repolarization subtype, horizontal/descending ST segment was more common in group 1 than group 2 (46.2% vs. 14.5%, p = 0.011). Recurrent SCD events developed in 13 (19.1%) patients. Kaplan– Meier estimation showed that patients with horizontal/descending ST segment experienced significantly higher recurrent SCD events than those patients without horizontal/descending ST segment (42.9% vs. 13.0%, log rank p = 0.005, Fig. 1). Cardiovascular risk factors including age, sex, hypertension, diabetes mellitus and smoking did not predict recurrent SCD events before and after covariate adjustment. Early repolarization with horizontal/descending STsegment (adjustedhazard ratio [HR]4.41, 95% confidence interval [CI] 1.26 to 15.40, p = 0.020) and right coronary artery diffuse type vasospasm (adjusted HR 4.03, 95% CI 1.09–14.96, p = 0.037) were associated with recurrent SCD events before and after covariate adjustment (Table 1). Coronary vasospasm without obstructive lesion may trigger fatal ventricular arrhythmia. Although medical therapy including calcium channel blockers and nitrates has been known to be effective in preventing coronary vasospasm and related ventricular arrhythmias, some of them experience recurrent SCD events.

One-year clinical impact of cardiac arrest in patients with first onset acute ST-segment elevation myocardial infarction

BACKGROUND Cardiac arrest complicating acute ST elevation myocardial infarction (STEMI) is known to be associated with increased in-hospital mortality. However, little is known about the long-term outcomes after cardiac arrest complicating first onset STEMI in contemporary percutaneous coronary intervention (PCI) era. METHODS We analyzed 7942 consecutive patients who were diagnosed with STEMI and had no previous history of MI. They were divided into two groups according to the presence of cardiac arrest (group I, patients with cardiac arrest; n=481, group II, patients without cardiac arrest; n=7641). RESULTS In a stepwise multivariate model, previous history of chronic kidney disease, high serum level of glucose and low high density lipoprotein-cholesterol was an independent predictor of cardiac arrest complicating STEMI. Group I had significantly higher in-hospital mortality (adjusted hazard ratio [HR] 3.06, 95% confidence interval [CI] 2.08-4.51, p<0.001) and 30-day mortality after hospital discharge (adjusted HR 2.92, 95% CI 1.86-4.58, log-rank p<0.001). However, there was no significant increase in mortality beyond 30 days (6-month, adjusted HR 1.46, 95% CI 0.45-4.77, log rank p=0.382; 1-year, adjusted HR 1.84, 95% CI 0.83-4.05, log-rank p=0.107). Also, there were no significant differences in 6-month and 1-year major adverse cardiac events in 30-day survivors. Performing PCI was associated with decreased 12-month mortality in 30-day survivors. CONCLUSIONS Although patients with cardiac arrest complicating first onset STEMI had higher in-hospital and 30-day mortality after hospital discharge, cardiac arrest itself did not have any residual impact on mortality as well as clinical outcomes.