Once ischemic necrosis occurs in the tissue below an injury site after trauma, a vascular injury is suspected first. On the other hand, it is not common for a blood vessel to become obstructed after a delay of a few days after the initial trauma. The authors experienced a case where the blood flow was maintained at the time of a femoral fracture injury and immediately after surgery, but the femoral artery was occluded later. On the 5th day after surgery, ischemic necrosis of the lower limb was confirmed and treated. This case is reported with a review of the relevant literature.

Purpose: Neuroinflammation is considered an important pathway associated with several diseases that result in cognitive decline. 18F-THK5351 positron emission tomography (PET) signals might indicate the presence of neuroinflammation, as well as Alzheimer’s disease-type tau aggregates. β-amyloid (Aβ)-negative (Aβ–) amnestic mild cognitive impairment (aMCI) may be associated with non-Alzheimer’s disease pathophysiology. Accordingly, we investigated associations between 18F-THK5351 PET positivity and cognitive decline among Aβ– aMCI patients. Materials and Methods: The present study included 25 amyloid PET negative aMCI patients who underwent a minimum of two follow-up neuropsychological evaluations, including clinical dementia rating-sum of boxes (CDR-SOB). The patients were classified into two groups: 18F-THK5351-positive and -negative groups. The present study used a linear mixed effects model to estimate the effects of 18F-THK5351 PET positivity on cognitive prognosis among Aβ– aMCI patients. Results: Among the 25 Aβ– aMCI patients, 10 (40.0%) were 18F-THK5351 positive. The patients in the 18F-THK5351-positive group were older than those in the 18F-THK5351-negative group (77.4±2.2 years vs. 70.0±5.5 years; p<0.001). There was no difference between the two groups with regard to the proportion of apolipoprotein E ε4 carriers. Interestingly, however, the CDR-SOB scores of the 18F-THK5351-positive group deteriorated at a faster rate than those of the 18F-THK5351-negative group (B=0.003, p=0.033). Conclusion The results of the present study suggest that increased 18F-THK5351 uptake might be a useful predictor of poor prognosis among Aβ– aMCI patients, which might be associated with increased neuroinflammation (ClinicalTrials.gov NCT02656498).

BACKGROUND AND OBJECTIVES: Although anticoagulation with warfarin is recommended as an international normalized ratio (INR) of prothrombin time between 2.0 and 3.0 and mean time in the therapeutic range (TTR) ≥70%, little has been proven that universal criteria might be suitable in Korean atrial fibrillation (AF) patients. METHODS: We analyzed 710 patients with non-valvular AF who took warfarin. INR value and clinical outcomes were assessed during 2-year follow-up. Intensity of anticoagulation was assessed as mean INR value and TTR according to target INR range. Primary net-clinical outcome was defined as the composite of new-onset stroke and major bleeding. Secondary net-clinical outcome was defined as the composite of new-onset stroke, major bleeding and death. RESULTS: Thromboembolism was significantly decreased when mean INR was over 1.6. Major bleeding was significantly decreased when TTR was over 70% and mean INR was less than 2.6. Mean INR 1.6–2.6 significantly reduced thromboembolism (adjusted hazard ratio [HR], 0.40; 95% confidence interval [CI], 0.19–0.85), major bleeding (HR, 0.43; 95% CI, 0.23–0.81), primary (HR, 0.50; 95% CI, 0.29–0.84) and secondary (HR, 0.45; 95% CI, 0.28–0.74) net-clinical outcomes, whereas mean INR 2.0–3.0 did not. Simultaneous satisfaction of mean INR 1.6–2.6 and TTR ≥70% was associated with significant risk reduction of major bleeding, primary and secondary net-clinical outcomes. CONCLUSIONS Mean INR 1.6–2.6 was better than mean INR 2.0–3.0 for the prevention of thromboembolism and major bleeding. However, INR 1.6–2.6 and TTR ≥70% had similar clinical outcomes to INR 2.0–3.0 and TTR ≥70% in Korean patients with non-valvular AF.

Background/Aims: Many patients with acute myocardial infarction (AMI) suffer from heart failure due to progressive ischemic left ventricular (LV) remodeling. This study investigated the predictors of ischemic cardiomyopathy (ICMP) in patients with AMI who underwent successful percutaneous intervention. Methods: A total of 547 patients with AMI were divided into two groups: ICMP (n = 66, 67.1 ± 11.9 years, 78.8% males) and non-ICMP (n = 481, 62.5 ± 12.2 years, 70.1% males). Results: On echocardiography, the LVEF was significantly decreased (41.7 ± 10.5 vs. 55.4 ± 10.3%, p < 0.001) but the LV end-diastolic (54.1 ± 7.2 vs. 49.3 ± 5.3 mm, p < 0.001) and systolic (42.1 ± 8.0 vs. 33.5 ± 6.0 mm, p < 0.001) dimensions significantly increased in the ICMP group compared with the non-ICMP group. According to multivariate logistic regression analysis, LVEF < 50% (odds ratio [OR] 8.722, 95% confidence interval [CI] 2.986–25.478, p < 0.001), LV end-diastolic dimension > 55 mm (OR 4.511, 95% CI 1.561–13.038, p = 0.005), and ratio of early mitral inflow velocity to mitral annular early diastolic velocity (E/e’) ≥ 15 (OR 3.270, 95% CI 1.168–9.155, p = 0.024) were independent predictors of ICMP development. Conclusions The present study demonstrates that a larger LV size, lower LV function, and increased E/e’ (≥ 15) were independent predictors of ICMP. Therefore, the development of ICMP should be carefully monitored in AMI patients with these features.

Background/Aims: Left ventricular hypertrophy (LVH) on clinical outcomes in patients with acute myocardial infarction (AMI) is not clear. This study was performed to investigate the effect of abnormal left ventricular geometry on clinical outcomes in Korean patients with AMI. Methods: A total of 852 consecutive patients with AMI were divided into two groups: normal left ventricular geometry (n = 470; 389 males) and LVH (n = 382; 214 males) groups. Major adverse cardiac events (MACEs) were defined as cardiac death, recurrent myocardial infarction, and rehospitalization. Results: During the clinical follow-up period of 21 ± 7.8 months, MACEs developed in 173 patients (20.0%), and the rate was higher in the LVH than normal left ventricular geometry groups (25.5% vs. 16.0%, respectively, p = 0.001). According to Kaplan-Meier survival curves, the MACE-free survival rate was significantly lower in the LVH group than in the left ventricular geometry group (p = 0.008). The rates of MACEs and all-cause mortality differed among the AMI with concentric remodeling, concentric hypertrophy, and eccentric hypertrophy subgroups (11.2% vs. 15.5% vs. 22.1%, respectively, p = 0.046). Eccentric hypertrophy was a predictive factor of MACE according to Cox proportional hazards analysis (hazard ratio 1.804, confidence interval 1.034-3.148, p = 0.038). Conclusions LVH is a predictor of poor outcomes in patients with AMI, and eccentric hypertrophy is associated with a worse prognosis compared with concentric remodeling and concentric hypertrophy. Therefore, Korean patients with AMI and LVH, especially eccentric hypertrophy, require more careful observation and intensive treatment.

Background/Aims: Left ventricular hypertrophy (LVH) on clinical outcomes in patients with acute myocardial infarction (AMI) is not clear. This study was performed to investigate the effect of abnormal left ventricular geometry on clinical outcomes in Korean patients with AMI. Methods: A total of 852 consecutive patients with AMI were divided into two groups: normal left ventricular geometry (n = 470; 389 males) and LVH (n = 382; 214 males) groups. Major adverse cardiac events (MACEs) were defined as cardiac death, recurrent myocardial infarction, and rehospitalization. Results: During the clinical follow-up period of 21 ± 7.8 months, MACEs developed in 173 patients (20.0%), and the rate was higher in the LVH than normal left ventricular geometry groups (25.5% vs. 16.0%, respectively, p = 0.001). According to Kaplan-Meier survival curves, the MACE-free survival rate was significantly lower in the LVH group than in the left ventricular geometry group (p = 0.008). The rates of MACEs and all-cause mortality differed among the AMI with concentric remodeling, concentric hypertrophy, and eccentric hypertrophy subgroups (11.2% vs. 15.5% vs. 22.1%, respectively, p = 0.046). Eccentric hypertrophy was a predictive factor of MACE according to Cox proportional hazards analysis (hazard ratio 1.804, confidence interval 1.034-3.148, p = 0.038). Conclusions LVH is a predictor of poor outcomes in patients with AMI, and eccentric hypertrophy is associated with a worse prognosis compared with concentric remodeling and concentric hypertrophy. Therefore, Korean patients with AMI and LVH, especially eccentric hypertrophy, require more careful observation and intensive treatment.

BACKGROUND AND OBJECTIVES: Although anticoagulation with warfarin is recommended as an international normalized ratio (INR) of prothrombin time between 2.0 and 3.0 and mean time in the therapeutic range (TTR) ≥70%, little has been proven that universal criteria might be suitable in Korean atrial fibrillation (AF) patients.METHODS: We analyzed 710 patients with non-valvular AF who took warfarin. INR value and clinical outcomes were assessed during 2-year follow-up. Intensity of anticoagulation was assessed as mean INR value and TTR according to target INR range. Primary net-clinical outcome was defined as the composite of new-onset stroke and major bleeding. Secondary net-clinical outcome was defined as the composite of new-onset stroke, major bleeding and death.RESULTS: Thromboembolism was significantly decreased when mean INR was over 1.6. Major bleeding was significantly decreased when TTR was over 70% and mean INR was less than 2.6. Mean INR 1.6–2.6 significantly reduced thromboembolism (adjusted hazard ratio [HR], 0.40; 95% confidence interval [CI], 0.19–0.85), major bleeding (HR, 0.43; 95% CI, 0.23–0.81), primary (HR, 0.50; 95% CI, 0.29–0.84) and secondary (HR, 0.45; 95% CI, 0.28–0.74) net-clinical outcomes, whereas mean INR 2.0–3.0 did not. Simultaneous satisfaction of mean INR 1.6–2.6 and TTR ≥70% was associated with significant risk reduction of major bleeding, primary and secondary net-clinical outcomes.CONCLUSIONS: Mean INR 1.6–2.6 was better than mean INR 2.0–3.0 for the prevention of thromboembolism and major bleeding. However, INR 1.6–2.6 and TTR ≥70% had similar clinical outcomes to INR 2.0–3.0 and TTR ≥70% in Korean patients with non-valvular AF.
Atrial Fibrillation ; Follow-Up Studies ; Hemorrhage ; Humans ; International Normalized Ratio ; Prothrombin Time ; Risk Reduction Behavior ; Stroke ; Thromboembolism ; Warfarin

Objective: High-quality intensive care, including targeted temperature management (TTM) for patients with postcardiac arrest syndrome, is a key element for improving outcomes after out-of-hospital cardiac arrest (OHCA). We aimed to assess the status of postcardiac arrest syndrome care, including TTM and 6-month survival with neurologically favorable outcomes, after adult OHCA patients were treated with TTM, using data from the Korean Hypothermia Network prospective registry. Methods: We used the Korean Hypothermia Network prospective registry, a web-based multicenter registry that includes data from 22 participating hospitals throughout the Republic of Korea. Adult comatose OHCA survivors treated with TTM between October 2015 and December 2018 were included. The primary outcome was neurological outcome at 6 months. Results: Of the 1,354 registered OHCA survivors treated with TTM, 550 (40.6%) survived 6 months, and 413 (30.5%) had good neurological outcomes. We identified 839 (62.0%) patients with preClinsumed cardiac etiology. A total of 937 (69.2%) collapses were witnessed, shockable rhythms were demonstrated in 482 (35.6%) patients, and 421 (31.1%) patients arrived at the emergency department with prehospital return of spontaneous circulation. The most common target temperature was 33°C, and the most common target duration was 24 hours. Conclusion The survival and good neurologic outcome rates of this prospective registry show great improvements compared with those of an earlier registry. While the optimal target temperature and duration are still unknown, the most common target temperature was 33°C, and the most common target duration was 24 hours.

BACKGROUND/AIMS: The aim of this study was to investigate useful cardiac biomarkers in the differential diagnosis of acute pulmonary embolism (APE) with troponin elevation from acute non-ST elevation myocardial infarction (NSTEMI). METHODS: A total of 771 consecutive NSTEMI patients with D-dimer measurements and 90 patients with troponin-I (TnI) elevation out of 233 APE patients were enrolled, and cardiac biomarkers were compared. RESULTS: D-dimer elevation was noted in 382 patients with NSTEMI (49.5%), and TnI elevation was noted 90 out of 233 APE patients (38.6%). Unnecessary coronary angiography was performed in 10 patients (11.1%) among 90 APE patients with TnI elevation. D-dimer was significantly elevated in APE than in NSTEMI (9.9 ± 11.6 mg/L vs. 1.8 ± 4.3 mg/L, p < 0.001), whereas TnI was significantly elevated in NSTEMI (22.4 ± 41.5 ng/mL vs. 0.7 ± 1.4 ng/mL, p < 0.001). D-dimer/TnI ratio was significantly higher in APE than in NSTEMI (50.6 ± 85.3 vs. 1.6 ± 5.7, p < 0.001). On receiver operation characteristic curve analysis, the optimal cut-off value for differentiating APE from NSTEMI was 1.12 mg/L for D-dimer (sensitivity 81.1%, specificity 70.2%), 0.72 ng/mL for TnI (sensitivity 80.6%, specificity 78.9%), and 1.82 for D-dimer/TnI ratio (sensitivity 93.3%, specificity 86.6%). CONCLUSIONS D-dimer/TnI ratio would be a simple and useful parameter for differentiating APE with cardiac troponin elevation from NSTEMI. Optimal cardiovascular imaging to identify APE should be considered in patients with D-dimer/TnI ratio > 1.82 before performing coronary angiography to avoid unnecessary invasive procedure.

BACKGROUND AND OBJECTIVES: Although current guidelines recommend early initiation of statin in patients with acute myocardial infarction (AMI), there is no consensus for optimal timing of statin initiation. METHODS: A total of 3,921 statin-naïve patients undergoing percutaneous coronary intervention were analyzed, and divided into 3 groups according to statin initiation time: group 1 (statin initiation <24 hours after admission), group 2 (24–48 hours) and group 3 (≥48 hours). We also made 3 stratified models to reduce bias: model 1 (<24 hours vs. ≥24 hours), model 2 (<48 hours vs. ≥48 hours) and model 3 (<24 hours vs. 24–48 hours). The endpoint was major adverse cardiac events (MACE; composite of cardiac death, myocardial infarction and target-vessel revascularization) during median 3.8 years. RESULTS: During follow-up, incidence of MACE was lower in early statin group in both model 1 (14.3% vs. 18.4%, hazard ratio [HR], 0.77; 95% confidence interval [CI], 0.66–0.91; p=0.002) and model 2 (14.6% vs. 19.7%, HR, 0.81; 95% CI, 0.67–0.97; p=0.022). After propensity-score matching, results remained unaltered. Statin initiation <24 hours reduced MACE compared to statin initiation ≥24 hours in model 1. Statin initiation <48 hours also reduced MACE compared to statin initiation later in model 2. However, there was no difference in incidence of MACE between statin initiation <24 hours and 24–48 hours) in model 3. CONCLUSIONS Early statin therapy within 48 hours after admission in statin-naïve patients with AMI reduced long-term clinical outcomes compared with statin initiation later.TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT02385682