Background/Aims: Omalizumab is the first biologic known to be effective in patients with severe allergic asthma. Methods: This study was conducted as a multicenter, single-group, open trial to evaluate the improvement in the quality of life with the additional administration of omalizumab for 24 weeks in Korean patients with severe persistent allergic asthma. Results: Of the 44 patients, 31.8% were men and the mean age was 49.8 ± 11.8 years. A score improvement of 0.5 points or more in the Quality of Life Questionnaire for Korean Asthmatics (KAQLQ) was noted in 50.0% (22/44) of the patinets. In the improved group, the baseline total immunoglobulin E (IgE) level and the amount of omalizumab used were higher, and the day and night asthma symptoms were more severe, compared to those in the non-improved group. According to the Global Evaluation of Treatment Effectiveness, favorable outcomes were found in 78.6% of patients. The Korean asthma control test (p < 0.005) and forced expiratory volume in 1 second % predicted (FEV1%; p < 0.01) improved significantly in patients who received omalizumab treatment, compared to that at week 0, and the total dose of rescue systemic corticosteroids significantly decreased (p < 0.05). The improved group on KAQLQ showed a significant improvement in FEV1% (p < 0.001). Conclusions Omalizumab can be considered a biological treatment for Korean patients with severe allergic asthma. It is recommended to consider omalizumab as add-on therapy in patients with high baseline total IgE levels and severe asthma symptoms.

Background/Aims: Omalizumab is the first biologic known to be effective in patients with severe allergic asthma. Methods: This study was conducted as a multicenter, single-group, open trial to evaluate the improvement in the quality of life with the additional administration of omalizumab for 24 weeks in Korean patients with severe persistent allergic asthma. Results: Of the 44 patients, 31.8% were men and the mean age was 49.8 ± 11.8 years. A score improvement of 0.5 points or more in the Quality of Life Questionnaire for Korean Asthmatics (KAQLQ) was noted in 50.0% (22/44) of the patinets. In the improved group, the baseline total immunoglobulin E (IgE) level and the amount of omalizumab used were higher, and the day and night asthma symptoms were more severe, compared to those in the non-improved group. According to the Global Evaluation of Treatment Effectiveness, favorable outcomes were found in 78.6% of patients. The Korean asthma control test (p < 0.005) and forced expiratory volume in 1 second % predicted (FEV1%; p < 0.01) improved significantly in patients who received omalizumab treatment, compared to that at week 0, and the total dose of rescue systemic corticosteroids significantly decreased (p < 0.05). The improved group on KAQLQ showed a significant improvement in FEV1% (p < 0.001). Conclusions Omalizumab can be considered a biological treatment for Korean patients with severe allergic asthma. It is recommended to consider omalizumab as add-on therapy in patients with high baseline total IgE levels and severe asthma symptoms.

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

BACKGROUND/AIMS: The impact of the timing of anemia during hospitalization on future clinical outcomes after surviving discharge from an index heart failure (HF) has been poorly studied in patients with acute decompensated heart failure (ADHF). METHODS: A total of 384 surviving patients with acute ADHF were divided into two groups: an anemia group (n = 270, 199 anemia at admission and 71 pre-discharge anemia) and a no anemia group (n = 114). All-cause mortality and HF re-hospitalization were compared between groups. RESULTS: During the follow-up period (median, 528 days), death occurred in 60 patients (15.6%) and HF re-hospitalization occurred in 131 patients (34.1%). Overall anemia was associated with increased mortality (hazard ratio [HR], 1.74; 95% confidence interval [CI], 1.03 to 3.01; p = 0.039), but not HF re-hospitalization (HR, 0.92; 95% CI, 0.59 to 1.42; p = 0.707). Pre-discharge anemia was significantly associated with increased mortality (HR, 1.68; 95% CI, 1.01 to 2.82; p = 0.048), but anemia at admission did not predict increased mortality or re-hospitalization. CONCLUSIONS Pre-discharge anemia, rather than anemia at admission, was identified as an independent predictor of mortality in patients with ADHF after surviving discharge. The results of the present study suggest that the identification and optimal management of anemia during hospitalization are important in patients with ADHF.

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
Bias (Epidemiology) ; Consensus ; Death ; Follow-Up Studies ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Incidence ; Myocardial Infarction ; Percutaneous Coronary Intervention

No abstract available.
Alopecia Areata ; Alopecia ; Epidermal Growth Factor ; Genes, erbB-1

We evaluated the efficacy of fimasartan on perfusion defects and infarction size in an animal model of myocardial infarction (MI), with echocardiography and positron emission tomography (PET) using a ¹⁸F-labeled phosphonium cation (5-[¹⁸F]-fluoropentyl-triphenylphosphonium salt, [¹⁸F]FPTP) as a mitochondrial voltage sensor for myocardial imaging. We induced MI in 33 rats by ligation of the left coronary artery, and checked their cardiac PET image using [¹⁸F]FPTP for evaluation of myocardial perfusion. Rats were grouped into 3 groups according to their administered drugs: no drug (n=11), fimasartan 3 mg/kg (n=10), and fimasartan 10 mg/kg (n=12). Each designated drug was administered for 4 weeks, and follow-up PET and histologic examinations were done. In the PET analysis, a perfusion defect size was markedly improved in fimasartan 10 mg/kg group (35.9±7.0% to 28.4±6.9%, p<0.001), whereas treatment with fimasartan 3 mg/kg induced only an insignificant reduction of perfusion defect size (35.9±7.9% to 33.9±7.3%, p=0.095). Using 2, 3, 5-triphenyltetrazolium chloride staining, infarction size was the largest in the control group (36.5±8.3%), and was insignificantly lower in the fimasartan 3 mg/kg group (31.5±6.5%, p for the difference between the control group=0.146) and was significantly lower in the fimasartan 10 mg/kg group (26.3±7.6%, p for the difference between the control group=0.011). PET imaging using a ¹⁸F-labeled mitochondrial voltage sensor, [¹⁸F]FPTP, is useful in evaluation and monitoring of myocardial perfusion states, and treatment with fimasartan decreases the infarction size in animal MI model.
Angiotensin Receptor Antagonists ; Animals ; Coronary Vessels ; Echocardiography ; Electrons ; Follow-Up Studies ; Infarction ; Ligation ; Models, Animal ; Myocardial Infarction ; Perfusion ; Positron-Emission Tomography ; Rats