The Committee on Pediatric Bone Health of the Korean Society of Pediatric Endocrinology has newly developed evidence-based clinical practice guidelines for optimizing bone health in Korean children and adolescents. These guidelines present recommendations based on the Grading of Recommendations, which includes the quality of evidence. In the absence of sufficient evidence, conclusions were based on expert opinion. These guidelines include processes of bone acquisition, definition, and evaluation of low bone mineral density (BMD), causes of osteoporosis, methods for optimizing bone health, and pharmacological treatments for enhancing BMD in children and adolescents. While these guidelines provide current evidence-based recommendations, further research is required to strengthen these guidelines.

Background: Evidence regarding the association between variabilities in obesity measures and health outcomes is limited. We aimed to examine the association between variabilities in obesity measures and cardiovascular outcomes and all-cause mortality. Methods: We identified 4,244,460 individuals who underwent health examination conducted by the Korean National Health Insurance Service during 2012, with ≥3 anthropometric measurements between 2009 and 2012. Variabilities in body weight (BW) and waist circumference (WC) were assessed using four indices including variability independent of the mean (VIM). We performed multivariable Cox proportional hazards regression analyses. Results: During follow-up of 4.4 years, 16,095, 18,957, and 30,200 cases of myocardial infarction (MI), stroke, and all-cause mortality were recorded. Compared to individuals with the lowest quartiles, incrementally higher risks of study outcomes and those of stroke and all-cause mortality were observed among individuals in higher quartiles of VIM for BW and VIM for WC, respectively. The multivariable adjusted hazard ratios and 95% confidence intervals comparing the highest versus lowest quartile groups of VIM for BW were 1.17 (1.12 to 1.22) for MI, 1.20 (1.16 to 1.25) for stroke, and 1.66 (1.60 to 1.71) for all-cause mortality; 1.07 (1.03 to 1.12) for stroke and 1.29 (1.25 to 1.33) for all-cause mortality regarding VIM for WC. These associations were similar with respect to the other indices for variability. Conclusion This study revealed positive associations between variabilities in BW and WC and cardiovascular outcomes and allcause mortality. Our findings suggest that variabilities in obesity measures are associated with adverse health outcomes in the general population.

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

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.

We investigated predictors of major adverse cardiac events (MACE) with two years after medical treatment for lesions with angiographically intermediate lesions with intravascular ultrasound (IVUS) minimum lumen area (MLA) <4 mm² in non-proximal epicardial coronary artery. We retrospectively enrolled 104 patients (57 males, 62±10 years) with angiographically intermediate lesions (diameter stenosis 30–70%) with IVUS MLA <4 mm² in the non-proximal epicardial coronary artery with a reference lumen diameter between 2.25 and 3.0 mm. We evaluated the incidences of major adverse cardiovascular events (MACE including death, myocardial infarction, target lesion and target vessel revascularizations, and cerebrovascular accident) two years after medical therapy. During the two-year follow-up, 15 MACEs (14.4%) (including 1 death, 2 myocardial infarctions, 10 target vessel revascularizations, and 2 cerebrovascular accidents) occurred. Diabetes mellitus was more prevalent (46.7% vs. 18.0%, p=0.013) and statins were used less frequently in patients with MACE compared with those without MACE (40.0% vs. 71.9%, p=0.015). Independent predictors of MACEs with two years included diabetes mellitus (odds ratio [OR]=3.41; 95% CI=1.43–8.39, p=0.020) and non-statin therapy (OR=3.11; 95% CI=1.14–6.50, p=0.027). Long-term event rates are relatively low with only medical therapy without any intervention, so the cut-off of IVUS MLA 4 mm² might be too large to be applied for defining significant stenosis. The predictors of long-term MACE were diabetes mellitus and statin therapy in patients with angiographically intermediate lesions in non-proximal epicardial coronary artery.
Constriction, Pathologic ; Coronary Artery Disease ; Coronary Vessels* ; Diabetes Mellitus ; Follow-Up Studies ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Incidence ; Male ; Myocardial Infarction ; Plaque, Atherosclerotic ; Retrospective Studies ; Ultrasonography* ; Ultrasonography, Interventional

BACKGROUND/AIMS: Coronary vasospasms are one of the important causes of sudden cardiac death (SCD). Provocation of coronary vasospasms can be useful, though some results may lead to false positives, with patients potentially experiencing recurrent SCD despite appropriate medical treatments. We hypothesized that it is not coronary vasospasms but inherited primary arrhythmia syndromes (IPAS) that underlie the development of SCD. METHODS: We analyzed 74 consecutive patients (3.8%) who survived out-of-hospital cardiac arrest among 1,986 patients who had angiographically proven coronary vasospasms. Electrical abnormalities were evaluated in serial follow-up electrocardiograms (ECGs) during and after the index event for a 3.9 years median follow-up. Major clinical events were defined as the composite of death and recurrent SCD events. RESULTS: Forty five patients (60.8%) displayed electrocardiographic abnormalities suggesting IPAS: Brugada type patterns in six (8.2%), arrhythmogenic right ventricular dysplasia patterns in three (4.1%), long QT syndrome pattern in one (2.2%), and early repolarization in 38 (51.4%). Patients having major clinical events showed more frequent Brugada type patterns, early repolarization, and more diffuse multivessel coronary vasospasms. Brugada type pattern ECGs (adjusted hazard ratio [HR], 4.22; 95% confidence interval [CI], 1.16 to 15.99; p = 0.034), and early repolarization (HR, 2.97; 95% CI, 1.09 to 8.10; p = 0.034) were ultimately associated with an increased risk of mortality. CONCLUSIONS: Even though a number of aborted SCD survivors have coronary vasospasms, some also have IPAS, which has the potential to cause SCD. Therefore, meticulous evaluations and follow-ups for IPAS are required in those patients.
Arrhythmias, Cardiac* ; Arrhythmogenic Right Ventricular Dysplasia ; Coronary Vasospasm* ; Death, Sudden, Cardiac* ; Electrocardiography ; Follow-Up Studies ; Heart Arrest ; Humans ; Long QT Syndrome ; Masks* ; Mortality ; Out-of-Hospital Cardiac Arrest ; Survivors

BACKGROUND AND OBJECTIVES: There is limited information on the transient or persistent no reflow phenomenon in patients with acute myocardial infarction (AMI) undergoing percutaneous coronary intervention (PCI). SUBJECTS AND METHODS: The study analyzed 4329 patients with AMI from a Korean multicenter registry who underwent PCI using coronary stents (2668 ST-elevation and 1661 non-ST-elevation myocardial infarction [MI] patients): 4071 patients without any no reflow, 213 with transient no reflow (no reflow with final thrombolysis in myocardial infarction [TIMI] flow grade 3), and 45 with persistent no reflow (no reflow with final TIMI flow grade≤2). The primary endpoint was all-cause mortality during 3-year follow-up. We also analyzed the incidence of cardiac mortality, non-fatal MI, re-hospitalization due to heart failure, target vessel revascularization, and stent thrombosis. RESULTS: The persistent no reflow group was associated with higher all-cause mortality (hazard ratio [HR] 1.98, 95% confidence interval [CI] 1.08-3.65, p=0.028) and cardiac mortality (HR 3.28, 95% CI 1.54-6.95, p=0.002) compared with the normal reflow group. Transient no reflow increased all-cause mortality only when compared with normal reflow group (HR 1.58, 95% CI 1.11-2.24, p=0.010). When comparing transient and persistent no reflow, persistent no reflow was associated with increased all-cause mortality (46.7 vs. 24.4%, log rank p=0.033). CONCLUSION: The persistent no reflow phenomenon was associated with a poor in-hospital outcome and increased long-term mortality mainly driven by increased cardiac mortality compared to the transient no reflow phenomenon or normal reflow.
Follow-Up Studies ; Heart Failure ; Humans ; Incidence ; Mortality ; Myocardial Infarction* ; No-Reflow Phenomenon ; Percutaneous Coronary Intervention* ; Stents ; Thrombosis

BACKGROUND: Hemodynamic and functional evaluation with Doppler and tissue Doppler study as a part of comprehensive echocardiography is essential but normal reference values have never been reported from Korean normal population especially according to age and sex. METHODS: Using Normal echOcaRdiographic Measurements in a KoreAn popuLation study subjects, we obtained normal reference values for Doppler and tissue Doppler echocardiography including tricuspid annular velocities according to current guidelines and compared values according to gender and age groups. RESULTS: Mitral early diastolic (E) and late diastolic (A) velocity as well as E/A ratio were significantly higher in women compared to those in men. Conversely, mitral peak systolic and late diastolic annular velocity in both septal and lateral mitral annulus were significantly lower in women compared to those in men. However, there were no significant differences in both septal and lateral mitral early diastolic annular (e') velocity between men and women. In both men and women, mitral E velocity and its deceleration time as well as both E/A and E/e' ratio considerably increased with age. There were no significant differences in tricuspid inflow velocities and tricuspid lateral annular velocities between men and women except e' velocity, which was significantly higher in women compared to that in men. However, changes in both tricuspid inflow and lateral annular velocities according to age were similar to those in mitral velocities. CONCLUSION: Since there were significant differences in Doppler and tissue Doppler echocardiographic variables between men and women and changes according to age were even more considerable in both gender groups, normal Doppler echocardiographic values should be differentially applied based on age and sex.
Deceleration ; Echocardiography* ; Echocardiography, Doppler ; Female ; Hemodynamics ; Humans ; Male ; Reference Values