Background: and Purpose Previous research on patients with acute ischemic stroke (AIS) has shown a 0.5% incidence of major gastrointestinal bleeding (GIB) requiring blood transfusion during hospitalization. The existing literature has insufficiently explored the long-term incidence in this population despite the decremental impact of GIB on stroke outcomes. Methods: We analyzed the data from a cohort of patients with AIS admitted to 14 hospitals as part of a nationwide multicenter prospective stroke registry between 2011 and 2013. These patients were followed up for up to 6 years. The occurrence of major GIB events, defined as GIB necessitating at least two units of blood transfusion, was tracked using the National Health Insurance Service claims data. Results: Among 10,818 patients with AIS (male, 59%; mean age, 68±13 years), 947 (8.8%) experienced 1,224 episodes of major GIB over a median follow-up duration of 3.1 years. Remarkably, 20% of 947 patients experienced multiple episodes of major GIB. The incidence peaked in the first month after AIS, reaching 19.2 per 100 person-years, and gradually decreased to approximately one-sixth of this rate by the 2nd year with subsequent stabilization. Multivariable analysis identified the following predictors of major GIB: anemia, estimated glomerular filtration rate <60 mL/min/1.73 m2 , and a 3-month modified Rankin Scale score of ≥4. Conclusion Patients with AIS are susceptible to major GIB, particularly in the first month after the onset of AIS, with the risk decreasing thereafter. Implementing preventive strategies may be important, especially for patients with anemia and impaired renal function at stroke onset and those with a disabling stroke.

Background: and Purpose Previous research on patients with acute ischemic stroke (AIS) has shown a 0.5% incidence of major gastrointestinal bleeding (GIB) requiring blood transfusion during hospitalization. The existing literature has insufficiently explored the long-term incidence in this population despite the decremental impact of GIB on stroke outcomes. Methods: We analyzed the data from a cohort of patients with AIS admitted to 14 hospitals as part of a nationwide multicenter prospective stroke registry between 2011 and 2013. These patients were followed up for up to 6 years. The occurrence of major GIB events, defined as GIB necessitating at least two units of blood transfusion, was tracked using the National Health Insurance Service claims data. Results: Among 10,818 patients with AIS (male, 59%; mean age, 68±13 years), 947 (8.8%) experienced 1,224 episodes of major GIB over a median follow-up duration of 3.1 years. Remarkably, 20% of 947 patients experienced multiple episodes of major GIB. The incidence peaked in the first month after AIS, reaching 19.2 per 100 person-years, and gradually decreased to approximately one-sixth of this rate by the 2nd year with subsequent stabilization. Multivariable analysis identified the following predictors of major GIB: anemia, estimated glomerular filtration rate <60 mL/min/1.73 m2 , and a 3-month modified Rankin Scale score of ≥4. Conclusion Patients with AIS are susceptible to major GIB, particularly in the first month after the onset of AIS, with the risk decreasing thereafter. Implementing preventive strategies may be important, especially for patients with anemia and impaired renal function at stroke onset and those with a disabling stroke.

Background: and Purpose Previous research on patients with acute ischemic stroke (AIS) has shown a 0.5% incidence of major gastrointestinal bleeding (GIB) requiring blood transfusion during hospitalization. The existing literature has insufficiently explored the long-term incidence in this population despite the decremental impact of GIB on stroke outcomes. Methods: We analyzed the data from a cohort of patients with AIS admitted to 14 hospitals as part of a nationwide multicenter prospective stroke registry between 2011 and 2013. These patients were followed up for up to 6 years. The occurrence of major GIB events, defined as GIB necessitating at least two units of blood transfusion, was tracked using the National Health Insurance Service claims data. Results: Among 10,818 patients with AIS (male, 59%; mean age, 68±13 years), 947 (8.8%) experienced 1,224 episodes of major GIB over a median follow-up duration of 3.1 years. Remarkably, 20% of 947 patients experienced multiple episodes of major GIB. The incidence peaked in the first month after AIS, reaching 19.2 per 100 person-years, and gradually decreased to approximately one-sixth of this rate by the 2nd year with subsequent stabilization. Multivariable analysis identified the following predictors of major GIB: anemia, estimated glomerular filtration rate <60 mL/min/1.73 m2 , and a 3-month modified Rankin Scale score of ≥4. Conclusion Patients with AIS are susceptible to major GIB, particularly in the first month after the onset of AIS, with the risk decreasing thereafter. Implementing preventive strategies may be important, especially for patients with anemia and impaired renal function at stroke onset and those with a disabling stroke.

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

We report on a 64-year-old man with leptomeningeal metastasis (LM) from an epidermal growth factor receptor (EGFR)-mutated adenocarcinoma of the lung. He was treated with paclitaxel, cisplatin. After completion of chemotherapy, he complained of headache, nausea, and vomiting. EGFR-mutated tumor cells were identified from the cerebrospinal fluid (CSF). Second-line therapy with gefitinib, methotrexate was started. After receiving gefitinib for 4 weeks, he had no more headaches or vomiting. Eleven months after initiation of gefitinib, he developed headache and nausea. Chest computed tomography showed aggravation of bone metastasis. Third-line therapy was started with gemcitabine and carboplatin. Two weeks later, he experienced disorientation. After a fourth relapse within the central nervous system, the therapy was switched to erlotinib and significant improvement of LM was achieved. This case shows that LM can be diagnosed by detecting EGFR mutation in CSF and EGFR tyrosine kinase inhibitors are effective for LM from EGFR mutant non-small cell lung cancer.
Adenocarcinoma ; Carboplatin ; Carcinoma, Non-Small-Cell Lung ; Central Nervous System ; Cerebrospinal Fluid ; Cisplatin ; Drug Therapy ; Epidermal Growth Factor* ; Erlotinib Hydrochloride ; Headache ; Humans ; Lung Neoplasms* ; Lung* ; Methotrexate ; Middle Aged ; Nausea ; Neoplasm Metastasis* ; Paclitaxel ; Phosphotransferases* ; Protein-Tyrosine Kinases ; Receptor, Epidermal Growth Factor* ; Recurrence ; Thorax ; Vomiting