Background: Hypertrophic cardiomyopathy (HCM) needs careful differentiation from other cardiomyopathies. Current guidelines recommend genetic testing, but genetic data on differential diagnoses and their relation with clinical outcomes in HCM are still lacking.This study aimed to investigate the prevalence of genetic variants and the proportion of other cardiomyopathies in patients with suspected HCM in Korea and compare the outcomes of HCM according to the presence of sarcomere gene mutation. Methods: We enrolled 1,554 patients with suspected HCM having left ventricular hypertrophy on transthoracic echocardiography between April 2012 and February 2023. Patients who declined genetic testing or who had pure apical HCM without a familial history were excluded. Genetic testing was performed using a next-generation sequencing panel or wholeexome sequencing for cardiomyopathies. We performed cardiovascular magnetic resonance if the diagnosis was inconclusive. Genotype-positive HCM was defined as sarcomere gene mutations of pathogenic or likely pathogenic variants. Adverse clinical outcomes were defined as a composite of all-cause death, resuscitated cardiac arrest, heart failure-related admission, appropriate implantable cardioverter defibrillator shocks, and stroke. Results: Of 492 patients (mean age 49.6 ± 14.7 years, 29.4% women) who underwent genetic testing, 214 (43.5%) had disease-causing gene mutations. After combining gene tests, multi-imaging modality, and clinical information, 447 (90.9%) had HCM, and 27 (5.5%) had Fabry disease. Among the HCM patients, 182 (40.7%) were genotype-positive, and 265 (59.3%) were genotype-negative. Kaplan–Meier curve analysis showed that genotype-positive HCM patients experienced more composite outcomes (log-rank, P < 0.001). In multivariable Cox analysis, non-sustained ventricular tachycardia (NSVT) (hazard ratio [HR], 1.91; 95% confidence interval [CI], 1.17–3.12; P = 0.010), left ventricular ejection fraction (LVEF) < 50% (HR, 5.50; 95% CI, 2.68–11.27; P < 0.001), LA reservoir strain (HR, 0.96; 95% CI, 0.93–0.99;P = 0.037), and positive sarcomere gene mutation (HR, 1.70; 95% CI, 1.04–2.78; P = 0.034) were significantly association with composite outcomes. Sarcomere gene mutation had incremental value for predicting adverse outcomes added on NSVT and LVEF < 50%. Conclusion Genetic testing is helpful in diagnosing HCM, and sarcomere gene mutations in HCM are significantly associated with clinical outcomes.

Background: Hypertrophic cardiomyopathy (HCM) needs careful differentiation from other cardiomyopathies. Current guidelines recommend genetic testing, but genetic data on differential diagnoses and their relation with clinical outcomes in HCM are still lacking.This study aimed to investigate the prevalence of genetic variants and the proportion of other cardiomyopathies in patients with suspected HCM in Korea and compare the outcomes of HCM according to the presence of sarcomere gene mutation. Methods: We enrolled 1,554 patients with suspected HCM having left ventricular hypertrophy on transthoracic echocardiography between April 2012 and February 2023. Patients who declined genetic testing or who had pure apical HCM without a familial history were excluded. Genetic testing was performed using a next-generation sequencing panel or wholeexome sequencing for cardiomyopathies. We performed cardiovascular magnetic resonance if the diagnosis was inconclusive. Genotype-positive HCM was defined as sarcomere gene mutations of pathogenic or likely pathogenic variants. Adverse clinical outcomes were defined as a composite of all-cause death, resuscitated cardiac arrest, heart failure-related admission, appropriate implantable cardioverter defibrillator shocks, and stroke. Results: Of 492 patients (mean age 49.6 ± 14.7 years, 29.4% women) who underwent genetic testing, 214 (43.5%) had disease-causing gene mutations. After combining gene tests, multi-imaging modality, and clinical information, 447 (90.9%) had HCM, and 27 (5.5%) had Fabry disease. Among the HCM patients, 182 (40.7%) were genotype-positive, and 265 (59.3%) were genotype-negative. Kaplan–Meier curve analysis showed that genotype-positive HCM patients experienced more composite outcomes (log-rank, P < 0.001). In multivariable Cox analysis, non-sustained ventricular tachycardia (NSVT) (hazard ratio [HR], 1.91; 95% confidence interval [CI], 1.17–3.12; P = 0.010), left ventricular ejection fraction (LVEF) < 50% (HR, 5.50; 95% CI, 2.68–11.27; P < 0.001), LA reservoir strain (HR, 0.96; 95% CI, 0.93–0.99;P = 0.037), and positive sarcomere gene mutation (HR, 1.70; 95% CI, 1.04–2.78; P = 0.034) were significantly association with composite outcomes. Sarcomere gene mutation had incremental value for predicting adverse outcomes added on NSVT and LVEF < 50%. Conclusion Genetic testing is helpful in diagnosing HCM, and sarcomere gene mutations in HCM are significantly associated with clinical outcomes.

Background: Hypertrophic cardiomyopathy (HCM) needs careful differentiation from other cardiomyopathies. Current guidelines recommend genetic testing, but genetic data on differential diagnoses and their relation with clinical outcomes in HCM are still lacking.This study aimed to investigate the prevalence of genetic variants and the proportion of other cardiomyopathies in patients with suspected HCM in Korea and compare the outcomes of HCM according to the presence of sarcomere gene mutation. Methods: We enrolled 1,554 patients with suspected HCM having left ventricular hypertrophy on transthoracic echocardiography between April 2012 and February 2023. Patients who declined genetic testing or who had pure apical HCM without a familial history were excluded. Genetic testing was performed using a next-generation sequencing panel or wholeexome sequencing for cardiomyopathies. We performed cardiovascular magnetic resonance if the diagnosis was inconclusive. Genotype-positive HCM was defined as sarcomere gene mutations of pathogenic or likely pathogenic variants. Adverse clinical outcomes were defined as a composite of all-cause death, resuscitated cardiac arrest, heart failure-related admission, appropriate implantable cardioverter defibrillator shocks, and stroke. Results: Of 492 patients (mean age 49.6 ± 14.7 years, 29.4% women) who underwent genetic testing, 214 (43.5%) had disease-causing gene mutations. After combining gene tests, multi-imaging modality, and clinical information, 447 (90.9%) had HCM, and 27 (5.5%) had Fabry disease. Among the HCM patients, 182 (40.7%) were genotype-positive, and 265 (59.3%) were genotype-negative. Kaplan–Meier curve analysis showed that genotype-positive HCM patients experienced more composite outcomes (log-rank, P < 0.001). In multivariable Cox analysis, non-sustained ventricular tachycardia (NSVT) (hazard ratio [HR], 1.91; 95% confidence interval [CI], 1.17–3.12; P = 0.010), left ventricular ejection fraction (LVEF) < 50% (HR, 5.50; 95% CI, 2.68–11.27; P < 0.001), LA reservoir strain (HR, 0.96; 95% CI, 0.93–0.99;P = 0.037), and positive sarcomere gene mutation (HR, 1.70; 95% CI, 1.04–2.78; P = 0.034) were significantly association with composite outcomes. Sarcomere gene mutation had incremental value for predicting adverse outcomes added on NSVT and LVEF < 50%. Conclusion Genetic testing is helpful in diagnosing HCM, and sarcomere gene mutations in HCM are significantly associated with clinical outcomes.

Background: Hypertrophic cardiomyopathy (HCM) needs careful differentiation from other cardiomyopathies. Current guidelines recommend genetic testing, but genetic data on differential diagnoses and their relation with clinical outcomes in HCM are still lacking.This study aimed to investigate the prevalence of genetic variants and the proportion of other cardiomyopathies in patients with suspected HCM in Korea and compare the outcomes of HCM according to the presence of sarcomere gene mutation. Methods: We enrolled 1,554 patients with suspected HCM having left ventricular hypertrophy on transthoracic echocardiography between April 2012 and February 2023. Patients who declined genetic testing or who had pure apical HCM without a familial history were excluded. Genetic testing was performed using a next-generation sequencing panel or wholeexome sequencing for cardiomyopathies. We performed cardiovascular magnetic resonance if the diagnosis was inconclusive. Genotype-positive HCM was defined as sarcomere gene mutations of pathogenic or likely pathogenic variants. Adverse clinical outcomes were defined as a composite of all-cause death, resuscitated cardiac arrest, heart failure-related admission, appropriate implantable cardioverter defibrillator shocks, and stroke. Results: Of 492 patients (mean age 49.6 ± 14.7 years, 29.4% women) who underwent genetic testing, 214 (43.5%) had disease-causing gene mutations. After combining gene tests, multi-imaging modality, and clinical information, 447 (90.9%) had HCM, and 27 (5.5%) had Fabry disease. Among the HCM patients, 182 (40.7%) were genotype-positive, and 265 (59.3%) were genotype-negative. Kaplan–Meier curve analysis showed that genotype-positive HCM patients experienced more composite outcomes (log-rank, P < 0.001). In multivariable Cox analysis, non-sustained ventricular tachycardia (NSVT) (hazard ratio [HR], 1.91; 95% confidence interval [CI], 1.17–3.12; P = 0.010), left ventricular ejection fraction (LVEF) < 50% (HR, 5.50; 95% CI, 2.68–11.27; P < 0.001), LA reservoir strain (HR, 0.96; 95% CI, 0.93–0.99;P = 0.037), and positive sarcomere gene mutation (HR, 1.70; 95% CI, 1.04–2.78; P = 0.034) were significantly association with composite outcomes. Sarcomere gene mutation had incremental value for predicting adverse outcomes added on NSVT and LVEF < 50%. Conclusion Genetic testing is helpful in diagnosing HCM, and sarcomere gene mutations in HCM are significantly associated with clinical outcomes.

Purpose: Several previous studies and case reports have reported ethanol-induced symptoms in patients receiving anticancer drugs containing ethanol. Most docetaxel formulations contain ethanol as a solvent. However, there are insufficient data on ethanol-induced symptoms when docetaxel-containing ethanol is administered. The primary purpose of this study was to investigate the frequency and pattern of ethanol-induced symptoms during and after docetaxel administration. The secondary purpose was to explore the risk factors for ethanol-induced symptoms. Materials and Methods: This was a prospective, multicenter, observational study. The participants filled out ethanol-induced symptom questionnaire on the day of chemotherapy and the following day. Results: Data from 451 patients were analyzed. The overall occurrence rate of ethanol-induced symptoms was 44.3% (200/451 patients). The occurrence rate of facial flushing was highest at 19.7% (89/451 patients), followed by nausea in 18.2% (82/451 patients), and dizziness in 17.5% (79/451 patients). Although infrequent, unsteady walking and impaired balance occurred in 4.2% and 3.3% of patients, respectively. Female sex, presence of underlying disease, younger age, docetaxel dose, and docetaxel-containing ethanol amount were significantly associated with the occurrence of ethanol-induced symptoms. Conclusion The occurrence of ethanol-induced symptoms was not low in patients receiving docetaxel-containing ethanol. Physicians need to pay more attention to the occurrence of ethanol-induced symptoms and prescribe ethanol-free or low-ethanol-containing formulations to high-risk patients.

Palinacousis is a rare auditory phenomenon characterized by the persistence of sounds beyond their actual duration. It has been associated with various brain conditions such as stroke, tumor, and seizure in the temporoparietal lobe. We present a case report of a 43-yearold man who developed palinacousis following cerebral venous thrombosis and seizure with lesions including the left auditory cortex. This case highlights the intriguing relationship between cerebral venous infarction, seizure, and the development of palinacousis in specific brain regions.

Background: and Purpose Moderate-intensity statin plus ezetimibe versus high-intensity statin alone may provide a greater low-density lipoprotein cholesterol (LDL-C) reduction in patients with recent ischemic stroke. Methods: This randomized, open-label, controlled trial assigned patients with recent ischemic stroke <90 days to rosuvastatin/ezetimibe 10/10 mg once daily (ROS10/EZT10) or to rosuvastatin 20 mg once daily (ROS20). The primary endpoint was LDL-C reduction ≥50% from baseline at 90 days. Key secondary endpoints were LDL-C <70 mg/dL and multiple lipid goal achievement, and composite of major vascular events. Results: Of 584 randomized, 530 were included in the modified intention-to-treat analysis. The baseline LDL-C level was 130.2±34.7 mg/dL in the ROS10/EZT10 group and 131.0±33.9 mg/dL in the ROS20 group. The primary endpoint was achieved in 198 patients (72.5%) in the ROS10/EZT10 group and 148 (57.6%) in the ROS20 group (odds ratio [95% confidence interval], 1.944 [1.352–2.795]; P= 0.0003). LDL-C level <70 mg/dL was achieved in 80.2% and 65.4% in the ROS10/EZT10 and ROS20 groups (P=0.0001). Multiple lipid goal achievement rate was 71.1% and 53.7% in the ROS10/EZT10 and ROS20 groups (P<0.0001). Major vascular events occurred in 1 patient in the ROS10/EZT10 group and 9 in the ROS20 group (P=0.0091). The adverse event rates did not differ between the two groups. Conclusion Moderate-intensity rosuvastatin plus ezetimibe was superior to high-intensity rosuvastatin alone for intensive LDL-C reduction in patients with recent ischemic stroke. With the combination therapy, more than 70% of patients achieved LDL-C reduction ≥50% and 80% had an LDL-C <70 mg/dL at 90 days.

The Korean Society of Radiology and Medical Guidelines Committee amended the existing 2016 guidelines to publish the “Korean Clinical Practice Guidelines for Adverse Reactions to Iodide Contrast for Injection and Gadolinium Contrast for MRI: The Revised Clinical Consensus and Recommendations (2022 Third Edition).” Expert members recommended and approved by the Korean Society of Radiology, the Korean Academy of Asthma, Allergy and Clinical Immunology, and the Korean Nephrology Society participated together. According to the expert consensus or systematic literature review, the description of the autoinjector and connection line for the infection control while using contrast medium, the acute adverse reaction, and renal toxicity to iodized contrast medium were modified and added. We would like to introduce the revised contents.

Endoscopic ultrasound (EUS)-guided tissue acquisition of pancreatic solid tumor requires a strict recommendation for its proper use in clinical practice because of its technical difficulty and invasiveness. The Korean Society of Gastrointestinal Endoscopy (KSGE) appointed a Task Force to draft clinical practice guidelines for EUS-guided tissue acquisition of pancreatic solid tumor. The strength of recommendation and the level of evidence for each statement were graded according to the Minds Handbook for Clinical Practice Guideline Development 2014. The committee, comprising a development panel of 16 endosonographers and an expert on guideline development methodology, developed 12 evidence-based recommendations in 8 categories intended to help physicians make evidence-based clinical judgments with regard to the diagnosis of pancreatic solid tumor. This clinical practice guideline discusses EUS-guided sampling in pancreatic solid tumor and makes recommendations on circumstances that warrant its use, technical issues related to maximizing the diagnostic yield (e.g., needle type, needle diameter, adequate number of needle passes, sample obtaining techniques, and methods of specimen processing), adverse events of EUS-guided tissue acquisition, and learning-related issues. This guideline was reviewed by external experts and suggests best practices recommended based on the evidence available at the time of preparation. This guideline may not be applicable for all clinical situations and should be interpreted in light of specific situations and the availability of resources. It will be revised as necessary to cover progress and changes in technology and evidence from clinical practice.

Endoscopic ultrasound (EUS)-guided tissue acquisition of pancreatic solid tumor requires a strict recommendation for its proper use in clinical practice because of its technical difficulty and invasiveness. The Korean Society of Gastrointestinal Endoscopy (KSGE) appointed a task force to draft clinical practice guidelines for EUS-guided tissue acquisition of pancreatic solid tumor. The strength of recommendation and the level of evidence for each statement were graded according to the Minds Handbook for Clinical Practice Guideline Development 2014. The committee, comprising a development panel of 16 endosonographers and an expert on guideline development methodology, developed 12 evidence-based recommendations in eight categories intended to help physicians make evidence-based clinical judgments with regard to the diagnosis of pancreatic solid tumor. This clinical practice guideline discusses EUS-guided sampling in pancreatic solid tumor and makes recommendations on circumstances that warrant its use, technical issues related to maximizing the diagnostic yield (e.g., needle type, needle diameter, adequate number of needle passes, sample obtaining techniques, and methods of specimen processing), adverse events of EUS-guided tissue acquisition, and learning-related issues. This guideline was reviewed by external experts and suggests best practices recommended based on the evidence available at the time of preparation. This guideline may not be applicable for all clinical situations and should be interpreted in light of specific situations and the availability of resources. It will be revised as necessary to cover progress and changes in technology and evidence from clinical practice.