Background: Sarcopenia, a multifactorial disorder involving metabolic disturbance, suggests potential for metabolite biomarkers. Carnitine (CN), essential for skeletal muscle energy metabolism, may be a candidate biomarker. We investigated whether CN metabolites are biomarkers for sarcopenia. Methods: Associations between the CN metabolites identified from an animal model of sarcopenia and muscle cells and sarcopenia status were evaluated in men from an age-matched discovery (72 cases, 72 controls) and a validation (21 cases, 47 controls) cohort. Results: An association between CN metabolites and sarcopenia showed in mouse and cell studies. In the discovery cohort, plasma C5-CN levels were lower in sarcopenic men (P=0.005). C5-CN levels in men tended to be associated with handgrip strength (HGS) (P=0.098) and were significantly associated with skeletal muscle mass (P=0.003). Each standard deviation increase in C5-CN levels reduced the odds of low muscle mass (odd ratio, 0.61; 95% confidence interval [CI], 0.42 to 0.89). The area under the receiver operating characteristic curve (AUROC) of CN score using a regression equation of C5-CN levels, for sarcopenia was 0.635 (95% CI, 0.544 to 0.726). In the discovery cohort, addition of CN score to HGS significantly improved AUROC from 0.646 (95% CI, 0.575 to 0.717; HGS only) to 0.727 (95% CI, 0.643 to 0.810; P=0.006; HGS+CN score). The improvement was confirmed in the validation cohort (AUROC=0.563; 95% CI, 0.470 to 0.656 for HGS; and AUROC=0.712; 95% CI, 0.569 to 0.855 for HGS+CN score; P=0.027). Conclusion C5-CN, indicative of low muscle mass, is a potential circulating biomarker for sarcopenia in men. Further studies are required to confirm these results and explore sarcopenia-related metabolomic changes.

Background: Sarcopenia, a multifactorial disorder involving metabolic disturbance, suggests potential for metabolite biomarkers. Carnitine (CN), essential for skeletal muscle energy metabolism, may be a candidate biomarker. We investigated whether CN metabolites are biomarkers for sarcopenia. Methods: Associations between the CN metabolites identified from an animal model of sarcopenia and muscle cells and sarcopenia status were evaluated in men from an age-matched discovery (72 cases, 72 controls) and a validation (21 cases, 47 controls) cohort. Results: An association between CN metabolites and sarcopenia showed in mouse and cell studies. In the discovery cohort, plasma C5-CN levels were lower in sarcopenic men (P=0.005). C5-CN levels in men tended to be associated with handgrip strength (HGS) (P=0.098) and were significantly associated with skeletal muscle mass (P=0.003). Each standard deviation increase in C5-CN levels reduced the odds of low muscle mass (odd ratio, 0.61; 95% confidence interval [CI], 0.42 to 0.89). The area under the receiver operating characteristic curve (AUROC) of CN score using a regression equation of C5-CN levels, for sarcopenia was 0.635 (95% CI, 0.544 to 0.726). In the discovery cohort, addition of CN score to HGS significantly improved AUROC from 0.646 (95% CI, 0.575 to 0.717; HGS only) to 0.727 (95% CI, 0.643 to 0.810; P=0.006; HGS+CN score). The improvement was confirmed in the validation cohort (AUROC=0.563; 95% CI, 0.470 to 0.656 for HGS; and AUROC=0.712; 95% CI, 0.569 to 0.855 for HGS+CN score; P=0.027). Conclusion C5-CN, indicative of low muscle mass, is a potential circulating biomarker for sarcopenia in men. Further studies are required to confirm these results and explore sarcopenia-related metabolomic changes.

Background: Sarcopenia, a multifactorial disorder involving metabolic disturbance, suggests potential for metabolite biomarkers. Carnitine (CN), essential for skeletal muscle energy metabolism, may be a candidate biomarker. We investigated whether CN metabolites are biomarkers for sarcopenia. Methods: Associations between the CN metabolites identified from an animal model of sarcopenia and muscle cells and sarcopenia status were evaluated in men from an age-matched discovery (72 cases, 72 controls) and a validation (21 cases, 47 controls) cohort. Results: An association between CN metabolites and sarcopenia showed in mouse and cell studies. In the discovery cohort, plasma C5-CN levels were lower in sarcopenic men (P=0.005). C5-CN levels in men tended to be associated with handgrip strength (HGS) (P=0.098) and were significantly associated with skeletal muscle mass (P=0.003). Each standard deviation increase in C5-CN levels reduced the odds of low muscle mass (odd ratio, 0.61; 95% confidence interval [CI], 0.42 to 0.89). The area under the receiver operating characteristic curve (AUROC) of CN score using a regression equation of C5-CN levels, for sarcopenia was 0.635 (95% CI, 0.544 to 0.726). In the discovery cohort, addition of CN score to HGS significantly improved AUROC from 0.646 (95% CI, 0.575 to 0.717; HGS only) to 0.727 (95% CI, 0.643 to 0.810; P=0.006; HGS+CN score). The improvement was confirmed in the validation cohort (AUROC=0.563; 95% CI, 0.470 to 0.656 for HGS; and AUROC=0.712; 95% CI, 0.569 to 0.855 for HGS+CN score; P=0.027). Conclusion C5-CN, indicative of low muscle mass, is a potential circulating biomarker for sarcopenia in men. Further studies are required to confirm these results and explore sarcopenia-related metabolomic changes.

Background: Sarcopenia, a multifactorial disorder involving metabolic disturbance, suggests potential for metabolite biomarkers. Carnitine (CN), essential for skeletal muscle energy metabolism, may be a candidate biomarker. We investigated whether CN metabolites are biomarkers for sarcopenia. Methods: Associations between the CN metabolites identified from an animal model of sarcopenia and muscle cells and sarcopenia status were evaluated in men from an age-matched discovery (72 cases, 72 controls) and a validation (21 cases, 47 controls) cohort. Results: An association between CN metabolites and sarcopenia showed in mouse and cell studies. In the discovery cohort, plasma C5-CN levels were lower in sarcopenic men (P=0.005). C5-CN levels in men tended to be associated with handgrip strength (HGS) (P=0.098) and were significantly associated with skeletal muscle mass (P=0.003). Each standard deviation increase in C5-CN levels reduced the odds of low muscle mass (odd ratio, 0.61; 95% confidence interval [CI], 0.42 to 0.89). The area under the receiver operating characteristic curve (AUROC) of CN score using a regression equation of C5-CN levels, for sarcopenia was 0.635 (95% CI, 0.544 to 0.726). In the discovery cohort, addition of CN score to HGS significantly improved AUROC from 0.646 (95% CI, 0.575 to 0.717; HGS only) to 0.727 (95% CI, 0.643 to 0.810; P=0.006; HGS+CN score). The improvement was confirmed in the validation cohort (AUROC=0.563; 95% CI, 0.470 to 0.656 for HGS; and AUROC=0.712; 95% CI, 0.569 to 0.855 for HGS+CN score; P=0.027). Conclusion C5-CN, indicative of low muscle mass, is a potential circulating biomarker for sarcopenia in men. Further studies are required to confirm these results and explore sarcopenia-related metabolomic changes.

The main mechanism of Takotsubo cardiomyopathy (TCM) is catecholamine-induced acute myocardial stunning. Pheochromocytoma, a catecholamine-secreting tumor, can cause several cardiovascular complications, including hypertensive crisis, myocardial infarction, toxic myocarditis, and TCM. A 29-year-old woman presented to our hospital with general weakness, vomiting, dyspnea, and chest pain. The patient was nullipara, 28 weeks’ gestation, and had a cachexic morphology. Her cardiac enzyme levels were elevated and bedside echocardiography showed apical akinesia, suggesting TCM. The next day, she could not feel the fetal movement, and an emergency cesarean section was performed. After delivery, the patient experienced cardiac arrest and was transferred to the intensive care unit for cardiopulmonary resuscitation (CPR). Spontaneous circulation returned after 28 minutes of CPR, but cardiogenic shock continued, and extracorporeal membrane oxygenation (ECMO) was initiated. On the third day of ECMO maintenance, left ventricular ejection fraction improved and blood pressure stabilized. On the eighth day after ECMO insertion, it was removed. However, complications of the left leg vessels occurred, and several surgeries and interventions were performed. A left adrenal gland mass was found on computed tomography and was removed while repairing the leg vessels. Pheochromocytoma was diagnosed and left adrenalectomy was performed.

The main mechanism of Takotsubo cardiomyopathy (TCM) is catecholamine-induced acute myocardial stunning. Pheochromocytoma, a catecholamine-secreting tumor, can cause several cardiovascular complications, including hypertensive crisis, myocardial infarction, toxic myocarditis, and TCM. A 29-year-old woman presented to our hospital with general weakness, vomiting, dyspnea, and chest pain. The patient was nullipara, 28 weeks’ gestation, and had a cachexic morphology. Her cardiac enzyme levels were elevated and bedside echocardiography showed apical akinesia, suggesting TCM. The next day, she could not feel the fetal movement, and an emergency cesarean section was performed. After delivery, the patient experienced cardiac arrest and was transferred to the intensive care unit for cardiopulmonary resuscitation (CPR). Spontaneous circulation returned after 28 minutes of CPR, but cardiogenic shock continued, and extracorporeal membrane oxygenation (ECMO) was initiated. On the third day of ECMO maintenance, left ventricular ejection fraction improved and blood pressure stabilized. On the eighth day after ECMO insertion, it was removed. However, complications of the left leg vessels occurred, and several surgeries and interventions were performed. A left adrenal gland mass was found on computed tomography and was removed while repairing the leg vessels. Pheochromocytoma was diagnosed and left adrenalectomy was performed.

The main mechanism of Takotsubo cardiomyopathy (TCM) is catecholamine-induced acute myocardial stunning. Pheochromocytoma, a catecholamine-secreting tumor, can cause several cardiovascular complications, including hypertensive crisis, myocardial infarction, toxic myocarditis, and TCM. A 29-year-old woman presented to our hospital with general weakness, vomiting, dyspnea, and chest pain. The patient was nullipara, 28 weeks’ gestation, and had a cachexic morphology. Her cardiac enzyme levels were elevated and bedside echocardiography showed apical akinesia, suggesting TCM. The next day, she could not feel the fetal movement, and an emergency cesarean section was performed. After delivery, the patient experienced cardiac arrest and was transferred to the intensive care unit for cardiopulmonary resuscitation (CPR). Spontaneous circulation returned after 28 minutes of CPR, but cardiogenic shock continued, and extracorporeal membrane oxygenation (ECMO) was initiated. On the third day of ECMO maintenance, left ventricular ejection fraction improved and blood pressure stabilized. On the eighth day after ECMO insertion, it was removed. However, complications of the left leg vessels occurred, and several surgeries and interventions were performed. A left adrenal gland mass was found on computed tomography and was removed while repairing the leg vessels. Pheochromocytoma was diagnosed and left adrenalectomy was performed.

The main mechanism of Takotsubo cardiomyopathy (TCM) is catecholamine-induced acute myocardial stunning. Pheochromocytoma, a catecholamine-secreting tumor, can cause several cardiovascular complications, including hypertensive crisis, myocardial infarction, toxic myocarditis, and TCM. A 29-year-old woman presented to our hospital with general weakness, vomiting, dyspnea, and chest pain. The patient was nullipara, 28 weeks’ gestation, and had a cachexic morphology. Her cardiac enzyme levels were elevated and bedside echocardiography showed apical akinesia, suggesting TCM. The next day, she could not feel the fetal movement, and an emergency cesarean section was performed. After delivery, the patient experienced cardiac arrest and was transferred to the intensive care unit for cardiopulmonary resuscitation (CPR). Spontaneous circulation returned after 28 minutes of CPR, but cardiogenic shock continued, and extracorporeal membrane oxygenation (ECMO) was initiated. On the third day of ECMO maintenance, left ventricular ejection fraction improved and blood pressure stabilized. On the eighth day after ECMO insertion, it was removed. However, complications of the left leg vessels occurred, and several surgeries and interventions were performed. A left adrenal gland mass was found on computed tomography and was removed while repairing the leg vessels. Pheochromocytoma was diagnosed and left adrenalectomy was performed.

OBJECTIVES: The escalating burden of cardiovascular disease (CVD) is a critical public health issue worldwide. CVD, especially acute myocardial infarction (AMI) and stroke, is the leading contributor to morbidity and mortality in Korea. We aimed to develop algorithms for identifying AMI and stroke events from the National Health Insurance Service (NHIS) database and validate these algorithms through medical record review. METHODS: We first established a concept and definition of “hospitalization episode,” taking into account the unique features of health claims-based NHIS database. We then developed first and recurrent event identification algorithms, separately for AMI and stroke, to determine whether each hospitalization episode represents a true incident case of AMI or stroke. Finally, we assessed our algorithms’ accuracy by calculating their positive predictive values (PPVs) based on medical records of algorithm- identified events. RESULTS: We developed identification algorithms for both AMI and stroke. To validate them, we conducted retrospective review of medical records for 3,140 algorithm-identified events (1,399 AMI and 1,741 stroke events) across 24 hospitals throughout Korea. The overall PPVs for the first and recurrent AMI events were around 92% and 78%, respectively, while those for the first and recurrent stroke events were around 88% and 81%, respectively. CONCLUSIONS We successfully developed algorithms for identifying AMI and stroke events. The algorithms demonstrated high accuracy, with PPVs of approximately 90% for first events and 80% for recurrent events. These findings indicate that our algorithms hold promise as an instrumental tool for the consistent and reliable production of national CVD statistics in Korea.

OBJECTIVES: Cardiovascular diseases are a leading cause of mortality worldwide, and acute myocardial infarction (AMI) is particularly fatal condition. We evaluated the incidence and case fatality rates of AMI in Korea from 2011 to 2020. METHODS: We utilized data from the National Health Insurance Services to calculate crude, age-standardized, and age-specific incidence rates, along with 30-day and 1-year case fatality rates, of AMI from 2011 to 2020. Age-standardized incidence rates were determined using direct standardization to the 2005 population. RESULTS: The crude incidence rate of AMI per 100,000 person-years consistently increased from 44.7 in 2011 to 68.3 in 2019, before decreasing slightly to 66.2 in 2020. The age-standardized incidence rate of AMI displayed a 19% rise from 2011 to 2019, followed by a slight decline in 2020. The increasing trend for AMI incidence was more pronounced in males than in females. Both 30-day and 1-year case fatality rates remained stable among younger individuals but showed a decrease among older individuals. There was a minor surge in case fatality in 2020, particularly among recurrent AMI cases. CONCLUSIONS Over the past decade, the AMI incidence rate in Korea has consistently increased, with a slight downturn in 2020. The case fatality rate has remained relatively stable except for a minor increase in 2020. This study provides data for continuous surveillance, the implementation of targeted interventions, and the advancement of research aimed at AMI in Korea.