Spontaneous coronary artery dissection (SCAD) is a condition in which an intramural hematoma within the coronary artery leads to acute coronary syndrome without atherosclerosis, trauma, or iatrogenic causes. It predominantly affects middle-aged women and is associated with several predisposing conditions, including fibromuscular dysplasia, systemic inflammatory disorders, connective tissue diseases, and coronary artery spasms. We report the case of a 64-year-old male with a history of hypertension who died of SCAD. His death occurred suddenly and without preceding trauma while the decedent was working overtime at a construction site. On gross examination, a thrombus-like material was identified in a branch of the left anterior descending artery and was initially presumed to be a postmortem clot. However, microscopic examination revealed an intramural hemorrhage, medial dissection, and formation of a false lumen within the coronary artery. This case report highlights the importance of a thorough histopathological examination of the coronary arteries during autopsy, even in the absence of atherosclerosis.

Spontaneous coronary artery dissection (SCAD) is a condition in which an intramural hematoma within the coronary artery leads to acute coronary syndrome without atherosclerosis, trauma, or iatrogenic causes. It predominantly affects middle-aged women and is associated with several predisposing conditions, including fibromuscular dysplasia, systemic inflammatory disorders, connective tissue diseases, and coronary artery spasms. We report the case of a 64-year-old male with a history of hypertension who died of SCAD. His death occurred suddenly and without preceding trauma while the decedent was working overtime at a construction site. On gross examination, a thrombus-like material was identified in a branch of the left anterior descending artery and was initially presumed to be a postmortem clot. However, microscopic examination revealed an intramural hemorrhage, medial dissection, and formation of a false lumen within the coronary artery. This case report highlights the importance of a thorough histopathological examination of the coronary arteries during autopsy, even in the absence of atherosclerosis.

Spontaneous coronary artery dissection (SCAD) is a condition in which an intramural hematoma within the coronary artery leads to acute coronary syndrome without atherosclerosis, trauma, or iatrogenic causes. It predominantly affects middle-aged women and is associated with several predisposing conditions, including fibromuscular dysplasia, systemic inflammatory disorders, connective tissue diseases, and coronary artery spasms. We report the case of a 64-year-old male with a history of hypertension who died of SCAD. His death occurred suddenly and without preceding trauma while the decedent was working overtime at a construction site. On gross examination, a thrombus-like material was identified in a branch of the left anterior descending artery and was initially presumed to be a postmortem clot. However, microscopic examination revealed an intramural hemorrhage, medial dissection, and formation of a false lumen within the coronary artery. This case report highlights the importance of a thorough histopathological examination of the coronary arteries during autopsy, even in the absence of atherosclerosis.

Spontaneous coronary artery dissection (SCAD) is a condition in which an intramural hematoma within the coronary artery leads to acute coronary syndrome without atherosclerosis, trauma, or iatrogenic causes. It predominantly affects middle-aged women and is associated with several predisposing conditions, including fibromuscular dysplasia, systemic inflammatory disorders, connective tissue diseases, and coronary artery spasms. We report the case of a 64-year-old male with a history of hypertension who died of SCAD. His death occurred suddenly and without preceding trauma while the decedent was working overtime at a construction site. On gross examination, a thrombus-like material was identified in a branch of the left anterior descending artery and was initially presumed to be a postmortem clot. However, microscopic examination revealed an intramural hemorrhage, medial dissection, and formation of a false lumen within the coronary artery. This case report highlights the importance of a thorough histopathological examination of the coronary arteries during autopsy, even in the absence of atherosclerosis.

Background/Aims: Noninvasive methods have become increasingly critical in the diagnosis of fibrosis in chronic liver diseases. Herein, we compared the diagnostic performance of serum Mac2 binding protein glycosylation isomer (M2BPGi) and other serological panels for fibrosis in patients with nonalcoholic fatty liver disease (NAFLD) and proposed an improved two-step diagnostic algorithm for advanced fibrosis. Methods: We enrolled 231 patients diagnosed with NAFLD who underwent a liver biopsy. We subsequently evaluated the diagnostic performance of serological panels, including serum M2BPGi, a fibrosis index based on four factors (FIB-4), aspartate aminotransferase-to-platelet ratio index (APRI), and NAFLD fibrosis score (NFS), in predicting the stage of liver fibrosis. We then constructed a two-step algorithm to better differentiate advanced fibrosis. Results: The areas under the receiver operating characteristic curves of serum M2BPGi, FIB-4, APRI, and NFS for advanced fibrosis (≥F3) were 0.823, 0.858, 0.779, and 0.827, respectively. To reduce the performance of unnecessary liver biopsy, we propose a two-step algorithm using FIB-4 as an initial diagnostic tool and serum M2BPGi (≥0.6) as an additional diagnostic method for patients classified as intermediate (23%). Using the proposed algorithm, the sensitivity, specificity, accuracy, positive predictive value, and negative predictive value were 0.812, 0.814, 0.814, 0.600, and 0.927, respectively. Conclusions Serum M2BPGi is a simple and effective test for advanced fibrosis in patients with NAFLD. Application of the two-step algorithm based on FIB-4 and M2BPGi proposed here can improve diagnostic performance and reduce unnecessary tests, making diagnosis easily accessible, especially in primary medical centers.

Viral load and the duration of viral shedding of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are important determinants of the transmission of coronavirus disease 2019.In this study, we examined the effects of viral doses on the lung and spleen of K18-hACE2 transgenic mice by temporal histological and transcriptional analyses. Approximately, 1×105 plaque-forming units (PFU) of SARS-CoV-2 induced strong host responses in the lungs from 2 days post inoculation (dpi) which did not recover until the mice died, whereas responses to the virus were obvious at 5 days, recovering to the basal state by 14 dpi at 1×102 PFU. Further, flow cytometry showed that number of CD8+ T cells continuously increased in 1×102 PFU-virusinfected lungs from 2 dpi, but not in 1×105 PFU-virus-infected lungs. In spleens, responses to the virus were prominent from 2 dpi, and number of B cells was significantly decreased at 1×105PFU; however, 1×102 PFU of virus induced very weak responses from 2 dpi which recovered by 10 dpi. Although the defense responses returned to normal and the mice survived, lung histology showed evidence of fibrosis, suggesting sequelae of SARS-CoV-2 infection. Our findings indicate that specific effectors of the immune response in the lung and spleen were either increased or depleted in response to doses of SARS-CoV-2. This study demonstrated that the response of local and systemic immune effectors to a viral infection varies with viral dose, which either exacerbates the severity of the infection or accelerates its elimination.

Background/Aims: We used next-generation sequencing (NGS) to analyze resistance-associated substitutions (RASs) and retreatment outcomes in patients with chronic hepatitis C virus (HCV) infection who failed direct-acting antiviral agent (DAA) treatment in South Korea. Methods: Using prospectively collected data from the Korean HCV cohort study, we recruited 36 patients who failed DAA treatment in 10 centers between 2007 and 2020; 29 blood samples were available from 24 patients. RASs were analyzed using NGS. Results: RASs were analyzed for 13 patients with genotype 1b, 10 with genotype 2, and one with genotype 3a. The unsuccessful DAA regimens were daclatasvir+asunaprevir (n=11), sofosbuvir+ribavirin (n=9), ledipasvir/sofosbuvir (n=3), and glecaprevir/pibrentasvir (n=1). In the patients with genotype 1b, NS3, NS5A, and NS5B RASs were detected in eight, seven, and seven of 10 patients at baseline and in four, six, and two of six patients after DAA failure, respectively. Among the 10 patients with genotype 2, the only baseline RAS was NS3 Y56F, which was detected in one patient. NS5A F28C was detected after DAA failure in a patient with genotype 2 infection who was erroneously treated with daclatasvir+asunaprevir. After retreatment, 16 patients had a 100% sustained virological response rate. Conclusions NS3 and NS5A RASs were commonly present at baseline, and there was an increasing trend of NS5A RASs after failed DAA treatment in genotype 1b. However, RASs were rarely present in patients with genotype 2 who were treated with sofosbuvir+ribavirin. Despite baseline or treatment-emergent RASs, retreatment with pan-genotypic DAA was highly successful in Korea, so we encourage active retreatment after unsuccessful DAA treatment.

Background: Fractional flow reserve (FFR) based on computed tomography (CT) has been shown to better identify ischemia-causing coronary stenosis. However, this current technology requires high computational power, which inhibits its widespread implementation in clinical practice. This prospective, multicenter study aimed at validating the diagnostic performance of a novel simple CT based fractional flow reserve (CT-FFR) calculation method in patients with coronary artery disease. Methods: Patients who underwent coronary CT angiography (CCTA) within 90 days and invasive coronary angiography (ICA) were prospectively enrolled. A hemodynamically significant lesion was defined as an FFR ≤ 0.80, and the area under the receiver operating characteristic curve (AUC) was the primary measure. After the planned analysis for the initial algorithm A, we performed another set of exploratory analyses for an improved algorithm B. Results: Of 184 patients who agreed to participate in the study, 151 were finally analyzed.Hemodynamically significant lesions were observed in 79 patients (52.3%). The AUC was 0.71 (95% confidence interval [CI], 0.63–0.80) for CCTA, 0.65 (95% CI, 0.56–0.74) for CT-FFR algorithm A (P = 0.866), and 0.78 (95% CI, 0.70–0.86) for algorithm B (P = 0.112). Diagnostic accuracy was 0.63 (0.55–0.71) for CCTA alone, 0.66 (0.58–0.74) for algorithm A, and 0.76 (0.68–0.82) for algorithm B. Conclusion This study suggests the feasibility of automated CT-FFR, which can be performed on-site within several hours. However, the diagnostic performance of the current algorithm does not meet the a priori criteria for superiority. Future research is required to improve the accuracy.

Human Q fever, a zoonosis caused by Coxiella burnetii, presents with diverse clinical manifestations ranging from mild self-limited febrile illnesses to life-threatening complications such as endocarditis or vascular infection. Although acute Q fever is a benign illness with a low mortality rate, a large-scale outbreak of Q fever in the Netherlands led to concerns about the possibility of blood transfusion-related transmission or obstetric complications in pregnant women. Furthermore, a small minority (< 5%) of patients with asymptomatic or symptomatic infection progress to chronic Q fever. Chronic Q fever is fatal in 5–50% of patients if left untreated. In South Korea, Q fever in humans was designated as a notifiable infectious disease in 2006, and the number of Q fever cases has increased sharply since 2015. Nonetheless, it is still considered a neglected and under-recognized infectious disease. In this review, recent trends of human and animal Q fever in South Korea, and public health concerns regarding Q fever outbreaks are reviewed, and we consider how a One Health approach could be applied as a preventive measure to prepare for zoonotic Q fever outbreaks.