Browsing UMB Open Access Articles by Author "Guo, Liang"
APOL1 Genetic Variants Are Associated With Increased Risk of Coronary Atherosclerotic Plaque Rupture in the Black PopulationCornelissen, Anne; Fuller, Daniela T; Fernandez, Raquel; Zhao, Xiaoqing; Kutys, Robert; Binns-Roemer, Elizabeth; Delsante, Marco; Sakamoto, Atsushi; Paek, Ka Hyun; Sato, Yu; et al. (Lippincott Williams and Wilkins, 2021-05-27)Objective: Reported associations between kidney risk variants (G1 and G2) in APOL1 (apolipoprotein L1), encoding APOL1, and cardiovascular disease have been conflicting. We sought to explore associations of APOL1 risk variants with cause of sudden death using the CVPath Sudden Death Autopsy Registry. Approach and Results: APOL1 haplotypes and causes of sudden death, as determined through autopsy and histopathology, were obtained for 764 Black subjects. Genotyping revealed APOL1 risk alleles in 452 of 764 (59%) subjects with 347 (77%) subjects carrying one risk allele and 105 (23%) subjects harboring 2 risk alleles. APOL1 risk allele carrier status was associated with a significantly increased risk of coronary thrombosis due to plaque rupture, versus noncarriers (odds ratio for rupture, 1.655 [95% CI, 1.079-2.539]; P=0.021). Histological examinations showed coronary plaques in carriers of 2 APOL1 risk alleles had larger necrotic cores compared with noncarriers (necrotic core area/total plaque area: 46.79%±6.47% versus 20.57%±5.11%; P=0.0343 in ruptured plaques, and 41.48%±7.49% versus 18.93%±3.97%; P=0.0342 in nonruptured plaques), and immunohistochemical and immunofluorescent staining revealed APOL1-positive areas localized primarily to the necrotic core. Conclusions: APOL1 risk alleles were independently associated with an increased risk of thrombotic coronary death due to plaque rupture. Our results suggest that carriers of both 1 and 2 APOL1 risk alleles have greater accumulation of APOL1 protein within culprit plaques and greater necrotic core sizes than noncarriers. These findings suggest that APOL1 plays a role in determining plaque stability. © 2021 Lippincott Williams and Wilkins. All rights reserved.
Pathological Evidence for SARS-CoV-2 as a Cause of Myocarditis: JACC Review Topic of the WeekKawakami, Rika; Sakamoto, Atsushi; Kawai, Kenji; Gianatti, Andrea; Pellegrini, Dario; Nasr, Ahmed; Kutys, Bob; Guo, Liang; Cornelissen, Anne; Mori, Masayuki; et al. (Elsevier Inc., 2021-01-18)To investigate whether severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2)–induced myocarditis constitutes an important mechanism of cardiac injury, a review was conducted of the published data and the authors’ experience was added from autopsy examination of 16 patients dying of SARS-CoV-2 infection. Myocarditis is an uncommon pathologic diagnosis occurring in 4.5% of highly selected cases undergoing autopsy or endomyocardial biopsy. Although polymerase chain reaction–detectable virus could be found in the lungs of most coronavirus disease-2019 (COVID-19)–infected subjects in our own autopsy registry, in only 2 cases was the virus detected in the heart. It should be appreciated that myocardial inflammation alone by macrophages and T cells can be seen in noninfectious deaths and COVID-19 cases, but the extent of each is different, and in neither case do such findings represent clinically relevant myocarditis. Given its extremely low frequency and unclear therapeutic implications, the authors do not advocate use of endomyocardial biopsy to diagnose myocarditis in the setting of COVID-19.