Faculty of Medicine, University of Belgrade, 11000 Belgrade, Serbia.
Clinic of Cardiology, Clinical Centre of Serbia, 11000 Belgrade, Serbia.
Int J Mol Sci. 2023 Jun 16;24(12):10234. doi: 10.3390/ijms241210234.
Although disturbance of redox homeostasis might be responsible for COVID-19 cardiac complications, this molecular mechanism has not been addressed yet. We have proposed modifying the effects of antioxidant proteins polymorphisms (superoxide dismutase 2 (), glutathione peroxidase 1 (), glutathione peroxidase 3 () and nuclear factor erythroid 2-related factor 2, ()) in individual susceptibility towards the development of cardiac manifestations of long COVID-19. The presence of subclinical cardiac dysfunction was assessed via echocardiography and cardiac magnetic resonance imaging in 174 convalescent COVID-19 patients. SOD2, , and polymorphisms were determined via the appropriate PCR methods. No significant association of the investigated polymorphisms with the risk of arrhythmia development was found. However, the carriers of variant *T, *C or *A alleles were more than twice less prone for dyspnea development in comparison with the carriers of the referent ones. These findings were even more potentiated in the carriers of any two variant alleles of these genes (OR = 0.273, and = 0.016). The variant alleles were significantly associated with left atrial and right ventricular echocardiographic parameters, specifically LAVI, RFAC and RV-EF ( = 0.025, = 0.009, and = 0.007, respectively). Based on the relation between the variant *T allele and higher levels of LV echocardiographic parameters, EDD, LVMI and GLS, as well as troponin T ( = 0.038), it can be proposed that recovered COVID-19 patients, who are the carriers of this genetic variant, might have subtle left ventricular systolic dysfunction. No significant association between the investigated polymorphisms and cardiac disfunction was observed when cardiac magnetic resonance imaging was performed. Our results on the association between antioxidant genetic variants and long COVID cardiological manifestations highlight the involvement of genetic propensity in both acute and long COVID clinical manifestations.
尽管氧化还原平衡失调可能是导致 COVID-19 心脏并发症的原因,但这一分子机制尚未得到解决。我们提出通过改变抗氧化蛋白多态性(超氧化物歧化酶 2 ()、谷胱甘肽过氧化物酶 1 ()、谷胱甘肽过氧化物酶 3 () 和核因子红细胞 2 相关因子 2 ())的作用,来修饰个体对长 COVID-19 心脏表现的易感性。通过超声心动图和心脏磁共振成像评估 174 名康复 COVID-19 患者的亚临床心功能障碍。通过适当的 PCR 方法确定 SOD2 、 、 和 多态性。研究多态性与心律失常发生风险之间没有显著关联。然而,与携带参考等位基因的携带者相比,携带变体 *T、*C 或 *A 等位基因的携带者发生呼吸困难的风险降低了两倍以上。在这些基因的任何两个变体等位基因的携带者中,这种情况更为明显(OR = 0.273, = 0.016)。变体 等位基因与左心房和右心室超声心动图参数显著相关,具体为 LAVI、RFAC 和 RV-EF( = 0.025, = 0.009, = 0.007)。基于变体 *T 等位基因与 LV 超声心动图参数较高水平之间的关系,EDD、LVMI 和 GLS,以及肌钙蛋白 T( = 0.038),可以提出携带这种遗传变异的康复 COVID-19 患者可能存在轻微的左心室收缩功能障碍。当进行心脏磁共振成像时,未观察到研究多态性与心功能障碍之间存在显著关联。我们关于抗氧化遗传变异与长 COVID 心脏表现之间关联的研究结果强调了遗传倾向在急性和长 COVID 临床表现中的作用。