Spontaneous coronary artery dissection with hypothyroidism in a 45-year-old man: A case report

Spontaneous coronary artery dissection (SCAD) is a rare cause of acute coronary syndrome in young persons, rarely found in men. There are currently no known direct causes of this condition, although some correlations have been found. We report the case of a 45-year-old man with unstable angina pectoris secondary to spontaneous diffuse spiral dissection in the right coronary artery. In addition, the patient was diagnosed with other autoimmune related diseases, for example hypothyroidism, chronic atrophic gastritis, lung emphysema, which suggesting that autoimmune mechanism is an important mechanism for the occurrence of SCAD

Possible Mechanisms of SARS-CoV2-Mediated Myocardial Injury

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has rapidly become a global health emergency. In addition to causing respiratory effects, SARS-CoV-2 can result in cardiac involvement leading to myocardial damage, which is increasingly being explored in the literature. Myocardial injury is an important pathogenic feature of COVID-19. The angiotensin-converting enzyme-2 receptor plays a key role in the pathogenesis of the virus, serving as a “bridge” allowing SARS-CoV-2 to invade the body. However, the exact mechanism underlying how SARS-CoV-2 causes myocardial injury remains unclear. This review summarizes the main possible mechanisms of myocardial injury in patients with COVID-19, including direct myocardial cell injury, microvascular dysfunction, cytokine responses and systemic inflammation, hypoxemia, stress responses, and drug-induced myocardial injury. Understanding of the underlying mechanisms would aid in proper identification and treatment of myocardial injury in patients with COVID-19

Correlation between serum uric acid to high-density lipoprotein cholesterol ratio and atrial fibrillation in patients with NAFLD.

BackgroundNon-alcoholic fatty liver disease (NAFLD) is independently associated with atrial fibrillation (AF) risk. The uric acid (UA) to high-density lipoprotein cholesterol (HDL-C) ratio (UHR) has been shown to be closely associated with cardiovascular disease (CVD) and NAFLD. The aim of this study is to clarify whether elevated UHR is associated with the occurrence of AF in patients with NAFLD and to determine whether UHR predicted AF.MethodsPatients diagnosed with NAFLD in the Department of Cardiovascular Medicine of the Second Hospital of Shanxi Medical University from January 1, 2020, to December 31, 2021, were retrospectively enrolled in this study. The study subjects were categorized into AF group and non-AF group based on the presence or absence of combined AF. Logistic regression was performed to evaluate the correlation between UHR and AF. Sensitivity analysis and subgroup interaction analysis were performed to verify the robustness of the study results. Receiver operating characteristic (ROC) curve analysis was used to determine the optimal cutoff value for UHR to predict the development of AF in patients with NAFLD.ResultsA total of 421 patients with NAFLD were included, including 171 in the AF group and 250 in the non-AF group. In the univariate regression analysis, NAFLD patients with higher UHR were more likely to experience AF, and the risk of AF persisted after confounding factors were adjusted for (OR: 1.010, 95%CI: 1.007-1.013, PConclusionIncreased UHR level was independently correlated with a high risk of AF in NAFLD patients

Gαq-PKD/PKCμ signal regulating the nuclear export of HDAC5 to induce the IκB expression and limit the NF-κB-mediated inflammatory response essential for early pregnancy

Decidualization, denoting the transformation of endometrial stromal cells into specialized decidual cells, is a prerequisite for normal embryo implantation and a successful pregnancy in human. Here, we demonstrated that knockout of Gαq lead to an aberrantly enhanced inflammatory state during decidualization. Furthermore, we showed that deficiency of Gαq resulted in over-activation of nuclear factor (NF)-κB signaling, due to the decreased expression of NFκBIA, which encode the IκB protein and is the negative regulator for NF-κB. Mechanistically, Gαq deficiency decreased the Protein kinase D (PKD, also called PKCμ) phosphorylation levels, leading to attenuated HDAC5 phosphorylation and thus its nuclear export. Aberrantly high level of nuclear HDAC5 retarded histone acetylation to inhibit the induced NFκBIA transcription during decidualization. Consistently, pharmacological activation of the PKD/PKCμ or inhibition of the HDAC5 restored the inflammatory state and proper decidual response. Finally, we disclosed that over-active inflammatory state in Gαq-deficient decidua deferred the blastocyst hatching and adhesion in vitro, and the decidual expression of Gαq was significantly lower in women with recurrent pregnancy loss compared with normal pregnancy. In brief, we showed here that Gαq as a key regulator of the inflammatory cytokine’s expression and decidual homeostasis in response to differentiation cues, which is required for successful implantation and early pregnancy