The glycosylated hemoglobin level and the severity of cardiovascular involvement in patients with the first episode of acute coronary syndrome.

Background: The current study was carried out aiming at investigating the relationship between glycosylated hemoglobin level and coronary atherosclerosis in patients with the first episode of acute coronary syndrome. Methods: This case-control study evaluated 450 patients with the first episode of acute coronary syndrome in Ayatollah Rouhani Hospital in Babol (Iran) from 2011 to 2018. Based on glycosylated hemoglobin, patients were divided into three groups of non-diabetic, pre-diabetic, and diabetic (n=150 in each group). Since SYNTAX score and Gensini score are employed to evaluate the extent of cardiovascular disease and predict CVD in patients with CAD over long-term follow-up, we calculated SYNTAX score and Gensini score based on angiographic results. Results: Concerning the factors related to the severity of cardiovascular involvement, the results revealed no significant difference between the diabetic and pre-diabetic groups in terms of the frequency of patients in terms of SYNTAX score, Gensini score, and the number of vessels involved (0.142 and 87, respectively, and P=0.102). However, this difference between the diabetic and non-diabetic groups, as well as between the pre-diabetic and non-diabetic groups was statistically significant (respectively for SYNTAX score, p< 0.001 and P=0.001; for Gensini score, P=0.013 and P=0.019; and for the number of vessels involved P=0.001and p<0.001). Conclusion: According to the findings of the current study, since there was no significant difference between diabetic and pre-diabetic patients in terms of the components indicating the severity of cardiovascular involvement, pre-diabetes itself may be associated with the severity of cardiovascular involvement as a predisposing factor.

Empagliflozin treatment of cardiotoxicity: A comprehensive review of clinical, immunobiological, neuroimmune, and therapeutic implications.

Cancer and cardiovascular disorders are known as the two main leading causes of mortality worldwide. Cardiotoxicity is a critical and common adverse effect of cancer-related chemotherapy. Chemotherapy-induced cardiotoxicity has been associated with various cancer treatments, such as anthracyclines, immune checkpoint inhibitors, and kinase inhibitors. Different methods have been reported for the management of chemotherapy-induced cardiotoxicity. In this regard, sodium-glucose cotransporter-2 inhibitors (SGLT2i), a class of antidiabetic agents, have recently been applied to manage heart failure patients. Further, SGLT2i drugs such as EMPA exert protective cardiac and systemic effects. Moreover, it can reduce inflammation through the mediation of major inflammatory components, such as Nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasomes, Adenosine 5'-monophosphate-activated protein kinase (AMPK), and c-Jun N-terminal kinase (JNK) pathways, Signal transducer and activator of transcription (STAT), and overall decreasing transcription of proinflammatory cytokines. The clinical outcome of EMPA administration is related to improving cardiovascular risk factors, including body weight, lipid profile, blood pressure, and arterial stiffness. Intriguingly, SGLT2 suppressors can regulate microglia-driven hyperinflammation affecting neurological and cardiovascular disorders. In this review, we discuss the protective effects of EMPA in chemotherapy-induced cardiotoxicity from molecular, immunological, and neuroimmunological aspects to preclinical and clinical outcomes.

Pheochromocytoma triggered by coronavirus disease 2019: a case report.

BACKGROUND: Coronavirus disease 2019 is an infectious disease with many presentations, and many of its effects on the human body are still unknown. Pheochromocytoma is a neuroendocrine tumor that may occur sporadically or be a manifestation of a hereditary disease line multiple endocrine neoplasia type 2. CASE PRESENTATION: In this study, we report a case of an Iranian patient infected with coronavirus disease 2019, causing unusual presentations of pheochromocytoma, including myocarditis and cerebrovascular involvement. CONCLUSIONS: We discovered a case of pheochromocytoma as an unusual presentation of COVID-19. In further investigations we also discovered thyroid medullary carcinoma and at the end MEN 2 syndrome was diagnosed. After proper treatment many symptoms were eliminated.

Effect of Hydroxychloroquine and Azithromycin on QT Interval Prolongation and Other Cardiac Arrhythmias in COVID-19 Confirmed Patients.

BACKGROUND: Hydroxychloroquine with or without azithromycin was one of the common therapies at the beginning of the COVID-19 pandemic. They can prolong QT interval, cause torsade de pointes, and lead to sudden cardiac death. We aimed to assess QT interval prolongation and its risk factors in patients who received hydroxychloroquine with or without azithromycin. METHODS: This study was a retrospective cohort study. One hundred seventy-two confirmed COVID-19 patients were included in this study, hospitalized at Babol University of Medical Sciences hospitals between March 5, 2020, and April 3, 2020. Patients were divided into two groups: hydroxychloroquine alone and hydroxychloroquine with azithromycin. Electrocardiograms were used for outcome assessment. RESULTS: 83.1% of patients received hydroxychloroquine plus azithromycin vs. 16.9% of patients who received only hydroxychloroquine. The mean age of patients was 59.2 ± 15.4.The mean of posttreatment QTc interval in the monotherapy group was shorter than the mean of posttreatment QTc interval in the combination therapy group, but it had no significant statistical difference (462.5 ± 43.1 milliseconds vs. 464.3 ± 59.1 milliseconds; p = 0.488). Generally, 22.1% of patients had a prolonged QTc interval after treatment. Male gender, or baseline QTc ≥ 450 milliseconds, or high-risk Tisdale score increased the likelihood of prolonged QTc interval. Due to QTc prolongation, fourteen patients did not continue therapy after four days. CONCLUSIONS: Hospitalized patients treated by hydroxychloroquine with or without azithromycin had no significant difference in prolongation of QT interval and outcome. The numbers of patients with prolonged QT intervals in this study emphasize careful cardiac monitoring during therapy, especially in high-risk patients.

Fc-Gamma Receptor 3B Copy Number Variation Is Not a Risk Factor for Behçet's Disease.

Behçet's disease (BD) is an immune-mediated systemic vasculitis associated with HLAB51. Other gene associations are likely and may provide further insight into the pathogenesis of this disease. Fc-gamma receptors play an important role in regulating immune function. Copy number variation (CNV) of the Fc-gamma receptor 3B (FCGR3B) gene is associated with other inflammatory conditions and may also play a role in BD. The aim of this study was to determine whether CNV of the FCGR3B gene is associated with BD or its clinical features. FCGR3B copy number was determined for 187 Iranian patients and 178 ethnicity-matched controls using quantitative real-time PCR. The genotype frequencies were comparable in both BD patients and controls. The odds ratio for low copy number (<2CN) was 0.6 (P = 0.16) and the odds ratio for high copy number (>2CN) was 0.75 (P = 0.50). There was no association found between high or low CN of the FCGR3B gene and BD or its clinical features in this Iranian population. We are the first to report this finding which, when looked at in the context of other genetic studies, gives us further insight into the complex pathogenesis of BD.

Association of interleukin-2, interleukin-4 and transforming growth factor-beta gene polymorphisms with Behcet's disease.

Behçet's disease (BD) is a chronic immune-mediated disease, characterised by oral and genital lesions and ocular inflammation. As cytokines seem to have important roles in the pathogenesis of BD and production of cytokines could be affected by genetic polymorphisms, this study was performed to investigate gene polymorphisms of a number of cytokines in the patients with BD in comparison with control subjects. One hundred and fifty patients with BD were enrolled in this study. Interleukin (IL)-2 (-330, +166), IL-4 (-1098, -590, -33), IL-10 (-1082, -819, -592), IL-12 (-1188), IFN-γ (5644), transforming growth factor (TGF)-ß (codon 10, 25), and IL-4RA (+1902) typing were performed by polymerase chain reaction with sequence-specific primers. In the patients with BD, there were significantly increased frequency of IL-2 (-330) GG genotype (p<0.001), IL-4 (-33) CC genotype (p<0.001), and TGF-ß (codon 10) CC genotype (p=0.004). Meanwhile a significant decrease in the frequency of IL-4 (-33) TC genotype (p<0.001) was detected in the patient group in comparison with normal controls. The genotype CC of TGF-ß at codon 10 was also significantly overrepresented in the patient group (p=0.004). Haplotype frequencies of IL-4 (-1098, -590, -33) showed that the frequency of TTC haplotype was significantly increased in the patients (p<0.001), whereas TTT haplotype was significantly decreased in this group of patients (p<0.001). There was not any significant difference in allele and genotype frequencies of IL-10, IL-12, IFN-γ, and IL-4RA between patient and control groups. Cytokine single nucleotide polymorphisms could play a role in the pathophysiology of BD. The results of this study could suggest a tendency towards higher production of IL-2 and lower production of IL-4 in the patients with BD.

Proinflammatory cytokine gene polymorphisms in Behçet's disease.

Behçet's disease (BD) is a chronic, systemic disease, characterized by oral and genital lesions, and ocular inflammation. There is evidence indicating altered levels of proinflammatory cytokines, such as interleukin (IL)-6 and tumor necrosis factor alpha (TNF-α) in patients with BD. This study involved 150 patients with BD and 140 healthy controls, and investigated the role of proinflammatory cytokine gene polymorphisms in the disease. The frequency of the TNF-α (-238) G/G genotype was significantly higher in the patient group, compared to the controls (p < 0.001), whilst the G/A genotype was significantly lower in the patients with BD (p < 0.001). Patients with BD showed a significant increase in the TNF-α (- 308, - 238) GG haplotype (p < 0.001), whilst there was a significant decrease in the GA haplotype (p < 0.001). The heterozygous, IL-6 (- 174) C/G genotype (p = 0.005), and the IL-6 (- 174, nt565) haplotype CG (p < 0.001), were significantly decreased in the patient group. The increased production of proinflammatory cytokines in BD could be a consequence of specific, cytokine gene polymorphisms. Particular genotypes and haplotypes in TNF-α were over-represented in BD, which may, in turn, predispose individuals to this disease.