Effects of Vitamin D Levels on Long-Term Coronary Events in Patients with Proven Coronary Artery Disease: Six-Year Follow-Up.

Although some clinical studies have claimed that low-dose vitamin D (Vit-D) increases the risk of long-term cardiac events, in others, no association was found. To better understand the impact of Vit-D levels on long-term cardiac events in coronary artery disease patients, this study was designed. There were 408 patients with coronary artery disease (CAD). The patients were separated into three groups based on their Vit-D levels: group 1 had levels below 10 ng/mL, group 2 had levels between 10 and 20, and group 3 had levels above 20 ng/mL. Six years were spent monitoring the patients for non-fatal MI, death, vascular revascularization, and stable course data. Mortality was found to be similar between groups (group 1: 24.5%; group 2: 13.8%; group 3: 17.4%; p > 0.05). In group 3, 47.8% of the patients did not experience any cardiac event, while 28.7% in group 2 and 27.6% in group 1 did not experience any cardiac event, and these values were found to be significant in favor of group 3 (p = 0.006). Group 3 was found to have considerably lower rates of non-ST-elevated myocardial infarction (non-STEMI) and unstable angina (UA) than the other groups did (group 1: 49%; group 2: 38%; group 3: 27%; p = 0.001). In conclusion, although vitamin D deficiency does not accompany an increase in mortality, it is associated with an increase in non-STEMI and UA in patients who have previously been diagnosed with CAD.

Evaluation of the inflammatory parameters for predicting stent thrombosis.

OBJECTIVES: Recent research demonstrated that classic inflammatory mediators were responsible for the development of stent thrombosis. We aimed to examine the relationship between predictors such as basophils, mean platelet volume (MPV), and vitamin D, which represented allergic, inflammatory, and anti-inflammatory states, and stent thrombosis after percutaneous coronary intervention. METHODS: In this observational case-control study, patients (n: 87) with ST-elevated myocardial infarction (STEMI) with stent thrombosis formed group 1, and (n = 90) with STEMI without stent thrombosis formed group 2. 25-OH vitamin-D and other laboratory values were obtained at the time of admission to the emergency room. RESULTS: In comparison to group 2, MPV was higher in group 1(9.05 ± 0.89 vs 8.17 ± 1.37 fL, respectively; p = 0.002). Group 2 had a higher basophil count than group 1(0.03 ± 0.05 vs 0.07 ± 0.080; p = 0.001). In comparison to group 2, group 1 had a greater vitamin-D level (p = 0.014). The MPV and basophil count were found as predictors for stent thrombosis in the multivariable logistic analyses. When MPV increased by one unit, the risk of stent thrombosis increased 1.69-times (95% CI: 1.038-3.023). Basophil counts below 0.02 increased the risk of stent thrombosis 12.74-times (95% CI: 4.22-36.00). CONCLUSION: Increased MPV and basophil depletion might be predictors for coronary stent thrombosis following percutaneous coronary intervention (Tab. 4, Fig. 2, Ref. 25). Text in PDF www.elis.sk Keywords: MPV; basophil; vitamin D; stent thrombosis.

The association between QT interval changes and the treatment protocols of COVID-19 patients.

OBJECTIVE: This study aimed to investigate the QT, QTc, and QTc dispersion changes that may occur with the use of hydroxychloroquine (HCQ), favipiravir, and moxifloxacin in combination or alone in COVID 19 patients. METHODS: This study was retrospectively conducted on 193 inpatients diagnosed with COVID-19. We divided the patients into four separate groups due to their medications as, group-1: favipiravir, group-2: favipiravir + HCQ, group-3: favipiravir + moxifloxacin, and group-4: favipiravir + moxifloxacin + HCQ. We recorded their pre and post-treatment QT parameters of each group and evaluated the changes of these parameters with the SPSS statistical program. RESULTS: The mean age of the patients was 63.1±17.7. In group 1 and 2, although there were slight changes in QT parameters, these results were not statistically significant. In group 3, significant increases in QT and QTc dispersion occurred (p=0.005 and p=0.018). In the 4th group where the triple therapy was applied, there was a significant increase only in the QTc values (p=0.027). When we compared the changes of QT parameters for each group, a significant difference was found in ΔQTc dispersion, and post hoc analysis showed that it was due to changes in the third group (p=0.047). CONCLUSION: We thought that, if there is a COVID-19 infection with an additional bacterial infection, and if there is a need of using moxifloxacin alone or together with HCQ, additional risk factors that may cause QT interval prolongation should be reviewed and ECG monitoring of the patients should be performed during the treatment period.

COX-1, COX-2 and CYP2C19 variations may be related to cardiovascular events due to acetylsalicylic acid resistance.

BACKGROUND: In some stent implanted patients, cardiovascular events (CE) may occur. Acetylsalicylic acid (ASA) is routinely administered to these patients in order to prevent the occurrence of CE. CE may be related to gene variations which cause ASA resistance (AR). Therefore, it was aimed to investigate the relationship between COX-1, COX-2, CYP2C9 and CYP2C19 variations with CE due to AR. MATERIALS AND RESULTS: Seventy-four stent implanted patients, using 100 mg of ASA per day during five years were enrolled into the study. Following stent implantation, thirty-eight patients who had a CE within five years due to AR and 36 patients without CE were enrolled in patient and control group, respectively. AR was confirmed by platelet aggregation testing. After DNA isolation from blood; COX-1, COX-2, CYP2C19 and CYP2C9 variations were investigated with real-time polymerase chain reaction. At the end of this study, heterozygous genotype of COX-1 was found statistically high in patients whereas heterozygous genotype of CYP2C19*17 was found statistically high in controls. The presence of C and G allele in COX-1 and COX-2 were found statistically high in patients, respectively. The presence of T allele in CYP2C19*17 was found statistically high in controls. Heterozygous genotype of COX-1 variation was found statistically high in patients who have AR. Additionally heterozygous genotype of CYP2C19*17 was found statistically high in patients who have low thrombosis risk. CONCLUSIONS: COX-1 and COX-2 gene mutations may increase the risk of CE due to AR whereas CYP2C19*17 may have a protective effect in this process.