Systemic immune-inflammation index (SII), on the basis of lymphocyte, neutrophil and platelet counts had been published to be a good prognostic factor in coronary artery disease. Nevertheless, the ...

Cardioneuroablation is one of the emerging therapies in vasovagal syncope. In this study, we present a simple method of cardioneuroablation performed via a right-sided approach, targeting anterior-right and right-inferior ganglionated plexi, along with procedural and follow-up data. Patients who had underwent cardioneuroablation between March 2018 and September 2019 with vasovagal syncope in 2 clinics were enrolled in the study. All patients underwent radio-anatomically guided radiofrequency ablation targeting anterior-right ganglionated plexi and right-inferior ganglionated plexi. Syncope and symptom burden, 24-hour ambulatory electrocardiogram data at presentation, and at follow-up were assessed along with procedural data. A total of 23 patients underwent modified right-sided cardioneuroablation. Mean basal cycle length decreased significantly from 862.3 ± 174.5 ms at the beginning of the procedure 695.8 ± 152.1 ms following the final radiofrequency ablation (P < .001). Mean 24-hour ambulatory heart rate increased significantly from 66.4 ± 10.7 bpm at baseline to 80 ± 7.6 bpm at follow-up (P < .001). Only 1 patient had 1 episode of syncope following the procedure at the mean follow-up period of 10 ± 2.9 months. The same patient had recurrent presyncope. The right-sided cardioneuroablation approach was found to be an effective treatment for vasovagal syncope and may be regarded as a default initial cardioneuroablation technique.

Background. Fenofibrate, a peroxisome proliferator-activated receptor-alpha (PPAR alpha) agonist, is used to treat patients with hypercholesterolemia and hypertriglyceridemia in order to reduce the risk of development of the atherosclerotic cardiovascular disease. However, it exerts pleiotropic effects beyond correcting atherogenic dyslipidemia to treat hypercholesterolemia. Objectives. The aim of this study was to investigate the potential effects of fenofibrate on endothelial function by analyzing the serum nitric oxide (NO) levels in patients with hypertriglyceridemia. Material and methods. Lipid profiles and serum NO levels were assessed in 56 healthy adults aged 29 to 84 years, before and after 12 weeks of fenofibrate (250 mg/d; n = 30) or placebo (n = 26). Appropriate dietary suggestions for hypertriglyceridemia were made for all patients. This study was randomized, double-blind and placebo-controlled in design. Results. Total cholesterol, low-density lipoprotein (LDL), very low-density lipoprotein (VLDL) and triglyceride levels significantly decreased; high-density lipoprotein (HDL) and NO levels significantly increased after 12 weeks of fenofibrate therapy. We observed a statistically significant correlation between the increase in serum NO levels and decrease in serum triglyceride levels (r = -0.42, p = 0.02) in the fenofibrate group. Conclusions. The positive effect of short-term fenofibrate treatments on vascular endothelial functions in patients with hypertriglyceridemia has been demonstrated by increasing the serum NO levels. Agents such as fenofibrate targeting PPAR alpha-associated signaling pathways show promise as an alternative treatment of vascular dysfunction related to advanced age and hyperlipidemia.

Coronary artery ectasia (CAE) is associated with increased risk of mortality, equivalent to that of patients with obstructive coronary artery disease (CAD). Considering the role of inflammation in the pathogenesis of CAE, we aimed to investigate whether there is an association between systemic immune-inflammation index (SII) and isolated CAE. The study population included 510 patients of which 170 patients with isolated CAE, 170 patients with obstructive CAD and 170 patients with normal coronary angiograms (NCA). The severity of CAE was determined according to the Markis classification. Patients with isolated CAE had significantly higher SII values compared to those with obstructive CAD and NCA [median 550 IQR (404–821), median 526 IQR (383–661), and median 433 IQR (330–555), respectively, p < .001]. In multivariate analysis, SII (OR 1.032, 95% CI 1.020–1.044, p = .003), male gender (OR 2.083, p = .008), eGFR (OR 0.979, p = .016), and CRP (OR 1.105, p = .005) were independent factors of isolated CAE. Moreover, in the Spearman correlation analysis, there was a moderate but significant positive correlation between SII and CRP (r = 0.379, p < .001). In conclusion, higher SII levels were independently associated with the presence of isolated CAE. This result suggests that a more severe inflammatory process may play a role in the development of this variant of CAD.

Nonalcoholic fatty liver disease (NAFLD) is the most common liver pathology in the developed world. Nonalcoholic fatty liver disease is associated with a higher risk of cardiovascular disease. We investigated the impact of ranolazine on liver tests in patients with NAFLD and coronary artery disease (CAD). Patients who had established CAD and NAFLD (as assessed by raised serum transaminase activity, sonographic criteria, and the absence of any other obvious liver disease) were allocated to “on ranolazine” (n = 40) or “not on ranolazine” (n = 35) groups. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured in all patients at baseline and at the end of the study. After 6 months of ranolazine treatment, both ALT and AST activities were significantly lower in patients in the “on ranolazine” group compared with “not on ranolazine” patients (change from baseline: ALT, −11.0 ± 1.7 IU/L, P < .001; AST, −5.2 ± 1.9 IU/L, P =.009). In conclusion, the present study showed that treatment with ranolazine for 6 months led to a significant reduction in the activities of both serum aminotransferases in patients with stable CAD and NAFLD.