Effect of fenofibrate on serum nitric oxide levels in patients with hypertriglyceridemia.

BACKGROUND: Fenofibrate, a peroxisome proliferator-activated receptor-α (PPARα) 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 PPARα-associated signaling pathways show promise as an alternative treatment of vascular dysfunction related to advanced age and hyperlipidemia.

Serum nitric oxide levels in patients with coronary artery ectasia.

OBJECTIVE: Serum levels of nitric oxide (NO) are decreased in patients with atherosclerosis and also are a risk factor for the development of atherosclerosis. Endothelial dysfunction and diffuse atherosclerosis have been proposed for the etiology of coronary artery ectasia (CAE). The purpose of this clinical trial was to determine the relationship between CAE and serum NO levels. METHODS: This prospective controlled study was conducted between January 2008 and March 2012. Serum levels of NO were compared in 40 patients with CAE (mean age 60.1±7.3 years) and 40 patients with normal coronary arteries (mean age 57.6±5 years) as a control group. CAE was diagnosed when a segment of coronary artery was more than 1.5 times the diameter of the adjacent healthy segment. Patients with stenotic atherosclerotic plaques, slow coronary flow, previous history of revascularization, acute coronary syndromes, left ventricular dysfunction, valvular heart disease, and systemic diseases were not included in the study. The effect of NO on the outcome was studied by constructing a receiver operating characteristic (ROC) curve with CAE as the primary variable. Effects of different variables on CAE were calculated using binary logistics regression analysis. RESULTS: Serum NO concentrations were significantly lower in patients with CAE than in the control group (42.1±20.1 µmol/L vs. 77.3±15.7 µmol/L, p<0.001). According to the results of the multivariate regression analysis, LDL and NO levels were identified as independent factors associated with CAE (OR=1.02, 95% CI 1-1.04, p=0.02 and OR=0.88, 95% CI 0.83-0.93, p=0.001, respectively). ROC analysis revealed that using a cut-off point of 63.3, NO level predicts CAE with a sensitivity of 87.5% and specificity of 90%. CONCLUSION: Our study indicates that decreased levels of NO are present in patients with CAE compared to patients with normal coronary arteries, supporting the hypothesis that decreased levels of NO might be associated with CAE development.

Relation of vitamin D deficiency and new-onset atrial fibrillation among hypertensive patients.

Vitamin D deficiency is associated with various cardiovascular disorders including hypertension, coronary artery disease, and heart failure. The renin-angiotensin-aldosterone system (RAS) axis is activated in vitamin D deficiency. The RAS axis also plays a role in the pathophysiology of atrial fibrillation (AF). We aimed to investigate whether vitamin D deficiency is a risk factor for the development of new-onset AF in hypertension. A total of 227 hypertensive patients were enrolled, of whom 137 had new-onset AF; 90 patients without AF were included in the control group. The age of the patient, left atrial diameter, and vitamin D deficiency increased the probability of new-onset AF independent from confounding factors (odds ratio [OR], 1.04; 95% confidence interval [CI], 1.01-1.08; P = .03 for age; OR, 1.88; 95% CI, 1.15-3.45; P = .03 for left atrial diameter; OR, 1.68; 95% CI, 1.18-2.64; P = .03 for vitamin D deficiency). Vitamin D deficiency is associated with new-onset AF in hypertension.

Successful intervention of an anomalous right coronary artery arising from the posterior left sinus of Valsalva.

Percutaneous coronary intervention (PCI) in an anomalous right coronary artery (RCA) arising from the left sinus of Valsalva can be technically difficult because selective cannulation of the vessel may not be easy. We present a case of two consecutive successful stent implantations in an anomalous RCA arising from the posterior left sinus of Valsalva. We used a Judkins left 5 guiding catheter, which provided excellent angiographic visualization and guide support for stent delivery throughout the procedure.

The relationship between angiotensin converting enzyme gene I/D polymorphism and QT dispersion in patients with hypertrophic cardiomyopathy.

INTRODUCTION: Hypertrophic cardiomyopathy (HCM) is characterized by disorganized myocardial architecture, and may cause ventricular arrhythmias and sudden death. The angiotensin-converting enzyme (ACE) with two deletion alleles (DD genotype) has been proposed to be associated with increased myocardial collagen content. We evaluated QT dispersion (QTd), which reflects regional differences in ventricular repolarization, in HCM patient and controls among the three different ACE genotypes. MATERIALS AND METHODS: Sixty-three patients with HCM and 20 healthy subjects were included in the study. QT parameters were measured from 12 lead electrocardiograms. ACE genotypes were determined from the DNA extracted from peripheral blood by a polymerase chain reaction (PCR) method. QT parameters were compared among the three ACE genotypes both in HCM patients and controls. RESULTS: Median ages were similar in HCM and control groups. QTd and corrected QTd (QTcd) were significantly greater in the HCM group compared with the controls. The frequencies of each genotype were similar in both groups. Although QTd and QTcd did not differ among the three genotypes in the control subjects, they were significantly greater in patients with DD genotype compared with other genotypes in the HCM group. CONCLUSION: QTd and QTcd are increased in patients with HCM, especially in those with the DD genotype.

Association between anticardiolipin antibodies and recurrent cardiac events in patients with acute coronary syndrome.

To determine whether the presence of anticardiolipin (aCL) antibodies in patients with acute coronary syndrome is predictive of recurrent cardiac events in hospital stay and follow-up. The study population consisted of 80 patients with acute coronary syndrome. IgM and IgG aCL levels were determined before hospital discharge. We divided the patients into those with an aCL IgG >or= 40 IgG phospholipid units (group I, n = 30) and those with an aCL IgG < 40 IgG phospholipid units (group II, n = 50). All patients underwent coronary angiography. Follow-up coronary angiography was performed 12 months after percutaneous coronary intervention (PCI). Infectious and autoimmune diseases were exclusion criteria. Patients were observed to determine overall mortality, reinfarction, and restenosis. There were no differences between the groups with respect to the prevalence of hypertension, diabetes mellitus, and cigarette smoking, sex, or ejection fraction. The prevalence of left ventricular thrombus was similar between the groups (group I: 16% versus group II: 16.7%, P > 0.05). Although the presence of left atrial thrombus was much more frequent in cardiolipin positive patients (13% versus 4%, respectively), the difference was not statistically significant (P = 0.19). Restenosis was observed in 40% of the cardiolipin positive patients and 14% of the cardiolipin negative patients (P < 0.01). There was no significant association between reinfarction and anticardiolipin positivity during follow-up (26% versus 10%, P > 0.05). In group I patients, in-hospital mortality was somewhat more frequent compared to group II patients (4% versus 10%), but the difference was not statistically significant (P = 0.27). One year mortality was similar between the groups. These results suggest that 1) restenosis occurs more frequently in anticardiolipin positive patients and 2) no association is evident between positive aCL and mortality, reinfarction, and intracardiac thrombus.

Tumour necrosis factor-alpha in diastolic dysfunction.

BACKGROUND: Active relaxation develops as a result of sequestration of calcium into the sarcoplasmic reticulum, and is controlled mainly by sarcoplasmic reticulum calcium ATPase (SERCA) and phospholamban.Tumour necrosis factor-alpha (TNF-alpha) downregulates both of these proteins, so it may play a role in the development of abnormal relaxation. However, a possible relationship between TNF-alpha and diastolic dysfunction has not been sufficiently evaluated in vivo. We investigated whether circulating levels of TNF-alpha increased in patients with relaxation abnormality. METHODS: Forty hypertensive patients with normal left ventricular systolic function were enrolled in the study. Age-adjusted values of echocardiographically measured mitral inflow velocities, E-wave deceleration time and isovolemic relaxation time were used to define normal and abnormal relaxation. Twenty of the patients (mean age 59.2 +/- 10.6) had a relaxation abnormality (group I), and the twenty other patients (mean age 45.9 +/- 7.9) had a normal diastolic function (group II). TNF-alpha levels were measured by ELISA. RESULTS: There were no significant differences between the two groups in terms of interventricular septal thickness, posterior wall thickness, left ventricular mass, ejection fraction, plasma creatinin level, and medication. Patients with a relaxation abnormality were older than those with a normal diastolic function (p < 0.001). TNF-alpha levels were similar in both groups (62.1 +/- 46.0 pg/ml for group I, and 48.7 +/- 51.4 pg/ml for group II, p = 0.089). CONCLUSION: In this preliminary study, we demonstrated that TNF-alpha levels did not increase in patients with a relaxation abnormality. However, we think that a possible relationship between TNF-alpha and diastolic dysfunction should be clarified by further studies involving a larger number of patients with a wider spectrum of diastolic dysfunction.