Effect of Continuous Positive Airway Pressure Therapy on Pro-Brain Natriuretic Peptide, C-Reactive Protein, Homocysteine, and Cardiac Markers in Patients with Obstructive Sleep Apnea.

OBJECTIVE: Obstructive sleep apnea is associated with increased morbidity and mortality, especially cardiovascular and cerebrovascular, and affects a significant proportion of the population. The study was aimed to determine the levels of pro-brain natriuretic peptide, C-reactive protein, homocysteine, and cardiac markers (creatine kinase, creatine kinase isoenzyme MB, troponin T) and evaluate the effectiveness of continuous positive airway pressure therapy in patients with obstructive sleep apnea. MATERIAL AND METHODS: Pro-brain natriuretic peptide, C-reactive protein, homocysteine, and cardiac markers (creatine kinase, creatine kinase isoenzyme MB, troponin T) were assessed in blood samples collected before and after continuous positive airway pressure treatment from the 30 patients included in the study, and their results were compared. RESULTS: There was a significant decrease between the baseline pro-brain natriuretic peptide and the 6-month pro-brain natriuretic peptide values after continuous positive airway pressure therapy (P < .05). There was a significant increase in creatine kinase-MB and troponin T values 6 months after continuous positive airway pressure therapy compared to baseline values (P < .05). CONCLUSIONS: A significant decrease was observed in pro-brain natriuretic peptide values after continuous positive airway pressure therapy in obstructive sleep apnea patients without cardiac failure, while a more significant decrease was especially observed among hypertension patients. This finding suggests that pro-brain natriuretic peptide may be used as an early indicator of cardiac dysfunction in obstructive sleep apnea patients without any heart diseases except for hypertension.

Galectin-3 and plasma cytokines in patients with acute myocardial infarction.

OBJECTIVE: To investigate the concentrations of plasma cytokines and Galectin-3 (Gal-3) as inflammatory markers in patients with acute myocardial infarction (AMI). METHODS: The study population consisted of 29 patients with AMI and 29 healthy control subjects. We measured Gal-3, tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6) levels in plasma using enzyme-linked immunosorbent assays (ELISAs). We measured levels of C-reactive protein (CRP) via the nephelometric method. RESULTS: Patients with AMI showed significantly higher plasma Gal-3, TNF-α, and IL-6 levels compared with controls. Gal-3 levels were positively and significantly correlated with plasma IL-6, TNF-α, and CRP levels in the control and patient groups. CONCLUSION: Our findings suggest that Gal-3 can be a new circulating biomarker of inflammation associated with AMI.

Levels of C-reactive protein and protein C in periodontitis patients with and without cardiovascular disease.

Since periodontitis is a chronic and inflammatory disease, a number of hypotheses have proposed that it has an etiological or modulating role in cardiovascular disease (CVD). This study aimed to ascertain the changes in the plasma levels of C-reactive protein (CRP) and protein C (PC), a natural anticoagulant also having an anti-inflammatory effect, in patients who have mild-to-severe periodontitis with or without CVD. The test group consisted of 26 patients with CVD and chronic periodontitis and the control group consisted of 26 patients with chronic periodontitis and no systemic disease. In both groups Community Periodontal Index of Treatment Needs scores were recorded and blood samples were collected. CRP levels were significantly high and PC activity was significantly low in the test group compared to the control group (p < 0.001). There was a negative correlation between tooth loss and PC and between CRP and PC. How PC is affected by the inflammatory events and its association with CRP is an active area of investigation.

Serum and saliva sialic acid in periodontitis patients with and without cardiovascular disease.

Serum total sialic acid (sTSA) has recently been shown to be a cardiovascular risk factor. However, there is little information about the role of sTSA and TSA in saliva in periodontitis, a chronic and inflammatory disease known to be a risk factor for cardiovascular disease (CVD). We aimed to investigate the changes in sTSA and TSA levels in saliva in patients having both periodontitis and CVD versus periodontitis patients without diagnosed CVD. The study group consisted of 26 patients with proven periodontitis and 26 controls with no diagnosed systemic disease but periodontitis. sTSA and saliva TSA levels were determined by the thiobarbituric acid method, and C-reactive protein (CRP) was evaluated by the nephelometric method. The severity of periodontitis has been determined by the community periodontal index of treatment needs (CPITN). TSA in blood and saliva and CRP levels in blood were significantly increased in CVD patients compared with the control group. CPITN ranged from 2 to 4 in both groups. Significant and positive correlations were found between sTSA and saliva SA levels in patients and controls and between tooth loss and TSA both in blood and saliva. Therefore, TSA in saliva may be a useful marker similar to sTSA in CVD patients.

Extraordinary cause of ischemic chest pain in a young man: congenital ostial atresia of the right coronary artery.

Chest pain in a young person without cardiovascular risk factors is usually attributed to noncoronary causes; however, if the history suggests ischemic pain, the potential presence of unusual cardiovascular abnormalities should not be disregarded. The present case describes a young man with solitary congenital ostial atresia of right coronary artery, who to our knowledge is only the second case in the medical literature. Manifestation of ischemic symptoms in a relatively advanced age in patients with coronary artery atresia may mislead clinicians to interpret them as signs of atherosclerotic coronary artery disease. Therefore congenital coronary artery atresia should be a part of the differential diagnosis particularly in young patients with ischemic symptoms and no cardiovascular risk factors.

The relation between plasma tissue factor and oxidized LDL levels in acute coronary syndromes.

AIM: Tissue factor (TF) is a low-molecular-weight glycoprotein responsible for the initiation of the coagulation cascade. The relation between oxidized low-density lipoprotein (Ox-LDL), that has been shown to be involved in atherogenesis, and TF has not been evaluated before in circulating plasma. The aim of this study was to determine plasma levels of TF and Ox-LDL in acute coronary syndrome (ACS) and stable coronary artery disease (SCAD). METHODS: The study group consisted of 41 patients with ACS and 26 patients with SCAD. Among the ACS patients, 12 were diagnosed with unstable angina pectoris (UAP) and 29 were diagnosed with acute myocardial infarction (AMI). The control group consisted of 30 healthy volunteers. TF and Ox-LDL levels were evaluated by ELISA kits. RESULTS: Ox-LDL levels were significantly higher in UAP and AMI patients compared with the control (p < 0.001) and SCAD (p < 0.01 and p < 0.001, respectively) groups. TF levels were significantly higher in the UAP, AMI and SCAD groups compared with the control group (p < 0.001, p < 0.001 and p < 0.01, respectively). In the AMI group a significant increase was observed in TF levels when compared with the SCAD group (p < 0.01). Plasma Ox-LDL levels were significantly and positively correlated with TF levels in the UAP and AMI groups (p < 0.05, r = 702, and p < 0.0001, r = 0.679, respectively). CONCLUSION: The potential link between Ox-LDL and TF in circulating blood in ACS may strengthen the evidence supporting a relationship between oxidant stress, lipids and thrombosis and consequently may contribute to understanding the mechanism through which Ox-LDL and TF may mediate the pathogenesis of CAD.

Short-term effects of rilmenidine on left ventricular hypertrophy and systolic and diastolic function in patients with essential hypertension: comparison with an angiotensin converting enzyme inhibitor and a calcium antagonist.

The short-term (three months) effects of rilmenidine on systemic hypertension induced left ventricular hypertrophy (LVH) and left ventricular systolic and diastolic functions in comparison with those of perindopril and nifedipine-slow release (SR) formulation were studied. The short-term effects of rilmenidine on biochemical parameters and lipid profiles were evaluated. Sixty patients (39 men, 21 women) with a mean age of 59 +/- 14 years and with mild to moderate systemic arterial hypertension were enrolled in three groups. The first group received 1 mg/day of rilmenidine, the second group 4 mg/day of perindopril, and the third group 20 mg/day of nifedipine SR. All drugs induced a similar decrease in systolic and diastolic blood pressure (BP) values. Left ventricular mass (LVM) and LVM index decreased equally in all groups associated with a significant increase in the E/A ratio. The ratio between the reduction in LVM and decrease in mean arterial pressure (LVM/mmHg) was higher in groups 1 and 2. Negative correlations between LVM and LVMI. E/A, and the dv/dt ratio were obtained. Rilmenidine did not change the blood chemistry and lipid profile values. Despite its neutral effect on lipid profile and biochemical parameters. rilmenidine is as effective as perindopril and nifedipine in controlling hypertension and decreasing left ventricular hypertrophy.

Effects of low and high doses of atorvastatin on arterial compliance.

At the beginning of atherosclerosis before evidence of morphological lesions or plaques, vascular distensibility or arterial compliance decreased gradually. This endothelial dysfunction is regarded as an early feature of atherosclerosis. In a randomized, double-blind study design, group 1 (12 patients; 7 males, 5 females) with serum LDL-C levels higher than 170 mg/dL and without any other risk factor for atherosclerosis received three months of 20 mg/day atorvastatin treatment while group 11 (8 males, 4 females) with the same characteristics received 80 mg/day. Baseline and posttreatment serum lipid fractions and arterial compliance were measured. Arterial compliance was measured noninvasively in the left common carotid artery with color Doppler ultrasound. Atorvastatin reduced total cholesterol (TC), LDL-C, and triglyceride levels by 32% (P < 0.001), 40.8% (P < 0.001), and 19% (P < 0.001), respectively, and increased HDL-C by 6.9%, (P = 0.002) in the first group. In the second group these reductions were 38.5% (P < 0.001), 46.2% (P < 0.001), and 26.78% (P < 0.001), respectively, and the increase in HDL was 7.8% (P = 0.03). It was observed that the decrease in serum TC, LDL-C and triglyceride levels were significantly higher in the second group than the first group. With atorvastatin, the distensibility coefficient (DC) and compliance coefficient (CC) increased from 18.7 +/- 3.4 to 21.3 +/- 2.9 10(-3) x kPa(-1) (P < 0.001) and from 0.69 +/- 0.05 to 0.77 +/- 0.03 mm2 x kPa(-1) (P < 0.001) in the first group while they changed from 18.3 +/- 3.6 to 21.9 +/- 3.0 10(-3) x kPa(-1) (P < 0.001) and from 0.70 +/- 0.04 to 0.81 +/- 0.01 mm2 x kPa(-1) (P < 0.001) respectively, in the second group. DC and CC increased in both groups, but the differences between the groups were not significant. High doses of atorvastatin reduce blood lipid levels more than conventional doses, however, the change in compliance is not dose-dependent. As endothelial dysfunction is regarded as an early feature of atherosclerosis, there would be no need to administer aggressive doses in a patient without any risk factors other than hyperlipidemia.