Increased release of nitric oxide associated with nebivolol may counteract the detrimental effect of beta-blockade on penile erection, thereby allowing maintenance of sexual activity in previously untreated hypertensive men compared with a significant decrease observed in the sexual activity of men receiving atenolol-based treatment.

Results of this study indicate that lower serum PON1 activity is associated with oxidative stress and the activity of PON1 is not related to HDL-cholesterol.

Ischemia leads to impaired ATP metabolism, with increased production of purine degradation products, such as hypoxanthine and xanthine, which are useful markers of tissue hypoxia. These extracellular markers of ischemia have been studied extensively in many clinical conditions of oxidative stress, including perinatal asphyxia, acute respiratory distress syndrome, cerebral ischemia, and preeclampsia. The aim of this study was to explore the usefulness of urinary hypoxanthine and xanthine as ischemia markers in acute coronary syndromes. Urinary excretion of hypoxanthine and xanthine was assessed by high-performance liquid chromatography in 30 patients with acute coronary syndromes and in 30 age- and sex-matched controls. Serum and urine uric acid, creatinine, and urea concentrations were also determined. Hypoxanthine excretion was significantly elevated in patients compared with healthy controls (84.37+/-8.63 and 42.70+/-3.97 nmol/mg creatinine, mean+/-SEM, P<0.0001). Urinary xanthine levels were also increased in patients with acute coronary syndromes (100.13+/-12.14 and 34.74+/-4.07 nmol/mg creatinine patients and controls, respectively; P<0.0001). Hypoxanthine and xanthine excretion showed a strong positive correlation in both groups. Significant negative correlations between urinary hypoxanthine and uric acid and xanthine and uric acid were observed in the patients, but not in controls. In conclusion, increased levels of ATP degradation products hypoxanthine and xanthine are observed in various hypoxic clinical conditions. This study suggests that these parameters may be useful markers of ischemia in patients with acute coronary syndromes.

Objectives: Although the pathophysiology of syndrome X (angina pectoris, positive ECG test findings and normal coronary arteriogram) is unclear, it is generally accepted that intracellular metabolic changes resulting from abnormal constriction of prearteriolar vessels due to endothelium-dependent vasodilation abnormalities may play a role in the pathogenesis. We established the effect of long-term treatment with cilazapril, an angiotensin-converting enzyme inhibitor, which prevents the effect of angiotensin II in the tonic control of vascular resistance. Methods: 18 patients (15 women and 3 men, mean age 43.2 ± 4.6 years) with syndrome X were included in this study. A randomized double-blind crossover placebo-controlled trial was done. After a 1-week washout period, patients received either cilazapril 2 × 2.5 mg or placebo for 3 weeks, followed by 3 weeks of the other therapy. At the end of two periods, an exercise ECG test (modified Bruce protocol) was employed. Results: The magnitude of ST segment depression was significantly decreased during treatment with cilazapril compared with placebo. On the other hand, total exercise time and time to 1 mm ST segment depression were significantly prolonged by cilazapril. However, rate pressure products were not significantly different at peak exercise at or at 1 mm of ST segment depression during both therapies. Conclusion: Cilazapril exerted a beneficial therapeutic effect in cases with syndrome X. The possible mechanism of this effect may be a modulation of coronary tone at the microcirculation level.

The aim of this study was to estimate the incidence of silent myocardial ischaemia in patients with mild to moderate hypertension, white-coat hypertension (WCH) and those with normal blood pressure. Ambulatory electrocardiographic (ECG) monitoring was carried out in 272 cases with normal blood pressure, 164 cases with mild to moderate hypertension (diastolic blood pressure Ͼ95 and Ͻ114 mm Hg), and 106 cases with white-coat hypertension who were diagnosed with ambulatory blood pressure monitoring. The ages of the patients of all groups were between 42-61 years. There were no differences between the groups according to age, gender

Objective: Anatomical differences in coronary orifices (CO) are important as they are associated with myocardial ischemia and sudden death. The location of coronary orifices to the aortic valve has been studied since it is a determining point in surgical and radiological attempts. Methods: The number, position, and shape of the CO, and their relation to the sinotubular junction (SJ), were studied in 100 normal adult hearts. Student-t test, one-and two-way ANOVA with posthoc Tukey's HSD tests were applied for statistical analysis. Results: The mean height of the right, non-and left coronary sinuses were 18.75±1.71, 17.86±1.55 and 16.41±1.21 mm, respectively. The mean height of the right, non-and left coronary cusps were measured as 16.2±1.2, 15.9±1.1 and 12.3±2.1 mm, respectively. The left coronary artery (LCA) was observed to arise from the lower part of the SJ in 58% of the patients, while in 29% of them it originated from the SJ, and in 13% of the cases it arose from the upper part of the SJ. The right coronary artery (RCA) arising from the lower part of the SJ was seen in 78% of the patients, while it originated from the SJ in 13% of the patients, and it was observed to arise from the upper part of the SJ in 9 specimens. The diameters of the LCA and RCA were measured as 4.22±0.72 and 3.32±0.82 mm, respectively. An accessory orifice was found on the left in 47 specimens, while it was seen on the right in 54 of them. Conclusions: The location of the CO should be identified according to the vertical and horizontal surfaces of the sinus. In this study, the frequency of the coronary artery orifices with different locations was provided. Such data will increase the success of coronary interventions and decrease complication rate.

Hyperhomocysteinemia is currently regarded as an independent and modifiable risk factor for ischemic vascular diseases and thrombosis. We measured fasting plasma total homocysteine levels by HPLC with fluorescence detection in 30 patients presenting with acute coronary syndromes and 30 age and sex-matched control subjects. Demographic data, classical risk factors (systolic blood pressure, diabetes mellitus, smoking, ethanol intake, family history of ischaemic heart disease) and life-style habits were recorded. Lipid fractions including total cholesterol, triglycerides, HDL-cholesterol, total cholesterol/HDL-cholesterol ratio, serum creatinine, LDL-cholesterol and vitamins involved in the metabolism of homocysteine, folic acid and vitamin B12 were also assessed. Total fasting homocysteine concentrations were significantly higher in the patient group (12.2 +/- 1.01 micromol/l) than in the control subjects (7.05 +/- 0.36 micromol/l; p < 0.0001). Homocysteine correlated positively with age (r = 0.617; p < 0.01) and serum creatinine (r = 0.457; p < 0.01) in the patient group. Hyperhomocysteinemia was not associated with vitamin B12 or folate deficiency states. Vitamin B12 concentration was 273 +/- 16.4 ng/l in the control group and 284.3 +/- 32.2 ng/l in the patient group (p = NS). Serum folate concentration also was not significantly different between controls and patients; 7.57 +/- 0.58 microg/l and 8.05 +/- 0.72 microg/l, respectively. Since no significant difference was observed in the lipid parameters between patients and controls, the hyperhomocysteinemia in the patient group supports the view that homocysteine is an independent risk factor for cardiovascular diseases. Our results strongly suggest that elevated homocysteine levels are among the interacting factors in the complex, multifactorial pathophysiology of ischemic heart disease.

The role of reactive oxygen products in myocardial damage caused by ischemia-reperfusion has been established in a number of studies performed in animals models. However, studies showing the development of increased free radicals following effective myocardial reperfusion in humans are scarce. In the present study, both the increase of lipid peroxidation (LPO) following early stage thrombolytic therapy which is the current treatment issue performed after acute myocardial infarct (AMI) and the plasma levels of vitamin E and C (chain braker antioxidants) were investigated parallel to time. Forty patients with AMI who were admitted to hospital within six hours from the beginning of symptoms were included in the study and divided into two groups; group 1 (recombinant tissue-Plasminogen Activator, rt-PA group) and group 2 (streptokinase group). Serial serum specimens were drawn before and 30, 90 minutes and 24 hours after thrombolytic therapy for the investigation of LPO, vitamin E and C levels. Echocardiographic examination was performed on the tenth day to evaluate the functions of the left ventricle. Plasma levels of lipid peroxides (LPO) were found to increase 90 minutes after thrombolytic therapy in each group, while the levels of vitamins E and C showed significant decreases. The difference between the two groups was not significant. Similar to this finding, no significant difference in the ejection fraction values was observed between the groups. Further, no correlation was observed between the ejection fraction and LPO values at the 90th minute which is considered to be the time of successful thrombolysis. In conclusion, the occurrence of a series of biochemical changes confirming an increase in free radical development of peripheral blood was observed. Although the decrease in vitamin E and C levels suggests the need for supplementation of these vitamins along with the thrombolytic therapy, the fact that at least a week is needed for an increase of tissue levels of vitamin E confirms the opinion that the daily prophylactic doses of these vitamins is suitable for the decrease of AMI risk.