The prevalence of silent myocardial ischaemia in patients with white-coat hypertension.

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 >95 and <114 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 and other parameters. There were no anginal symptoms, and resting ECGs were in normal limits in all cases. The diagnosis of silent ischaemia was considered to be present if there was ST depression >2 mm/at least 120 sec in ambulatory ECG examination without angina or its equivalent cardiac symptoms. The incidence of silent ischaemia was 6.4%, 18.8%, and 26.2% in cases with normal blood pressure, WCH, and hypertension, respectively. The differences between groups were significant. It was concluded that WCH is not a benign condition, but shares some characteristics with essential hypertension.

Therapeutic benefits of cilazapril in patients with syndrome X.

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 x 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.

Plasma homocysteine levels in acute coronary syndromes.

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 efficacy of felodipine ER on regression of left ventricular hypertrophy in patients with primary hypertension.

The aim of the study was to evaluate the efficacy over 1 year of of felodipine ER 5 and 10 mg once daily (od) in 12 Caucasian patients with left ventricular hypertrophy secondary to primary hypertension. After a placebo period of 20 days, a physical examination and an echocardiography were performed in each patient. All patients started treatment with felodipine ER 5 mg. In 3 of the 12 patients the dose was increased to 10 mg od to control blood pressure (BP). BP was recorded every 2 weeks during the first 3 months, and at monthly intervals from the 3rd to the 12th months. An echocardiogram was taken at the end of the 3rd, 6th, 9th and 12th months. At the end of the placebo period, the mean SBP/DBP (+/-SD) was 178 +/- 11/104 +/- 5 mmHg. Mean SBP and DBP decreased significantly (p < 0.001) during the first 2 months to 138 +/- 10/86 +/- 3 mmHg and remained at this level until the end of the study. Mean left ventricular mass index (LVMI) decreased from 170 +/- 33 g/m2 after the placebo period to 115 +/- 19 g/m2 after 1 year (p < 0.01). It is concluded that felodipine ER 5 and 10 mg od over 1 year statistically significantly reduced both BP and LVMI.

The state of lipid peroxidation and antioxidants following thrombolytic therapy with rt-PA and streptokinase in acute myocardial infarction.

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.

Urinary hypoxanthine and xanthine levels in acute coronary syndromes.

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.

Prevalence of Chlamydia pneumoniae specific antibodies in different clinical situations and healthy subjects in Izmir, Turkey.

Serological markers for Chlamydia pneumoniae were investigated by using the microimmunofluorescence (MIF) test in various age and patient groups in a specific area in Turkey. IgG seropositivity to C. pneumoniae was 64.3% and 18.7% in healthy adults and children, respectively. The highest positivity rate (77%) was in the 15-19 age group. Among the groups investigated, serological findings revealed a possible etiological association between C. pneumoniae and the clinical condition in the groups with acute myocardial infarction, atypical pneumoniae and chronic obstructive pulmonary disease.