[The psychometric properties of the Turkish version of Myocardial Infarction Dimensional Assessment Scale (MIDAS)]. / Miyokart Enfarktüsü Boyutsal Degerlendirme Ölçegi (MIDAS) Türkçe sürümünün psikometrik özellikleri.

OBJECTIVE: The purpose of this study was to describe the psychometric properties of the Myocardial Infarction Dimensional Assessment Scale (MIDAS). METHODS: This is a methodological cultural adaptation study. The MIDAS consists of 35-items covering seven domains: physical activity, insecurity, emotional reaction, dependency, diet, concerns over medication, and side effects which are rated on a five-point Likert scale from 1: never to 5:always. The highest score of MIDAS is 100.Quality of life (QOL) decreases as the score of scale increases. Overall 185 myocardial infarction (MI) patients were enrolled in this study. Cronbach alpha was used for the reliability analysis. The criterion validity, structural validity, and sensitivity analysis approach was used for validity analysis. New York Heart Association (NYHA) and the Canadian Cardiovascular Society Functional Classifications (CCSFC) for testing the criterion validity; SF-36 for construct validity testing of the Turkish version of the MIDAS were used. RESULTS: The range of Cronbach alpha values is 0.79-0.90 for seven domains of the scale. No problematic items were observed for the entire scale. Medication related domains of the MIDAS showed considerable floor effects (35.7%-22.7%). Confirmatory Factor analysis indicators [Comparative Fit Index (CFI) =0.95 and Root Mean Square Error of Approximation (RMSEA) =0.075] supported the construct validity of MIDAS. Convergent validity of the MIDAS was confirmed with correlation of SF-36 scale where appropriate. Criterion validity results was also satisfactory by comparing different stages of the NYHA and the CCSFC (p<0.05). CONCLUSION: Overall results revealed that Turkish version of the MIDAS is a reliable and valid instrument.

Effect of monocyte chemoattractant protein-1 (MCP-1) gene polymorphism in Turkish patients with premature coronary artery disease.

OBJECTIVES: It has been suggested that monocyte chemoattractant protein-1 (MCP-1) is important in the initiation of atherosclerosis and crucial in monocyte recruitment into the subendothelial lesions. Recent studies have demonstrated that MCP-1 -2518 A>G polymorphism is associated with susceptibility to coronary artery disease (CAD). Since there are conflicting reports on the possible association of MCP-1 -2518 A>G polymorphism with CAD, we investigated the role of this polymorphism in Turkish patients with premature CAD. MATERIAL AND METHODS: Genomic DNA was collected from 171 premature CAD patients and 151 healthy individuals. MCP-1 -2518 A>G polymorphism was genotyped using the PCR-RFLP method. RESULTS: There were no differences between genotype distribution and allele frequencies in the premature CAD and control groups (AA: 49.7 %; AG: 40.3 %; GG: 10.0 % in premature CAD groups and AA: 53.7 %; AG: 34.4 %; GG: 11.9 % in controls; p = 0.53). The prevalence of the G allele was 0.302 in patients and 0.291 in controls. CONCLUSIONS: Our data demonstrate that MCP-1 -2518 A>G polymorphism is not associated with premature CAD in Turkish patients. Further studies are needed to elucidate the role of this polymorphism in the pathogenesis of CAD in various populations.

Effect of losartan on exercise tolerance and echocardiographic parameters in patients with mitral regurgitation.

OBJECTIVES: The aim of this study was to assess the effects of losartan treatment on exercise tolerance and echocardiographic parameters in patients with mitral regurgitation (MR) secondary to mitral valve prolapse or rheumatic heart disease. METHODS: Twenty-seven patients (14 males, 13 females, mean age 51+/-11, range 21-76) with moderate MR due to mitral valve prolapse or rheumatic heart disease were examined by means of Doppler echocardiography. The subjects were submitted to treadmill exercise tests using the modified Bruce protocol at baseline, after six hours and after the six-week treatment period to be evaluated based on their exercise tolerance. Mitral Regurgitant Volume (MRV), effective regurgitant orifice diameter, left atrial volume, left ventricle (LV) end-diastolic volume index, LV end-systolic volume index, LV ejection fraction (LVEF), left ventricle mass index were calculated at baseline and after six weeks of treatment with single dose of losartan (50 mg/day). RESULTS: Total treadmill exercise time increased from 477.7+/-147.9 to 535.7+/-149.0 seconds after six hours (p<0.01) and to 559.6+/-142.8 seconds after six weeks of treatment. Also, metabolic equivalent values increased following six hours of first dose and six weeks of losartan treatment (from 10.9+/-2.9 to 11.8+/-3.1, p=0.006 and 12.4+/-3.1, p=0.002; respectively). However, peak exercise systolic blood pressure (BP) was reduced after six hours and six weeks of treatment, and resting diastolic BP did not change after six hours but reduced at the end of the treatment period. MR volume decreased significantly from 29.3+/-14.1 ml to 25.1+/-14.8 ml, (p=0.025) without significant change in regurgitant orifice diameter (0.72+/-0.37 cm vs. 0.66+/-0.37 cm, p=NS), left atrium diameter and area while LVEF increased from 51.70+/-13.37 to 54.11-11.75 (p=0.015) with losartan. CONCLUSION: We conclude that the angiotensin II receptor antagonist losartan improves exercise tolerance and echocardiographic parameters in patients with moderate MR.

No association of interleukin-6 gene polymorphism (-174 G/C) with premature coronary artery disease in a Turkish cohort.

OBJECTIVES: Interleukin-6 (IL-6) may contribute to the inflammatory response by activating endothelial cells and stimulating the synthesis of fibrinogen. It might thus be important in the pathogenesis of inflammation associated with coronary artery disease (CAD). Several studies suggested that the -174 C allele was associated with an increased prevalence of coronary heart disease. The aim of this study was to investigate further the association of the IL-6 -174 G/C allele status with premature CAD. METHODS: A total of 120 patients and 105 controls were included in the study. The IL-6 -174 G/C polymorphism was genotyped using PCR-restriction fragment length polymorphism. RESULTS: The genotype distribution of the -174 G/C polymorphism was not different in premature CAD patients (GG: 53%; GC: 42.6%; CC: 4.3%) and controls (GG: 54.3%; GC: 39%; CC: 6.7%) (P=0.72). The prevalence of the C allele was 25.6% in patients and 26.1% in controls. By multiple regression analysis, family history, smoking, diabetes, and hypertension were independent risk factors of premature CAD, but not IL-6 genotype. CONCLUSIONS: We conclude that the IL-6 -174 G/C polymorphism is not associated with the risk of premature CAD, and does not contribute to cardiovascular risk stratification.

Association of platelet-activating factor acetylhydrolase gene polymorphism with premature coronary artery disease in Turkish patients.

OBJECTIVE: Platelet-activating factor (PAF) is a phospholipid with multiple actions that is involved in inflammatory diseases as well as in atherogenesis. It is inactivated by a plasma enzyme, PAF-acetylhydrolase (PAF-AH). Deficiency of this enzyme in plasma is caused by a missense mutation in the gene (G994T). The aim of this study was to investigate association of this mutation with premature coronary artery disease (CAD). METHODS: One hundred and fifteen unrelated Turkish patients with a diagnosis of premature CAD and 128 unrelated healthy subjects were enrolled in this study. Genotyping was performed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). RESULTS: The prevalence of the G994T mutation in the patients was 2.60 % (heterozygote), and 0 % in the controls. There was no significant difference in allele frequency and genotype distribution among the study groups. CONCLUSION: The G9943T mutation in the plasma PAF acetylhydrolase gene is not associated with premature CAD in Turkish subjects.

The role of ATP sensitive K+ channels and of nitric oxide synthase on myocardial ischemia/reperfusion-induced apoptosis.

During ischemia, ATP-sensitive K+ channels (KATP channels) open, and this triggers necrotic processes and apoptosis. In this study, we investigated whether selective sarcoplasmic and mitochondrial KATP channel blockers affected myocardial apoptosis and nitric oxide synthase (NOS) activity in a rat model of myocardial ischemia/reperfusion in vitro. Isolated rat hearts were subjected to 30 min of coronary artery occlusion followed by 30 min of reperfusion. A selective sarcKATP channel blocker, HMR1098 and a selective mitoKATP channel blocker, 5-hydroxydecanoate, were added to the perfusion fluid 10 min before occlusion. Myocardial apoptosis was detected immunohistochemically using the TUNEL method. Myocardial inducible NOS (iNOS) and endothelial NOS (eNOS) were determined immunohistochemically. In control hearts, apoptosis induction was associated with a greater immunoreactivity of iNOS than eNOS. Treatment with HMR1098, at a concentration of 3 micromol/l, significantly reduced the TUNEL-positive cardiomyocytes and this was associated with decreased iNOS and increased eNOS immunoreactivity. When this drug was administered at a higher concentration, at 30 micromol/l, a more marked reduction in apoptosis was observed but, in contrast to the effects observed at the lower drug concentration, eNOS immunoreactivity was almost completely abolished while iNOS was strong. Moreover, ischemia-induced cardiac dysfunction (e.g. contractile force and recovery of coronary flow) was increased by the higher concentration of HMR 1098. In hearts treated with 5-hydroxydecanoate, myocyte apoptosis was slightly reduced, and this was associated with an almost equal increase in both iNOS and eNOS immunoreactivity. These findings suggest that iNOS appears to be more important than eNOS in the reduction of apoptosis. However, the further inhibition of apoptosis by the higher concentration of HMR 1098 was associated with poorer cardiac function.

Renin-angiotensin system gene polymorphisms and premature coronary heart disease.

INTRODUCTION: Experimental and clinical studies demonstrated that the renin-angiotensin system (RAS) affects the pathogenesis of atherosclerosis and prognosis of coronary heart disease (CHD). The aim of this study was to investigate the genotype distribution and the allele frequencies of three RAS genes polymorphisms and their effects on premature CHD in a Turkish population. MATERIALS AND METHODS: One-hundred and fifteen Turkish patients with premature CHD and 128 controls were included into the study. Angiotensin-converting enzyme (ACE), angiotensin II type 1 (AT1) receptor and angiotensinogen (AGT) gene polymorphisms were analysed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). RESULTS: The patients group showed an increased frequency of the ACE D allele compared with controls (65% vs. 35%, p = 0.0001). There was a significant association between the DD genotype and premature CHD (ACE DD vs. ID and II; odds ratio [OR] = 2.82 [CI 95% 1.33 2.91, p = 0.002]). Also, we observed increased premature CHD risk associated with higher frequencies of the AGT MM genotype in patients when compared with controls (AGT MM vs. TT and MT, OR = 1.92 [CI 95% 1.11-3.33, p = 0.018]). We found a significant association between AT1-receptor AA genotype and decreased risk of premature CHD (AT1R AA vs. AC and CC, OR = 0.57[CI 95% 0.34-0.95, p = 0.03]). CONCLUSIONS: We demonstrated that increased premature CHD risk is associated with higher frequencies of the ACE DD and AGT MM genotypes. These findings indicate a synergistic contribution of ACE DD and AGT MM polymorphisms to the development of premature CHD. Also, our results suggest that family history, smoking, diabetes, hypertension, obesity and ACE DD genotype were independent risk factors for premature CHD.

The G894T polymorphism on endothelial nitric oxide synthase gene is associated with premature coronary artery disease in a Turkish population.

INTRODUCTION: The aim of the present study was to investigate the association between premature coronary artery disease and Glu298Asp polymorphism of the endothelial nitric oxide synthase gene. MATERIALS AND METHODS: The eNOS gene polymorphism was analysed in 115 (mean age, 48.1+/-7.9 years) Turkish patients with a diagnosis of premature coronary artery disease and 83 (mean age, 44.6+/-1.4 years) control subjects. The Glu298Asp polymorphism of the endothelial nitric oxide synthase gene was determined by polymerase chain reaction and restriction fragment length polymorphism. RESULTS: The patients group showed an increase in the frequency of the T allele compared to controls (0.456 versus 0.169, p=0.0001). There was a significant association between the TT genotype and premature coronary artery disease [eNOS TT vs. TG and GG; OR=17.000 (CI 95% 3.952-73.125, p=0.0001)]. The eNOS T/G genotypes were not associated with the number of affected vessels (p>0.05). In addition, the family history of premature coronary artery disease, smoking, diabetes, obesity, dyslipidemia and eNOS TT genotype were independent risk factors of coronary artery disease. The patients with eNOS TT genotype had 15 fold risk of coronary artery disease compared with the control group [OR=15.356(CI 95% 3.262-77.289, p=0.001)]. CONCLUSIONS: These results suggest that premature coronary artery disease is associated with the Glu298Asp polymorphism of the endothelial nitric oxide synthase gene in our population.

Association between the ACE I/D gene polymorphism and physical performance in a homogeneous non-elite cohort.

BACKGROUND: I/D polymorphism of the ACE gene may be associated with better endurance performance and a stronger response to exercise training. The aim of this study was to investigate the association between ACE gene polymorphism and athletic performance in a homogeneous cohort. METHODS: Eighty-eight male non-elite Caucasian Turkish athletes with similar training backgrounds for at least for 6 months were studied for ACE gene polymorphisms by PCR analysis. Performance on the 60-meter sprint and middle-distance running tests were evaluated. RESULTS: The distributions of the ACE I/D genotypes were 20.5%, 40.9%, and 38.6% for II, ID, and DD polymorphisms in the whole group (N = 88), respectively. The ACE DD genotype frequency was significantly higher in the superior group (56.7%) than in the poor (37.9%) and mediocre (20.7%) group in middle-distance running performance (chi2 = 11.778; p = 0.019). CONCLUSION: The ACE DD genotype may be related to better short-duration aerobic endurance performance. Larger homogeneous cohorts may help clarify the association between ACE I/D polymorphism and physical performance.

Association between the eNOS (Glu298Asp) and the RAS genes polymorphisms and premature coronary artery disease in a Turkish population.

BACKGROUND: The renin-angiotensin system (RAS) and endothelial nitric oxide (NO) affect the pathogenesis of atherosclerosis and prognosis of coronary artery disease (CAD). Previous epidemiologic data suggested that genetic factors are more likely to affect young rather than old people. Our objective was to investigate the association between the polymorphisms of eNOS (Glu298Asp) and the RAS genes and premature CAD in a Turkish population. METHODS: A total of 115 Turkish patients with premature CAD and 83 controls were included in the study. ACE I/D, AT1R A/C, AGT T/M and eNOS Glu298Asp gene polymorphisms were analysed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). RESULTS: It was found that increased premature CAD risk is associated with higher frequencies of the ACE DD [OR: 2.600 (CI 95% 1.395-4.847, p=0.002)], AGT MM [OR=2.407 (CI 95% 1.267-4.573, p=0.007)] and eNOS 894TT [OR=17.000 (CI 95% 3.952-73.125, p<0.001)] genotypes. Carriers of ACE DD+eNOS 894TT (p=0.002), AGT MM+eNOS 894TT (p=0.001), AT1R AA+eNOS 894TT and AT1R non-AA+eNOS 894TT (p=0.002) genotypes were significantly associated with the risk of premature CAD. CONCLUSIONS: This study indicates a synergistic contribution of RAS genes (ACE I/D, AGT T/M, AT1R T/C) and eNOS Glu298Asp polymorphisms to the development of the premature CAD.

[Evaluation of diastolic function by transmitral color M-mode flow propagation velocity in hypertensive patients]. / Hipertansif olgularda transmitral renkli M-mod akim yayilma hizi ile diyastolik fonksiyonlarin degerlendirilmesi.

OBJECTIVE: Diastolic dysfunction is considered as the most important cause of heart failure and morbidity in hypertensives. This study was designed to evaluate the relationship between the transmitral diastolic color M-mode flow propagation velocity (FPV) and left ventricular relaxation by using Doppler echocardiography. METHODS: In the present study, thirty-nine patients (21 male, 58.3%, age mean 52.7+/-5.9 years) with hypertension stage-I and over, were included. Transmitral diastolic E and A velocities, E-deceleration time (DT) and isovolumic relaxation time (IVRT) were measured by pulse Doppler method. We performed color M-mode technique for measurement of FPV of transmitral diastolic flow in the apical four-chamber view. We measured slope of aliasing velocity (blue aliasing) determined by color M-mode images. RESULTS: Flow propagation velocity values were not statistically related with age and gender, whereas differentiation of age groups were estimated as poor parabolic relationship, specially in patients over fifty years, FPV is estimated to be decreasing. Color M-mode FPV is correlated with DT, (r=-0.715, p<0.01), IVRT (r=-0.736, p<0.01) and interventricular septum thickness (r=-0.498, p<0.01), but not correlated with E/A ratio. CONCLUSION: Color M-mode FPV is correlated with DT and IVRT, which are important parameters for evaluation of diastolic function in hypertensive patients. This parameter is related with left ventricular relaxation and should be considered as a routine echocardiographic evaluation, because it is not affected by minimal changes in left ventricular filling pressure.

Elevated levels of matrix metalloprotein-3 in patients with coronary aneurysm: A case control study.

BACKGROUND: Matrix metalloproteinases (MMPs) have been implicated in the pathogenesis of arterial aneurysms through increased proteolysis of extracellular matrix proteins. Increased proteolysis due to elevated matrix degrading enzyme activity in the arterial wall may act as a susceptibility factor for the development of coronary aneurysms. The aim of this study was to investigate the association between MMPs and presence of coronary aneurysms. METHODS: Thirty patients with aneurysmal coronary artery disease and stable angina were enrolled into study (Group 1). Fourteen coronary artery disease patients with stable angina were selected as control group (Group 2). MMP-1, MMP-3 and C-reactive protein (CRP) were measured in peripheral venous blood and matched between the groups. RESULTS: Serum MMP-3 level was higher in patients with aneurismal coronary artery disease compared to the control group (20.23 +/- 14.68 vs 11.45 +/- 6.55 ng/ml, p = 0.039). Serum MMP-1 (13.63 +/- 7.73 vs 12.15 +/- 6.27 ng/ml, p = 0.52) and CRP levels (4.78 +/- 1.47 vs 4.05 +/- 1.53 mg/l, p = 0.13) were not significantly different between the groups. CONCLUSION: MMPs can cause arterial wall destruction. MMP-3 may play role in the pathogenesis of coronary aneurysm development through increased proteolysis of extracellular matrix proteins.

Decreased plasminogen activator inhibitor-1 levels in coronary artery aneurysmatic patients.

BACKGROUND: Matrix metalloproteinases (MMPs) have been implicated in the pathogenesis of arterial aneurysms through increased proteolysis of extracellular matrix proteins. Increased proteolysis due to elevated matrix degrading enzyme activity in the arterial wall may act as a susceptibility factor for the development of coronary aneurysms. Plasmin strongly stimulates pro-MMP enzyme conversion to the active form. Plasmin hyperactivity due to decreased plasminogen activator inhibitor-1 (PAI-1) may cause MMP over activity and coronary aneurysms. The aim of this study was to investigate the association between PAI-1 and presence of coronary aneurysms. METHODS: Twenty-three patients with aneurysmal coronary artery disease and stable angina were enrolled into study (Group 1). Twenty-two patients without coronary aneurysm were selected as a control group (Group 2). PAI-1 was measured in peripheral venous blood. RESULTS: The plasma PAI-1 level was lower in the coronary artery aneurysmatic patients compared to the control group (8.41 +/- 4.28 vs. 13.32 +/- 10.05 ng/ml, p = 0.037). Serum C-reactive protein (CRP) values were not significantly different between groups (3.83 +/- 1.08 vs. 4.01 +/- 1.35 mg/l, p >0.05). CONCLUSION: Increased matrix degrading enzyme activity can cause arterial wall destruction through increased proteolysis of extracellular matrix proteins. Unregulated plasmin hyperactivity due to decreased inhibition by PAI-1 may play an important role in coronary aneurysm formation.

[Serum level of insulin-like growth factor-1 and insulin-like growth factor binding protein-3 in acute coronary syndromes and relationship with prognosis]. / Akut Koroner Sendromlarda Insülin Benzeri Büyüme Faktörü-I ve Insülin Benzeri Büyüme Faktörü Baglayici Protein-3 Düzeyleri ve Prognozla Iliskisi.

OBJECTIVE: The aim of the present study was to examine the levels of insulin-like growth factor (IGF-I) and binding protein-3 (IGFBP-3) in acute coronary syndrome (ACS) and their relationship with prognosis. METHODS: Thirty patients with ACS (22 male, 8 female) were included in our study. Patient's population included 20 patients with ST elevation myocardial infarction (STEMI) and 10 with non-ST-elevation ACS. Death, re-infarction, revascularization and malignant arrhythmia were monitored during 3 months. Study group was compared with 20 healthy subjects (Controls). Blood samples were collected in the first 24 hours and at the end of third month. Serum IGF-I and IGFBP-3 levels were determined by radioimmunoassay method. RESULTS: We found decreased level of IGF-I only in the STEMI group (105+/-84 ng/ml vs. 715+/-150 ng/ml, p<0.0001). There were no significant differences in IGFBP-3 levels between two groups. Serum IGF-I levels were significantly increased after 3rd month in the STEMI group (356+/-72 ng/ml vs. 105+/-84 ng/ml, p=0.025). There was no relationship between IGF-I, IGFBP-3 levels and cardiovascular events occurred during 90 days of follow-up. CONCLUSION: These data allows to suggest that significantly decreased level of IGF-I in STEMI group of ACSs can be used as a marker of myocardial necrosis. There was no relationship between IGF-I level and cardiovascular events occurred in 90 days, so this parameter can not be used as a negative prognostic factor.

[The effects of clarithromycin treatment on cardiac events in acute coronary syndrome patients]. / Akut Koroner Sendromlu Hastalarda Klaritromisin Tedavisinin Kardiyak Olaylar Uzerine Etkisi.

OBJECTIVE: The assessment of short duration early clarithromycin treatment on major cardiac events in acute coronary syndrome patients. METHODS: One hundred and thirteen patients with acute coronary syndrome had been enrolled in the study in a prospective manner. Fifty-seven of 113 patients received peroral clarithromycin 1g/day for 14 days in addition to standard therapy. The remaining 56 patients were considered as control group. The treatment and control groups had similar major cardiac risk factors such as diabetes, hypertension, dyslipidemia and smoking habits. The occurrence of unstable angina pectoris, non-ST elevation myocardial infarction and ST elevation myocardial infarction was comparable in both groups. The use of thrombolytic therapy and glycoprotein IIb/IIIa receptor blockers administration was also similar in both groups. The patients were followed for major cardiac events for 6 months. RESULTS: During the follow-up, no difference was observed between groups in the occurrence of unstable angina pectoris, myocardial infarction, the need for revascularization with percutaneous coronary intervention or cardiac surgery and cardiac death. We observed a reduction of myocardial infarction and cardiac death occurrence and an increase in the necessity of percutaneous interventions in the treatment group even though this difference did not reach statistical significance. CONCLUSION: No benefit of short duration early clarithromycin therapy was observed in the occurrence of major cardiac events in acute coronary syndromes. Studies with longer treatment and follow-up period using different antibiotics are necessary to elucidate the possible effect of antibiotics on major cardiac events in patients with acute coronary syndrome.

[Doppler index of myocardial performance and its relationship with mitral E wave deceleration time in acute Q-wave myocardial infarction]. / Akut Q-Dalgali Miyokard Infarktüsünde Miyokardiyal Performans Indeksi ve Mitral E Dalga Deselerasyon Zamani Arasindaki Iliski.

OBJECTIVE: The objectives of the study were to assess myocardial systolic and diastolic functions by myocardial performance index (MPI) and its relationship with E - wave deceleration time (DT) in early phase of acute Q-wave myocardial infarction (MI). METHODS: We performed nongeometric Doppler-derived echocardiography to assess combined systolic and diastolic functions using myocardial performance index in 50 patients with acute Q-wave MI at early phase of events, (25 pts with anterior MI and 25 pts with inferior MI). The index is defined as the sum of the isovolumic contraction and isovolumic relaxation times divided by ventricular ejection time and was obtained by Doppler measurement from the diastolic mitral inflow and left ventricular outflow velocity-time intervals. RESULTS: As a result, the index was 0.54+/-0.1 in all patients with MI. We also estimated the higher MPI and DT values in anterior than in inferior MI (MPI: 0.61+/-0.07 vs. 0.46+/-0.06, p<0.001; DT: 244+/-64 msec vs. 204+/-31.2 msec, p=0.005, respectively). Myocardial performance index was positively correlated with DT in inferior MI (r=0.42, p<0.035) and negatively correlated with anterior MI; (r=- 0.72, p=0.0001). CONCLUSION: These data suggest that Doppler-derived MPI reflects severity of global left ventricular dysfunction in early phase of acute MI and may be a useful parameter in these patients.

Decreased soluble cell adhesion molecules after tirofiban infusion in patients with unstable angina pectoris.

AIM: The inflammatory response, initiated by neutrophil and monocyte adhesion to endothelial cells, is important in the pathogenesis of acute coronary syndromes. Platelets play an important role in inflammatory process by interacting with monocytes and neutrophils. In this study, we investigated the effect of tirofiban on the levels of cell adhesion molecules (soluble intercellular adhesion molecule-1, sICAM-1, and vascular cell adhesion molecule-1, sVCAM-1) in patients with unstable angina pectoris (AP). METHODS: Thirty-five patients with unstable AP (Group I), ten patients with stable AP (Group II) and ten subjects who had angiographycally normal coronary arteries (Group III) were included the study. Group I was divided into two subgroups for the specific treatment regimens: Group IA (n = 15) received tirofiban and Group IB (n = 20) did not. Blood samples for investigating the cell adhesion molecules were drawn at zero time (baseline; 0 h) in all patients and at 72 h in Group I. RESULTS: The baseline levels of sICAM-1 and sVCAM-1 were higher in Group I than in Groups II and III. They were higher in Group IA than in Group IB. However, the sICAM-1 and sVCAM-1 levels decreased significantly in Group IA after tirofiban infusion. In contrast, these levels remained unchanged or were increased above the baseline value in Group IB at 72 h. CONCLUSION: The levels of cell adhesion molecules in patients with unstable AP decreased significantly after tirofiban infusion. Inhibition of platelet function by specific glycoprotein IIb/IIIa antagonists may decrease platelet-mediated inflammation and the ischemic end-point.

Cardiovascular disease risk factors in post-menopausal women in West Anatolia.

Cardiovascular risk factors are important causes of morbidity and mortality in postmenopausal women. The aim of this cross-sectional study was to evaluate the cardiovascular risk factors in 207 postmenopausal Turkish women over 45 years old in a rural district of West Anatolia, Manisa Muradiye district. A questionnaire on socioeconomic and sociodemographic characteristics was conducted in the women followed by the measurement of blood pressure, fasting blood glucose, cholesterol levels, and waist-hip ratio along with an electrocardiogram (ECG). The European Cardiology Society risk index was used for cardiovascular risk evaluation. The results showed that 86% percent of the women will be carrying more than a 5% probability of developing a cardiovascular risk in the next 10 years. Moreover, the results proved 7% of the women are at high risk for a cardiovascular condition. Hypertension, hypercholesterolemia, and impaired glucose tolerance, were observed in 62%, 35.3%, and 13.5% of the women, respectively. Seven percent had smoked for at least six months. Fourteen cases had complained of exercise angina and pathologic ECG signs were diagnosed in one-third of these 14 cases. The waist-hip ratio measured 0.8 or more in 66.2% of the cases, with a range of 68-147 cm (mean; 95.6 +/- 11.55). The results indicate that the risk of a cardiovascular condition developing is extremely high in postmenopausal West Anatolian women and increases with age. Morever, the prevalance of hypertension increased with age and was very closely related with low socioeconomic levels. These hazardous cardiovascular disease risk factors should be considered as high priority health problems in rural and low socioeconomic areas of developing communities. Intervention to modify the cardiovascular risk factors should be included in routine primary health care programs.

Retinal artery macroaneurysm as initial presentation of hypertension.

A case of uncontrolled hypertension with a vitreoretinal hemorrhage due to a retinal artery macroaneurysm of the right eye and chorio-retinal scars of the left eye as initial symptom of hypertension is presented. End organ damage was undiagnosed until an intraocular hemorrhage appeared in the right eye. The hemorrhage and retinal macroaneursym disappeared spontaneously with proper medical therapy for hypertension.