Objective: Caffeic acid phenethyl ester (CAPE) is a natural product with potent anti-inflammatory, antitumor and antioxidant activities and attenuates inflammation and lipid peroxidation induced by ischemia-reperfusion injury. The purpose of the present study was to investigate the effects of CAPE on isoproterenol (ISO) -induced myocardial infarction. Methods: A randomized controlled experimental design was used in this study. Rats were divided into four groups and treated with saline, CAPE, ISO and ISO+CAPE. Rats were treated with CAPE (10 μmol kg/day i.p.) or saline starting 3 days before injecting ISO (150 mg /kg s.c., 24 hours). Seven days later, rats were sacrificed and the hearts were excised for biochemical analyses and microscopic examination. One-way ANOVA test with post hoc multiple comparisons using LSD method were used for statistical analysis of the data. Results: The administration of ISO alone resulted in higher myeloperoxidase (MPO) activity, lipid peroxidation, superoxide dismutase (SOD) and catalase (CAT) than in the control. The enzyme activities did not change in rat given CAPE alone. CAPE treatment prevented the increase in MPO activity and malondialdehyde, but did not affect the activities SOD and CAT enzymes. Conclusion: In light of these results, we conclude that CAPE prevents MPO-and lipid peroxidation-mediated myocardial injury via inhibition of neutrophil’s MPO activity.

Objective: The observation that Bop null allele mice show underdeveloped right ventricle and excessive development of left ventricle, suggests the possible relationship between human BOP gene and hypertrophic cardiomyopathy (HCMP). In our study, we investigated this possible relationship between BOP gene variations and QT dispersion, a noninvasive arrhythmic risk marker for HCMP. Methods: This cross-sectional study consisted of 50 patients clinically diagnosed with HCMP and 60 healthy subjects. Exonic regions of BOP gene were amplified by polymerase chain reaction and amplified exonic regions were analyzed by Single-Strand Conformation Polymorphisms (SSCP). The samples with different migration patterns were sequenced through an automated sequencing system. Continuous variables were compared by unpaired t-test for independent samples or Mann-Whitney U test. Genotype-disease relationship was tested by Chi-square test. Results: The nucleotide substitutions G275>A and C965>A in exon 2 and 7 were determined only in HCMP group. The G707>C, C710>T, T761>C, T1217>C SNPs in exon 6 and 9 are also found in the control group. Significant differences were found between two groups (p=0.002 and p<0.001). It was found that SNPs in exon 6 constitute a haplotype and that QT dispersion and corrected QT dispersion in the rare homozygote (707C/710T/761C) type carriers of HCMP patients for this haplotype were significantly lower than other genotypes (p=0.032 and p=0.030, respectively). Conclusion: The human BOP gene was analyzed for the first time in HCMP to investigate possible association. The result that homozygosity of 707C/710T/761C haplotype is associated with lower QT dispersion and corrected QT dispersion supports the modifier role of BOP gene in HCMP.

Ob jec ti ve: Levosimendan is a relatively new inotropic agent. Unlike other inotropic agents, Levosimendan does not increase cellular calcium intake, so that, does not cause intracellular calcium overload and related arrhythmias. Atrial fibrillation (AF) was shown to be an independent risk factor for mortality and morbidity in large heart failure (HF) trials. Heart failure induces AF, AF aggravates HF and therefore they generally coexist. We conducted a study to investigate if there is any differential effect of Levosimendan in HF patients with chronic AF and without AF. Methods: This is a prospective study. Consecutive patients, who were hospitalized because of acutely decompensated HF due to systolic dysfunction and decided Levosimendan administration, were enrolled. Patients were classified into two as those with AF (group A) and those with sinus rhythm (control group, group S). All patients had echocardiography before and after administration. Echocardiographic data were evaluated by ANOVA repeated measurements test. Results: Baseline left ventricle ejection fraction (LVEF) was poorer in group with AF (mean LVEF for group A: 20.9%, for group S: 26.4%, p=0.04). Baseline diastolic parameters were equally impaired. After infusion, diastolic parameters like velocity of propagation (Vp) and isovolumic relaxation time (IVRT) improved almost to same extent in both groups but deceleration time (DT) did not. IVRT values decreased (p=0.012) both in group S (from 108.6±23.2 msec to 100.4±28.4 msec) and group A (from 117.3±25.1 msec to 92.0±20.9 msec) without a significant difference between groups (p=0.180 for interaction). Another valuable diastolic parameter, Vp was also similarly improved (p<0.01) in both groups to similar extent (for group A, from 35.4±8.8 cm/sec to 41.1±7.7 cm/sec, for group S, from 33.7±7.5 cm/sec to 37.8±7.6 cm/sec; p=0.498 for interaction). Conclusion: We have shown that in patients with chronic HF and AF, levosimendan improves left ventricular systolic and diastolic functions as good as those with HF and sinus rhythm. We suggest that a positive electrophysiological effect of levosimendan on failing myocardial tissue seems to fill the absence of atrial booster in patients with AF who are on beta-blocker therapy.

Objective: Renin-angiotensin system may be activated during atrial fibrillation (AF). Our aim was to evaluate plasma renin activity (PRA) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels in patients with different AF types who had normal left ventricular (LV) systolic function. Methods: This cross-sectional study included 97 patients with recent (≤7 days), persistent (7 days to 12 months) and permanent AF (>12 months), and age- and sex-matched 30 controls with sinus rhythm. Plasma levels of PRA and NT-pro-BNP were measured and presented as median (25th-75th percentiles). Echocardiographic examination was performed in all population. Variance and logistic regression analyses were also used for multiple comparisons and independent predictors, respectively. Results: Median NT-proBNP levels were higher in overall patients with AF than in controls [114 (63-165) vs 50 (38-58) pg/ml, p<0.001), but PRA level was comparable in both groups. Similarly, NT-proBNP levels were also higher in all subtypes of AF compared with controls (p<0.05). In addition, there was a significant difference in NT-proBNP level among recent, persistent and permanent AF subtypes (p=0.001). This difference mainly derived from the recent AF subtypes. Whereas PRA level was similar in all AF subtypes and controls. Age was an independent predictor of PRA level ≥1.9 ng/ml/hour (OR=1.1, 95% CI 1.01-1.23, p=0.03). With NT-proBNP level ≥52 pg/ml, independent predictors were age (OR=1.1, 95% CI 1.01-1.19, p=0.02), presence of persistent and/or permanent AF (OR=6.8, 95% CI 1.03-45.7, p=0.04) and left atrial dimension (OR=1.2, 95% CI 1.03-1.36, p=0.02). Conclusion: Plasma NT-proBNP levels can be associated with AF and its subtypes in patients with normal LV systolic function, whereas there was no association between PRA levels and AF.

Objective: The most important sequel of acute rheumatic fever is mitral stenosis in long-term. The aim of the study is to determine left ventricular (LV) functions by tissue Doppler imaging (TDI) and strain/strain rate echocardiography (SE/SRE) in mitral stenosis patients who had no clinical signs of heart failure. Methods: Our study was designed as cross-sectional study. The study population consisted of 32 patients with isolated mitral stenosis and mitral valve area < 2.0 cm2 (Group 1) and 25 healthy control subjects (Group 2). In addition to standard echocardiographic methods, TDI and SE/SRE were performed to assess LV functions in all participants. Student’s t-test was used to compare continuous variables. Fisher- exact test was used to compare categorical variables. Results: Systolic myocardial velocity (Sm) were significantly lower in Group 1 than in Group 2 (6.0±1.4 cm/sec vs 7.9±1.8 cm/sec, p<0.001) also, early diastolic myocardial velocity (Em) were significantly lower in Group 1 than in Group 2 (4.4±1.5 cm/sec vs 10.8±2.1 cm/sec, p<0.001). But there was no significant difference in late diastolic myocardial velocity (Am) between two groups. Peak systolic strain and strain rate of septal wall in Group 1 were significantly lower than Group 2 (p<0.001 for both). Besides, peak systolic strain and strain rate of lateral wall in Group 1 were significantly lower than in Group 2 (p<0.001 for both). Conclusion: Although, global ejection fraction were normal and there were no symptoms of heart failure clinically in the patients with mitral stenosis, LV dysfunction demonstrated that using by echocardiography. TDI and strain/strain rate imaging to be new echocardiographic methods may be used reliably for detection LV function in early stage of mitral stenosis.

Objective: To evaluate longitudinal function of ischemic and nonischemic myocardial tissue detected by Tc-99m MIBI single photon emission computed tomography (SPECT) prior to coronary revascularization in patients with stable angina pectoris. Methods: We studied 24 consecutive patients (mean age 62±9 years; 5 women) with stable angina pectoris. All patients underwent myocardial perfusion SPECT. Tissue Doppler imaging (TDI) was performed to detect myocardial systolic velocities of anterior, inferior, septum and lateral walls at rest and peak dobutamine stress. Results: A total of 96 segments were visualized with SPECT study. Maximum mean septal, lateral, anterior and inferior TDI systolic velocities were similar in ischemic and nonischemic segments (6.73±1.04 cm/sec, 6.93±1.34 cm/sec, respectively) at rest. At peak stress, maximum mean TDI systolic velocities were lower in the 37 ischemic segments (11.00±2.03 cm/sec) than 59 nonischemic segments (13.76±1.97cm/sec, p < 0.001). Because we detected ischemia in whole group using both diagnostic tests, coronary angiography was decided. Critical coronary artery stenosis related to ischemic segments was detected and coronary revascularization decided. Conclusion: TDI with dobutamine stress can be used in patients with stable angina pectoris. In this study, we observed that quantitative data by TDI associated with SPECT showed an agreement for coronary revascularization.

Objective: The purpose of this study was to compare the intravenous bolus dose of tirofiban with intracoronary bolus dose in primary percutaneous coronary intervention (PCI) with regard to in hospital and six months clinical outcomes and peak cardiac enzyme levels. Methods: We retrospectively examined 84 ST elevation myocardial infarction (STEMI) patients who underwent primary PCI from March 2006 to February 2007. All patients received the systemic bolus dose of tirofiban 10 mcg/kg either via intracoronary (IC) or intravenous (IV) route, followed by a 36 hours of IV infusion at 0.15 mcg/kg/min. Thirty six patients in IC group were compared with 48 patients in IV group in terms of peak cardiac enzyme levels, in-hospital and six months major adverse cardiac events (MACE) rates (death, myocardial infarction and repeat revascularization). Fisher’s exact test, Yates Chi-square, unpaired Student’s t-test and Mann-Whitney U test were used for statistical analysis. Results: There was no difference in cardiovascular risk profile or cardiac history between two groups. At six months the incidence of MACE was 6.25% in IV group and 11.1% in IC group (p=0.45). Peak cardiac phosphokinase (CPK) levels between IV and IC groups were also statistically non significant (2657±2181 U/L in IV group and 2529±1929 U/L in IC group) (p=0.92). Conclusion: Intracoronary bolus application of tirofiban was not associated with reduction in MACE rates compared to intravenous administration in patients with STEMI who underwent primary PCI. Future prospective trials with higher bolus doses of IC tirofiban should addressed to clarify this issue.

Objective: To investigate possible relationship between the D-dimer and ischemia-modified albumin (IMA) levels and radiological imaging-based severity scores in pulmonary embolism (PE) based on two different radiological characteristics; the pulmonary arterial obstruction index (PAOI) and the right ventricle/left ventricle (RV/LV) ratio. Methods: In this prospective cohort study, forty-seven patients presenting to the emergency department and definitively diagnosed with PE using spiral computerized tomography (CT) were initially enrolled in the study. Levels of IMA and D-dimer were assessed colorimetrical and immuno-turbidimetric methods, respectively. The PAOI and RV/LV ratios were calculated from CT images. The levels of biochemical parameters between the groups were compared with use of Mann-Whitney U and Kruskal-Wallis tests and relationship between the radiological scores were assessed using the Spearman correlation test. Results: Analysis of the calculated PAOI and RV/LV ratio revealed a significant correlation between them (r=0.36, p=0.023). D-dimer levels differed considerably among the mild (<40%), moderate (40%-60%) and severe (60%) groups constituted on the basis of PAOI (p=0.039). This difference stemmed from those in D-dimer levels in the mild group, PAOI <40 % and the severe group, PAOI 60% (p=0.02; Z= -2.328). In addition, D-dimer levels and PAOI revealed a positive correlation, but no similar correlation was determined between D-dimer levels and RV/LV. There were no significant correlations between IMA and D-dimer levels, PAOI and RV/LV ratios. Conclusion: In the biochemical determination of severity of PE based on radiological characteristics, D-dimer may be a more relevant marker than IMA, which has been proposed as a new marker.

Objective: This study aimed to compare the results of angiocardiography and cardiovascular magnetic resonance imaging in the assessment of pulmonary regurgitation following repair of tetralogy of Fallot. Methods: We prospectively studied 37 patients with repaired tetralogy of Fallot. After routine examination cardiovascular magnetic resonance imaging (CMR) and cardiac catheterization and angiography were performed. Pulmonary regurgitation (PR) was classified according to the following criteria, using a left lateral angiogram of the main pulmonary artery; insufficiency jet is limited to right ventricular outflow tract (mild); jet reaches the body of right ventricle (moderate); jet fills the apex of the right ventricle (severe). Results: Pulmonary regurgitation determined by angiocardiography and CMR was severe in 51.4% and 32.4%, moderate in 27% and 40.5%, and none or mild in 21.6% and 27% of patients respectively. The ability of semi-quantitative estimation of PR determined by cardiac catheterization to distinguish between mild, moderate and severe pulmonary regurgitation was shown to have significant correlation with pulmonary regurgitant fraction obtained by CMR. Conclusions: Angiography obtained during invasive study can be used for the diagnosis and follow-up of pulmonary regurgitation confidently in patients with repaired tetralogy of Fallot and residual pulmonary regurgitation.

Objective: We aimed to identify characteristics differentiating patients undergoing mitral valve replacement versus valve repair for mitral regurgitation (MR) and to investigate retrospectively mid-term clinical and functional outcomes. Methods: From January, 2004 to January, 2009 146 patients underwent mitral valve surgery (62 male / 84 female; age: 55.9±13.6 [18-80] years) by one surgical team. Mitral valve replacement was performed in 101 patients (69.2 %) and valve repair was performed in 45 patients (30.8%). Mean follow-up time was 586±413 days. Life tables were constructed for the analysis of 5-year complication free survival and comparisons were performed between the groups using Log-rank test within 95%CI. Results: The choice of surgical technique depended on the etiology of MR. Degenerative (p<0.001) and ischemic (p=0.014) MR were more common in patients undergoing repair whereas patients with complex rheumatic mitral valve disease (p<0.001) with subvalvular involvement commonly underwent replacement. Overall 30-day mortality was 3.2% (replacement, 3.96%vs repair, 2.22%, p=0.59). Although there was no significant difference between the groups regarding baseline left ventricular ejection fraction (EF) (ischemic p=0.61; non-ischemic p=0.34), improvement was more pronounced in the repair group for both etiologies (ischemic MR, p=0.001; non- ischemic MR p=0.002). Survival at 5-years was 91.7±4.7% after repair and 83.5±9.2% after replacement, respectively (p=0.83). Freedom from grade 2 or more mitral regurgitation, reoperation, endocarditis, and thromboembolism were 95±5% vs 97±3% (p=0.71); 95±4% vs 98±2% (p=0.98); 94±4% vs 100% (p=0.16); and 85±8% vs 100% (p=0.095) in replacement and repair groups, respectively. Conclusion: This study demonstrates that mitral valve repair is associated with an acceptable operative mortality, satisfactory mid-term survival and better preservation of left ventricular function. Significant differences in favor of repair are expected in long-term follow-up particularly regarding freedom from thromboembolism and endocarditis.

Health is considered as important due to its impacts on individuals’ lives. Although individual health level is determined partly by the accessibility of the services and their quality, there are many other factors that may influence an individual’s health condition, which are mainly social determinants. Since there are many factors that determine health conditions of the individuals, it would be wrong to hold someone totally responsible for her health condition on the basis of her life-style; such as prudency. Indeed, before deciding about whether the patient was prudent or not; first, we have to look at those determinants of health, and investigate whether there is an effective intervention to avoid those determinants. Furthermore, life-styles of the individuals, which are thought to be the personal choices, are just one of the relatively less effective factors that may influence a person’s health and also the autonomy of those choices is controversial. In our paper, we will endeavor to develop an argument showing that since health is one of our primary goods that needs to be protected as one of our basic human rights, and since the health status of individuals are not determined only by their personal choices, we claim that it would be unfair to consider accessing healthcare as something removable or limitable based on conditions other than medical criteria.