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Correction to: Wien Klin Wochenschr 2015 https://doi.org/10.1007/s00508-015-0854-z The original version of this article unfortunately contained a mistake. The first names of Dr. Ismail Dogu Kilic were interchanged.

Background. Adiponectin is an adipocytes-derived hormone which has been shown to possess insulin-sensitizing, antiatherogenic, and anti-inflammatory properties. In acromegaly, the data on adiponectin is contradictory. The relationship between adiponectin levels and cardiac parameters has not been studied. Objectives. The aim of this study was to find out how adiponectin levels were affected in acromegalic patients and the relationship between adiponectin levels and cardiac parameters. Material and Methods. We included 30 subjects (15 male, 15 female), diagnosed with acromegaly and 30 healthy (10 male, 20 female) subjects. Serum glucose, insulin, GH, IGF-1 and adiponectin levels were obtained and the insulin resistance of the subjects was calculated. Echocardiographic studies of the subjects were performed. Results. We determined that adiponectin levels were significantly higher in the acromegalic group than the control group. In the acromegalic group, there was no statistically significant relation between serum adiponectin and growth hormone (GH), or insulin-like growth factor-1 (IGF-1) levels (p = 0.3, p = 0.1). We demonstrated that cardiac function and structure are affected by acromegaly. IVST, PWT, LVMI, E/A ratio, DT, ET, IVRT, VPR, and LVESV values were increased and the results were statistically significant. In the acromegalic group, adiponectin levels were positively related with left ventricle mass index (LVMI) but this correlation was found to be statistically weak (p = 0.03). In our study, there was a positive correlation between VAI and LVM. We also could not find any correlation between VAI and adiponectin levels. Conclusions. Although insulin resistance and high insulin levels occur in active acromegaly patients, adiponectin levels were higher in our study as a consequence of GH lowering therapies. Our study showed that adiponectin levels may be an indicator of the cardiac involvement acromegaly. However, the usage of serum adiponectin levels in acromegalic patients as an indicator of cardiac involvement should be supported with other, wide, multi-centered studies. © Copyright by Wroclaw Medical University.

Purpose To find out how resistin and leptin levels were affected in patients with acromegaly and whether there is a relation between resistin levels and cardiac parameters. We also aimed to investigate whether resistin and leptin may be a link between insulin resistance and cardiac functions as well as these affected cardiac functions in the patients with acromegaly. Methods We included 30 subjects (15 men and 15 women) who had a diagnosis of acromegaly and 30 healthy (10 men and 20 women) subjects. Serum glucose, insulin, growth hormone, insulinlike growth factor 1 (IGF-1), resistin, and leptin levels were obtained, and insulin resistance of subjects were calculated. Echocardiographic studies of the subjects were performed. Results Resistin levels of the patients with acromegaly were found lower than controls. This difference was statistically significant ( P = 0.001). Leptin levels were lower in the patients with acromegaly than in the controls, but this difference was not statistically significant. Resistin and leptin levels were not correlated with growth hormone, IGF-1, and with insulin-like growth factor binding protein 3 levels. Homeostasis model assessment of insulin resistance was positively correlated with resistin levels. ( P = 0.03; r = 0.531) but not correlated with leptin levels. There was a positive correlation between body mass index and leptin levels in the patients with acromegaly ( P = 0.007; r = 0.482). Interventricular septum thickness, posterior wall thickness, left ventricle mass index, peak early mitral inflow velocity–peak late mitral inflow velocity ratio, deceleration time, ejection time, isovolumetric relaxation time, velocity propagation, and left ventricular end-systolic volume values were significantly greater in the patients with acromegaly. Leptin levels in the acromegalic patients were not correlated with any of them. Conclusions We found biventricular hypertrophy and impairment of diastolic and systolic function in the patients with acromegaly. We conclude that changes in resistin and leptin levels are unlikely to account for the insulin resistance of acromegaly. They do not also seem to be contributing factors of cardiovascular changes in patients with acromegaly.

Introduction: Cardiovascular system is rich in thyroid hormone receptors and is one of the major sites of action for thyroid hormones. However, the effect of subclinical hypothyroidism (SCH) on atherosclerosis has not been cleared yet. Materials and Methods: SCH is defined as high thyroid-stimulating hormone (TSH) levels in the presence of normal serum T4 and T3 levels. A total of 32 patients with SCH and 29 controls were included in the study. Carotid intima-media thickness, flow-mediated dilatation, and aortic distensibility were compared between the groups. Results: FMD was lower in patients with SCH than in controls. GTN-induced vasodilatation was similar in the patients with SCH and controls. There was no statistically significant difference between the patients with SCH and controls with respect to CIMT and aortic distensibility. Conclusion: SCH is associated with endothelial dysfunction as established by FMD. Inconsistent results of CIMT and aortic stiffness can be explained by these parameters being measures of structural changes whereas FMD is a dynamic measure that reflects the impact of both acute and chronic influences on endothelial function.

ObjectivesAlthough hypertension has been shown to be one of the most important risk factors for atherosclerosis, data about the presence of subclinical atherosclerosis in normotensive offspring with parental history of hypertension are scarce. Accordingly, the current study was designated to evaluate flow-mediated dilatation and aortic stiffness, which are early signs of atherosclerosis in young subjects with parental history of hypertension.MethodsA total of 102 healthy, non-obese subjects in the age group of 18–22 years were included in this study and divided into two groups. The first group included 70 offspring of hypertensive parents and the second group included 70 offspring of normotensive parents as controls. In all subjects, endothelium-dependent and endothelium-independent vasodilatation of the brachial artery and aortic elastic parameters were investigated using high-resolution Doppler echocardiography.ResultsOffspring of hypertensive parents demonstrated higher values of aortic stiffness (7.1 plus or minus 1.88 and 6.42 plus or minus 1.56, respectively) but lower distensibility (9.47 plus or minus 1.33 and 11.8 plus or minus 3.36 square centimetres per dyne per 106) and flow-mediated dilatation (4.57 plus or minus 1.3 versus 6.34 plus or minus 0.83 percent, p equals 0.0001, respectively) than offspring of hypertensive parents.ConclusionWe observed blunted endothelium-dependent dilatation and aortic stiffness in offspring of hypertensive parents compared with offspring of hypertensive parents. This is evident in the absence of overt hypertension and other diseases, suggesting that parental history of hypertension is a risk for subclinical atherosclerosis and it may contribute to the progression to hypertension and overt atherosclerosis in later life.

Myocardial injury may complicate allergic reactions caused by several medications. We evaluated a case of a myocardial injury with transient ST segment elevation in a 72 year-old man presenting with collapse caused by sulbactam-ampicilllin assumption. The purpose of this report is to present this interesting case and revise the classification of Kounis syndrome. © 2008 Elsevier Ireland Ltd. All rights reserved.

Increase in carotid artery intima-media thickness (IMT) is an early sign of atherosclerosis. Slow coronary flow (SCF) is characterized by delay of opacification of coronary arteries in coronary angiography in the absence of any evident obstructive lesion, but its etiopathogenesis remains unclear. Genes that regulate the renin angiotensin system also play a role in developing cardiovascular system disorders. The presence of deletion (D) allele in angiotensin converting enzyme (ACE) gene polymorphism is associated with coronary artery disease. The aim of this study was to investigate the carotid artery IMT measurement, as an early sign of atherosclerosis, in patients with SCF and without SCF and also to assess the effect of the renin-angiotensin gene system on carotid IMT. Forty-four patients with angiographically proven SCF and 44 cases with normal coronary flow (NCF) pattern with similar risk profile were enrolled in the study. Coronary flow patterns of the cases were determined by thrombolysis in myocardial infarction (TIMI) frame count method. Intima-media thickness was measured by recording ultrasonographic images of both the left and right common carotid artery with a 12-MHz linear array transducer. ACE I/D polymorphism and Angiotensin II tip 1 receptor (AT1R) A/C gene polymorphism were determined by polymerase chain reaction (PCR) amplification. Demographic characteristics and coronary artery disease risk factors of SCF and NCF groups were similar. Mean TIMI frame count and carotid IMT (mm) were significantly higher in the SCF group than controls (45.9 ± 12 vs 23.3 ± 3.7, P = 0.0001; 0.75 ± 0.08 vs 0.69 ± 0.06, P = 0.0001, respectively). Mean TIMI frame count was positively correlated with IMT of carotid artery in correlation analysis (r = 0.45, P = 0.0001). When analyzed in regard to ACE genotype in all subjects, IMT values were statistically different (0.78 ± 0.06 for DD genotype, 0.72 ± 0.05 for ID genotype, and 0.64 ± 0.06 for II genotype, P = 0.0001). This difference remained significant in subgroup analyses for each genotype. No association could be observed between the AT1R A/C1166 polymorphism and IMT of carotid artery measurement (P > 0.05). Lack of association was still observed with analysis carried out when genotype effect was assumed to be inherited as additive (CC versus AA versus AC) or dominant (AA versus AC+CC). Increased IMT in patients with SCF shows that subclinical atherosclerosis may play role in this phenomenon. This increase was most marked in the presence of D allele of ACE genotype, which is associated with vascular hypertrophy. © Springer-Verlag Tokyo 2007.

Background: Reduced heart rate recovery (HRR) in coronary artery disease (CAD) is predictive of increased cardiovascular mortality and is related to reduced parasympathetic tonus. Objective: To investigate HRR and heart rate variability (HRV) measured at steady state condition and the relationship between these two parameters in CAD. Materials and Methods: In our study, we enrolled 33 (28 males, mean age 52.4 ± 9.6 years) patients with CAD who did not have heart failure, atrial fibrillation, pacemaker, and any disease state that could affect the autonomic functions and 38 age-matched healthy subjects (21 males, mean age 48.3 ± 7.8 years). All the patients underwent submaximal treadmill exercise testing (Bruce protocol). HRR was calculated by subtracting the heart rate values at the 1st, 2nd, and 3rd minutes of the recovery phase from the peak heart rate (HRR1, HRR 2, HRR3). Before exercise testing, short-term steady state HRV analyses of all subjects were obtained with the time- and frequency-domain methods and were correlated to HRR. For frequency-domain analysis, low-frequency HRV (LF, 0.004-0.15 Hz), high-frequency HRV (HF, 0.15-0.5 Hz), and LF/HF ratio were measured for 5 minutes in the morning. For time-domain analysis, standard deviation of the normal-to-normal NN intervals (SDNN), square root of the mean squared differences of successive N-N intervals (RMSSD), and proportion derived by dividing the number of interval differences of successive N-N intervals greater than 50 ms by the total number of N-N intervals (pNN50) were obtained. Only HRR3 was used for the correlation analysis. Results: In CAD groups, the HF, an indicator of parasympathetic activation, was significantly reduced, whereas the LF and LF/HF values, which are indicators of sympathetic activity, were increased (P = 0.0001 for each parameter). The time-domain parameters SDNN, RMSSD, and pNN50 were significantly reduced in the patient group (P = 0.0001, P = 0.009, and P = 0.0001, respectively). Similar to the HRV parameters, the HRR1, HRR2, and HRR3 values were significantly reduced in the patient group (P = 0.0001 for each parameter). We observed a significant negative correlation between HRR3 and LF (r =-0.67, P = 0.0001) and between HRR3 and LF/HF (r =-0.62, P < 0.0001), while there was a significant positive correlation between HRR 3 and HF, SDNN, RMSSD, and pNN50 (r = 0.69, P = 0.0001; r = 0.41, P = 0.0001; r = 0.31, P = 0.008; and r = 0.44, P = 0.0001). Conclusions: HRR and HRV are significantly reduced in CAD. The reduction in HRR is parallel to the changes in HRV parameters. HRR, which can be measured easily in the recovery phase of exercise testing, can be used to detect the depression of parasympathetic tonus and to evaluate the basal autonomic balance in this patient group. ©2006, Copyright the Authors.

BACKGROUND: Obstructive sleep apnea (OSA) syndrome has a critical association with cardiovascular mortality and morbidity. Aortic elastic parameters are important markers for left ventricular (LV) function and are deteriorated in cardiovascular disease. METHODS AND RESULTS: Aortic elastic parameters and LV functions and mass were investigated in 40 patients with OSA (apnea - hypopnea index (AHI) >or=5) (mean age 51.3 +/-9 years, 32 males) and 24 controls (AHI

Both left ventricular (LV) hypertrophy and insulin resistance (IR) have often been demonstrated in patients with essential hypertension (EH). Insulin may exert a direct growth promoting effect on cardiomyocytes rather than affecting the LV internal diameter. The purpose of this study was to examine the effect of IR on LV geometry. We enrolled 105 patients (71 females, mean age, 49.2 +/- 13.6 years) with recently diagnosed and untreated hypertension (blood pressure > 140 and/or 90 mmHg, fasting glucose < 110 mg/dL), and grouped them as normal (N) (39 patients, 26 females, mean age, 48.5 +/- 14.7 years) if all M-mode echocardiographic measurements were within normal limits, concentric remodeling (CR) (22 patients, 15 females, mean age, 50.5 +/- 14.8 years) if relative wall thickness was increased but left ventricular mass index (LVMI) was normal, concentric hypertrophy (CH) (13 patients, 9 females, mean age, 50.3 +/- 10.8 years) if both ventricular thicknesses and the LVMI were increased, and eccentric hypertrophy (EH) (31 patients, 21 females, mean age, 48.6 +/- 12.9 years) if ventricular thicknesses were normal, but LVMI was increased. Transthoracic echocardiography was performed in all subjects, and interventricular septal thickness (IVS), posterior wall thickness (PWT), sum of wall thickness (SWT), left ventricular end-diastolic internal diameter (LVED), relative wall thickness (RWT), and LVMI were recorded. Blood samples for routine biochemical examination and fasting insulin levels were obtained and then the homeostasis model assessment (HOMA) index was calculated by the formula: HOMA Index = Fasting Blood Glucose (mg/dL) x Immunoreactive Insulin (microU/mL)/405, for the assessment of IR. There were no significant differences among the groups with respect to age, blood pressure (BP) levels, fasting blood glucose (FBG), LDL-cholesterol (LDL-C), HDL-cholesterol (HDL-C), total cholesterol (TC), or triglyceride (TG) levels. Insulin levels were significantly higher in the CR and CH groups in comparison with the N group (P = 0.004), and the HOMA index was higher in the CH group compared to the N group (P = 0.024). In Pearson's correlation analysis, insulin was found to be directly correlated with IVS (r = 0.29, P = 0.002), SWT (r = 0.25, P = 0.009), and RWT (r = 0.33, P = 0.0001). The HOMA index was also directly correlated with IVS (r = 0.33, P = 0.001), SWT (r = 0.29, P = 0.002), and RWT (r = 0.29, P = 0.003). Cardiac changes in hypertensive patients include increased LVMI and altered LV geometry. The concentric LV geometry seen in hypertensive patients might be mediated, at least in part, by increased insulin levels and the HOMA index.

Background and Objective: Obstructive sleep apnea (OSA) has a critical association with cardiovascular mortality and morbidity. Carotid intima-media thickness (IMT), flow-mediated dilatation (FMD) and aortic stiffness are early signs of atherosclerosis. The presence of subclinical atherosclerosis was assessed in OSA patients using these parameters. Methods: 40 patients with OSA showing an apnea-hypopnea index (AHI) ≧5 (mean age 51.3 ± 9 years, 32 males) and 24 controls (AHI < 5, mean age 51.9 ± 5.2 years, 19 males) were enrolled in the study. In all subjects, polysomnographic examination and recordings were performed during sleep. IMT of the carotid artery, endothelium-dependent/-independent vasodilation of the brachial artery and aortic elastic parameters were investigated using high-resolution Doppler echocardiography. Results: The demographic data of the patients with OSA and controls were not significantly different. Subjects with OSA demonstrated higher values of aortic stiffness (7.1 ± 1.88 vs. 6.42 ± 1.56, respectively) and IMT (0.85 ± 0.13 vs. 0.63 ± 0.11 mm, p = 0.0001, respectively) but lower distensibility (9.47 ± 1.33 vs. 11.8 ± 3.36 cm2/dyn/106) and FMD (4.57 ± 1.3 vs. 6.34 ± 0.83%, p = 0.0001, respectively) than the controls. The respiratory disturbance index correlated positively with aortic stiffness and IMT and negatively with distensibility and FMD. Conclusion: We observed blunted endothelium-dependent dilatation, increased carotid IMT and aortic stiffness in patients with OSA compared with matched control subjects. This is evident in the absence of other diseases, suggesting that OSA is an independent cause of atherosclerosis. These simple and non-invasive methods help to detect subclinical atherosclerosis in OSA.

BACKGROUND QT dispersion (QTd) is a measure of inhomogeneous repolarization of myocardium and is used as an indicator of arrhythmogenicity. QTd is increased in myocardial hypertrophy secondary to systemic hypertension. The relation between left ventricular (LV) enlargement in endurance trained subjects and QTd is unknown. The cloning of the angiotensin-converting enzyme (ACE) gene has made it possible to identify a deletion (D)-insertion (I) polymorphism that appears to affect the level of serum ACE activity. The aim of this study was to assess whether physiologic left ventricular hypertrophy as a result of physical training is associated with an increased QT length or dispersion depending on ACE I/D polymorphism. METHODS 56 endurance athletes and 46 sedentary subjects were included in this study, and they underwent both complete echocardiographic and electrocardiographic examination, the QT interval was measured manually as an average based on a 12-lead ECG. We also analysed ACE I and D allele frequencies in all patients. RESULTS Athletes had a significantly increased LV mass (235.1 +/- 68.5 g vs. 144.9 +/- 44.5 g, p < 0.001) and corrected QTd (QTcd) (55.5 +/- 18.1 ms vs. 42.9 +/- 17.2 ms, p < 0.001) in comparison to control subjects. There was a positive correlation between left ventricular mass index and QTcd in athletes (r = 0.3, p = 0.024). Left ventricular mass and mass index in ACE DD, DI and II genotypes were significantly different (p < 0.001). QTcd was significantly different between ACE DD (63.2 +/- 12.8 ms) and ACE II (44.9 +/- 17.6 ms) genotypes in athletes (p < 0.05). CONCLUSION These data show that myocardial hypertrophy induced by exercise training might be associated with increased QTd as observed in systemic hypertension and might be affected by ACE I/D polymorphism.

Objectives - Angiotensin-converting enzyme (ACE) is a key enzyme in the production of angiotensin II and thus may participate in the modulation of cardiac growth. The cloning of the ACE gene has made it possible to identify a deletion (D)-insertion (I) polymorphism that appears to affect the level of serum ACE activity. The aim of the study is to analyse the ACE gene I/D polymorphisms in healthy young subjects and to evaluate its relationship to left ventricular mass and functions. Methods - 38 women and 40 men (mean age 21.1 +/- 1.7 and 21.4 +/- 1.7 years) were studied. They underwent complete echocardiographic assessment and analysis of ACE insertion (I) and deletion (D) allele frequencies in peripheral blood by polymerase chain reaction. Thickness of interventricular septum (IVS) and posterior wall (LVPW) and left ventricular mass (LVM) and LVM index (LVMI) were measured by M-mode. Left ventricular ejection fraction (LVEF) was calculated by Simpson's method. Results - There was no statistically significant difference among the DD, DI and II genotypes, concerning age, body mass index, heart rate, systolic and diastolic blood pressures. The thickness of IVS (9.5 mm), LVPW (9.0 mm), LVM (204.5 g) and LVMI (105.5 g/m(2)) in DD genotypes were higher than both DI (8.3 mm; 8.1 mm; 168.1 g; 90.9 g/m(2)) and II genotypes (8.2 mm; 7.0 mm; 141.7 g; 77.8 g/m(2)) in men, but not in women. LVEF among the 3 genotypes were not statistically different. Conclusion - Our findings suggest that left ventricular hypertrophy is partially determined by genetic disposition especially in men but not in women. C1 Pamukkale Univ, Fac Med, Dept Cardiol, Denizli, Turkey. Pamukkale Univ, Fac Med, Dept Physiol, Denizli, Turkey.

Heart rate variability (HRV) is a useful tool for the detection of sympathetic-parasympathetic balance of autonomic nervous system in patients at risk of sudden death (SD). SD is more common in patients with epilepsy and the exact mechanisms of SD are unknown. Autonomic nervous system involvement in patients with epilepsy has rarely been studied and has shown conflicting results. Our purpose was to determine if HRV showed any changes in patients with epilepsy in comparison with normal population. A short period analysis of HRV was performed for both the frequency and time domain in 43 epilepsy patients who had generalized tonic-clonic seizures (GTCS) and who were not taking any medications and also in 43 age and sex matched controls. In the time domain analysis, patients displayed higher SDNN (standard deviation of all R-R intervals), SDANN (standard deviation of mean NN intervals in 5 min recordings) and HRV triangular index than did healthy subjects (p < 0.0001). Patients tended to display higher pNN50 (number of R-R intervals differed by >50 ms from adjacent interval divided by the total number of all R-R intervals) and RMSSD (root-mean-square of successive differences) values than did healthy subjects, but the differences were not statistically significant (p > 0.05). In the frequency domain analysis, the spectral measures of HRV showed a reduction of high frequency (HF) values (is a marker of parasympathetic activity) and an increase of low frequency (LF) values (is a measure of sympathetic activity); as a result, the ratio between low and high frequencies (LF/HF) was significantly increased (p < 0.0001, p < 0.0001 and p < 0.001, respectively). Our data suggests an increase in the sympathetic control of the heart rate in epilepsy patients who have GTCS. This increased sympathetic activity could play a key role in the development of ventricular tachyarrhythmias in patients with epilepsy and may be related to the higher incidence of sudden death in this disorder as compared to controls. © 2005 Elsevier B.V. All rights reserved.

Objective: Changes in lipid profiles, Lp(a) lipoprotein, and acute phase reactants are associated with early atherosclerosis in rheumatoid arthritis (RA). The associations of Lp(a) levels with atherosclerotic disorders, diabetes, RA, and renal diseases suggest that Lp(a) might be involved in autoimmune reactions. Methods: Eighty-seven women with RA diagnosed according to American Rheumatism Association criteria (mean age 45.4±9.4 years) were recruited and 50 healthy women (mean age 44±10.7 years) included as a control group. Serum Lp(a), total cholesterol (TC), triglyceride (TG), LDL cholesterol (LDL-C), HDL cholesterol (HDL-C), and C-reactive protein levels were analyzed. Results: In the RA and C groups, serum Lp(a) levels were 39.2±20.6 mg/dl and 14.8±9.7 mg/dl, respectively (P0.05), TG levels were 124.5±50.1 mg/dl and 94.6±24.9 mg/dl (P0.05). While serum CRP levels showed a positive correlation with Lp(a), they correlated negatively with HDL-C levels (r=0.83 and P

WOS: 000220464100002, PubMed ID: 14973346, Late potentials (LP) detected on the signal-averaged electrocardiogram (SAECG) predict arrhythmic events after acute myocardial infarction (AMI). It is also well established that successful thrombolytic therapy reduces the incidence of LP. Our aim was to evaluate the effects of a beta-blocker on LP in patients receiving thrombolytic therapy. We Studied 40 patients presenting with anteroseptal AMI (< 6 hours). All patients received thrombolytic therapy and were evaluated with coronary angiography at predischarge. Eighteen patients received metoprolol (5 mg IV on admission followed by 50 mg BID). SAECG recordings were obtained serially using an ART system (40-250 Hz filter, noise < 0.5 mV) prior to thrombolytic therapy, after 48 hours and after 10 days. LP was defined as positive if the SAECG met at least 2 of the Gomes criteria. Changes observed in SAECG recordings after thrombolytic therapy were correlated with angiographic and clinical data with regard to the usage of BB. The frequencies of LP before and after thrombolytic therapy were compared with the McNemar test. There were no significant differences between the clinical characteristics, risk factors, and angiographic findings (including infarct related artery patency and LV functions) of the groups. Baseline SAECG findings were also similar between the groups. The incidence of LP significantly decreased after TT in the BB group, however, this change was not observed in patients who did not receive BB (P = 0.012, McNemar test). Beta-blockers reduce the incidence of LPs following thrombolytic therapy in patients with anterior AMI. This might be explained by the possible beneficial effect of BB on the arrhythmogenic substrate.

Background: Metabolic syndrome (MS) refers to a group of cardiovascular risk factors associated with endothelial dysfunction and impaired coronary blood flow (CBF). Homocysteine (Hcy) is another risk factor for the development of insulin resistance and endothelial dysfunction. However, the relationship between Hcy levels and CBF in patients with MS has not been investigated specifically. In the present study, we aimed to evaluate the relationship between Hcy levels and CBF in MS patients with normal coronary arteries. Methods: The study population included 36 patients with MS (20 males, 16 females; mean age = 55 ± 9 years) and 36 control subjects (20 males, 16 females; mean age = 51 ± 7 years). All subjects had angiographically proven normal coronary arteries. Plasma Hcy concentrations were evaluated after a fast of 12 h or longer. The CBF rates of all subjects were documented by the thrombolysis in myocardial infarction (TIMI) frame count method. Results: The TIMI frame counts for each major epicardial coronary artery and mean TIMI frame count were found to be significantly higher in the MS group compared with the control group (left anterior descending coronary artery (LAD): 53 ± 26 vs. 39 ± 17; p = 0.01, left circumflex artery (LCx): 32 ± 12 vs. 26 ± 11; p = 0.01, right coronary artery (RCA): 33 ± 14 vs. 26 ± 12; p = 0.02, mean TIMI frame count: 39 ± 16 vs. 20 ± 12; p = 0.01). Plasma Hcy levels in patients with MS were significantly higher compared with controls (MS group = 11.6 ± 4 and control group = 9.6 ± 2.6; p = 0.01). Additionally, plasma Hcy levels were positively correlated with each calculated TIMI frame count value in the MS group (LAD, r: 0.28 and p = 0.006; LCx, r: 0.25 and p = 0.022; RCA, r: 0.26 and p = 0.042; mean TIMI frame count, r: 0.28 and p = 0.004). Conclusion: Plasma Hcy levels and TIMI frame counts were significantly higher in patients with MS. Impaired CBF in MS may be related to elevated levels of Hcy, even if Hcy levels are normal. © 2015, Springer-Verlag Wien.

Neurofibromatosis is an autosomal dominant multi-system genetic disorder. Extra-cardiac vascular manifestations of neurofibromatosis have been previously described in many reports. However, coronary arterial involvements have been rarely described. A 17-year-old girl with neurofibromatosis presented to our institute with subacute myocardial infarction. Coronary angiogram revealed an aneurysm with thrombus in the left anterior descending artery.

Left-ventricular non-compaction (LVNC) represents an arrest in the normal process of myocardial compaction, resulting in multiple, prominent, persistant trabeculations and deep inter-trabecular recesses communicating with the ventricular cavity. LVNC is a rarely encountered cardiomyopathy and few cases have been reported in pregnancy. In this case report we present a patient who referred to our clinic with symptoms of heart failure during pregnancy and whose echocardiographic examination revealed prominent trabeculations in the left ventricle.

Spontaneous coronary dissections (SCAD) can be asymptomatic or can manifest itself as any of the clinical spectrum of the ischemic heart disease. In this report, we present a 65 year old man presented with myocardial infarction in whom coronary angiography a nonocclusive SCAD was noticed in addition to a very late stent thrombosis and make a brief overview of the treatment for SCAD.

An extremely rare case of myxomas originating from the mitral leaflets was diagnosed in a 64-year-old man presented with a history of exertion dyspnea and palpitations. Two masses originating from the anterior and posterior mitral leaflets in the left ventricular (LV) cavity, causing LV outflow obstruction, were detected by echocardiography. The myxomas were successfully removed with the mitral leaflets via left atriotomy and mitral valve replacement. No embolic events occurred in the preoperative or postoperative period. In this article, we wanted to present. (Circ J 2008; 72: 1709 - 1711)

Background: Glycosylated hemoglobin (HbA1c) level on admission is a prognostic factor for mortality in patients with and without diabetes after myocardial infarction. In the present study, the authors examined the relationship between admission HbA1c level and myocardial perfusion abnormalities in patients with acute myocardial infarction. Methods: One hundred consecutive patients with acute myocardial infarction who were treated with thrombolytic therapy were included in the present prospective study. Blood glucose and HbA1c levels of all patients were measured within 3 h of admission. Patients were divided into three groups according to HbA1c level: 4.5% to 6.4% (n=25), 6.5% to 8.5% (n=28) and higher than 8.5% (n=47). All patients then underwent exercise thallium-201 imaging and coronary angiography to determine ischemic scores and the number of diseased coronary arteries four weeks after admission. Results: Seven patients died within the four-week follow-up period. There was a significant relationship between admission HbA1c level and mortality (P=0.009). Furthermore, there was a significant relationship between HbA1c level and total ischemic scores in patients with acute myocardial infarction (r=0.482; P=0.001). Ischemic scores increased as HbA1c levels increased in patients with acute myocardial infarction. Conclusions: The results demonstrated that admission plasma glucose and HbA1c levels are prognostic factors associated with mortality after acute myocardial infarction. ©2008 Pulsus Group Inc. All rights reserved.

Endothelial dysfunction is an early marker of atherosclerosis. Angiotensin II and nitric oxide have important roles in maintaining the vascular tone. The existence of the angiotensin converting enzyme (ACE) gene polymorphisms has been known, and deletion (D) of the allele has been associated with coronary artery disease. As ACE genotype affects endothelial functions in the patients with risk factors for coronary artery disease, it may also be a determinant of atherosclerosis. In this study, the relationship between endothelial function and ACE gene polymorphisms was investigated in healthy young subjects.Forty-six healthy young subjects were included in this cross-sectional, randomized study. Participants were further divided into three groups according with ACE genotypes: DD genotype--24 subjects, DI genotype--13 subjects and II genotype--9 subjects. All patients underwent brachial artery ultrasonographic examination. We analyzed ACE insertion (I) and D allele frequencies in all subjects. Kruskal-Wallis test was used to compare continuous variables, and the Chi-square test was used to compare proportions among groups.Demographic features were similar except gender between the groups according to the ACE genotypes. Total cholesterol levels were lower in the DD genotype comparing with the others (p0.05). High-density lipoprotein cholesterol levels, baseline brachial artery diameter, baseline blood flow and the increase in the blood flow during the reactive hyperemia were also similar. The changes in flow-mediated dilatation (endothelium dependent) were 4.9+/-1.3% in DD genotype, 5.5+/-1.7% in DI genotype and 5.5+/-1.9% in II genotype groups. Flow mediated dilatation was lower in DD genotype group as compared with ID and II genotype groups, however, this result did not reach statistical significance (p0.05). Endothelium independent dilatations were similar among different ACE genotypes.Our data showed that ACE genotype has no effect on endothelial functions in patients without risk factors for coronary artery disease.

Introduction: We investigated the probable role of free-radical damage in the pathogenesis of slow coronary flow (SCF) by using oxidative stress parameters. Methods: Sixty-four patients with angiographically proven SCF and 63 patients with normal coronary flow (NCF) pattern with similar risk profiles were enrolled in this study. We measured erythrocyte superoxide dismutase (SOD), reduced glutathione (GSH), serum malondialdehyde (MDA), catalase and myeloperoxidase (MPO) levels in all subjects. Results: There were statistically significant differences in the levels of erythrocyte SOD, GSH and serum MDA between the 2 groups. Serum MDA (P = 0.003) and erythrocyte SOD levels (P = 0.0001) were increased in the SCF group. The level of erythrocyte GSH (P = 0.010) was lower in patients with SCF. There were no differences between the groups' serum catalase (P = 0.682) and MPO levels (P = 0.070). Conclusion: Our data showed that in patients with SCF, serum MDA and erythrocyte SOD levels were increased while erythrocyte GSH levels were decreased significantly, compared with NCF patients. These results indicate that free-radical damage may play a role in the pathogenesis of SCF. © Springer Healthcare Communications 2008.

Background: The slow coronary flow (SCF) phenomenon is a coronary microvascular disorder characterized by the delayed passage of contrast in the absence of obstructive epicardial coronary disease. Recent studies showed the possible role of endothelial dysfunction, diffuse atherosclerosis and inflammation in the pathogenesis of this phenomenon. We aimed to investigate the effect of statin on myocardial perfusion in patients with SCF. Methods and Results: The study population consisted of 97 patients with SCF. Coronary flow patterns of the cases are determined by thrombolysis in myocardial infarction (TIMI) frame count method. Single-photon emission computed tomographic myocardial perfusion imaging studies and lipid parameters of the patients were obtained before and after 6 months of simvastatin treatment period. During the study, daily single dose of 40 mg simvastatin has been given to each subject. We found a significant positive correlation between mean TIMI frame count and basal reversibility score (r = 0.84, p = 0.0001). In addition, analysis of the reversibility scores demonstrates that simvastatin treatment has significantly improved the myocardial perfusion abnormality at the end of the follow-up period. Conclusion: Present findings allow us to conclude that simvastatin improved myocardial perfusion in patients with SCF.

Background The purpose of the present study was to investigate the elastic characteristics of the aorta in patients with coronary ectasia (CE) and the relationship between these characteristics and echocardiographic left ventricular (LV) diastolic functions. Methods and Results In the first group there were 35 patients with CE, the second group consisted of 35 patients with coronary artery disease (CAD) and the third group consisted of 35 patients with normal coronary arteries. Echocardiographic investigation was carried out for the assessment of the LV diastolic functions. Aortic strain, β index and aortic distensibility were used as aortic elasticity parameters. LV diastolic functions were impaired in both the ectasia group and the CAD group as compared with patients with normal coronary arteries. Beta index and aortic distensibility measurements were similar between the CAD and CE groups. The values obtained for aortic strain, β index and aortic distensibility were lower in the CAD and ectasia groups when compared with the values of the normal group. On performing the stepwise linear multivariable analyses, aortic elastic parameters have been determined to possess the strongest diagnostic power for LV diastolic functions. Conclusions The results of the current study show that stiffness parameters of aorta are impaired in the patients with CE as in the patients with CAD. The increase in aortic stiffness might be responsible for LV diastolic dysfunction. (Circ J 2007; 71: 506 - 510)

A 55-year-old man with acute myocardial infarction and no heart failure, had episodes of severe oxygen desaturation and apnea, while his hemodynamic parameters were stable. Sleep recordings revealed severe sleep apnea, and pulmonary function tests showed bronchial obstruction. Apnea and desaturation resolved on bilevel positive airway pressure. Patients with acute myocardial infarction who have apnea and hypoxemia without evident heart failure should be evaluated for sleep disorders. © 2007, SAGE Publications. All rights reserved.

Background and Objective: The slow coronary flow (SCF) phenomenon is an angiographic observation and a well-recognized clinical entity characterized by delayed opacification of vessels in a normal coronary angiogram due to reasons yet unclear. Thyroid hormones exert significant effects on plasma homocysteine (Hcy) levels and microvascular resistance. Recently, several investigators have consistently reported that elevation of the plasma Hcy level can severely disturb vascular endothelial function and play a role in the pathogenesis of SCF. Accordingly, we investigated the levels of plasma Hcy and thyroid hormones and their relationship in patients with SCF. Method: Forty-four patients with angiographically proven SCF (Group I) (mean age 55.5 ± 10.4 years, 26 males) and 44 cases with normal coronary flow (NCF) pattern (Group II) (mean age 53.9 ± 11 years, 22 males) with similar risk profiles were enrolled in the study. Coronary flow patterns of the cases were determined by the thrombolysis in myocardial infarction (TIMI) frame count method. The coronary TIMI frame counts were calculated separately for each coronary artery and their average was determined as the mean TIMI frame count for each subject. Serum levels of free tri-iodothyronine (fT3), free thyroxine (fT4), thyroid stimulating hormone (TSH) and Hcy were measured. Patients with thyroid disease or on medications with a potential to affect thyroid functions were excluded. Results: There were no statistically significant differences between the groups concerning the demographic characteristics and major cardiovascular risk factors. Mean TIMI frame counts of SCF and NCF groups were 45.9 ± 12 and 23.3 ± 3.7, respectively. fT4 (ng/dl) and TSH (µIU/ml) levels of the two groups were similar (p > 0.05). The level of fT3, the active metabolite of the thyroid hormone family, was dramatically reduced in the SCF group when compared to the NCF group (2.3 ± 0.2 vs. 3.0 ± 0.3, p = 0.0001, respectively). Plasma Hcy levels of patients with SCF were found to be significantly higher than controls (12.2 ± 4.9 vs. 8.5 ± 2.9, p = 0.0001, respectively). Correlation analysis showed a significant negative correlation between the plasma fT3 and Hcy levels and the mean TIMI frame counts (r = –0.31, p = 0.003 vs. r = –0.66, p = 0.0001). Moreover, there was a significant positive correlation between the plasma Hcy levels and the mean TIMI frame counts (r = 0.58, p = 0.0001). Also, fT3 was the only significant determinant of the variance of Hcy in multiple regression analysis (r = –0.30, p = 0.005). Conclusion: fT3 levels were decreased and plasma Hcy levels were increased significantly in patients with SCF as compared to controls. This finding suggests that thyroid hormones and/or (?) a possible disturbance in their metabolism may be responsible for the elevated levels of plasma Hcy in patients with SCF and may play a role in the pathogenesis of the SCF phenomenon.

Background and Objective: Coronary slow-flow (CSF) phenomenon is characterized by delayed opacification of vessels in a normal coronary angiogram, but its etiopathogenesis remains unclear. Plasma homocysteine (Hcy) level can severely disturb vascular endothelial function and may play a role in the pathogenesis of CSF. In our study, endothelial function in patients with CSF and their relationship with Hcy and oxidative stress parameters are investigated. Method: Forty-four patients with angiographically proven CSF and 44 cases with normal coronary flow pattern with similar risk profile were enrolled in the study. Coronary flow patterns of the cases are determined by Thrombolysis in Myocardial Infarction (TIMI) frame count method. Endothelium dependent flow mediated dilatation (FMD) and independent vasodilatation characteristics are evaluated by high frequency ultrasound over the brachial artery. Superoxide dismutase (SOD) and reduced glutathione (GSH) and reduction of oxidative material in the body and the end product of lipid peroxidation, malondialdehyde (MDA) are measured as oxidative stress markers in blood samples. Results: Plasma Hcy level (µmol/l) of patients with CSF was found to be significantly higher than in controls (12.2 ± 4.9 vs. 8.5 ± 2.8, p = 0.0001). FMD was 7.87 ± 2.0% in controls and 4.98 ± 1.1% in patients with CSF (p = 0.0001). GSH was reduced in patients with CSF. SOD and MDA activity were found higher in patients with CSF than control subjects. Plasma Hcy level was significantly positively correlated with mean TIMI frame count and negatively correlated with FMD in correlation analysis (r = 0.58, p = 0.0001; r = –0.41, p = 0.022; respectively). Conclusion: The present findings allow us to conclude that patients with CSF have increased levels of Hcy and oxidative stress markers and impaired endothelial cell function.

Background and objective Elevation of plasma homocysteine (Hcy) level has been implicated in the pathogenesis of slow coronary flow (SCF) as it can severely disturb vascular endothelial function. Helicobacter pylori chronically infect the human stomach and causes malabsorption of vitamin B(12) and folate in food, leading ultimately to an increase in circulating Hcy levels. Methods Forty-three patients with angiographically proven SCF (group I) were enrolled in this study; 43 cases with normal coronary flow pattern (group II) served as controls. Fasting plasma levels of Hcy, vitamin B(12), and folate were measured in all subjects. Presence of H. pylori infection was defined as positive 14 C urea breath test. Coronary flow patterns for each major epicardial coronary artery were determined with the Thrombolysis in Myocardial Infarction (TIMI) frame count method. Results Mean TIMI frame count was 46.3 +/- 8.7 in group I and 24.3 +/- 2.9 in Group II (p = .0001). Vitamin B(12) levels were similar, whereas folate levels were dramatically reduced in group I compared to group II (13.2 +/- 4.3 vs. 17.1 +/- 5.2, p = .0001). Plasma Hcy levels were significantly higher in group I compared to group II (13.4 +/- 5.6 vs. 7.9 +/- 2.5, p = .0001) as was the prevalence of H. pylori infection (90.7% in group I vs. 58.1% in group II, p = .001). Hcy levels were elevated (11.7 +/- 5.3 vs. 7.5 +/- 2.7, p = .0001) and folate levels were reduced (13.9 +/- 4.7 vs. 18.6 +/- 4.9, p = .0001) in patients with H. pylori infection, while vitamin B(12) levels were similar in patients with and without H. pylori infection. Correlation analysis revealed a significant negative correlation between plasma folate and Hcy levels and also between folate levels and mean TIMI frame counts (r = -.33, p = .002 vs. r = -.33, p = .003). Moreover, there was a significant positive correlation between plasma Hcy levels and mean TIMI frame counts (r = .66, p = .0001). In addition, the folate level was the only significant determinant of the variance of Hcy in multiple regression analysis (r = -.21, p = .03). Conclusion Our data showed that plasma folate levels were decreased and plasma Hcy levels were increased in patients with SCF compared to controls. Also, the prevalence of H. pylori infection was increased in patients with SCF. These findings suggest that elevated levels of plasma Hcy, possibly caused by H. pylori infection, and/or a possible disturbance in its metabolism may play a role in the pathogenesis of SCF.

Both left ventricular (LV) hypertrophy and insulin resistance (IR) have often been demonstrated in patients with essential hypertension (EH). Insulin may exert a direct growth promoting effect on cardiomyocytes rather than affecting the LV internal diameter. The purpose of this study was to examine the effect of IR on LV geometry. We enrolled 105 patients (71 females, mean age, 49.2 +/- 13.6 years) with recently diagnosed and untreated hypertension (blood pressure140 and/or 90 mmHg, fasting glucose110 mg/dL), and grouped them as normal (N) (39 patients, 26 females, mean age, 48.5 +/- 14.7 years) if all M-mode echocardiographic measurements were within normal limits, concentric remodeling (CR) (22 patients, 15 females, mean age, 50.5 +/- 14.8 years) if relative wall thickness was increased but left ventricular mass index (LVMI) was normal, concentric hypertrophy (CH) (13 patients, 9 females, mean age, 50.3 +/- 10.8 years) if both ventricular thicknesses and the LVMI were increased, and eccentric hypertrophy (EH) (31 patients, 21 females, mean age, 48.6 +/- 12.9 years) if ventricular thicknesses were normal, but LVMI was increased. Transthoracic echocardiography was performed in all subjects, and interventricular septal thickness (IVS), posterior wall thickness (PWT), sum of wall thickness (SWT), left ventricular end-diastolic internal diameter (LVED), relative wall thickness (RWT), and LVMI were recorded. Blood samples for routine biochemical examination and fasting insulin levels were obtained and then the homeostasis model assessment (HOMA) index was calculated by the formula: HOMA Index = Fasting Blood Glucose (mg/dL) x Immunoreactive Insulin (microU/mL)/405, for the assessment of IR. There were no significant differences among the groups with respect to age, blood pressure (BP) levels, fasting blood glucose (FBG), LDL-cholesterol (LDL-C), HDL-cholesterol (HDL-C), total cholesterol (TC), or triglyceride (TG) levels. Insulin levels were significantly higher in the CR and CH groups in comparison with the N group (P = 0.004), and the HOMA index was higher in the CH group compared to the N group (P = 0.024). In Pearson's correlation analysis, insulin was found to be directly correlated with IVS (r = 0.29, P = 0.002), SWT (r = 0.25, P = 0.009), and RWT (r = 0.33, P = 0.0001). The HOMA index was also directly correlated with IVS (r = 0.33, P = 0.001), SWT (r = 0.29, P = 0.002), and RWT (r = 0.29, P = 0.003). Cardiac changes in hypertensive patients include increased LVMI and altered LV geometry. The concentric LV geometry seen in hypertensive patients might be mediated, at least in part, by increased insulin levels and the HOMA index.

Potentially hazardous short ischemic episodes increase the tolerance of myocardium to ischemia paradoxically. This condition decreases the infarct area markedly caused by a longer duration of coronary occlusion. This phenomenon is known as 'ischemic preconditioning' and its powerful cardioprotective effect has been shown in experimental and clinical studies. Ischemic preconditioning decreases cardiac mortality markedly by preventing the development of left ventricular dysfunction and ventricular and supraventricular arrhythmias after acute myocardial infarction. Ischemia-induced opening of ATP-sensitive potassium channels and synthesis of stress proteins via activation of adenosine, bradykinin and prostaglandin receptors seem to be the possible mechanisms. By understanding the underlying mechanisms of ischemic preconditioning, it may be possible to develop new pharmacologic agents that cause ischemic preconditioning with antiischemic and antiarrhythmic properties without causing myocardial ischemia.

Coronary artery fistula is a rare heart defect found in approximately 0.2% of the adult population undergoing coronary angiography. The diagnosis is usually made by aortography and selective coronary angiography. We report here an adult patient with rheumatic mitral stenosis and left anterior descending coronary artery and pulmonary conus branch of right coronary artery-pulmonary artery fistulas detected by coronary angiography. © 2005 Elsevier Ireland Ltd. All rights reserved.

Single atrium or common atrium is a rare, isolated defect. We report here an adult patient with single atrium detected by transthoracic echocardiography. C1 Univ Pamukkale, Fac Med, Dept Cardiol, Kinikli Denizli, Turkey.

BACKGROUND AND OBJECTIVE: Coronary slow-flow phenomenon is characterized by delayed opacification of coronary vessels in a normal coronary angiogram. Although clinical and pathological features have been previously described, the underlying pathophysiology has not been fully elucidated. Thus, it still remains to be determined whether either microvascular or epicardial diffuse atherosclerotic disease is related to slow flow. In this study, we aimed to determine the carotid artery intima-media thickness, which is a marker of atherosclerosis in patients with coronary slow flow, and its possible relationship with the total homocysteine level. METHOD: The study population consisted of 88 patients who underwent coronary angiography because of typical and quasi-typical symptoms of angina. Forty-four patients with angiographically proven coronary slow flow and 44 individuals with normal coronary flow pattern with similar risk profiles were enrolled in the study. Coronary flow patterns of the latter were determined by the thrombolysis in myocardial infarction frame count method. Intima-media thickness was measured by recording ultrasonographic images of both the left and the right common carotid artery with a 12-MHz linear array transducer. Plasma homocysteine, folate and B12 levels were measured from blood samples. RESULTS: Plasma homocysteine levels (μmol/l) and carotid intima-media thickness (mm) of patients with coronary slow flow were found to be significantly higher than that of controls (12.4±4.9 vs. 8.5±2.8, P=0.0001; 0.75±0.08 vs. 0.69±0.06, P=0.0001, respectively). The plasma folate level (ng/ml) was lower in coronary slow-flow patients than in controls (13.8±4.4 vs. 16.5±5.6, P=0.014). The plasma homocysteine level was significantly positively correlated with the mean thrombolysis in myocardial infarction frame count and intima-media thickness of the carotid artery in correlation analysis (r=0.58, P=0.0001; r=0.41, P=0.0001; respectively). CONCLUSION: Homocysteine levels and carotid intima-media thickness increased but folate levels decreased in patients with coronary slow flow. The present findings allow us to conclude that the possible disturbance in the metabolism of homocysteine in patients with coronary slow flow may have a role in the etiopathogenesis of this phenomenon by causing generalized atherosclerosis. © 2006 Lippincott Williams & Wilkins.

Objectives: Congenitally corrected transposition of great arteries with dextrocardia is an extremely rare lesion in adulthood. This group of patients does not live long enough for atherosclerotic coronary artery disease processes, because of existing comorbid anomalies. Methods: We report a 47-year-old man with isolated congenitally corrected transposition of great arteries, dextrocardia, and athersclerotic coronary artery disease. The patient underwent coronary artery revascularization with cardiopulmonary bypass. The free left internal mammary artery (LIMA) was grafted to the tiny left anterior descending artery (LAD), and the reversed saphenous vein Y graft was anastomosed to the posterior descending and posterolateral branches of the morphologic right coronary artery. Results: The patient recovered uneventfully. He is alive and well 24 months after the surgery. Conclusions: To our knowledge, the present case is the first congenitally corrected transposition of great arteries with dextrocardia treated with grafted coronary artery bypass. Early and full revascularization is very important for the systemic right ventricle exposed to a systemic workload. The vessel pathologies and technical details of this unusual case are discussed in this paper.

Metabolic syndrome (MS) is a condition, which is recognized as raising the risk of cardiovascular disease. The aim of our study is to estimate the left ventricular functions by atrioventricular plane displacement (AVPD), myocardial performance index (MPI) and conventional methods in patients with MS who were diagnosed according to NCEP (ATP III) criteria.Fifty-three female patients with MS (mean age 53.1+/-6.9 years) and 30 healthy female subjects (mean age 52.8+/-6.3 years, p0.05) underwent complete echocardiographic assessment. All of the subjects had no heart and pulmonary diseases. The systolic mitral AVPD was recorded at 4 sites (septal, lateral, anterior, and posterior) by M-mode echocardiography and left ventricle ejection fraction (LVEF) was calculated from the AVPD-mean (EF-AVPD). The LVEF was also established by biplane Simpson's (EF-2D) and Teichholz's methods (EF-T). Left ventricular MPI was calculated as (isovolumic contraction time + isovolumic relaxation time) / aortic ejection time by Doppler echocardiography.Patients with MS showed mild left ventricular diastolic dysfunction (DD) in comparison to healthy subjects. The EF-2D and EF-T in patients with MS and healthy subjects were not different significantly and were within normal limits. Patients with MS showed LV global dysfunctions compared to healthy subjects (MPI: 0.56+/-0.12 and 0.46+/-0.11 respectively, p0.01). Both the septal, anterior, lateral and posterior part of the atrioventricular plane values and also AVPD-mean during systole were statistically lower in patients with MS (12.85+/-1.76 mm) as compared with controls (14.65+/-2.19 mm, p0.05). The EF-AVPD in patients with MS was statistically lower (65.58+/-11.95%) as compared with healthy subjects (74.45+/-11.07%, p0.01).Female patients with MS had both left ventricular DD and a global dysfunction with an increased MPI. The EF-2D and EF-T were not different significantly between patients and controls, but patients with MS had a relatively reduced EF-AVPD. The AVPD method may indicate a systolic dysfunction with a relatively lower AVPD-mean and relatively lower EF-AVPD. The presence of global dysfunction in patients with MS may lead to heart failure.

Preinfarction angina (PA) and early reperfusion of infarct-related arteries have been shown to reduce infarct size in patients with acute myocardial infarction (AMI). The beneficial effects of PA on infarct size have been attributed to the development of ischemic preconditioning and faster coronary recanalization in patients treated with thrombolytic therapy (TT).To evaluate the effect of PA on clinical coronary reperfusion time in patients with AMI receiving successful TT.Seventy-five patients presenting with AMI (within 6 h after the initial onset of symptoms) were studied. All patients received TT and were evaluated with coronary angiography (CA) at predischarge. The patients were divided into two groups: group 1 (PA-positive) comprised those who experienced a new onset of prodromal angina within 72 h before the onset of AMI. Group 2 (PA-negative) comprised those who had a sudden onset of AMI without the preceding angina. The successful myocardial reperfusion criteria after TT were ST segment resolution of 50% or greater, the appearance of reperfusion arrhythmias and the resolution of chest pain. The time of reperfusion criteria was recorded after TT. CA was performed in all patients at predischarge. Patients with no patent infarct-related arteries on CA and clinical failure of reperfusion were excluded from the study.Clinical characteristics, risk factors and angiographic findings did not differ significantly between the groups. The time interval from the start of continuous chest pain to TT was also similar between the groups. The left ventricular ejection fraction was higher and there were less frequent ventricular arrhythmias in patients with PA than in those without PA (47.9+/-7.4 versus 44.4+/-8.1, P=0.041, and 17.1% versus 37.5%, P=0.043, respectively). The clinical reperfusion time was significantly shorter in the patients with PA than in those without PA (68.2+/-24.5 min versus 81.4+/-19.3, P=0.012). The clinical reperfusion time was positively correlated with age and the time interval from the start of continuous chest pain to TT but inversely related to the presence of PA.In patients with AMI preceded by PA, TT resulted in more rapid clinical reperfusion than in patients without PA. Thus, earlier myocardial reperfusion may account for smaller infarct size and better prognosis in patients with PA.

Angiotensin converting enzyme (ACE) is a key enzyme in angiotensin II production which causes myocardial hypertrophy and hyperplasia. In this study we aimed to investigate the relation between ACE I/D gene polymorphism and left ventricular mass (LVM), dimensions and systolic functions calculated by mitral annular motion (MAM) in young healthy male subjects.Complete echocardiographic examination was performed in 49 male healthy subjects (mean age 22.9+/-2.1 years) consisting of 18 ACE DD, 18 ACE DI and 13 ACE II genotypes. We calculated LVM and mass index (LVMI) by M-Mode echocardiography. The systolic MAM was recorded at 4 sites (septal, lateral, anterior, and posterior) by M-mode echocardiography and the MAM-ejection fraction (EF) was calculated from above four sites. Ejection fraction was also calculated by Simpson's method.There was no significant difference among the three genotypes according to age, body mass index, systolic and diastolic blood pressure and heart rate. Interventricular septum (IVS) and left ventricular posterior wall (LVPW) diastolic thickness, LVM and LVMI were found significantly different among 3 ACE genotypes. Those measurements were higher in DD genotype in comparison to the DI and II genotypes. There was no significant difference among the three genotypes according to EF-MAM and EF by Simpson's method.In young healthy male subjects having ACE DD genotype, even though LVM and LVMI were within normal limits, their measurements were found to be higher than in subjects with ACE DI and II genotypes respectively. There was no difference among the three genotypes according to left ventricular systolic functions.

Obstructive sleep apnea (OSA) has a critical association with cardiovascular mortality and morbidity. Carotid intima-media thickness (IMT), flow-mediated dilatation (FMD) and aortic stiffness are early signs of atherosclerosis. The presence of subclinical atherosclerosis was assessed in OSA patients using these parameters.40 patients with OSA showing an apnea-hypopnea index (AHI)or =5 (mean age 51.3 +/- 9 years, 32 males) and 24 controls (AHI5, mean age 51.9 +/- 5.2 years, 19 males) were enrolled in the study. In all subjects, polysomnographic examination and recordings were performed during sleep. IMT of the carotid artery, endothelium-dependent/-independent vasodilation of the brachial artery and aortic elastic parameters were investigated using high-resolution Doppler echocardiography.The demographic data of the patients with OSA and controls were not significantly different. Subjects with OSA demonstrated higher values of aortic stiffness (7.1 +/- 1.88 vs. 6.42 +/- 1.56, respectively) and IMT (0.85 +/- 0.13 vs. 0.63 +/- 0.11 mm, p = 0.0001, respectively) but lower distensibility (9.47 +/- 1.33 vs. 11.8 +/- 3.36 cm(2)/dyn/10(6)) and FMD (4.57 +/- 1.3 vs. 6.34 +/- 0.83%, p = 0.0001, respectively) than the controls. The respiratory disturbance index correlated positively with aortic stiffness and IMT and negatively with distensibility and FMD.We observed blunted endothelium-dependent dilatation, increased carotid IMT and aortic stiffness in patients with OSA compared with matched control subjects. This is evident in the absence of other diseases, suggesting that OSA is an independent cause of atherosclerosis. These simple and non-invasive methods help to detect subclinical atherosclerosis in OSA.