Objective: Acute coronary syndromes are usually the disease of people over 45 years old; however, a number of younger patients are also diagnosed with acute coronary syndrome. In this study, it was aimed to elucidate the relationship between genetic hypercoagulable and atherosclerotic states and acute coronary syndromes in the young adults. Material and Methods: Between January 2008 and June 2010, 68 young adult patients with acute coronary syndrome (62 men, mean age: 36.8±6.4) and 69 healthy individuals (56 men, mean age: 35.1±5.9) were recruited in this cross-sectional study. The diagnosis of acute coronary syndrome was based on the criteria of the European Society of Cardiology/American College of Cardiology Foundation/American Heart Association/Word Heart Federation Task Force the definition of MI definition. Blood samples were obtained during the first hour after admission to the Coronary Care Unit. Plasma samples were stored at -80°C until used. Polymerase chain reaction was used for the genotype analysis. Results: Statistically significant difference was found between groups for factor V Leiden and methylenetetrahydrofolate reductase gene mutation (for both mutation p:0.006); whereas there was no statistically significant difference for prothrombin gene mutation, plasminogen activator inhibitor-1 4G/5G polymorphism and angiotensin converting enzyme I/D polymorphism (p:0.551, p:0.291 and p:0.469, respectively). The study group had significantly higher homocysteine levels than control group (14.45±5.50 μmol/L versus 11.17±3.79 μmol/L, p<0.001). Conclusion: Factor V Leiden and methylenetetrahydrofolate reductase gene mutations might play a part in the pathophysiology of acute coronary syndromes in the young adult patients. Also, it was found that Turkey looks like a factor V Leiden mutation region as opposite to known current literature in this study.

Objective: We aimed to examine the relationship between serum uric acid levels and left atrial appendage (LAA) peak flow velocity, an indicator of the mechanical functions of the LAA, and atrial fibrillation (AF). Subjects and Methods: Transesophageal echocardiography was performed before cardioversion in 153 patients with AF. The patients were categorized into 2 groups based on their LAA blood flow velocity. Group 1 included 87 patients with a low LAA flow velocity (<35 cm/s), and group 2 comprised 66 patients with a normal LAA flow velocity (≥35 cm/s). The χ2 and Student's t tests were used to compare categorical and quantitative data between the groups. Linear regression analyses were performed to demonstrate the independent association between serum uric acid levels and LAA peak flow velocity. Results: The LAA blood flow velocity was 24.62 ± 5.90 cm/s in group 1 and 49.28 ± 13.72 cm/s in group 2, respectively (p < 0.001). The serum uric acid levels were 6.88 ± 1.85 mg/dl in group 1 and 5.97 ± 1.51 mg/dl in group 2, and the difference was statistically significant (p = 0.001). There was a negative correlation between serum uric acid levels and LAA blood flow velocity (r = -0.216, p = 0.007). Multivariate regression analysis showed that serum uric acid levels, age and gender differences were significant predictors of the LAA peak flow velocity. Conclusions: High serum uric acid levels were associated with a low contractile function of the LAA and could provide additional prognostic information on future thromboembolic events in patients with AF.

The bicuspid aortic valve (BAV) is a common congenital cardiac anomaly. The BAV may function normally throughout life, and usually unobserved until valvec stenosis or regurgitation appears. Furthermore, the BAV is a potential substrate for infective endocarditis (IE), especially in young male patients. The risk of developing IE on a BAV is 10-30% over a lifetime. Staphylococci (12% coagulase negative) and viridans streptococci accounted for nearly three-quarters of the cases of IE affecting BAVs. Most patients necessitate surgery, frequently on a emergency basis. Transthoracic (TTE) or transesophageal (TEE) echocardiography plays a critical role in diagnosis and addressing the patient to cardiac surgery. A 21-year-old male patient without any history of cardiovascular disease was admitted to our hospital for dyspnea and fever (>=39°C). He had moderate dyspnea (New York Heart Association functional class III). On his physical examination, orthopnea, tachycardia (118/min), roughed lung sounds, and aortic 2-3/4 diastolic murmur were present. We suspected IE with the present findings. Blood and urine cultures were obtained, and then wide-spectrum antibiotherapy was started. TTE examination revealed a severe aortic regurgitation, bicuspid aortic valve with suspected vegetation. In addition to elucidate the findings of 2D TTE, 3D TEE was performed and provided additional information. To clarify this pathology, 3D-TEE was carried out and precisely delineated the lesion by showing a major perforation in the anterior aortic cusp of the BAV. Patient underwent then aortic valve replacement. Intraoperative examination of the aortic valve confirmed the findings of the 3D TEE. Although 2D TTE and TEE are the conventional procedures for the diagnosis of valvular heart disease, 3D TEE is a better noninvasive tool to define more accurately the intracardiac anatomy. In our case, the images that we obtained with use of 3D TEE helped us to conclusively recognize the identification of perforation on BAV.

Pulmonary hypertension (PH) is a chronic, progressive debilitating disease and associated with poor prognosis despite the novel numerous treatment options. Beta-blockers constitute a cornerstone in left heart failure treatment; however, we still don't know the role of beta-blockers on PH and they are considered relatively contraindicated in patients with PH because of the possible negative effect on these patients' hemodynamics and exercise capacity. On the other hand, animal models of PH and non-randomized clinical trials have shown that beta-blockers may improve right ventricular function and prevent remodeling in the heart muscle. As it is well-known, right heart function is the main prognostic determinants of the PH. The purpose of this chapter is to present the use of beta-blockers for the treatment of PH, the purported mechanisms of action, previously conducted animal studies and clinical trials.

There is increasing evidence of importance of evaluating right ventricular function (RV) for risk stratification and prognosis in various diseases. There is paucity of data regarding with the effect of age on Doppler echocardiographic parameters of RV diastolic performance during rest or exercise. In this study, we aimed to evaluate the effect of treadmill exercise test on tricuspid inflow and tissue Doppler velocity of tricuspid annulus in healthy people in different age groups. A total of 54 healthy persons with normal clinical examination, negative treadmill stress test at target heart rate, and normal echocardiographic examination were enrolled to this study. For the analysis of effectiveness of exercise on RV filling patterns in the different age groups, the patients were divided into two groups: Group 1 (young patients <= 45 years old) and Group 2 (old patients > 45 years old). Peak systolic (Sa), early (Ea), and late (Aa) tricuspid annular Doppler velocities are obtained both at rest and immediately after the end of exercise, and then analyzed. Group 1 was consisted of 28 patients (mean age 26.28 ± 5.49 years, 15 male) nad group 2 was consisted of 26 patients (mean age 57.26 ± 7.69 years, 12 male). In the group 2, BMI (23.41 ± 3.16 kg/m2 vs. 26.07 ± 4.03 kg/m2, p=0.009) and systolic blood pressure (116.78 ± 11.88 mmHg vs. 129.03 ± 13.71 mmHg, p<0.001) was higher while exercise duration (12.14 ± 2.72 min vs. 8.86 ± 3.18 min, p<0.001) and achieved METs level 14.15 ± 2.74 ± 10.44 ± 3.27, p<0.001) was lower compared to group 1. Following exercise, A-wave velocity was increased, E-wave deceleration time and isovolumic relaxation time were significantly decreased. However, E-wave velocity and E' velocity were not significantly changed. This resulted in reduction in E/A ratio and E'/A' ratio, while E/E' ratio was not changed. Interestingly, we observed that these changes were more evident in the young group as compared to elderly (Table). These exercise induced changes of tissue Doppler velocity of tricuspid annulus (increased A-wave and unchanged E-wave velocity) suggested that increased right ventricle filling is substantially formed by right atrial contraction rather than early filling of right ventricle RV on exercise, and more prominent in the young ones compared to old ones, probably because of the ageing of myocardium.Table

Being at risk for overweight has been associated with increased cardiovascular risk factors. We examine the aortic stiffness index and left ventricular tissue Doppler parameters in young adults who are at risk for obesity. Twenty-three young adults with a body mass index (BMI) > 25 kg/m2 and 39 young adults with a BMI < 25 kg/m2 were enrolled in this study. The presence of aortic stenosis was accepted as exclusion criteria. Aortic strain (AS), aortic distensibility (DIS) and aortic stiffness index (βSI) were derived from M-mode echocardiography at the AAo together with cuff blood pressure recordings using the following previously described formulas. Left and right ventricular tissue Doppler parameters were also evaluated. AS (11.31 ± 6.76 vs. 24.07 ± 11.51) was and DIS (10.24 ± 6.37 vs. 20.42 ± 10.79) were significantly lower and βSI (2.83 ± 0.66 vs. 1.98 ± 0.51) was significantly higher in young adults who were at risk for obesity (BMI > 25 kg/m2) than in control subjects (BMI < 25 kg/m2) (for all p < 0.001). AS (r=-0.454, p<0.001), DIS (r=-0.418, p=0.001) and βSI (r=0.557, p<0.001) were significantly correlated to BMI. There were no significant differences for left and right ventricular tissue Doppler parameters between two groups. We concluded that elasticity of ascending aorta is impaired in young adults at risk for obesity. Assessment of aortic elasticity by transthoracic echocardiography in young obese patients may help to early detection of possible future cardiovascular complications.Tabled 1Results of the study

With respect to a common embryologic origin of the aortic and pulmonary roots, we hypothesized that similar pathologic changes and biomolecular changes in the media of the pulmonary artery media identical to those caused in the aorta could be existed. We therefore performed a study to investigate whether the dimensions of main, right and left pulmonary artery measured with computed tomography were affected in patients ascending aorta aneurysm (AAA). Patients with AAA and without any history of cardiovascular disease were enrolled to this study. After a transthoracic echocardiography and standard biochemical tests, a computed tomography (CT) of the thorax with contrast was performed. The pulmonary artery was measured at 3 sites as recommended in the guidelines: main pulmonary artery, right and left pulmonary artery. All measurements were done by two observers, which do not have any information about the patients. Forty male patients (mean age 39.75 ± 8.12 years) were enrolled to this study. The mean height was 171.02 ± 6.71 cm, mean weight was 82.92 ± 10.27 kilograms, mean systolic blood pressure was 138.37 ± 17.77 mmHg and mean diastolic blood pressure was 82.37 ± 10.12 mmHg. The measurement of aorta was as follows: at the aortic valve annulus 25.42 ± 2.19 mm, at the sinus of valsalva 43.75 ± 4.81 mm, at the sinotubular junction 40.85 ± 6.60 mm, at the ascending aorta 45.36 ± 7.46 mm, at the arcus aorta 29.26 ± 2.57 mm and at the descending aorta 26.58 ± 2.76 mm. The pulmonary artery was measured at the sites. The mean dimensios of pulmonary artery were 25.15 ± 3.00 mm for main pulmonary artery, 19.24 ± 2.43 mm for right pulmonary artery and 19.74 ± 2.35 mm for left pulmonary artery. The obtained values from the measurement of pulmonary artery were within the normal limits. We found that the dimensions of the pulmonary artery measured by CT seemed to be not affected in patients with AAA. However, it should be kept in mind that hemodynamic stress of the pulmonary circulation is lower than the systemic circulation and pre-existing medial abnormalities of the pulmonary artery possibly likely might predispose to dilatation of pulmonary artery after its exposure to the hemodynamic stress of the systemic circulation, such as in the dilation of the pulmonary autograft in patients undergoing Ross procedure.

We read the article titled “Importance of epicardial adipose tissue thickness measurement in obese adolescents, its relationship with carotid intima-media thickness, and echocardiographic findings” by Boyraz et al1 with great interest. However, we would like to make a few suggestions regarding the analysis and presentation of data. First, in Table I the standard deviation (SD) of some parameters, for example HOMA-IR, LDL-C and triglyceride levels are so large that it renders interpretation of data ambiguous. Such large SD would bring the normal distribution of the data into question, which in turn, would alter the selection of statistical tests. Also, the authors1 indicate that unpaired Student’s t-test was used to evaluate the three groups within the cohort; namely lean, mild-moderate obese and severe obese patients, in pairs. However, in cases with more than three independent groups, the preferred methodology must be an Analysis of Variance (ANOVA) followed by post-hoc analysis if statistical significance is achieved. This further complicates interpretation of the p-values, which we would have preferred to be provided in a separate column next to the data analyzed; rather than at the bottom of the table. Second, the title of Table III is “Tissue Doppler echocardiography measurements in lean, and mildmoderate and severely obese groups”. However, there is no data provided regarding lean patients. Furthermore, instead of measurements, a bunch of “r” correlation coefficients and their respective pvalues are provided. In another words, the title of the table and the contents are irrelevant. Last, although the multivariate regression analysis of the epicardial adipose tissue thickness is provided in Table IV, their correlation with measurements made within groups is not present. We are deducing that Table III was actually aiming to provide the correlations between epicardial adipose thickness and other measured parameters. Is this the case? We believe that Boyraz et al1 selected a great topic for exploration and would like to congratulate them for their efforts in shedding more light on this important matter.

The accurate underlying pathogenic mechanism behind the spontaneous echo contrast (SEC) is complex and poorly understood. The aim of this study is to characterize the relationship between mean platelet volume (MPV) and left atrium SEC. We screened retrospectively the records of 172 patients with AF in whom transesophageal echocardiography was performed. Patients were categorized according to the presence of the left atrial SEC. Group 1 was consisted of patients with AF and left atrial SEC (-), and group 2 was consisted of patients with AF and left atrial SEC (+). Basal demographic, laboratory and echocardiographic features of the patients were compared between two groups. Multivariate regression analysis was established to identify the independent association between MPV levels and other potential variables. The study group included 105 men (61%) and 67 women (39%), and the mean age of the patients was 64.48 ± 13.90 years. Group 1 was consisted of 97 patients (70 (72.2%) men and mean age 61.90 ± 15.75 years) and Group 2 was consisted of 75 patients (35 (46.7%) men and mean age 67.82 ± 10.23 years). We observed that SEC (+) patients had higher MPV values (8.94 ± 0.98 fL vs. 8.52 ± 1.15 fL, p value 0.012). The mean MPV values for 8.65 fL for patients with SEC (+), 8.93 fL for patients with SEC (++) and 9.15 fL for SEC patients with (+++). (p value between groups was 0.038). In multivariate regression analysis, only the association between MPV level and the degree of SEC remained statistically significant (β= 0.165, p = 0.042). We conclude that AF patients with SEC have significantly higher MPV levels compared with AF patients without SEC. Elevated MPV may be helpful for the better recognition and/or managing of ongoing pathologies due to the future thromboembolic events in patients with AF and SEC.Tabled 1Results of the study

We read the article titled “The influence of angiotensin converting enzyme-2 gene polymorphisms on type 2 diabetes mellitus and coronary heart disease” by Chaoxin et al1 with great interest. However, we would like to make a few suggestions regarding the analysis and presentation of data. As it is known, the types of variables are nominal, ordinal, and numeric. If the variables are numeric, they should be defined whether it’s compatible with normal distribution or not2,3. Normal distribution may control with both visual tests and functional tests. Visual tests are graphical techniques including Q-Q plot, P-P plot, and histogram. Functional tests include statistical tests (Kolmogorov-Smirnov and Shapiro-Wilk), skewness and kurtosis2. The authors did not report any normalization tests in the paper. Furthermore, in Table II, the standard deviation (SD) of some parameters, for example urine microprotein and E/A ratio, are so large that it renders interpretation of data almost impossible. Such a large SD would bring the normal distribution of the data into question, which in turn, would alter the selection of statistical tests in favor of non-parametric tests like Wilcoxon Signed Rank test. Also, instead of SD, we recommend the authors use of standard of error of mean; as the prior shows how widely scattered some measurements and the latter focuses on indicating the uncertainty around the estimate of the mean measurement, and is also more useful in determining a confidence interval (CI). In addition, to better interpret the differences between groups, presentation of the p values of every parameter in a separate column would be very helpful. We would like to conclude by congratulating Chaoxin et al1 on their study and suggest that extension of this study to different populations would prove useful in finally establishing the place of angiotensin converting enzyme-2 (ACE-2) polymorphisms in this cohort of patients.

Pulmonary arterial stiffness (PAS) is a new noninvasive echocardiographic marker of pulmonary arterial vasculature. We tested the pulmonary arterial compliance in patients with chronic heart failure (CHF). Twenty patients with CHF (16 male) and 21 healthy subjects (16 male) without any history of cardiovascular disease were enrolled in this study. In all patients, pulmonary artery stiffness (PAS) was measured echocardiographically in parasternal short axis view. PAS (kHz/sec)= maximal frequency shift (MFS) / acceleration time of the pulmonary artery flow trace (AcT). As expected, patients with CHF were older and LVEF was significantly lower in CHF patients. The PAS was significantly increased in patients with CHF compared with control subjects (11.42 ± 2.77 vs. 7.94 ± 1.44, p < 0.001). In correlation analysis, duration of CHF (r = 0.967, p < 0.001), age (r = 0.730, p < 0.001) and LVEF (r = -0.608, p < 0.001) were found significantly correlated with PAS. To determine the independent variables that likely predict PAS, a backward multivariate linear regression model, including variables that correlated significantly with PAS and those that exhibited significant differences between the two groups, was performed. It was found that duration of CHF (β= 1.064, p < 0.001) was the only significant independent predictor of PAS. We demonstrated that pulmonary artery stiffness tend to be increased in patients with CHF and this increase seems to be related to the duration of CHF.Tabled 1Results of the study

In recent years, a growing interest has been directed towards the elevated prostate-specific antigen (PSA) levels in patients with cardiovascular conditions. However, there is conflicting data about the exact relationship between PSA level and cardiovascular disease. In this context, we investigated the factors that can affect the level of PSA in those with cardiovascular disease. Thirty-nine patients with a history of cardiovascular disease who admitted to our cardiology outpatient clinic and in whom serum PSA level was measured were enrolled to this study. The effect of basal demographic characteristics, echocardiographic findings, medications, and standard biochemical test results on PSA level were evaluated. Pearson's correlation analysis was used. The study was consisted of 39 male patients (mean age 57,67 ± 13,86 years). There was a moderate negative correlation between height and weight and PSA level (r= -0,431, p=0,008 and -0,446, p=0.006 respectively). However, there was statistically significant correlation for body mass index. When we evaluated the use of cardiovascular medications, we found a moderate positive correlation between calcium channel blocker usage and PSA level (r=0,446 and p =0.006), and a moderate negative correlation between beta-blocker and statin usages and PSA level (r= -0,356, p= 0,31 and r= -0,362, p = 0,028, respectively). Among the parameters of standard biochemical test results, the level of alanine amino transferase was negatively correlated with PSA level (r= -0,336, p= 0,042), monocyte and eosinophil counts were positively correlated with PSA level (r= 0,379 p=0,021 and r= 0,345 p=0,039, respectively). In terms of platelet indices, there was a positive correlation between platelet count and PSA level (r=0,420 and p=0,010) and a negative correlation between mean platelet volume and PSA level (r= -0,341 and p= 0,039). In this study of short number of patients, we found that, the height, weight, beta-blocker usage, statin usage, the level of alanine amino transferase and mean platelet volume were negatively correlated with PSA, whereas calcium channel blocker usage, monocyte, eosinophil and platelet counts were positively correlated. Without these knowledges, decision of any study will be limited. We strongly believe that these factors should be kept in mind when analyzing the relationship between PSA levels and the diagnosis and severity of cardiovascular diseases.

OBJECTIVES Vasovagal syncope (VVS) is supposed to be modulated by increased sympathetic tone following an orthostatic maneuver. Increased sympathetic activity may have an important role in mean platelet volume (MPV), either by peripheral activation or by effects on thrombocytopoiesis. We aimed to show the effects of increased sympathetic activity on platelet size in patients with VVS in the present study. PATIENTS AND METHODS Thirty-seven patients with VVS were compared with age- and sex-matched 33 patients without VVS. All patients have undergone 24 hour holter monitoring for heart rate variability (HRV) and time-domain HRV analysis. Blood samples for MPV measurements were taken before 24 hour holter monitoring. RESULTS Group 1 was consisted of 37 patients with VVS and group 2 was consisted of 33 patients without VVS. We observed that SDNN, SDNN index, SDSD, RMSDD, PNN50 count were significantly lower and MPV was found significantly higher in patients with VVS (p < 0.05 for all). Pearson's correlation analysis showed that MPV was moderately negatively correlated with SDNN (r = -0.421), SDSD (r = -0.396), NN50 count (r = -0.395) and RMSDD (r = -0.393). Multivariate regression analysis showed that SDNN was the only independent variable, which had a significant effect on increased MPV level (β = -0.295 , p = 0.016). CONCLUSIONS We found that MPV was closely associated with increased sympathetic activity in patients with VVS. Our analysis supports the hypothesis that alterations in autonomic status might play a role in the development of platelet size.

Several studies have shown the association between STEMI and circadian rhythm. Nonetheless, intrinsic circadian release or sequestering of platelets is controlled by various humoral factors, including hormones, endothelial-derived factors, platelet-derived factors and other blood-borne substances. We hypothesized that endogenous circadian rhythm in platelet function may play a partial role in the circadian rhythm of STEMI. A total of 205 patients with STEMI were enrolled into this study. Hospital's computerized database was used to obtain clinical and demographic characteristics of patients. The time in which chest pain had started was considered as the beginning of AMI; within ±30 min. Patients were then categorized into 4 6-h increments (12:00 AM–06:00 AM, 06:00 AM–12:00 PM; 12:00 PM–06:00 PM and 06:00 PM–12:00 AM hours). Basal demographic, laboratory and echocardiographic features of the patients were compared between two groups. The rate of anterior MI was higher in group 1 (61.7%), whereas inferior MI was higher in group 3 (67.9%). There was no significant difference for otherclinical characteristics between 4 groups. When we evaluated the platelet index, we had observed that MPV level was highest in group 1 and the lowest in group 3 (p = 0.002) (Table) We have found a circadian variation of MPV with morning peak in patients with STEMI. Endogenous circadian system on platelet function might affect circadian rhythm of MI and thereby, might play a causal role in the morning peak of adverse cardiovascular events.Table

Juvenile hyaline fibromatosis is a rare, autosomal-recessive connective tissue disorder with aberrant synthesis of glycosaminoglycans by fibroblasts. It is characterized by papular and nodular skin lesions, gingival hyperplasia, joint contractures and bone involvement in variable degrees. We report a female patient of juvenile hyaline fibromatosis with mitral valve prolapsus. A 9-year-old female patient of juvenile hyaline fibromatosis was admitted to child outpatient department for periodic routine controls. She was referred to our cardiology clinic for further evaluation of 2-3/6 left apical systolic murmur on her cardiac examination. Echocardiography revealed a mitral valve prolapsus accompanying with mild mitral insufficiency (Figure 1). Routine echocardiographic imaging was planned. Juvenile hyaline fibromatosis (JHF) is an extremely rare disease and less than 70 cases of JHF have been reported worldwide. It is progressive autosomal recessive disease that's characterized by papulonodular skin lesions, soft tissue masses, joint contractures, gingival hypertrophy and osteolytic bone lesions. Impaired collagen synthesis is thought to be the major pathogenetic mechanism that's responsible for this disease. Considering progressive nature of the disease, this case emphasizes that physicians should consider the probability of cardiac involvement and therefore, echocardiographic imaging should be considered in the routine controls of the disease. Thus, making an early diagnosis and administering early treatment, including the proper supportive care are important in these patients.