A comparison of postoperative complications following cardiac implantable electronic device procedures in patients treated with antithrombotic drugs.

BACKGROUND: The incidence of postoperative complications following cardiac implantable electronic device (CIED) procedures in patients treated with antithrombotic drugs has not been studied sufficiently. Here we present a comparison of complications after CIED implantations. METHODS: Using an observational study design, the study included 1807 patients with a taking antiplatelet drugs (n: 1601), nonvitamin K anticoagulants (NOAC) (n: 136), and warfarin (n: 70) undergoing CIED surgery. Primary endpoint was accepted as cumulative events including composite of clinically significant hematoma (CSH), pericardial effusion or tamponade, pneumothorax, and infection related to device system. Secondary outcomes included each compenent of cumulative events. Multivariable analysis was performed to identify predictors of cumulative events. RESULTS: The overall cumulative event rate was 3.7% (67 of 1807). Cumulative events occured 3.1% (50 of 1601) in the antiplatelet, 5.1% (7 of 136) NOAC, and 14.3% (10 of 70) warfarin groups (p < 0.001). CSH occurred in 2 of 70 patients (2.9%) in the warfarin group, as compared with 5 of 1601 (0.3%) in the antiplatelet group (p: 0.032). However, no significant differences were found between NOAC and warfarin groups in terms of CSH (0.7% vs. 2.9% respectively, p: 0.267). Warfarin treatment was an independent predictor of cumulative events and increased 2.9-fold the risk of cumulative events. Major surgical complications were rare and did not differ significantly between the study groups. CONCLUSIONS: The incidence and severity of complications may be lower in patients treated with periprocedurally antiplatelet or NOAC therapy when compared with warfarin therapy. Further randomized control studies are required to confirm our findings.

Association of pentraxin-3 with the severity of rheumatic mitral valve stenosis.

OBJECTIVE: Inflammation is involved in the pathogenesis of rheumatic mitral valve stenosis (RMVS). Pentraxin-3 (PTX3) indicates the inflammatory state of humans. However, circulating PTX3 levels in patients with RMVS, remain largely unknown. In this study, we investigated whether there is an association between the severity of RMVS and PTX3. METHODS: All patients diagnosed as rheumatic mitral valvular stenosis between December 2013 and April 2014 were included in the study. We investigated circulating PTX3 and high-sensitivity C-reactive protein (hsCRP) levels in patients with RMVS and healthy controls. RESUITS: The study population included 72 subjects (41 patients with RMVS and 31 healthy subjects, 56 female) with a mean age of 40 +/- 13 years. Patients with RMVS had higher left atrial diameters than healthy subjects. PTX3 and hsCRP were significantly higher in patients with RMVS when compared to control subjects and this difference was more significant in PTX3 compared to hsCRP (3.37 +/- 1.11 vs 2.86 +/- 0.59, P = 0.014 and 2.36 +/- 1.48 vs. 1.72 +/- 0.73, P = 0.019, respectively). PTX3 was positively correlated with Wilkins score, mitral valvular area, mitral pressure gradient and left atrium diameter. CONCLUSIONS: We demonstrated that plasma PTX3 and hsCRP levels were increased in patients with RMVS. Compared to hsCRP, PTX3 was more closely related with the severity of mitral valve stenosis. These findings suggest that PTX3 may participate in the pathophysiology of RMVS.

Simultaneous occurrence of a large asymptomatic prolapsing left atrial myxoma with a cutaneous squamous cell carcinoma.

Synchronous myxoma of the heart and other malignancies are extremely rare. We report a case of a 64-year-old man who had a large left atrial myxoma that obstructed the mitral valve, as well as an unrelated, coexistent cutaneous squamous cell carcinoma in the sacral area. During the preoperative evaluation for non-cardiac surgery, the tumor was diagnosed coincidentally by echocardiographic examination. Echocardiography findings were consistent with a large left atrial myxoma originating from the posterior wall and prolapsing into the left ventricular cavity through the mitral valve, causing mitral stenosis. The mass was successfully completely excised. Histologic examination of the mass confirmed the diagnosis of cardiac myxoma. We report a casual echocardiographic finding of a left atrial myxoma that obstructed the mitral valve outflow tract, and an unrelated, synchronous cutaneous squamous cell carcinoma in the sacral area.

The importance of hematologic indices in the risk stratification of patients with acute decompensated systolic heart failure.

OBJECTIVES: In patients with heart failure, a variety of hemogram parameters are known to be of prognostic significance. This study aimed to investigate which of these parameters is/are useful in predicting one-year all-cause mortality in patients with acute decompensated heart failure (ADHF). STUDY DESIGN: Patients who were hospitalized between September 2012-March 2013 in our hospital with systolic-ADHF with ejection fraction ≤40%, symptoms, and findings of congestion were enrolled retrospectively in the study. The study population was divided into two groups based on one-year-mortality. RESULTS: 119 patients with ADHF (mean-age 67±14 years; 55% male) were enrolled in the study. One-year-mortality occurred in 29% of patients. Hemoglobin levels, platelet, basophil and lymphocyte counts were significantly lower, while red-cell distribution width (RDW) was found to be significantly higher in the one-year-mortality group. Neutrophil, monocyte, and eosinophil counts were similar in the two groups. Furthermore, lower estimated glomerular-filtration-rate (eGFR) and unused angiotensin-converting enzyme inhibitors/angiotensin receptor blockers (ACEI/ARB) were associated with mortality. Age, presence of hypertension, right-ventricular diameter, eGFR, ACE/ARB treatment, hemoglobin levels, RDW and platelet, leukocyte, lymphocyte, basophil, neutrophil, monocyte, and eosinophil-counts were found to have prognostic significance in univariate analysis. In multivariate analysis, decreased platelet, lymphocyte-counts and hemoglobin level on admission and unused ACE/ARB treatment at discharge (p<0.05) were found to be independent factors predicting one-year-mortality. CONCLUSION: Among hematological indices; hemoglobin level, platelet and lymphocyte counts are readily available, useful and inexpensive markers for the prediction of one-year all-cause mortality in ADHF patients.

An epidemiological study to evaluate the use of vitamin K antagonists and new oral anticoagulants among non-valvular atrial fibrillation patients in Turkey- AFTER-2 study design.

OBJECTIVES: Atrial fibrillation (AF) is one of the most common causes of preventable ischemic stroke and is related to increased cardiovascular morbidity and mortality. There is a lack of data in Turkey on the use of new oral anticoagulants (NOACs), and time in therapeutic INR range (TTR) in vitamin K antagonist users and AF management modality. In this multi-center trial, we aimed to analyze, follow and evaluate the epidemiological data in non-valvular AF patients. STUDY DESIGN: Four thousand one hundred consecutive adult patients from 42 centers with at least one AF attack identified on electrocardiography will be included in the study. Patients with rheumatic mitral valve stenosis and prosthetic valve disease will be excluded from the study. At the end of one year, the patients will be evaluated in terms of major cardiac end points (death, transient ischemic attack, stroke, systemic thromboembolism, major bleeding and hospitalization). RESULTS: First results are expected in June 2015. Data about major cardiovascular end-points will be available in January 2016. CONCLUSION: The rates and kind of oral anticoagulant use, TTR in vitamin K antagonist users and main management modality applied in non-valvular AF patients will be determined by AFTER-2 study. In addition, the rate of major adverse events (MACEs) and the independent predictors of these MACEs will be detected (AFTER-2 Study ClinicalTrials.gov number, NCT02354456.).

Effect of sleep quality on hemodynamic response to exercise and heart rate recovery in apparently healthy individuals.

PURPOSE: Poor sleep quality has an unfavorable impact on autonomic nervous system activity, especially that of the cardiovascular (CV) system. The heart rate (HR) and blood pressure (BP) at rest and during exercise, along with the heart rate recovery (HRR), were examined in poor sleepers and compared with individuals with good sleep quality. METHODS: A total of 113 healthy individuals were enrolled to the study. All participants performed treadmill stress testing. Sleep quality of participants was assessed by using the Pittsburgh Sleep Quality Index (PSQI) questionnaire: 48 subjects were categorized as 'poor sleepers' (PSQI score > 6 points), and the rest were grouped as 'good sleepers'. RESULTS: The poor sleepers showed higher resting HR (p <0.001), higher diastolic BP (p=0.006), similar systolic BP (p=0.095), more frequent hypertensive response to exercise (p=0.046) and less HR increase with exercise (chronotropic incompetence) (p=0.002) compared with individuals who reported good sleep quality. In addition, the poor sleepers demonstrated reduced heart rate recovery at the 1st and 3rd minute of recovery (p=0.005 and 0.037, respectively) compared with good sleepers. Multivariate logistic regression analysis revealed that only resting diastolic BP was the independent predictor of HRE. The PSQI score was positively correlated with resting HR; while it was negatively correlated with HR response to exercise, HRR1 and HRR index-1. CONCLUSION: This cross-sectional study emphasizes the effect of poor sleep quality on unfavorable cardiovascular outcome indicators of the treadmill stress test.

Platelet-to-lymphocyte ratio is a predictor of long-term mortality in patients with acute coronary syndrome.

INTRODUCTION: Atherosclerosis is a chronic inflammatory process and inflammation is an important component of acute coronary syndrome (ACS). Platelet-to-lymphocyte ratio (PLR) is a useful parameter showing the degree of the inflammatory response. AIM: To explore the association between PLR and long-term mortality in patients with ACS. MATERIAL AND METHODS: A total of 538 patients who had a diagnosis of ACS between January 2012 and August 2013 were followed up to 60 months. On admission, blood sampling to calculate PLR and detailed clinical data were obtained. RESULTS: In total, 538 patients with a mean age of 61.5 ±13.1 years (69% male) were enrolled in the study. Median follow-up was 79 months (IQR: 74-83 months). Patients were divided into 3 tertiles based on PLR levels. Five-year mortality of the patients was significantly higher among patients in the upper PLR tertile when compared with the lower and middle PLR tertile groups (55 (30.7%) vs. 27 (15.0%) and 34 (19.0%); p < 0.001, p = 0.010 respectively). In the Cox regression analysis, a high level of PLR was an independent predictor of 5-year mortality (OR = 1.005, 95% CI: 1.001-1.008, p = 0.004). Kaplan-Meier analysis according to the long-term mortality-free survival revealed the higher occurrence of mortality in the third PLR tertile group compared to the first (p < 0.001) and second tertiles (p = 0.009). CONCLUSIONS: PLR, which is an easily calculated and universally available marker, may be useful in long-term risk classification of patients presenting with ACS.

Prognostic Significance of Serum Albumin in Patients With Acute Coronary Syndrome.

In patients with unstable angina pectoris (UAP) or non-ST elevation myocardial infarction (NSTEMI), long-term mortality remains high despite improvements in the diagnosis and treatment. In this study, we investigated whether serum albumin level is a useful predictor of long-term mortality in patients with UAP/NSTEMI. Consecutive patients (n = 403) who were hospitalized with a diagnosis of UAP/NSTEMI were included in the study. Patients were divided into 2 groups based on the presence of hypoalbuminemia and the relationship between hypoalbuminemia and mortality was analyzed. Hypoalbuminemia was detected in 34% of the patients. The median follow-up period was 35 months (up to 45 months). Long-term mortality rate was 32% in the hypoalbuminemia group and 8.6% in the group with normal serum albumin levels (P < .001). On multivariate analysis, hypoalbuminemia, decreased left ventricular ejection fraction, and increased age were found to be independent predictors of mortality (P < .05). The cutoff value of 3.10 g/dL for serum albumin predicted mortality with a sensitivity of 74% and specificity of 67% (receiver-operating characteristic area under curve: 0.753, 95% CI: 0.685-0.822). All-cause long-term mortality rates were significantly increased in patients with hypoalbuminemia. On-admission albumin level was an independent predictor of mortality in patients with UAP/NSTEMI.

Sympathetic overactivity in patients with pulmonary stenosis and improvement after percutaneous balloon valvuloplasty.

OBJECTIVE: Percutaneous balloon valvulotomy (PBV) is the procedure of choice for the treatment of valvular pulmonary stenosis (PS) with similar results comparable to surgical valvotomy but less invasive. METHODS AND RESULTS: Twenty-seven consecutive patients with PS being evaluated for PBV were enrolled in the study. Peak instantaneous transvalvular gradient, right ventricle (RV) diameter, mean atrial pressures, RV systolic pressure (RVSP), pro-brain natriuretic peptide (proBNP) levels significantly decreased immediately after PBV. Regarding heart rate variability (HRV) parameters, mean HR (heart rate), LF (low frequency) day and night, LF/HF day and night significantly decreased and standard deviation of all NN intervals (SDNN), root mean square of successive differences (RMSSD), P number of NN intervals that differed by more than 50 ms from adjacent interval divided by the total number of all NN intervals (PNN50), HF (High frequency) day and night significantly increased 1 day after PBV and these changes were shown to be preserved at the first month. The increase in SDNN was correlated with the decrease in right atrial pressure (RAP) (r =-0.5, P = 0.04); the increase in standard deviation of the 5-minute mean RR intervals (SDANN) was correlated with the decrease in proBNP (r =-0.4, P = 0.03). CONCLUSIONS: Sympathetic overactivity and increased proBNP levels were associated with the symptomatic status of patients with PS. Associated with a decrease in atrial pressures and proBNP levels, PBV yielded a decrease in adrenergic overactivity in the patients with PS.

The relationship between angiotensin-converting enzyme (insertion/deletion) gene polymorphism and left ventricular remodeling in acute myocardial infarction.

BACKGROUND: The development of left ventricular remodeling after acute myocardial infarction is a predictor of heart failure and mortality. The genetic influence on cardiac remodeling in the early period after acute myocardial infarction, is however, unclear. The aim ofthis study was to investigate the relationship between angiotensin-converting enzyme (ACE) gene polymorphism and left ventricular remodeling in the early period in patients with anterior myocardial infarction. METHOD: The study population consisted of 142 patients with their first attack of acute anterior myocardial infarction. Echocardiographic examinations were performed within 24 h of the first attack (first evaluation) and on the fifth day of acute myocardial infarction (second evaluation). Left ventricular end systolic and diastolic diameters, left ventricular end systolic and diastolic volumes, ejection fraction, mitral flow velocities (E, A, E/A), deceleration time, isovolumic relaxation time and myocardial performance index were calculated. ACE I/D polymorphism was determined using polymerase chain reaction amplification. RESULTS: On the basis of polymorphism of the ACE gene, the patients were classified into the three groups: group 1, deletion/deletion (n=59) genotype, group 2 insertion/deletion (n=69), and group 3 insertion/insertion (n=14) genotype. When the first and second sets of echocardiographic results of the groups were compared, all parameters were not different among three groups. In group analysis, Left ventricular systolic diameters, left ventricular diastolic diameters, left ventricular end diastolic diameters, left ventricular ejection fraction and myocardial performance index between first and second echocardiographic results were significantly different in deletion/deletion group and only myocardial performance index and left ventricular ejection fraction in insertion/deletion group (P<0.05). CONCLUSIONS: ACE gene polymorphism may influence early cardiac remodeling after acute myocardial infarction. Patients with the deletion/deletion-insertion/deletion genotype may be particularly more sensitive to ACE-I treatment possibly owing to the more prominent role of the renin-angiotensin system.

Elevated plasma N-terminal pro-brain natriuretic peptide levels in acute ischemic stroke.

BACKGROUND: B-type natriuretic peptide (BNP) is a neurohormone secreted mainly in the cardiac ventricles in response to volume expansion and pressure overload. The aim of this study was to assess plasma N-terminal proBNP (NT-proBNP) changes in acute ischemic stroke (AIS). METHODS: The study group consisted of 57 (37 women aged 64 +/- 12 years) patients who had their first AIS and no history or signs of cardiovascular disease. An age-matched control group was also included (n = 57, 36 women aged 61 +/- 6 years). NT-proBNP, troponin I (TnI), and creatine kinase-MB were evaluated. A thorough cardiovascular and neurological investigation, including imaging techniques and lesion size determination, was also performed. RESULTS: The log NT-proBNP peak levels, TnI, and creatine kinase-MB levels were significantly higher in AIS compared with controls (7.25 +/- 1.77 vs 3.48 +/- 0.76 pg/mL, P < .0001; 0.76 +/- 0.54 vs 0.5 +/- 0.0 ng/mL, P < .001; 57 +/- 37 vs 13 +/- 4 U/L, P < .001, respectively). The log NT-proBNP correlated positively with TnI (r = 0.29, P = .03) and heart rate (r = 0.41, P = .002), and negatively with left ventricular ejection fraction (r = -0.67, P < .0001). Patients with signs of marked myocardial ischemia and patients with insular cortex involvement had even higher NT-proBNP levels. After adjustment for relevant factors, the relation between the log NT-proBNP and AIS as well as insular cortex involvement was observed to be insignificant (P > .05 for both). CONCLUSIONS: Our results show that NT-proBNP plasma levels are significantly elevated in AIS and might be of clinical importance as a supplementary tool for the assessment of cardiovascular function in patients with AIS.

Serum Levels of IL-17 and IL-23 in Patients With Rheumatic Mitral Stenosis.

Rheumatic mitral valve stenosis (RMS) is a complication of rheumatic heart disease (RHD) and leads to significant morbidity and mortality. RHD is a chronic inflammatory and autoimmune disease that is associated with cytokine activities. The etiology of RMS is not fully understood yet. Interleukin (IL)-17 and IL-23 have a key role in development of the autoimmunity. The expression of these cytokines in RMS remains unclear. In this study, we investigated the serum levels of IL-17 and IL-23 in RMS patients compared to healthy subjects.A total of 35 patients admitted to cardiology outpatient clinic between December 2014 and May 2015 who were diagnosed with RMS formed the study group. Age- and gender-matched 35 healthy subjects were included as the control group. Statistical analyses were performed using SPSS 18.0 and P value <0.05 was considered as statistically significant.The patients with RMS had higher WBC count, hsCRP, systolic pulmonary artery pressure (PAPs), left atrial diameter (LAD), IL-17, and IL-23 levels compared to the control subjects. The levels of IL-17 (P = 0.012) and IL-23 (P = 0.004) were significantly higher in the RMS group. Correlation analysis revealed that IL-17 and IL-23 levels had a significant correlation with each other and with hsCRP and LAD.We demonstrated that serum levels of IL-17 and IL-23 are significantly higher in patients with RMS compared to those of healthy subjects. IL-17 and IL-23 expression may have a possible role in inflammatory processes that result in RMS development.

Complement activation in acute coronary syndromes.

The complement system is part of the host defence response. However, considerable evidence suggests that complement plays an important role in the pathophysiology of ischemic heart disease. The aim of this study was to evaluate complement activation in patients with all forms of acute coronary syndromes (ACS) and to examine the relationship between the degree of complement activation and myocardial injury. The study population included 152 subjects (26 females): 82 with ACS (35 acute myocardial infarction (AMI), 22 non-Q wave MI (NQMI), 25 unstable angina (UAP)) (Group A), 35 stable angina (SA) (Group B), and 35 healty control subjects (Group C). Complement 3 (C3), Complement 4 (C4), C-reactive protein (CRP), troponin I (TnI) as well as creatine kinase MB (CK-MB) were evaluated. Patients' blood samples were taken on admission (day 1) and after 2, 3 and 7 days in group A. However, only one measurement was performed in the groups B and C. Plasma C3 and C4 peak levels were significantly higher in patients with AMI (141+/-29 and 35+/-11 mg/dl) and NQMI (136+/-13 and 35+/-7 mg/dl) than in patients with SA (128+/-14 and 27+/-10 mg/dl) and the control subjects (114+/-22 and 22+/-7 mg/dl) (p<0.03). Also, C3 and C4 serum levels in patients with SA and UAP (126+/-16 and 31+/-7 mg/dl) were significantly higher than those in control subjects (p<0.01, p<0.03, respectively). At 1-week follow-up, there were no significant differences between the plasma levels of C3 and C4 in patients with UAP (p>0.05). However, plasma levels of C3 and C4 were significantly different between days in patients with AMI and NQMI (p<0.0001). Plasma C3 and C4 levels in ACS showed a relationship with peak CK-MB and Tn I levels (p<0.01). Plasma CRP level in ACS showed positive correlation with C3 (p<0.01) and C4 (p<0.001). In this study, we determined that plasma C3 and C4 levels were elevated in ACS and SA. Although C3 and C4 were higher in ACS and SA, the systemic levels of inflammatory markers in patients with SA and UAP were lower than those found in the AMI and NQMI groups. The relationship between C3, C4 levels and ACS further suggests that the complement activation is related to necrosis within the myocardium.

Clinical investigation: thyroid function test abnormalities in cardiac arrest associated with acute coronary syndrome.

INTRODUCTION: It is known that thyroid homeostasis is altered during the acute phase of cardiac arrest. However, it is not clear under what conditions, how and for how long these alterations occur. In the present study we examined thyroid function tests (TFTs) in the acute phase of cardiac arrest caused by acute coronary syndrome (ACS) and at the end of the first 2 months after the event. METHOD: Fifty patients with cardiac arrest induced by ACS and 31 patients with acute myocardial infarction (AMI) who did not require cardioversion or cardiopulmonary resuscitation were enrolled in the study, as were 40 healthy volunteers. The patients were divided into three groups based on duration of cardiac arrest (<5 min, 5-10 min and >10 min). Blood samples were collected for thyroid-stimulating hormone (TSH), tri-iodothyronine (T3), free T3, thyroxine (T4), free T4, troponin-I and creatine kinase-MB measurements. The blood samples for TFTs were taken at 72 hours and at 2 months after the acute event in the cardiac arrest and AMI groups, but only once in the control group. RESULTS: The T3 and free T3 levels at 72 hours in the cardiac arrest group were significantly lower than in both the AMI and control groups (P < 0.0001). On the other hand, there were no significant differences between T4, free T4 and TSH levels between the three groups (P > 0.05). At the 2-month evaluation, a dramatic improvement was observed in T3 and free T3 levels in the cardiac arrest group (P < 0.0001). In those patients whose cardiac arrest duration was in excess of 10 min, levels of T3, free T3, T4 and TSH were significantly lower than those in patients whose cardiac arrest duration was under 5 min (P < 0.001, P < 0.001, P < 0.005 and P < 0.05, respectively). CONCLUSION: TFTs are significantly altered in cardiac arrest induced by ACS. Changes in TFTs are even more pronounced in patients with longer periods of resuscitation. The changes in the surviving patients were characterized by euthyroid sick syndrome, and this improved by 2 months in those patients who did not progress into a vegetative state.

Iatrogenic left atrioventricular fistula after aortic valve re-replacement.

Left ventriculoatrial fistula is a very rare cardiac disorder. The case is reported of a male patient who was admitted to the authors' clinic with dyspnea and fatigue. The patient had an atrioventricular fistula between the left atrium and left ventricle, and had undergone aortic valve re-replacement for prosthesis malfunction about one year previously. The fistula was considered to be the result of iatrogenic injury related to valve re-replacement surgery.

N-terminal proBNP plasma levels correlate with severity of mitral stenosis.

BACKGROUND AND AIM OF THE STUDY: Brain natriuretic peptide (BNP), a neurohormone, is secreted predominantly from the ventricular myocardium. Studies investigating BNP secretion in diseases affecting the right side of the heart are scarce. The relationship between N-terminal proBNP (NT-proBNP) and echocardiographic and clinical findings was studied in cases with isolated moderate to severe rheumatic mitral stenosis (MS), and in patients with previous mitral valve replacement (MVR). METHODS: Thirty-two patients with MS (mean age 41.2 +/- 5.7 years), 20 with MVR (mean age 46.0 +/- 4.6 years) and 30 healthy individuals (mean age 40.3 +/- 4.9 years) were included in the study. In addition to NT-proBNP measurements, detailed transthoracic echocardiography was performed in all patients and healthy subjects. RESULTS: Plasma levels of NT-proBNP were significantly higher in patients with MS than in those with MVR or in controls (99.8 +/- 12.7 versus 74.7 +/- 6.9 and 48.5 +/- 10.5 pg/ml, respectively; p <0.0001 all groups). NT-proBNP levels showed a significantly greater increase in severe MS than in moderate MS (109.8 +/- 5.6 versus 88.3 +/- 7.6 pg/ml, p <0.0001). NT-proBNP levels also were higher in MVR patients than in controls (74.7 +/- 6.9 versus 48.5 +/- 10.5 pg/ml; p <0.0001). Although NT-proBNP levels did not correlate with left ventricular ejection fraction (LVEF) in patients with MS (r = -0.33; p >0.05), there was a positive correlation with pulmonary artery pressure (r = 0.87; p <0.001) and a negative correlation with mitral valve area (MVA) (r = -0.89; p <0.0001). However, multivariate analysis identified only MVA as an independent correlate of NT-proBNP (beta = -0.47; p = 0.02). CONCLUSION: In patients with rheumatic MS, NT-proBNP levels correlated positively with MS severity. Moreover, NT-proBNP levels increased significantly in patients with MS, but were significantly lower in those who underwent MVR.

The association between NT-proBNP levels, functional capacity and stage in patients with heart failure.

OBJECTIVE: Amino-terminal probrain natriuretic peptide (NT-proBNP), a biologically inactive derivative of BNP, is clinically more useful owing to its longer half-life, higher plasma concentrations, lesser variation among individuals, and higher in vitro stability. In this regard, NT-proBNP may be a better indicator of the severity of ventricular dysfunction. In this study, the association of NT-proBNP levels with functional capacity and stage of heart failure was explored in patients with CHF. Also, we particularly focused on the presence and significance of neurohormonal activation in the group of patients classified as stage-A according to ACC/AHA guidelines. METHODS AND RESULTS: 64 patients with CHF (31 men, 33 women; mean age 58.26 +/- 10.59 y) and 36 healthy controls (24 men, 12 women; mean age 57.47 +/- 10.83) were included in this study. The New York Heart Association (NYHA) classification system (I, II, III, IV) was used to define the functional capacity; and the stage of the heart failure was based on the ACC/AHA guidelines (A, B, C, D). Healthy female participants had higher NT-proBNP levels compared to their male counterparts (p < 0.001). Left ventricular ejection fraction (LVEF) did not correlate significantly with functional capacity and stage of the disease. CHF patients had higher NT-proBNP compared to controls (p < 0.001). There was a positive correlation between NT-proBNP and functional capacity in patients, and NT-proBNP increased significantly with each increasing class of the disease. Similarly, a positive correlation existed between the stage of heart failure and NT-proBNP levels, which increased significantly with increasing stages of the disease. Patients with NYHA I and stage A disease had higher NT-proBNP levels compared to controls (p = 0.04). CONCLUSIONS: The severity of CHF can be objectively assessed by measuring the circulating levels of NT-proBNP. Even in NYHA I and stage A disease, NT-proBNP levels are higher compared to controls (p = 0.04). NT-proBNP can provide objective information regarding the severity of the disease and also aid in treatment decisions in patients with CHF.

The serial changes in plasma homocysteine levels and it's relationship with acute phase reactants in early postmyocardial infarction period.

OBJECTIVE: We aimed to study the change in the plasma homocysteine concentration in the early stage of acute myocardial infarction and its relationship with the acute phase reactants. METHODS: We included into the study 33 patients who were admitted to the hospital with acute myocardial infarction within the first three hours after the onset of symptoms. The plasma samples were obtained on admission (within 3 hours onset of symptom) and at 6, 12, 24 hours and 2, 4, 7, 30 and 90th day after admission. RESULTS: The serial homocysteine measurements were as following: 11.87+/-0.71 micromol/L, 11.89+/-0.62 micromol/L, 11.37+/-0.83 micromol/L, 10.96+/-0.93 micromol/L, 11.37+/-0.89 micromol/L, 11.24+/-0.66 micromol/L, 13.09+/-0.64 micromol/L, 12.85+/-0.71 micromol/L, and 12.19+/-0.91 micromol/L, respectively (p=0.05). Statistically significant difference was found only between the hour 24 and the day 7 (p=0.04). However, there was no statistically significant difference between the admission level and none of the other time points. No correlation was identified between acute phase reactants and lipid parameters that were measured serially at the same time periods and homocysteine levels. CONCLUSION: Although homocysteine plasma values obtained during the sixth and twelfth hours of acute myocardial infarction provide reliable results as a risk markers, timing of blood sampling during the myocardial infarction does not have significant role since plasma values of homocysteine did not affect acute phase reactants.

The relationship between atrial electromechanical delay and left atrial mechanical function in stroke patients.

OBJECTIVE: The aim of this study was to evaluate the relationship between atrial electromechanical delay (EMD) measured with tissue Doppler imaging (TDI) and left atrial (LA) mechanical functions in patients with ischemic stroke and compare them with healthy controls. METHODS: Thirty patients with ischemic stroke were enrolled into this cross-sectional, observational study. The control group consisted of 35 age- and gender-matched apparently healthy individuals patients. Acute cerebral infarcts of probable embolic origin were diagnosed via imaging and were confirmed by a neurologist. Echocardiographically, time intervals from the beginning of P wave to beginning of A wave from the lateral and septal mitral and right ventricular tricuspid annuli in TDI were recorded. The differences between these intervals gave the mechanical delays (inter- and intra-atrial). Left atrial (LA) volumes were measured using the biplane area-length method, and LA mechanical function parameters were calculated. Statistical analysis was performed using student's t-test, chi-squared test, and Pearson's test. RESULTS: The laboratory and clinical characteristics were similar in the two groups. Increased left atrial EMD (21.36±10.38 ms versus 11.74±6.06 ms, p<0.001), right atrial EMD (13.66±8.62 ms versus 9.66±6.81 ms, p=0.040), and interatrial EMD (35.03±9.95 ms versus 21.40±8.47 ms, p<0.001) were observed in stroke patients as compared to controls. Active LA emptying volume and fraction and passive LA emptying volumes and fraction were similar between controls and stroke patients. Total LA emptying volumes were significantly increased in stroke patients as compared to healthy controls (33.19±11.99 mL/m2 versus 27.48±7.08 mL/m2, p=0.021). CONCLUSION: According to the results of our study, interatrial electromechanical delay may be a new predictor for ischemic stroke.