Pentraxin-3: A new parameter in predicting the severity of diabetic foot infection?

This study was undertaken to evaluate the diagnostic and prognostic values of pentraxin-3 (PTX-3) in patients with infected diabetic foot ulcers (IDFU) as well as to assess the association between PTX-3 levels and IDFU severity. This study included 60 IDFU patients (Group 1), 45 diabetic patients without DFU (Group 2), and 45 healthy controls. Patients with IDFU were divided into mild, moderate, and severe subgroups based on classification of clinical severity. Patients who underwent amputation were also documented. Blood samples were collected to determine PTX-3 levels. PTX-3 levels in healthy controls, Group 1, and Group 2 were 5.83 (3.41-20) ng/mL, 1.47 (0.61-15.13) ng/mL, and 3.26 (0.67-20) ng/mL, respectively. A negative correlation between plasma PTX-3 and glucose levels was found. There were significant differences in terms of procalcitonin (PCT) and PTX-3 levels in the subgroup analysis of Group 1. The PTX-3 level in patients who did or did not undergo amputation was 4.1 (0.8-13.7) and 1 (0.6-15.1) ng/mL, respectively. Results suggest that PTX-3 is a particularly effective marker in patients with IDFU, both in terms of predicting disease severity and assisting in the decision to perform amputation.

Circulating soluble lectin-like oxidized low-density lipoprotein receptor-1 levels are associated with erectile dysfunction in patients without known coronary artery disease.

AIM: Endothelial dysfunction and microvascular damage are involved in the pathogenesis of erectile dysfunction (ED). Soluble lectin-like oxidized low-density lipoprotein receptor-1 (sLOX-1) is identified endothelial receptor for oxidized low-density lipoprotein (ox-LDL) that plays a pivotal role in ox-LDL-induced endothelial dysfunction. The purpose of the current study was to determine the association between sLOX-1 and ED in patients without known coronary artery disease (CAD). MAIN OUTCOME MEASURES: Diagnosis of ED was based on the International Index of Erectile Function Score-5. Levels of sLOX-1 were measured in serum by enzyme-linked immunosorbent assay. METHODS: One hundred thirty-eight subjects with ED patients without known CAD (ED group) and 75 age-matched subjects without ED and known CAD (Non-ED Group) were included in this study. RESULTS: Plasma levels of sLOX-1 were significantly higher in ED than in Non-ED group (95±87 and 49±30 pg/mL, respectively, P<0.001). The levels of sLOX-1 highly negative correlated with score of ED (r=-0.618, P<0.001). The sLOX-1 levels>75 pg/mL predicts ED with 26.8% sensitivity and 96.0% specificity on receiver operator characteristic analysis. CONCLUSIONS: Our study demonstrated that serum sLOX-1 levels were associated with endothelial dysfunction that predicts ED. Moreover, the current study revealed that there was strong negative correlation between the levels of circulating sLOX-1 and score of ED. This study suggested sLOX-1 may be involved in the pathogenesis of ED in patients without known CAD.

An investigation of tenascin-C levels in rheumatic mitral stenosis and their response to percutaneous mitral balloon valvuloplasty.

OBJECTIVE: The purpose of this study was to evaluate the tenascin-C levels in severe rheumatic mitral stenosis before and after percutaneous mitral balloon valvuloplasty (PMBV). SUBJECTS AND METHODS: Forty patients with severe mitral stenosis requiring PMBV and 20 age-matched healthy subjects were included in the study. The mitral valve areas, mitral gradients and systolic pulmonary artery pressure (sPAP) were measured by echocardiography. The sPAP values and mitral gradients were also measured by catheterization before and after PMBV. The blood tenascin-C levels were measured before PMBV and 1 month after the procedure. RESULTS: The echocardiographic mean mitral gradients had a significant decrease after PMBV (11.7 ± 2.8 vs. 5.6 ± 1.7 mm Hg; p < 0.001) and also those of catheterization (13.9 ± 4.4 vs. 4.0 ± 2.4 mm Hg; p < 0.001). Mitral valve areas increased significantly after PMBV (from 1.1 ± 0.1 to 1.8 ± 0.2 cm(2), p < 0.001). Tenascin-C levels decreased significantly in patients after PMBV (from 15.0 ± 3.8 to 10.9 ± 3.1 ng/ml; p < 0.001). Tenascin-C levels were higher in patients with mitral stenosis before PMBV than in healthy subjects (15.0 ± 3.8 and 9.4 ± 2.9 ng/ml; p < 0.001, respectively). There were no significant differences between patients with mitral stenosis after PMBV and healthy subjects (10.9 ± 3.1 and 9.4 ± 2.9 ng/ml; p = 0.09, respectively). There was a significant positive correlation between tenascin-C levels and sPAP (r = 0.508, p < 0.001). In multivariant analysis, tenascin-C predicted mitral stenosis (p = 0.004, OR: 2.31). CONCLUSIONS: Tenascin-C was an independent predictor for rheumatic mitral stenosis.

The association between soluble lectin-like oxidized low-density lipoprotein receptor-1 levels and patients with isolated coronary artery ectasia.

Some evidence suggests that chronic inflammation plays a critical role in the development and progression of coronary artery ectasia. Lectin-like oxidized low-density lipoprotein receptor-1 is involved in multiple phases of vascular dysfunction, including endothelial dysfunction, atherogenesis, initiation of plaque rupture, and restenosis. The objectives was to study the purpose of the current study was to determine whether soluble lectin-like oxidized low-density lipoprotein receptor-1 is associated with isolated coronary artery ectasia patients. Forty-six patients with isolated coronary artery ectasia without stenosis and 46 control subjects with angiographically normal coronary arteries were included in this study. Lectin-like oxidized low-density lipoprotein receptor-1 levels were measured in serum by sandwich enzyme-linked immunosorbent assay. Baseline characteristics of the two groups were similar. Plasma levels of lectin-like oxidized low-density lipoprotein receptor-1 were significantly higher in the coronary artery ectasia group than normal coronary artery group (1.7 ± 0.8 ng/ml vs. 1.1 ± 0.3 ng/ml, P < 0.001, respectively). No correlation was found between plasma soluble lectin-like oxidized low-density lipoprotein receptor-1 levels and different types of ectasia in patients with coronary artery ectasia. In this study, we found significantly higher levels of soluble lectin-like oxidized low-density lipoprotein receptor-1 in coronary artery ectasia patients when compared to control subjects with normal coronary arteries, suggesting that soluble lectin-like oxidized low-density lipoprotein receptor-1 may be involved in the pathogenesis of coronary artery ectasia.

Circulating soluble lectin-like oxidized low-density lipoprotein receptor-1 levels predict percutaneous coronary intervention-related periprocedural myocardial infarction in stable patients undergoing elective native single-vessel PCI.

Percutaneous coronary intervention-related periprocedural myocardial infarction (PCI-RPMI) has now been definitively linked in large data sets to long-term adverse outcomes. It is more likely that the relationship is caused by the underlying predisposing factors that led to the PCI-RPMI, such as plaque vulnerability. Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is involved in multiple phases of vascular dysfunction, including atherosclerotic plaque formation and/or vulnerability. The purpose of this study was to determine whether soluble LOX-1 (sLOX-1) is associated with myocardial necrosis in elective native single-vessel PCI (NSV-PCI). From January 2010 to January 2012, 214 consecutive stable patients undergoing elective NSV-PCI were enrolled. Troponin T, CK and CK-MB were performed to screen for PCI-induced myocardial necrosis after the procedure, and PCI-RPMI was defined as three times the ULN of CK, which was confirmed by the elevation of the CK-MB and troponin T. According to the cardiac biomarkers result, patients were divided into two groups [PCI-RPMI(+) and PCI-RPMI(-)]. sLOX-1 levels were measured in serum by ELISA. Of the 214 patients who underwent NSV-PCI, 33 (15.4 %) patients developed PCI-RPMI. The results of this study showed that among patients undergoing elective NSV-PCI, those with PCI-RPMI had significantly higher circulating sLOX-1 levels than those without (167 ± 89 vs. 99 ± 68 pg/mL; p < 0 0.001). There were high correlations between sLOX-1 levels and CK and CK-MB values (r = 0.677 and r = 0.682, respectively; p < 0.001). Our study demonstrated that circulating sLOX-1 levels were associated with PCI-RPMI, which might predict periprocedural myocardial necrosis in elective NSV-PCI. Importantly, the study speculates that the level of sLOX-1 may help to identify patients at risk for PCI-RPMI before the procedure. sLOX-1 may provide new insights into not only risk stratification, but also therapeutic strategies for elective PCI.

Pregnancy followed by delivery may affect circulating soluble lectin-like oxidized low-density lipoprotein receptor-1 levels in women of reproductive age.

BACKGROUND/OBJECTIVE: It is known that menopause or lack of endogenous estrogen is a risk factor for endothelial dysfunction and CAD. Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is involved inmultiple phases of vascular dysfunction. The purpose of the current study was to determine the association between soluble LOX-1 (sLOX-1) and pregnancy followed by delivery in women of reproductive age. MATERIALS/METHODS: Sixty-eight subjects with pregnancy followed by delivery (group 1) and 57 subjects with nongravidity (group 2) were included in this study. Levels of sLOX-1 were measured in serum by EL SA. RESULTS: Plasma levels of sLOX-1 were significantly lower in Group 1 than Group 2 in women of reproductive age (0.52 ± 0.18 ng/mL and 0.78 ± 0.13, resp., P < 0.001). There were strong correlations between sLOX-1 levels and the number of gravida (r = -0.645, P < 0.001). The levels of sLOX-1 highly correlated with the number of parous (r = -0.683, P < 0.001). CONCLUSION: Our study demonstrated that serum sLOX-1 levels were associated with pregnancy followed by delivery that might predict endothelial dysfunction. We conclude that pregnancy followed by delivery may delay the beginning and progress of arteriosclerosis and its clinical manifestations in women of reproductive age.

MR-proADM and MR-proANP levels in patients with acute pulmonary embolism.

BACKGROUND: The aim of this study was to determine levels of Mid-regional Pro-adrenomedullin (MR-proADM) and Mid-regional Pro-atrial Natriuretic Peptide (MR-proANP) in patients with acute pulmonary embolism (PE), the relationship between these parameters and the risk classification in addition to determining the relationship between 1and 3month mortality. METHODS: 82 PE patients and 50 healthy control subjects were included in the study. Blood samples for Mr-proANP and Mr-proADM were obtained from the subjects prior to the treatment. Risk stratification was determined according to sPESI (Simplified Pulmonary Embolism Severity Index). Following these initial measurements, cases with PE were assessed in terms of all causative and PE related mortalities. RESULTS: The mean serum Mr-proANP and Mr-proADM levels in acute PE patients were found to be statistically higher compared to the control group (p < 0.001, p < 0.01; respectively) and statistically significantly higher in high-risk patients than low-risk patients (p < 0.01, p < 0.05; respectively). No statistical difference was determined in high-risk patients in case of sPESI compared to low-risk patients while hospital mortality rates were higher. It was determined that the hospital mortality rate in cases with Mr-proANP ≥ 123.30 pmol/L and the total 3-month mortality rate in cases with Mr-proADM ≥ 152.2 pg/mL showed a statistically significant increase. CONCLUSIONS: This study showed that Mr-proANP and MRproADM may be an important biochemical marker for determining high-risk cases and predicting the mortality in PE patients and we believe that these results should be supported by further and extensive studies.

Adiponectin levels in coronary artery ectasia.

Etiopathogenesis of coronary artery ectasia (CAE), which is defined as abnormal dilatation of a segment of the coronary artery to 1.5 times of an adjacent normal coronary artery segment, is unclear. However, it is speculated that CAE develops in the atherosclerosis process through degeneration of coronary artery media layer. Our objective in this study is to compare levels of adiponectin between cases with CAE and normal coronary anatomy, and to examine whether adiponectin plays a role in CAE etiopathogenesis. The study registered a total of 66 cases, consisting of CAE cases (group 1, n = 36) and cases with normal coronary anatomy (group 2, n = 30). Taking coronary artery diameters of the control group cases as the reference, patients with abnormal segments 1.5 times larger than the adjacent segments were accepted as CAE. Serum adiponectin levels were 4.31 +/- 2.02 microg/ml in group 1 and 6.73 +/- 4.0 microg/ml in group 2 (P = 0.02). High-sensitivity C-reactive protein was 4.8 +/- 3.8 mg/l in group 1 and 3.6 +/- 3.4 mg/l in group 2 (P > 0.05). There was a negative correlation between ectatic coronary artery diameter and plasma adiponectin level (P = 0.03; r = -0.339). It was known that adiponectin levels dropped in atherosclerotic heart disease. In this study we found low plasma adiponectin levels in acquired CAE, attributed to atherosclerosis. Therefore, we think that adiponectin might be playing a role in etiopathogenesis and progression of CAE. This in turn may indicate that hypo-adiponectinemia may be useful in revealing a realized risk in CAE. However, larger, randomized, multicenter studies are required to examine the role of adiponectin in the development of CAE.

Effect of Repeated Remote Ischemic Preconditioning on Peripheral Arterial Disease in Patients Suffering from Intermittent Claudication.

BACKGROUND/OBJECTIVE: Intermittent claudication (IC) is the symptom of peripheral artery disease (PAD) and causes functional disability. Remote ischemic preconditioning (RIPC), is a phenomenon in which a short period of sub-critical ischemia, protects tissues against ischemia/reperfusion/injury. We considered to test the hypothesis that RIPC in PAD patients suffering from IC would increase muscle resistance to ischemia and thus improve walking-capacity. MATERIALS/METHODS: A total of 63 patients with proven-IC underwent two treadmill tests (graded treadmill protocol) with a 28-day interval in between. Patients were consecutively assigned for the non/RIPC-group and RIPC-group procedure one by one. Patients received 5-cycles of alternating 5-minute inflation and 5-minute deflation of blood-pressure cuffs on nondominant upper-limb every day for four weeks. Initial claudication distance (ICD), total walking distance (TWD) and time to relief of claudication (TRC) were recorded during procedure. RESULTS: Patients receiving-RIPC exhibited a marked increase in ICD and TWD between basal and last tests: 209.1 ± 15.4 m vs. 226 ± 15.0 m and 368.8 ± 21.0 m vs. 394 ± 19.9 m, respectively (p < 0.001). In addition, patients receiving-RIPC represented a significant decrease in TRC between basal and last tests: 7.8 ± 1.3 min vs. 6.4 ± 1.1 min, respectively (p < 0.001). Patients not receiving-RIPC did not exhibit improvement in ICD, TWD, and TRC between basal and last tests: 205.2 ± 12.1 min vs. 207.4 ± 9.9 min, 366.5 ± 24.2 min vs. 369.4 ± 23.2 min and 7.9 ± 1.4 min vs. 7.7 ± 1.3 min, respectively (p > 0.05). CONCLUSION: A significant increase in ICD and TWD were observed in last/treadmill test in RIPC-group. In addition, a significant decrease in TRC was observed in last/treadmill test in RIPC-group. In non/RIPC-group, no improvement was observed in ICD, TWD and TRC.

Prognostic value of copeptin in patients with acute pulmonary thromboembolism.

BACKGROUND AND AIMS: The aim of this study was to determine the level of copeptin, which is one of the new cardiac markers in acute pulmonary thromboembolism (PE) cases, and to determine the relationship between the severity of the disease, risk classification and hospital, first month, third month and 3-month total mortality. METHODS: The study included 100 cases with PE and 60 healthy control subjects. Copeptin was measured in control group. The risk grade of the cases was determined according to the sPESI index. Patients survival data at the first and third months were determined. This study was performed in patients with strict exclusion criteria for comorbidities known to be associated with increased risk of PE. RESULTS: sPESI was ≥1 in 68 (68%) of patients with acute PE. Mean serum copeptin levels were found statistically higher in patients with high risk compared to low-risk cases and controls (9.18 ± 3.29, 6.47 ± 2.29, and 5.26 ± 2.15, P < 0.0001, respectively). When the cut-off value of copeptin was taken as ≥7.87 with ROC analysis for predicting high sPESI score, the sensitivity of the copeptin was 78% and the specificity was 62% (AUC = 0.74, 95% CI = 0.63-0.85, P < <0.0001). When cases divided in the groups according to the cut-off value as 7.87, first month hospital mortality and 3-month total mortality rate was found statistically higher in patients with copeptin ≥7.87 (χ2 = 5.33 P < 0.05, χ2 = 3.88, P < 0.05 and χ2 = 4.26, P < 0.05 respectively). CONCLUSIONS: The results of our study showed that increased serum copeptin levels might predict the severity of PE as well as a promising marker of early mortality in high-risk cases according to sPESI.

The effect of rapid blood pressure control on P-wave dispersion in hypertensive urgency.

INTRODUCTION: A sharp increase in blood pressure, increase in atrial pressure and atrial strain, left ventricular diastolic dysfunction, and left ventricular hypertrophy (LVH) lead to heterogeneity and instability in atrial conduction. The resulting physiopathological situation may elevate maximum Pwave duration (P(max)) and P-wave dispersion (PWD) in electrocardiography. The objective of our study was to explore the effect of the sudden change in atrial hemodynamics on P(max) and PWD, which may indicate the risk of atrial fibrillation (AF) development in hypertensive urgency. METHODS: The study included patients diagnosed as hypertensive urgency (systolic blood pressure > or =180 mmHg, diastolic blood pressure > or =110 mmHg). Nitroprusside was started at a dose of 0.2 microg/kg/min, and the ensuing dose was arranged according to blood pressure. Echocardiography and electrocardiography were used to noninvasively measure changes in diastolic function and PWD and P(max), respectively. RESULTS: The study enrolled 102 patients (mean age 57.9+/-11.6 years; 32 [31.4%] males, and 70 [68.6%] females). P(max) decreased from 99.9+/-11.1 msec (95% confidence intervals [CI] 97.7, 102) to 88.5+/-9.3 msec (95% CI 86.6, 90.3) (P<0.001), while PWD decreased from 60.1+/-7.4 msec (95% CI 58.7, 61.6) to 43.9+/-6.7 msec (95% CI 42.5, 45.2) (P<0.001). In addition, most patients had LVH and diastolic dysfunction. After nitroprusside treatment improvements in indicators of diastolic functions such as E/A ratio, deceleration time, and isovolumetric relaxation time were observed. CONCLUSION: The change observed in P(max) and PWD in hypertensive urgency may be associated with the rapid change in blood pressure and atrial strain, sympathetic nervous system activation, relative myocardial ischemia, and left ventricular diastolic dysfunction. Rapid regulation of blood pressure with nitroprusside brought about a marked decrease in P(max) and PWD in our patients. This improvement was interpreted as atrial conduction acquiring a stable and homogeneous character, which may reduce the risk of AF development in hypertensive urgency.

Can ADMA play a role in determining pulmonary hypertension related to chronic obstructive pulmonary disease?

BACKGROUND AND AIMS: Asymmetric dimethylarginine (ADMA) decreases the levels of nitric oxide by inhibiting nitric oxide synthases. In this study, the possible role of ADMA in determining pulmonary hypertension (PH) in chronic obstructive pulmonary disease (COPD) patients was investigated. METHODS: Stable COPD patients who were admitted to pulmonology outpatient clinic were involved in the study. Forty healthy volunteers, with similar ages and sexes, were accepted as the control group. COPD patients were divided into two groups: 40 patients without PH (COPD group) and 40 COPD-related PH patients (COPD-PH group). Pulmonary function test, echocardiography and arterial blood analyses of all patients were performed. RESULTS: The mean age of patients was 69.21 ± 10.62, and 15 of these patients were females. There was no significant difference between the two COPD groups in terms of age and sex (P > .05). There was no difference in PaO2 , SaO2 , FEV1 and FEV1 /FVC values between the two COPD groups (P > .05). Serum ADMA levels were similar in the control and the COPD group (0.42 ± 0.13 vs 0.43 ± 0.15), but it was significantly higher in the COPD-PH group compared to the control and the COPD group (0.49 ± 0.14). A negative correlation was determined between serum ADMA levels and SaO2 levels (r = -.247, P = .028). A significant positive correlation observed between ADMA and systolic pulmonary artery pressure values (r = .627, P < .001) CONCLUSIONS: In conclusion, high levels of serum ADMA levels may be able to determine the presence of PH.

P-wave dispersion in panic disorder.

BACKGROUND: P-wave dispersion (PWD) is defined as the difference between the maximum and the minimum P-wave (Pmax and Pmin, respectively) duration. Significant variation in cardiac atrial PWD has been correlated with changes in systemic autonomic tone such as during periods of anxiety. It is also known that the degree of PWD seen on 12-lead electrocardiogram (ECG) may be a predictor of susceptibility of the atrial myocardium to future atrial fibrillation (AF). Therefore, we firstly aimed to show an association between PWD and panic disorder, a state of high sympathetic tone. METHODS: PWD was measured in 40 outpatients with panic disorder and in 40 physically and mentally healthy age- and gender-matched controls. In addition, the Panic Agoraphobia Scale (PAS) and the Hamilton Depression Rating Scale (HDRS) were scored concomitantly. RESULTS: Both Pmax and Pmin were significantly higher than those of healthy controls. PWD was significantly greater in the panic disorder group than in the controls. As expected, the mean score on PAS was significantly higher for the panic disorder group than for the controls and correlated significantly with PWD. Heart rate (measured as RR intervals in milliseconds on electrocardiogram) did not differ significantly between the groups. CONCLUSIONS: The findings of the present study suggest that the disorder may be associated with an increase in PWD. This association may result from prolonged anxiety and increase in sympathetic modulation, which are main characteristics of panic disorder.

The level of hs-CRP in coronary artery ectasia and its response to statin and angiotensin-converting enzyme inhibitor treatment.

BACKGROUND/AIM: Coronary artery ectasia (CAE) was thought of as a variant of atherosclerosis. C-reactive protein (CRP) which is among the most sensitive markers of systemic inflammation, and elevation of systemic and local levels of this inflammatory marker which has been associated with an increased risk for cardiovascular disease in the obstructive coronary artery disease (O-CAD) are well known, but little was known in CAE. The anti-inflammatory effects of statins and the effect of angiotensin-converting enzyme (ACE) inhibitors on endothelial dysfunction are well established in atherosclerosis. The aim of the present study was to investigate CRP level and its response to statin and ACE inhibitor treatment in CAE. MATERIALS AND METHOD: We measured serum hs-CRP level in 40 CAE (26 males, mean age: 56.32 +/- 9 years) and 41 O-CAD (34 males, mean age: 57.19 +/- 10 years) patients referred for elective coronary angiography at baseline and after 3-month statin and ACE inhibitor treatment. RESULTS: Plasma hs-CRP levels were significantly higher in CAE group than O-CAD group at baseline (2.68 +/- 66 mg/L versus 1, 64 +/- 64, resp., P < .0001). Plasma hs-CRP levels significantly decreased from baseline 3 months later in the CE (from 2.68 +/- 0.66 mg/L to 1.2 +/- 0.53 mg/L, P < .0001) as well as in the O-CAD group (from 1.64 +/- 0.64 mg/L to 1.01 +/- 0.56 mg/L, P < .001). CONCLUSION: We think that hs-CRP measurement may be a good prognostic value in CAE patients as in stenotic ones. Further placebo-controlled studies are needed to evaluate the clinical significance of this decrease in hs-CRP.

Effect of diltiazem and metoprolol on left atrial appendix functions in patients with nonvalvular chronic atrial fibrillation.

OBJECTIVES: Thrombo-embolic events are the important cause of mortality and morbidity in patients with chronic atrial fibrillation (CAF). The origin of thromboembolism is often the left atrial appendix (LAA). Flow rate velocity (FRV) inside the LAA is the major determinant of thrombus formation. The aim of our study was to investigate the effects of diltiazem and metoprolol used for ventricular rate control on FRV of the LAA in CAF patients and thus to evaluate the positive or negative effects of these two drugs on thromboembolic events. METHODS: Sixty-four patients were included in the study. All patients were suffering from CAF for more than a year. The patients were allocated to two groups according with agent used for rate control- metoprolol (Group 1; n=31) and diltiazem (Group 2; n=33). Transesophageal echocardiography was applied to all patients and LAA FRV was measured by a pulse wave Doppler in the 1/3 proximal portion of the LAA. The measurements were repeated after applying 5 mg metoprolol to Group 1 and 25 mg diltiazem to Group 2 via venous cannula. RESULTS: In Group 1 after metoprolol LAA flow velocity changed from 0.25 +/- 0.90 m/s to 0.25 +/- 0.10 m/s (p>0.05). In group 2 after diltiazem left atrial appendix FRV decreased from 0.21 +/- 0.9 m/s to 0.19 +/- 0.6 m/s (p>0.05). CONCLUSIONS: In patients with CAF metoprolol used for ventricular rate control had no effect on LAA flow velocity and the observed decrease in LAA flow rate velocity with intravenous diltiazem was insignificant.

Deterioration of heart rate recovery index in patients after carotid artery stenting.

Objective Although carotid artery stenting (CAS) is an effective treatment for severe carotid stenosis, it has been associated with alterations in autonomic functions long term after the procedure. Patients with CAS have been reported to have autonomic nervous system (ANS) dysfunction. This study aimed to evaluate heart rate recovery (HRR) indices and exercise test parameters after CAS. Methods Patients (10 male, 11 female) suitable for CAS, without a history of hypertension, diabetes mellitus, severe coronary artery or valvular heart disease, were enrolled in our study. Basal electrocardiography, echocardiography, and treadmill exercise testing were performed in all patients pre- and post-procedure. The HRR index was defined as the reduction in the heart rate from the rate at peak exercise to the rate first minute (HRR1), second minute (HRR2), third minute (HRR3) and fifth minute (HRR5) after the cessation of exercise stress testing. Results The exercise time, maximal heart rate, maximal blood pressure and maximal metabolic equivalents values were significantly decreased after the procedure. The first- and second-minute HRR indices of patients before procedure were significantly lower than after procedure (23.5 ± 6.6 vs 25.8 ± 8.3; p < 0.001 and 41.8 ± 12.3 vs 50.2 ± 16.3; p < 0.001, respectively). Similarly, HRR indices after the third and fifth minutes of the recovery period were significantly lower in patients before procedure, when compared with those indices after procedure (52.9 ± 13.1 vs 60.7 ± 14.4; p < 0.001 and 62.4 ± 12.8 vs 71.9 ± 14.1; p < 0.001). Conclusion We have demonstrated that HRR indices increased in the first, second, third and fifth minutes of the recovery period after maximal exercise testing in patients after the CAS procedure, which may be a reflection of parasympathetic dominance after CAS.

The relationship between platelet collagen receptor glycoprotein VI and no-reflow phenomenon in patients with acute ST-segment elevation myocardial infarction.

OBJECTIVES: The purpose of this study was to determine whether admission soluble glycoprotein VI (sGP-VI) level is associated with no-reflow phenomenon (NRP) after primary percutaneous coronary intervention (P-PCI) in patients with acute ST-segment elevation myocardial infarction (STEMI). METHODS: A total of 178 consecutive patients admitted to our hospital for a first STEMI and undergoing P-PCI within 12 hours of onset of symptoms were enrolled. The patients were divided into 2 groups (NRP group and reflow group). Admission sGP-VI plasma levels were measured by enzyme-linked immunosorbent assay. RESULTS: Of the 178 patients who underwent P-PCI, 41 patients (23%) developed NRP. The patients in the reflow group had higher levels of sGP-VI compared with the patients in the NRP group (38.5 ± 21.0 vs 21.9 ± 11.9 ng/mL, P < 0.001). The sensitivity and specificity values of the sGP-VI levels were 90% and 49%, respectively (cutoff value was ≤ 25). In the multivariate logistic regression analyses, sGP-VI levels of 25 ng/mL or lower, higher peak troponin T levels and body mass index value, amount of opaque of greater than 250 mL, and lesion length of greater than 13.5 mm were independent predictors of angiographic NRP. CONCLUSIONS: Lower admission sGP-VI levels are associated with NRP in patients with STEMI undergoing P-PCI. This outcome may open new therapeutic facility in the setting of P-PCI.

The association between apelin-12 levels and paroxysmal supraventricular tachycardia.

AIMS: Our aim was to investigate the apelin-12 levels in patients with atrioventricular tachyarrhythmias and compare with those in patients with lone atrial fibrillation. METHODS: Forty four patients with supraventricular tachycardia as atrial fibrillation, 44 patients with paroxysmal supraventricular tachycardia (P-SVT) as atrioventricular tachyarrhythmias, including atrioventricular nodal reentrant tachycardia or atrioventricular reentrant tachycardia, and 30 age- and sex-matched healthy individuals were included in the study. RESULTS: The apelin-12 levels were significantly lower in both atrial fibrillation and P-SVT groups than control group. In post-hoc analysis, there was no significant difference in apelin-12 levels between atrial fibrillation and P-SVT groups (P = 0.9). Patients in atrial fibrillation group and patients in P-SVT group had significantly lower apelin-12 levels than control group, separately (P < 0.001 and P < 0.001, respectively). The sensitivity and specificity values of the apelin-12 levels for predicting SVT, including both atrial fibrillation and atrioventricular reentrant tachycardia or atrioventricular nodal reentrant tachycardia were 64.77 and 90%, respectively (cut-off value was 0.87). The area under the receiver operator characteristic curve was 0.834 for the apelin-12 levels (P = 0.0001). CONCLUSION: Apelin-12 levels are lower in patients with atrial fibrillation and P-SVT than control groups. Lower apelin levels in patients with atrial fibrillation and P-SVT would be expected to result in a decrease in the conduction velocity.

Deficiency of a new protein associated with cardiac syndrome X; called adropin.

The pathophysiology of cardiac syndrome X (CSX) is still unclear, but most patients with CSX have endothelial dysfunction. It has been shown that adropin uniquely effects the regulation of endothelial function. The purpose of the study was to evaluate the role of adropin in CSX. Eighty-six consecutive cardiac syndrome X-diagnosed patients and 86 age-sex matched healthy subjects were enrolled into the study. Serum adropin levels, nitrite/nitrate levels were measured in each subject. The adropin levels were significantly lower in patients with CSX than healthy subjects (1.7 ± 0.8 ng/mL and 3.4 ± 1.8 ng/mL, respectively; P < 0.001). The BMI values of patients with CSX were significantly higher than control subjects (28.1 ± 2.4 kg/m(2) and 26.0 ± 3.7 kg/m(2) , respectively; P < 0.001). Plasma nitrite/nitrate levels were lower in patients with CSX than control subjects (15.9 ± 1.6 µmol/L vs. 25.4 ± 2.8 µmol/L, respectively; P < 0.001), and they have a significantly positive correlation with plasma adropin levels (r = 0.463, P < 0.001). In the multiple linear regression analysis, nitrite/nitrate levels, BMI, and adropin were found to be independent risk factors for CSX. A ROC curve is used to identify the ability of adropin levels to predict the cardiac syndrome X. The area under the ROC curve was 0.854 for adropin levels (P = 0.0001). The sensitivity and specificity values of adropin levels were 90.7 and 70.9%, respectively (cut-off value 2.73). In conclusion, lower serum adropin levels were associated with CSX. Adropin is an independent risk factor for CSX.

The effect of nesfatin-1 levels on paroxysmal supraventricular tachycardia.

BACKGROUND: Nesfatin-1 was originally identified as a neuropeptide of the hypothalamus, which is a key integration area of the brain, where numerous neuropeptides and transmitters are released to participate in the control of essential body functions. In the literature, there are no studies showing the relationship between the nesfatin-1 level and paroxysmal supraventricular tachycardia. We hypothesize that the circulating levels of nesfatin-1 may increase during supraventricular tachycardia, to engage the vagal stimulation to terminate by the inhibition of neuropeptide-Y, and may activate oxytocin and the corticotropin-releasing hormone. MATERIALS AND METHODS: This study includes 120 cases (80 patients and 40 controls). Patients with paroxysmal supraventricular tachycardia were compared with the control group with regard to sex, nesfatin-1 level, comorbid diseases, serum renal function values, and patients' vital findings. RESULTS: The nesfatin-1 levels were significantly higher in the paroxysmal supraventricular tachycardia group than in the control group and positively correlated highly with heart rate (r = 0.634; P < 0.001). The area under the receiver operating characteristic curve was 0.644 for the nesfatin-1 levels (P = 0.0051). The sensitivity and specificity values of the nesfatin-1 levels were 41.2% and 95%, respectively (cutoff value >1743.7 pg/mL). CONCLUSION: At the end of this study, a statistically significant correlation was found between the serum nesfatin-1 level and supraventricular tachycardia. Although multifactorial causes may explain the relationship, we based our hypothesis on the relationship of the antagonistic effects of nesfatin-1 on the neuropeptide-Y and activated oxytocin.