Is lysosomal acid lipase activity associated with the presence and severity of coronary artery disease?

BACKGROUND: Lipid metabolism is considerably complex and there can be many critical steps in atherogenesis. The association between lysosomal acid lipase (LAL) activity and coronary artery disease (CAD) has not been elucidated in detail. We aimed to evaluate the association between LAL activity with the presence and severity of CAD in patients who are seen in daily clinical practice. METHODS: Patients who underwent coronary angiography were divided into groups according to the angiography results. Syntax scores and Gensini scores were calculated. The LAL activity was measured from dried blood spots. RESULTS: Median LAL activity values were similar in all study groups (normal coronary arteries: 0.40 nmol/punch/h; non-obstructive CAD: 0.44 nmol/punch/h; obstructive chronic CAD: 0.40 nmol/punch/h; obstructive acute coronary syndrome: 0.48 nmol/punch/h) and there was no correlation between coronary atherosclerotic burden and LAL activity (correlation coefficients Syntax score and LAL: -0.032; Gensini score and LAL: -0.030). In addition, no relationship between serum lipid levels and LAL activity was detected. CONCLUSION: The presence of CAD and its severity is not associated with the LAL activity in patients encountered in daily clinical practice.

Determination of microRNAs associated with adverse left ventricular remodeling after myocardial infarction.

Increasing evidence indicates that microRNA (miRNA) regulated mechanisms in myocardial healing and ventricular remodeling following acute myocardial infarction (AMI). We aim to comprehensively investigate changes of exosomal miRNA profile during the post-MI period and determine potential miRNAs associated to adverse left ventricular remodeling (ALVR). We prospectively evaluated ST-elevated MI patients with cardiac magnetic resonance imaging at the 2 weeks and 6 months after AMI (n = 10). ALVR was defined as an increase in LV end-diastolic and end-systolic volume > 13%. The blood samples were taken for miRNA measurements at the baseline, 2 and 6 weeks after AMI. In the miRNA profile assessment, 8 miRNAs were identified that were associated ALVR (miR-199a-5p, miR-23b-3p, miR-26b-5p, miR-301a-3p, miR-374a-5p, miR-423-5p, miR-483-5p and miR-652-3p). Three of them (miR-301a-3p, miR-374a-5p and miR-423-5p) differed significantly between patients with and without ALVR during follow-up period and the rest of them during the acute phase of AMI. The detection of these miRNAs, which have different role in various pathways, necessitate future mechanistic studies unravel the complex remodeling process after AMI.

The Role of Serum Resolvin D1 Levels in Determining the Presence and Prognosis of ST-Segment Elevation Myocardial Infarction.

BACKGROUND: Resolvin D1 (RvD1) can play a determining role in inflammatory cell migration and reduce the expression of inflammatory cytokines to enhance cardioprotection. The aim of this study was to compare serum RvD1 levels in patients with ST-segment elevation myocardial infarction (STEMI) and individuals with normal coronary arteries (NCAs) and to evaluate the association between serum RvD1 levels and prognostic markers of STEMI. METHODS: 140 subjects (88 patients diagnosed with the indication of STEMI and 52 healthy individuals with NCA) were studied. RESULTS: Regression analysis revealed that RvD1 levels were independently associated with STEMI. While RvD1 levels were negatively correlated with high-sensitivity C-reactive protein, pro-brain natriuretic peptide, peak troponin, and Thrombolysis in Myocardial Infarction thrombus grade, they were positively correlated with left ventricular ejection fraction. An RvD1 cut-off value of 5.07 (ng/mL) was effective in predicting STEMI with a sensitivity of 79.5% and specificity of 96.2%. CONCLUSION: Serum RvD1 levels were found to be lower in the group with STEMI compared to the control group. Levels of RvD1 at admission were associated with poor prognostic markers of STEMI.

Low sCD163/TWEAK Ratio at First Day After Acute Myocardial Infarction Associated with Adverse Cardiac Remodeling in Non-Elderly Patients.

Aim    In this study, we aimed to investigate the role of sCD163 / tumor necrosis factor-like weak apoptosis-inducing (TWEAK) ratio in cardiac remodeling in non-elderly patients diagnosed with first acute myocardial infarction (MI).Material and Methods    Forty-four patients (age ranges: 40-64 years) diagnosed with first-time acute ST-elevation MI in the emergency department were evaluated with cardiac magnetic resonance (CMR) imaging. Adverse remodeling (AR) was defined the increases of left ventricular end-diastolic volume by ≥12 % by CMR at 6­month post-MI TWEAK and sCD163 were measured at the first day (baseline), 2 weeks and 6 weeks post-MI.Results    The average age of patients included in the study was 53.6±5.1 years. AR was detected in 18 patients at the 6 months post-MI. At the first day post-MI, median sCD163 concentration (116 069 vs 86 394 pg / mL, p=0.040) and median TWEAK concentration (759.4 vs 220.1 pg / mL, p<0.001) were higher in AR group compared to group without AR (the non-AR group), median sCD163 / TWEAK ratio (101.4 vs. 406.8; p<0.001) was lower. At the first day post-MI, concentrations of TWEAK and sCD163 showed a positive correlation in AR group and group without AR s. At 2 weeks post-MI, positive correlation continued in the non-AR group, but no significant correlation was found in the AR group. At the first day post-MI, sCD163 / TWEAK ratio was higher diagnostic performance compared to TWEAK and sCD163.Conclusion    In the early phase post-MI, the relationship between sCD163 - TWEAK may have an important role in AR pathogenesis. A lower sCD163 / TWEAK ratio on the first day after MI was associated with an increase in left ventricular end-diastolic volume after 6 months of follow-up.

Relationship Between Prodromal Angina Pectoris and Neutrophil-to Lymphocyte Ratio in Patients With ST Elevation Myocardial Infarction.

BACKGROUND: The aim of this study was to investigate the relationship between prodromal angina (PA) with neutrophil-to-lymphocyte ratio (NLR) in patients with ST-segment elevation myocardial infarction (STEMI). METHODS: The study group included 145 patients with STEMI who underwent emergency coronary angiography (CA) within 24hours of symptom onset. Data were collected regarding whether patients had experienced PA before acute myocardial infarction. Seventy-three (73) patients (50.3%) had prodromal angina. Prodromal angina positive and negative groups were compared for demographic characteristics, complete blood count parameters including NLR, blood biochemistry parameters and left ventricular ejection fraction (LVEF). RESULTS: Neutrophil count, NLR, and troponin I levels were significantly higher in the PA negative group. LVEF after reperfusion and lymphocyte count were lower in the PA negative group. In multivariate regression analysis, NLR (ß=-0.419, p<0.001) and LVEF (ß=0.418, p<0.001) were found to be significantly associated with the presence of PA in STEMI patients. CONCLUSIONS: Absence of PA was significantly and independently associated with increased NLR and impaired LVEF after reperfusion, and increased NLR was found as a significant predictor for both lack of PA and impaired LVEF in STEMI patients.

Association of Serum Copeptin Levels with Patency of Infarct-Related Arteries in Patients with ST-Segment Elevation Myocardial Infarction.

BACKGROUND: Copeptin is widely used as a predictor of an adverse prognosis in many clinical conditions. Reduced antegrade coronary flow in an infarct-related artery (IRA) is associated with adverse clinical outcomes in patients with ST-segment elevation myocardial infarction (STEMI). The aim of this study was to investigate whether copeptin level on admission was associated with IRA patency in STEMI patients. METHODS: A total of 88 patients were enrolled into the study and divided into two groups according to TIMI flow grade in the IRA before primary percutaneous coronary intervention. RESULTS: White blood cell count (p = 0.015), neutrophils (p = 0.047), N-terminal pro-brain natriuretic peptide (NTproBNP) (p < 0.001), copeptin (p < 0.001) and peak troponin I (p = 0.001) were significantly higher in the occluded IRA group with a significantly lower serum sodium level (p < 0.001). Age- and gender-adjusted multivariate analysis revealed that copeptin (OR = 1.970; p = 0.001), peak troponin I (1.055; p = 0.005) and NTproBNP (OR = 1.003; p = 0.010) were independent predictors of an occluded IRA. A copeptin cut-off value of > 6.8 ng/mL was found to predict an occluded IRA with a sensitivity of 80% and specificity of 100% (area under the curve: 0.917; p < 0.001). Performance ranking of the biomarkers that could predict an occluded IRA showed copeptin > peak troponin I = NTproBNP. CONCLUSIONS: Copeptin levels were higher in the patients with an occluded IRA and STEMI. Higher levels of copeptin predicted an occluded IRA in the patients with STEMI who were admitted to the emergency department during the first three hours of chest pain.

Serum Sphingosine 1 Phosphate Levels in Patients with and without Coronary Collateral Circulation.

BACKGROUND: Sphingosine 1 phosphate, an active sphingolipid metabolite, functions in both healthy and diseased cardiovascular systems. It has been reported to play a role in angiogenesis and arteriogenesis in various tissues, which are the proposed mechanisms for the development of coronary collateral circulation. To the best of our knowledge, no data exist regarding serum sphingosine 1 phosphate levels and the presence of coronary collateral circulation in the literature. Thus this study aimed to investigate serum sphingosine 1 phosphate levels in patients with and without coronary collateral circulation. METHODS: A total of 140 patients were included (70 with coronary collateral circulation and 70 with normal coronary arteries and stable coronary artery disease without collaterals). Rentrop collateral grade and the number of coronary arteries with collateral circulation were recorded. RESULTS: Serum sphingosine 1 phosphate levels were higher in the collateral group than in the control group [186.6 (142.3-243.5) µg/l vs. 128.5 (105.0-161.6) µg/l, p < 0.001]. Multivariate logistic regression analysis revealed that the presence of multivessel disease, high serum sphingosine 1 phosphate levels and previous history of P2Y12 use were independent predictors of coronary collateral circulation. Median sphingosine 1 phosphate levels in different Rentrop grades in the collateral group were similar, and there was no significant difference in median serum sphingosine 1 phosphate level with a higher number of coronary arteries with collateral circulation. CONCLUSIONS: Our findings demonstrated higher levels of sphingosine 1 phosphate in the patients with coronary collateral circulation.

Association between plasma homocysteine levels and end-organ damage in newly diagnosed type 2 diabetes mellitus patients.

PURPOSE: The aim of the present study was to investigate the association between plasma homocysteine (Hcy) levels and carotid, cardiac, and renal end-organ damage in newly diagnosed type 2 diabetes mellitus (T2DM) patients. METHODS: Newly diagnosed normotensive T2DM patients (n = 390) were enrolled in this study. The patients were not taking any medications over the duration of the study. The left ventricular mass index (LVMI), carotid intima media thickness (CIMT), and creatinine levels and 24-h microalbuminuria were used to determine cardiac, carotid, and kidney end-organ diseases, respectively. RESULTS: Using univariate logistic regression analysis; age, 24-h microalbuminuria, fasting blood glucose, CIMT, creatinine level, and LVMI were found to be significantly associated with the Hcy level. When those six variables were included in a multivariate regression model, CIMT, LVMI, and creatinine were found to be significantly associated with the Hcy level. We determined that an Hcy level >12.5 µmol/L was predictive of high LVMI, with a sensitivity of 70.1% and a specificity of 68%. An Hcy level >13.5 µmol/L was predictive of high CIMT, with a sensitivity of 67.5% and a specificity of 63.1%. CONCLUSION: In this study, LVMI, CIMT, and creatinine level were positively correlated with the Hcy level. We believe that the Hcy level may be a useful predictor of end-organ damage, including cardiac, carotid, and renal diseases, in newly diagnosed T2DM patients.

Admission Value of Serum Cathepsin D Level Can be Useful for Predicting In-Hospital Mortality in Patients with NSTEMI.

BACKGROUND: We aimed to investigate the association of serum cathepsin D levels with in-hospital mortality and Syntax scores (SXscore) in non-ST elevation myocardial infarction (NSTEMI) patients. METHODS: A total of 88 patients were included in the study. The patients were divided into two groups: those with in-hospital mortality (-), and those with in-hospital mortality (+). The receiver operating characteristics curve was used to show the sensitivity and specificity of serum cathepsin D levels, and the optimal cut-off value for predicting in-hospital mortality and high SXscore. RESULTS: Patients with (+) in-hospital mortality and high SXscore had lower serum cathepsin D levels compared to the patients with (-) in-hospital mortality and low SXscore. Using a cutoff score of < 16 for the cathepsin D level, in-hospital mortality was predicted with a sensitivity and specificity of 73.4% and 77.6%, respectively, and also predicted high SXscore with a sensitivity and specificity of 72.4% and 67.6%, respectively. CONCLUSIONS: Serum cathepsin D levels established upon admission were significantly and independently lower in NSTEMI patients with high rate of mortality, high SXscores, and low left ventricular ejection fraction.

Association of thiol disulfide homeostasis with slow coronary flow.

Objective The aim of this study was to investigate the role of thiol disulfide homeostasis in the presence of slow coronary flow. Material and methods In this cross-sectional study, a total of 110 patients who admitted to our hospital between March 2014 and December 2015 were included in the study. There were 65 patients in the slow coronary flow, and 45 patients in the normal flow groups. Results We found significant differences between slow coronary flow and the normal flow groups for thiol disulfide homeostasis, and the results of our study indicated that hsCRP, and thiol disulfide ratio were independently associated with slow coronary flow. Conclusion Our study showed that thiol disulfide homeostasis was significantly and independently related to the presence of slow coronary flow.

Predictive Value of Neutrophil Lymphocyte Ratio and Platelet Lymphocyte Ratio in Patients with Coronary Slow Flow.

BACKGROUND: Increased microvascular resistance due to chronic inflammation is assumed to be one of the mechanisms associated with coronary slow flow (CSF). Previous studies have shown that the platelet-to-lymphocyte ratio (PLR) and the neutrophil-lymphocyte ratio (NLR) are markers of inflammation for various diseases. In this study we aimed to evaluate the relationship between CSF and PLR-NLR. METHODS: Seventy-eight patients with CSF and 50 patients with normal coronary flow were enrolled into this study. The study subjects underwent medical examination and testing, after which their platelet-to-lymphocyte ratios and NLR values were calculated. An independent observer measured the coronary flow rate by Thrombolysis in Myocardial Infarction Frame Count (TFC) method. The platelet-to-lymphocyte ratio and NLR values were compared between the groups and correlation analysis was performed to explore the relationship between mean TFC with PLR and NLR. RESULTS: Platelet-to-lymphocyte ratio and NLR values were significantly higher in patients with CSF (p < 0.001). There was a positive significant correlation between TFC with NLR and PLR (Spearman's Rho: 0.59, p < 0.001 and Spearman's Rho: 0.30, p = 0.001, respectively). Multivariate logistic regression analysis revealed that NLR is the one independent predictor for CSF. CONCLUSIONS: This study demonstrated an association between CSF and PLR-NLR. Although the exact mechanism could not be explained, our findings support the possible role of inflammation in CSF physiopathology.

Relationship between serum vitamin D levels and angiographic severity and extent of coronary artery disease.

BACKGROUND: Vitamin D is known for its effect in calcium and bone homeostasis. There is an increasing evidence for health benefits accomplished by activated vitamin D that go beyond these classical functions. Previous studies have suggested that lower vitamin D levels are associated with increased cardiovascular disease risk. Therefore, we aimed to evaluate relationship between vitamin D levels and extent and severity of coronary artery disease. MATERIALS AND METHODS: A total of 746 patients in whom coronary angiography was performed between August 2012 and July 2013 were enrolled in this study. Serum vitamin D levels were measured, and patients were grouped according to their serum vitamin D levels (vitamin D <20 ng/mL (n = 602) Group 1 versus >20 ng/dL (n = 144) Group 2). Gensini score system was used to evaluate the association between serum vitamin D levels and severity and extent of coronary artery disease. RESULTS: There was no significant difference between the groups in terms of baseline characteristics and demographic characteristics. Mean serum vitamin D levels of all patient cohort was 15.54 ± 7.46 ng/mL. Group 1 and Group 2 had an average serum vitamin D levels of 12.6 ± 3.3 ng/mL and 27.5 ± 7.8 ng/mL, respectively. Gensini score for all cohort was 26.25 ± 34.32. Group 1 had an average Gensini score of 26.4 ± 35.7; on the other hand, Gensini score was 25.5 ± 27.5 in Group 2 (P = 0.097). CONCLUSIONS: This study failed to demonstrate significant relationship between serum vitamin D levels and the severity and extent of coronary artery disease. Further studies with more participation and homogenous groups with comparable individual and environmental features are needed to evaluate the association of serum vitamin D levels and cardiovascular diseases.

Association of thiol/disulfide ratio with syntax score in patients with NSTEMI.

OBJECTIVE: The aim of this study was to investigate the relation between native thiol/disulfide ratio (TDR) and severity of coronary atherosclerosis as assessed by the Syntax score (SXscore) in patients with non-ST elevation myocardial infarction (NSTEMI) who underwent coronary angiography. MATERIAL AND METHODS: A total of 290 patients with NSTEMI who underwent coronary angiography, were included in the study between January and August 2014. Baseline coronary angiography determined the SXscore. The patients were divided into two groups: one with low SXscores (< 23) and the other with high SXscores (≥ 23). RESULTS: TDR was significantly lower in patients with high SXscores (p < 0.001). In-hospital mortality was higher in the group with low TDR and high SXscores. The cut-off value of TDR on admission that predicted a high SXscore in the groups combined was 14, with a sensitivity of 73% and a specificity of 68%. CONCLUSION: TDR can be determined by an easy, inexpensive, automated, or optionally manual spectrophotometric assay, and correlates inversely with SXscore in patients with NSTEMI.

A novel oxidative stress marker in acute myocardial infarction; thiol/disulphide homeostasis.

BACKGROUND: The aim of this study was to investigate a novel oxidative stress marker (thiol/disulphide homeostasis) in patients with acute myocardial infarction (AMI) and compare the results with healthy controls for the first time in literature. METHODS: A total of 450 participants including 300 patients with AMI and 150 healthy individuals were included in the study. Left ventricular ejection fraction, body mass index, peak troponin I levels, triglyceride, total cholesterol, low-density lipoprotein, high-density lipoprotein (HDL), native thiol, total thiol, and disulphide as well as disulphide/native thiol and disulphide/total thiol ratios were compared between the groups. RESULTS: There were significant differences between AMI patients and the controls for left ventricular ejection fraction and troponin, HDL, native thiol, total thiol, and disulphide levels as well as disulphide/native thiol and disulphide/total thiol ratios (P < .05). Stepwise logistic regression model indicated that HDL (odds ratio [OR] = 0.923, P < .001) and disulphide levels (OR = 0.548, P < .001) and disulphide/total thiol ratio (OR = 0.356, P < .001) were significantly and independently related to AMI. The cutoff value of disulphide/total thiol ratio percentage on admission to predict AMI in all population was 4.3, with a sensitivity of 70% and a specificity of 69%. CONCLUSION: Thiol/disulphide homeostasis may be used as a novel oxidative stress marker in patients with AMI because it is readily available, easily calculated, and relatively cheap. Further studies are needed to confirm the pathophysiologic role of thiol/disulphide homeostasis in AMI.

An Unusual Case of Loffler Endomyocarditis after Takotsubo Cardiomyopathy Induced by Deep Neck Infection.

UNLABELLED: In this case, we herein have described a 72-year-old female patient with deep neck infection induced Takotsubo cardiomyopathy and idiopathic hypereosinophilic syndrome with Loffler endocarditis characterized by right atrial thrombus and right ventricular fibrothrombotic obliteration within two months. KEY WORDS: Cardiac thrombi; Hypereosinophilic syndrome; Takotsubo cardiomyopathy.

Acetylsalicylic Acid resistance in patients with type 2 diabetes mellitus, prediabetes & non-diabetic coronary artery disease.

UNLABELLED: Objective : Several studies have demonstrated the beneficial role of antiplatelet therapy with acetylsalicylic acid (ASA) at atherosclerotic vascular disease. Antiaggregant effect of ASA is not uniform in all patients. Purpose of the present study is to evaluate the prevalence of ASA resistance in patients with type 2 diabetes mellitus (T2DM), pre-diabetes and non-diabetic coronary artery disease (CAD). METHODS: Effect of ASA was assessed using the platelet function analyzer (PFA-100) system. Resistance to ASA was defined as a normal collagen/epinephrine induced closure time after one week of ASA therapy. Patients with non-diabetic CAD, pre-diabetes and T2DM were compared. RESULTS: ASA resistance was found in 26 (37.1%), 6 (17.6%) and 41 (26.5%) patients in the groups, respectively (p=0.154). ASA resistance was found to be significantly higher in men, smokers and insulin users, besides this it was found to be significantly lower in beta blocker (BB) users, angiotensin converting enzyme inhibitor (ACEI) users with univariate analysis. However insulin usage was found to be the single effective parameter on ASA resistance in multivariate analysis. CONCLUSION: There was no difference with regard to ASA resistance between groups. While ASA resistance was higher in men, smokers and insulin users, it was lower in patients using BBs and ACEIs.

The Relationship between Pre-Infarction Angina and Serum Sphingosine-1-Phosphate Levels.

BACKGROUND: Pre-infarction angina reduces myocardial infarct size by preventing the myocardium from being subjected to ischemia reperfusion (I/R) injury. Ischemic preconditioning is the proposed mechanism for this effect. Sphingosine 1 phosphate (S1P) activates ischemic preconditioning pathways and may play a role in the presence of cardioprotective effects of pre-infarction angina. Therefore, we evaluated the relationship between pre-infarction angina and serum S1P levels. METHODS: Between May 2011 and January 2012, 79 patients with acute myocardial infarction were included in the study. In addition to taking routine medical histories, all of the patients were questioned as to whether or not they had pre-infarction angina. We determined patients serum levels of S1P at admission and discharge, and peak creatine kinase MB and troponin levels were also measured in the pre-infarction angina positive and negative groups. RESULTS: Of the 79 patients included in the study, 36 had pre-infarction angina and 43 had not. Baseline characteristics were similar between the groups. The median level of serum S1P in patients with pre-infarction angina was significantly higher than in those without pre-infarction angina both at admission and discharge [0.54 (0.14-1.35) vs. 0.26 (0.12-0.62) p = 0.014/0.51 (0.20-1.81) vs. 0.30 (0.13-0.68) p = 0.010]. Serum high sensitive troponin levels were significantly lower in patients with pre-infarction angina [0.97 (0.39-3.07) vs. 2.56 (0.9-6.51) p = 0.034]. Serum S1P levels both at admission and discharge tended to be higher in patients with more angina episodes, but the differences between these subgroups were not statistically significant. CONCLUSIONS: Patients who experienced pre-infarction angina had higher serum S1P levels than patients without pre-infarction angina. This study supported our hypothesis that the cardioprotective effects of pre-infarction angina may in part be mediated by S1P. KEY WORDS: Ischemic preconditioning; Pre-infarction angina; Sphingosine 1 phosphate.

Predictors of length of hospital stay and in-hospital adverse events in patients with acute decompensated heart failure: in-hospital 24-hour blood pressure monitoring data.

OBJECTIVE: Neurohumoral alterations in heart failure (HF) affect blood pressure variability (BPV) and vascular compliance, but little is known about this subject among patients admitted to the hospital with decompensated HF. This study sought to investigate in-hospital 24-h blood pressure monitoring (BPM)-derived BPV parameters and vascular compliance in patients with decompensated HF and explore the association of these parameters with hospitalization length and in-hospital adverse events. METHODS: A 24-h BPM was applied during the first 6 h of admission to the hospital in patients with decompensated HF. Circadian patterns were determined by the study patients. Average real variability (ARV), pulse pressure index (PPI), pulse stiffening ratio (PSR), and ambulatory arterial stiffness index (AASI) values were calculated from in hospital 24-h BPM recordings. Admission and discharge N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels, length of hospitalization, and in-hospital adverse events were recorded. RESULTS: A total of 167 patients with decompensated HF were included in the study. The dipper group exhibited a greater NT-proBNP decrease with the treatment than the non-dipper group and reverse dipper group. Hospitalization length was shorter in the dipper group than in the non-dipper and reverse dipper groups. Although ARV, AASI, and PSR were independently associated with the length of hospitalization, ARV, AASI, and PPI were independently associated with in-hospital adverse events. CONCLUSION: The post-admission in hospital 24-h BPM-derived parameters (dipper pattern, ARV, PPI, PSR, and AASI) of patients admitted to hospital with decompensated HF provide important prognostic information and predict the length of hospital stay.