Relationship between adiponectin and copeptin levels with long-term cardiovascular mortality in ST-segment elevation myocardial infarction after percutaneous coronary intervention.

OBJECTIVE: The aim of this study was to determine adiponectin and copeptin levels that might be prognostic for cardiovascular mortality (CvsM) in ST-segment elevation myocardial infarction (STEMI) patients who had percutaneous coronary intervention (PCI). METHODS: Patients who underwent PCI between November 2010 and April 2011 were enrolled and followed for more than eight years. The baseline, demographic and angiographic findings, in-hospital follow up, laboratory results including adiponectin and copeptin levels, and echocardiographic data of the patients were evaluated. RESULTS: There were 78 males and 20 females. The CvsM rate was 26.66% at 112 months of follow up. Some factors were significantly related to CvsM and adiponectin level was an independent predictor of mortality. A cut-off value of ≥ 8 950 ng/ml for adiponectin and ≥ 7.41 ng/ml for copeptin was related to a 3.01- and 2.83-times higher CvsM risk, respectively. CONCLUSION: Adiponectin level was a predictor for CvsM. Higher levels of adiponectin and copeptin could predict a higher risk of CvsM in STEMI patients.

Admission triglyceride-glucose index is predictor of long-term mortality and appropriate implantable cardiac defibrillator therapy in patients with heart failure.

Background: In this study, the main aim was to evaluate the relation of the triglyceride-glucose (TyG) index to long-term mortality and proper shock therapy in patients with an implantable cardiac defibrillator (ICD) implanted for heart failure with reduced ejection fraction. Methods: This retrospective study group consisted of 773 patients treated with ICD for heart failure with reduced ejection fraction. The long-term prognostic effect of the TyG index among tertiles was evaluated regarding mortality and appropriate ICD therapy. Results: In the adjusted model, the mortality rates were 14.0% (hazard ratio: 2.24; 95% CI: 1.42-6.88) in tertile 2 and 23.3% (hazard ratio: 3.88; 95% CI: 1.84-14.38) in tertile 3. Conclusion: The TyG index was found to be an independent predictive marker for both long-term mortality and appropriate ICD therapy.

Are inflammatory parameters predictors of amputation in acute arterial occlusions?

Background The aim of the present study was to investigate the role of inflammatory markers to predict amputation following embolectomy in acute arterial occlusion. Methods A total of 123 patients operated for arterial thromboembolectomy due to acute embolism were included in the study. The patients without an extremity amputation following thromboembolectomy were classified as Group 1 ( n = 91) and the rest were classified as Group 2 ( n = 32). These groups were compared in terms of clinical and demographic characteristics, C-reactive protein, complete blood count parameters, neutrophil-lymphocyte ratio, platelet-lymphocyte ratio and red cell distribution width. Results The average age was 68.0 ± 11.7 years. The most common thromboembolism localization was femoral artery. When preoperative mean C-reactive protein ( p = 0.0001), mean platelet volume ( p = 0.0001), platelet-lymphocyte ratio ( p = 0.0001), neutrophil-lymphocyte ratio ( p = 0.0001) and red cell distribution width ( p = 0.0001) were compared, a statistically significant difference was observed between groups. In univariate and multivariate regression analysis, higher levels of preoperative C-reactive protein ( p = 0.009) and mean platelet volume ( p = 0.04) were detected as independent risk factors of early extremity amputation. Conclusion We observed that preoperative mean platelet volume and C-reactive protein were predictors of amputation after thromboembolectomy in acute arterial occlusion.

Association of admission serum laboratory parameters with new-onset atrial fibrillation after a primary percutaneous coronary intervention.

OBJECTIVES: New-onset atrial fibrillation (NOAF) during hospitalization is considered a frequent complication associated with worse outcomes in the setting of ST-segment elevation myocardial infarction (STEMI). We aimed to investigate the association of admission serum laboratory parameters, neutrophil to lymphocyte ratio (NLR), and monocyte to high-density lipoprotein ratio (MHR) with NOAF in STEMI patients treated with a primary percutaneous coronary intervention (PCI). PATIENTS AND METHODS: A total of 621 patients who were hospitalized with a diagnosis of STEMI and treated with primary PCI were retrospectively enrolled in the study. NOAF during index hospitalization and overall mortality were reported as the clinical outcomes. RESULTS: In our study population, 40 (6.4%) patients developed NOAF during index hospitalization. Monocyte counts, mean platelet volume (MPV), red cell distribution width (RDW), NLR, MHR, C-reactive protein (CRP), creatinine, glucose, and uric acid levels were higher in the NOAF+ group compared with the NOAF- group. In multivariate regression analysis, age, left-ventricular ejection fraction, left atrial volumes, admission heart rate, multivessel disease, increased levels of CRP, MPV, RDW, uric acid, NLR, and MHR independently predicted NOAF. In addition, NOAF was found to be an independent predictor of overall mortality in the study population. CONCLUSION: For the first time in the literature, admission serum levels of MPV, RDW, uric acid, NLR, and MHR were found to be correlated independently with NOAF after primary PCI.

The neutrophil-to-lymphocyte ratio is associated with bare-metal stent restenosis in STEMI patients treated with primary PCI.

BACKGROUND: The clinical importance of complete blood count (CBC) parameters such as the neutrophil-to-lymphocyte ratio (NLR) has been shown in cardiovascular diseases. Stent restenosis (SR) is a major adverse event after stent implantation. In this study, we aimed to investigate the correlation of CBC parameters with SR rates after primary percutaneous coronary intervention (PCI). METHODS: Patients who had undergone primary PCI for ST-segment elevation myocardial infarction (STEMI) and control angiography during follow-up were retrospectively recruited. Patients were categorized according to admission NLR tertiles, and clinical, hematological, and angiographic data were compared. RESULTS: A total of 404 patients (207 patients with SR and 197 patients without SR) were included in the study. Patients were categorized into three groups according to the tertiles of admission NLRs; the NLR was less than 3.38 in tertile 1 (n=134), between 3.38 and 6.26 in tertile 2 (n=135), and greater than 6.26 in tertile 3 (n=135). During a follow-up period of a median of 14 months (minimum 6 months, maximum 60 months) SR developed in 80 patients of tertile 3 (59%), 74 patients of tertile 2 (55%), and 53 patients of tertile 1 (40%), which were significantly different (P=0.01). According to multivariate Cox regression analysis, male sex, stent length (odds ratio 1.04, 95% confidence interval 1.01-1.06, P=0.01), admission NLRs (odds ratio 1.13, 95% confidence interval 1.08-1.19, P=0.01), and white blood cell and neutrophil counts remained the independent predictors of SR in the study population. Other CBC parameters and admission C-reactive protein, creatinine, and fasting glucose levels were not independently correlated with SR. On receiver operating curve analysis, admission NLRs higher than 3.84 were found to predict SR with a sensitivity of 73.4% and a specificity of 50.8% (area under the curve 0.604, P=0.01). CONCLUSION: High NLR levels, white blood cell counts, and neutrophil counts at admission are independently correlated with SR after primary PCI.

Can the T-peak to T-end interval be a predictor of mortality in patients with ST-elevation myocardial infarction?

BACKGROUND: The interval between the peak and the end of the T wave (Tp-e interval) on 12-lead ECG is a measure of transmural dispersion of repolarization and may be related to malignant ventricular arrhythmias. The objective of this study was to investigate whether the Tp-e interval predicts in-hospital and long-term mortality in patients with ST-segment elevation myocardial infarction (STEMI) undergoing a primary percutaneous coronary intervention (pPCI). METHODS: This study included 488 consecutive patients with STEMI treated with pPCI. Electrocardiograms were obtained after pPCI and the Tp-e interval was measured in leads without ST-segment elevation. RESULTS: There were 46 (9.4%) deaths in the population, with a mean follow-up time of 21.1±10.2 months. The Tp-e interval was associated with not only in-hospital ventricular tachycardia/fibrillation, target vessel revascularization, and death but also long-term target vessel revascularization and death. Furthermore, the Tp-e interval measured using the tail method was found to be a significant predictor of long-term mortality in multivariable Cox analyses [odds ratio 1.018, 95% confidence interval (1.004-1.033)]. Findings were similar in the Tp-e interval and the heart rate-corrected Tp-e interval (cTp-e). CONCLUSION: Tp-e and cTp-e measured using the tail method were found to be predictors of both in-hospital and long-term mortality.

Evaluation of coronary microvascular function and nitric oxide synthase intron 4a/b polymorphism in patients with coronary slow flow.

OBJECTIVE: Slow coronary flow (SCF) is reported to be associated with increased risk of cardiovascular disease. We have used coronary flow reserve measurement by transthoracic Doppler echocardiography to determine coronary microvascular function in patients with SCF and to determine whether the intron 4a/b polymorphism of the eNOS gene influences coronary endothelial function. METHODS: Overall, 96 patients with SCF and 79 controls were enrolled in the study. Coronary flow was quantified according to the thrombolysis in myocardial infarction (TIMI) frame count (TFC) on angiogram. Coronary diastolic peak flow velocities (DPFV) were measured with color Doppler flow mapping at baseline and after dipyridamole infusion. Coronary flow reserve was calculated as the ratio of hyperemic to baseline DPFV. The eNOS 4a/b polymorphism was detected by PCR. Patients with diabetes were excluded from the study. RESULTS: The SCF group was comparable to the control group in terms of demographic and clinical characteristics, except for hemoglobin and HDL-cholesterol levels, TFC of the left anterior descending artery, the circumflex artery, and the right coronary artery; the mean TFC was higher in the SCF group. Hyperemic DPFV and the hyperemic/baseline DPFV ratio were significantly lower in the SCF group when compared with the control group. However, baseline DPFV were similar in both groups. The number of patients with eNOS4 a/a and eNOS4 a/b phenotypes was statistically higher in SCF groups. The frequency of allele 'a' of the eNOS4 gene was also statistically higher in the SCF group. When patients were grouped according to the presence or absence of allele 'a' of the eNOS4 gene, statistically significant differences were found in the TFC of the left anterior descending artery, the circumflex artery; mean TFC; baseline DPFV; and hyperemic/baseline DPFV. Univariate analysis in which eNOS4 b/b was used as the referent group showed that the presence of allele 'a' of the eNOS4 gene significantly predicted SCF (odds ratio: 2.79, 95% confidence interval: 1.32-5.89; P=0.007). In multivariate analysis using a model adjusted for variables with a P value lower than 0.10 in univariate analyses, the presence of allele 'a' of the eNOS4 gene was found to be an independent predictor of SCF (odds ratio: 3.22, 95% confidence interval: 1.28-8.82; P=0.013). CONCLUSION: The presence of allele 'a' may be a risk factor for microvascular endothelial dysfunction and higher TFCs in SCF patients.

Assessment of interleukin-1 gene cluster polymorphisms in lone atrial fibrillation: new insight into the role of inflammation in atrial fibrillation.

BACKGROUND: Systemic inflammation is accepted as one of the pathophysiological mechanisms of atrial fibrillation (AF). The role of inflammation has been shown previously. Interleukin (IL) system is the main modulator of the inflammatory responses and genetic polymorphisms of IL-1 cluster genes are associated with increased risk for inflammatory diseases. OBJECTIVES: To investigate the association between polymorphisms of IL-1 cluster genes and lone AF. SUBJECTS AND METHODS: DNA samples were collected from 70 proven lone AF patients and 70 healthy subjects. Genomic DNA was typed for the variable number of the tandem repeat (VNTR) IL-1 receptor antagonist (RN) gene polymorphism, IL-1B -511 C > T(rs16944) promoter polymorphism, and +3953 C > T(rs1143634) polymorphism in exon 5 by polymerase chain reaction. RESULTS: In lone AF group the frequency of IL-1RN2/2 and IL-1RN1/2 genotypes were higher than in the control group (7.2% vs 4.3% and 48.5% vs 22.8%, respectively; χ(2) = 14.1; P = 0.028). The frequency of allele 2 was significantly higher in the lone AF group (32.1% vs 15.7%; χ(2) = 10.7; P = 0.005). Allele and genotype distribution of IL-1B -511 C > T and +3953 C > T polymorphisms were not statistically different between the groups. C-reactive protein (CRP) levels were higher in lone AF patients compared to the control group (median = 1.25, interquartile range [IQR] = 0.85 vs median = 1.08, IQR 0.46 mg/L, respectively; P = 0.02). In multivariate regression analysis, presence of allele 2 of IL-1 VNTR polymorphism and elevated plasma high-sensitive-CRP levels were the independent predictors of lone AF. CONCLUSION: Presence of allele 2 of VNTR polymorphism of IL-1RN gene may cause increased risk for lone AF probably due to the inadequate limitation of inflammatory reactions.