Recep Kurt

Neutrophil to Lymphocyte Ratio is Predictor of Atrial Fibrillation Recurrence After Cardioversion With Amiodarone

Background: In this study, our aim is to examine the role of the neutrophil to lymphocyte ratio (NLR) in the predictions of recurrence under long-term follow-up in patients whose sinus rhythms (SRs) were restored with amiodarone in acute atrial fibrillation (AF). Methods: Retrospectively, patients with acute AF, which successfully converted to the SR with amiodarone treatment, were recruited into the study. Patients experiencing the first AF attack were enrolled to the study and followed up for 5 years (median 23 months, 25-75 percentiles 12-24 months). Neutrophil to lymphocyte ratio was computed as absolute neutrophil count divided by lymphocyte count. Results: A total of 218 patients were recruited into the study and followed up for 21.6 ± 13.9 months; 87 (40%) patients had ≥1 recurrent AF attack within this period. The follow-up of 131 (60%) patients resulted in persisted SR without any other AF attack. Groups were similar in terms of age and gender. Left atrium (LA) diameter and NLR were increased, and platelet count and lymphocyte count were decreased in patients with AF recurrence in univariate analysis (P < .05 for all). Only LA diameter (for per mm, 1.077 [1.021-1.136], P = .006) and NLR (1.584 [1.197-2.095], P = .001) were independent predictors of AF recurrence in the multivariate analysis. Conclusion: Increased NLR is a marker of increased inflammation and may serve as simple, cheap, and readily available predictors of recurrence in the long-term follow-up of patients admitted with acute AF and successfully converted to SR with amiodarone.

COHgb levels predict the long-term development of acute myocardial infarction in CO poisoning

BACKGROUND There are several studies evaluating the cardiac effects of carbon monoxide (CO) poisoning during the acute period; however, the number of studies evaluating the long-term cardiac effects is limited. OBJECTIVE The present study aimed to evaluate the effects of blood carboxyhemoglobin (COHb) levels, elevated due to CO poisoning on the long-term development of acute myocardial infarction (AMI). METHODS This cross-sectional cohort study included a total of 1013 consecutive patients who presented to the emergency department (ED) due to CO poisoning, between January 2005 and December 2007. The diagnosis of CO poisoning was made according to the medical history and a COHb level of greater than 5%. In terms of AMI development, the patients were followed up for an average of 56 months. RESULTS At the end of follow-up, 100 (10%) of 1013 patients experienced AMI. Carboxyhemoglobin levels at the time of poisoning were higher among those who were diagnosed with AMI compared to those who were not (55%±6% vs 30%±7%; P<.001). Using a multivariate Cox proportional hazards model with forward stepwise method, age, COHb level, CO exposure time, and smoking remained associated with an increased risk of AMI after adjustment for the variables found to be statistically significant in a univariate analysis. According to a receiver operating characteristic curve analysis, the optimal cutoff value of COHb used to predict the development of AMI was found to be greater than 45%, with 98% sensitivity and 94.1% specificity. CONCLUSION In patients presenting to the ED with CO poisoning, COHb levels can be helpful for risk stratification in the long-term development of AMI.

Association between oxidative stress index and post-CPR early mortality in cardiac arrest patients: A prospective observational study.

Objective: Cardiopulmonary resuscitation (CPR) is a series of lifesaving actions that improve the chance of survival following cardiac arrest (CA). Many clinical and laboratory parameters, such as the presence of asystole, out-of-hospital CPR, and duration of cardiac arrest, are associated with failed CPR in patients with CA. Asystole is a state of no cardiac electrical activity, along with the absence of contractions of the myocardium and absence of cardiac output. Oxidative stress index (OSI), which is the ratio of total oxidative status to total antioxidant status, increases by ischemia-reperfusion injury. We investigated whether OSI levels in patients with CA could predict early mortality after CPR. Methods: This study has a prospective observational cohort design. Five patients with a history of cancer, four patients who developed hemolysis in their blood, six patients who were transferred to our hospital from other hospitals, and six patients in whom blood samples for OSI could not be stored properly were excluded. Finally, a total of 90 in-hospital or out-of-hospital CA patients and 40 age- and sex-matched healthy volunteers as the control group were evaluated prospectively. The patients were classified according to the CPR response into a successful group (n=46) and a failed group (n=44). Comparisons between groups were performed using one-way ANOVA with post hoc analysis by Tukey’s HSD or independent samples t-test and the Kruskal-Wallis tests or Mann-Whitney U test for normally and abnormally distributed data, respectively. Also, we used chi-square test, Spearman’s correlation test, univariate and multible logistic regression analyses, and receiver operator characteristic curve analysis. Results: OSI was 3.0±4.0, 5.6±4.3, and 8.7±3.8 in the control group, the successful CPR group, and the failed CPR group, respectively (p<0.001 for the 2 comparisons). OSI on admission, ischemia-modified albumin, presence of asystole, mean duration of cardiac arrest, out-of-hospital CPR, pH, and potassium and sodium levels were found to have prognostic significance in the univariate analysis. In the multivariate logistic regression model, OSI on admission (OR=1.325, p=0.003), ischemia-modified albumin (OR=1.008, p=0.005), presence of asystole (OR=13.576, p<0.001), and sodium level (OR=1.132, p=0.029) remained associated with an increased risk of early mortality. In addition, the optimal cut-off value of OSI to predict post-CPR mortality was measured as >6.02, with 84.1% sensitivity and 76.1% specificity. Conclusion: Elevated OSI levels can predict failed CPR in CA patients.

The role of SCUBE1 in the pathogenesis of no-reflow phenomenon presenting with ST segment elevation myocardial infarction

Objective: SCUBE1 [signal peptide-CUB (complement C1r/C1 s)-EGF (epidermal growth factor)-like domain-containing protein 1] might function as a novel platelet-endothelial adhesion molecule and play pathological roles in cardiovascular biology. Acute myocardial infarction is one of the most common causes of death in modern society. The concept of “no reflow” (NR) refers to a state of myocardial tissue hypoperfusion in the presence of a patent epicardial coronary artery. The main mechanisms of this phenomenon are thought to be high platelet activity and much thrombus burden. So, we researched the role of SCUBE1 in the pathogenesis of NR. Methods: A total of 142 patients with ST elevation myocardial infarction (STEMI) (n=42 with NR and n=100 without NR) and 50 healthy individuals were prospectively case-control recruited between March 2015 and October 2016 from our outpatient clinics of cardiology department. Patients with STEMI were diagnosed according to American Heart Association (AHA) guideline for the management of STEMI. Results: The mean SCUBE1 levels of the control subjects were 34±8.4 ng/mL, the mean SCUBE1 levels of patients with STEMI who were treated successfully with primary percutaneous coronary intervention (PCI) were 51±6.2, and the mean SCUBE1 levels of patients with STEMI who had NR phenomenon after primary PCI procedure were 97.2±8.9 ng/mL. Conclusion: In our opinion, SCUBE1 might contribute to NR phenomenon via thrombus activation and aggregation. The pathophysiology of NR phenomenon is unclear. The present study is the first clinical study that demonstrated that serum SCUBE1 level was significantly higher in patients with NR and that serum SCUBE1 was an independent predictor for the presence of NR in our study population.

Giant Left Atrium

A 58-year-old woman with a history of mitral valve replacement (MVR) 17 years ago was admitted to our outpatient clinic with shortness of breath and a nonproductive cough. On physical examination, her blood pressure was 90/ 60 mmHg, and heart rate was 122 beats/min. Distended neck veins were noted, basal crepitations were heard in lungs, and there was grade I peripheral edema. A prosthetic valve sound and a grade III pansystolic murmur were present along the left mid-clavicular line. ECG (Cardioline Delta 60 Plus CP/1 version, Remco Italy Cardioline, Milan, Italy) showed atrial fibrillation with a ventricular rate of 110 beats/min. Laboratory evaluation revealed a creatinine level of 1.36 mg/dL (0.4–1.0), an albumin level of 3.8 mg/dL (3.2– 4.8), and pro-brain natriuteric peptide level of 3050 ng/L (12–133). Chest x-ray revealed marked cardiomegaly (Fig. 1). Echocardiographic examination (Vivid 7 pro, GE, Horten, Norway) showed normal functioning MVR with massive biatrial enlargement (left larger than right), moderate mitral regurgitation, severe tricuspid regurgitation, and mildly depressed left ventricular systolic function. The left atrium, measuring 209 9 96 mm, was so large that it was not possible to fit it to the screen in its entirety (Fig. 2). Giant left atrium is a condition in which the left atrial diameter exceeds 65 mm or one that touches the right lateral thoracic wall. This condition is commonly caused by rheumatic mitral disease and malfunctioning replaced mitral valve. Dilatation is the left atrial compensation mechanism due to the chronic pressure overload in mitral stenosis, to balance pulmonary capillary wedge pressure. It may be misdiagnosed as pleural effusion or a mass, so the clinician must be alert to avoid from further invasive examinations like pleurocentesis or biopsy, which may be associated with dangerous complications. References 1. Hurst JW: Memories of patients with giant left atrium. Circulation 2001;104:2630–2631. 2. Akdemir I, Davutoglu V, Aksoy M: Giant left atrium, giant thrombus, and left atrial prolapse in a patient with mitral valve replacement. Echocardiography 2002;19(8):691– 692. Figure 1. Increased cardiothoracic index and left atrial size in x-ray.

Spontaneous coronary artery dissection diagnosed by multislice computed tomography.

Spontaneous coronary artery dissection is a rare cause of acute coronary syndrome. Spontaneous coronary artery dissection can cause stable angina pectoris, unstable angina pectoris, acute myocardial infarction, cardiogenic shock and sudden cardiac death. It usually occurs in young to middle aged women. Atherosclerosis, peripartum period, and structural and inflammatory diseases affecting the artery wall are predisposing factors. It shows similar clinical presentation to coronary artery disease. Diagnosis and early treatment decrease mortality. Treatment options are medical treatment, percutaneous coronary intervention and surgery. The treatment decision is made according to the clinical presentation of the patient, the affected coronary artery and the length of the dissected segment. Diagnosis of the disease is usually made by coronary angiography. We present a patient who consulted our clinic with atypical chest pain and was diagnosed with spontaneous left anterior descending dissection by coronary computed tomography angiography.

Demonstration of ischemia in myocardial perfusion scintigraphy before coronary revascularization decreases acute coronary syndrome-related hospitalizations

In this study, we compared the patients who underwent coronary angiography (CAG), followed by revascularization by coronary artery stent implantation according to the CAG results without any evidence of ischemia with myocardial perfusion scintigraphy (MPS), and the patients who underwent revascularization by coronary artery stent implantation following the detection of ischemia in MPS before CAG in terms of the mortality and hospitalization due to acute coronary syndrome (ACS). Between January 2009 and January 2016, a total of 407 patients (52% males, 48% females; mean age: 66 ± 9 years; range: 40–85 years) who underwent CAG following diagnosis of stable angina and underwent coronary artery stenting were retrospectively analyzed. The patients were divided into two groups: Group 1 (n = 200) included those who had MPS before CAG and in whom ischemia was detected and stent was implanted, and Group 2 (n = 207) included those who had stent implantation according to the CAG results without prior MPS. The mean follow-up was 40 ± 18 months. Although there was no significant difference in the mortality rates between the groups, the rate of hospitalization due to ACS was significantly lower in Group 1 (P = 0.112 vs.P = 0.022, respectively). According to the multivariate Cox-regression analysis, demonstration of ischemia in MPS before revascularization, statin use, clopidogrel use, and higher high-density lipoprotein cholesterol levels were found to be associated with a reduced risk of ACS-related hospitalization, whereas the presence of diabetes mellitus and smoking was found to be associated with an increased risk of ACS-related hospitalization.

Cancer Antigen 125 is Associated with Length of Stay in Patients with Acute Heart Failure

Length of stay is the primary driver of heart-failure hospitalization costs. Because cancer antigen 125 has been associated with poor morbidity and mortality rates in heart failure, we investigated the relationship between admission cancer antigen 125 levels and lengths of stay in heart-failure patients. A total of 267 consecutive patients (184 men, 83 women) with acute decompensated heart failure were evaluated prospectively. The median length of stay was 4 days, and the patients were classified into 2 groups: those with lengths of stay ≤4 days and those with lengths of stay >4 days. Patients with longer lengths of stay had a significantly higher cancer antigen 125 level of 114 U/mL (range, 9-298 U/mL) than did those with a shorter length of stay (19 U/mL; range; 3-68) (P <0.001). The optimal cutoff level of cancer antigen 125 in the prediction of length of stay was >48 U/mL, with a specificity of 95.8% and a sensitivity of 96% (area under the curve, 0.979; 95% confidence interval [CI], 0.953-0.992). In the multivariate logistic regression model, cancer antigen 125 >48 U/mL on admission (odds ratio=4.562; 95% CI, 1.826-11.398; P=0.001), sodium level (P<0.001), creatinine level (P=0.009), and atrial fibrillation (P=0.015) were also associated with a longer length of stay after adjustment for variables found to be statistically significant in univariate analysis and correlated with cancer antigen 125 level. In addition, it appears that in a cohort of patients with acute decompensated heart failure, cancer antigen 125 is independently associated with prolonged length of stay.

Left atrial metastasis of Ewing's sarcoma mimicking atrial myxoma.

A 33-year-old male patient was admitted to our hospital with shortness of breath and fever. The patient’s past medical history was remarkable for Ewing’s sarcoma (ES) in the left kidney, for which the patient had received therapy 2 years previously. On physical examination, body temperature was 38.5°C, there were rales in the lungs, and a palpable supraclavicular mass was present. Echocardiography revealed a mobile, smooth shaped, hyperechoic mass in the left atrium (Figure A and Video*). At first glance, the lesion appeared to be a myxoma. Mitral valve flow was normal, and there was no gradient with positional change. Furthermore, examination exhibited local pericardial effusion adjacent to the left ventricle and a large mass lesion in the lung on the left posterior side of the left atrium (Figure B). Echocardiographic assessment of the patient 1 year prior to current admission had shown normal findings. Computed tomography scan of the thorax confirmed a large mass lesion that completely occupied the inferior lobe of the left lung. The mass lesion located in the left atrium appeared to arise from the pulmonary vein (Figure C). Histopathological findings of supraclavicular and lung mass lesion were all consisted with ES. Due to expectation of poor prognosis with surgery in patients with recurrent ES, the patient elected to undergo chemotherapy. ES is a malignant primary neoplasm of bone, which usually affects children and adolescents. ES without involvement of bone rarely develops from the soft tissues of the lower extremities, paravertebral region, gastrointestinal tract, kidney, uterus, and other areas of the body. Cardiac metastasis of ES is extremely rare. To our knowledge, the present case is the first example of extraskeletal ES metastasized to the left atrium and pulmonary structures, as indicated by echocardiographic examination. It must be considered that mass lesions may represent not only a primary cardiac tumor, thrombus formation, vegetative lesions, and foreign bodies, but also metastasis from a malignant tumor located in other organs. 88

Hemogram parameters for predicting pulmonary embolism in patients with deep venous thrombosis.

Dear editor We read the article of Sevuk et al,1 published in the August 2015 issue of your journal, with great interest. The authors concluded that percentage change in serial measurements of mean platelet volume (MPV) and platelet-distribution width (PDW) is valuable in predicting the development of pulmonary thromboembolism in patients with a previous history of deep venous thrombosis (DVT). In a similar study conducted by Braekkan et al2 (Tromso Study), MPV on admission was shown to predict pulmonary thromboembolism. In a study by Zorlu et al,3 red cell-distribution width (RDW) values >14%, which is another parameter included in complete blood count, were associated with increased risk of mortality in the early period after pulmonary thromboembolism. RDW can be easily measured in routine hemograms, and indicates changes in erythrocyte-distribution width.4 Certain inflammatory cytokines released in response to acute heart failure occurring in acute pulmonary embolism may cause an increase in RDW values through inhibition of erythrocyte maturation by affecting bone marrow.5–7 It is realized that the study by Sevuk et al1 did not include RDW in statistical analysis. Considering the fact that RDW has been previously documented to increase mortality in pulmonary thromboembolism,3 we suggest that RDW may be increased in patients with DVT due to acute pulmonary embolism and associated acute right heart failure and thus play a role in predicting the development of pulmonary embolism. In conclusion, RDW, which is measured in routine hemograms together with MPV and PDW, is an easy parameter to access, so authors might include RDW in statistical analysis. We think that if RDW levels were used for this study together with MPV and PDW, RDW might change the results of multivariate analysis and might be one of the predictors of pulmonary embolism in patients with DVT.