Hakan Güneş

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.

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.

Eltrombopag Induced Thrombosis: A Case with Acute Myocardial Infarction

Eltrombopag is a non-peptide thrombopoietin receptor agonist. Eltrombopag has originally been developed for conditions where therapy for thrombocytopenia is needed. Secondary to eltrombopag have been reported thrombotic events, chest pain, acute renal failure, neutropenia, ascites, retinal exudates, antiphospholipid syndrome. In this case, we present a 53 year-old patient who had diagnosis of Idiopathic Thrombocytopenic Purpura (ITP) for 30 years with splenectomy. Hes still having low thrombocyte counts despite the classical ITP therapy. He was treated with eltrombopag for the last 2 months and had inferior myocardial infarction despite that having no additional risk factors for coronary heart disease.

Ischemia-modified albumin levels in patients with acute decompensated heart failure treated with dobutamine or levosimendan: IMA-HF study.

Objective: Ischemia-modified albumin (IMA) is a sensitive biomarker of myocardial ischemia. However, data on IMA levels in acute heart failure (HF) are still lacking. In this study, we aimed to evaluate serum IMA levels in acute decompensated HF and the effects of dobutamine and levosimendan treatments on IMA levels. Methods: This was a prospective, multicenter study that included 70 patients hospitalized with acute decompensated HF and left ventricular ejection fraction <35%. Blood samples for IMA measurements were obtained on admission and 24-48 h after the initiation of HF therapy. Twenty-nine patients were treated with standard HF therapy, 18 received levosimendan, and 23 received dobutamine in addition to standard of care. A single serum specimen was also collected from 32 healthy individuals each. IMA concentrations were measured by the albumin cobalt binding colorimetric assay, and the results were given in absorbance units (AU). Independent and paired sample t-tests, Mann-Whitney U test, and Wilcoxon signed-rank test were used for the analysis. Results: In patients with acute decompensated HF, the serum concentration of IMA was significantly higher than those of healthy subjects (0.894±0.23 AU vs. 0.379±0.08 AU, p<0.001). Overall, the IMA levels significantly decreased after 24-48 h of HF therapy (0.894±0.23 AU and 0.832±0.18 AU, p=0.013). Furthermore, the IMA levels were also found to significantly decrease with standard HF therapy (1.041±0.28 vs. 0.884±0.15 AU, p=0.041), with levosimendan (0.771±0.18 vs. 0.728±0.18 AU, p=0.046) and also with dobutamine (0.892±0.18 vs. 0.820±0.13 AU, p=0.035). Conclusion: Patients with acute decompensated HF had elevated IMA levels, and appropriate HF therapy significantly reduced the serum IMA levels. Dobutamine or levosimendan did not increase the IMA levels, suggesting a lower potential in inducing myocardial ischemia when used in recommended doses.

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.

Association between multidrug resistance-1 C3435T gene polymorphism and right ventricular dysfunction in patients with chronic obstructive pulmonary disease: cross-sectional study

BACKGROUND Right ventricular (RV) dysfunction may develop over the course of chronic obstructive pulmonary disease (COPD) and is an important predictor of morbidity and mortality. Polymorphism of the multidrug resistance-1 (MDR-1) gene has been correlated with worse clinical findings among patients with COPD. Our aim here was to investigate the relationship between MDR-1 C3435T gene polymorphism and RV dysfunction in COPD patients. DESIGN AND SETTING This was a cross-sectional study investigating the relationship between RV dysfunction and genetic defects in COPD patients. METHODS Forty-one consecutive patients diagnosed with COPD and hospitalized due to acute exacerbation were enrolled. Polymorphism was analyzed using the strip assay technique. RV parameters were evaluated, and RV dysfunction was identified via transthoracic echocardiography. Patients were categorized into three groups according to gene polymorphism: MDR-1 CC (wild type, n = 9), MDR-1 CT (heterozygote mutant, n = 21) or MDR-1 TT (homozygote mutant, n = 11). RESULTS The study included 14 males and 27 females (mean age 65 ± 11 years). The mean systolic pulmonary artery pressure was 31.4 ± 8 mmHg in the wild-type group, 42.2 ± 12 mmHg in the heterozygote mutant group and 46.5±14 mmHg in the homozygote mutant group (P = 0.027). Presence of RV dilatation was significantly different among the three groups (33%, 71%, and 100%, respectively; P = 0.005). In multiple logistic regression analysis, MDR-1 C3435T gene polymorphism (OR = 9.000, P = 0.019) was an independent predictor of RV dysfunction after adjustment for potential confounders. CONCLUSION MDR-1 C3435T gene polymorphism was associated with RV dysfunction in patients with COPD.

What is the most appropriate method for coronary sinus cannulation? The telescopic method or the electrophysiologic method?

Objectives The most challenging stage of cardiac resynchronization therapy (CRT) is coronary sinus cannulation (CS). The aim of this study was to compare coronary sinus cannulation techniques using electrophysiology catheters and coronary angiography catheters. Methods In this observational, retrospective and non-randomized study, 87 patients who were eligible for CRT device implantation were screened at Kahramanmaras Sutcu Imam University Hospital between March 2014 and March 2018. Seventy-two patients who met the inclusion criteria were enrolled in the study. The study population was divided into 2 groups: the first group consisted of 36 patients whose coronary sinuses were cannulated via electrophysiology (EP) catheters and the second group included 36 patients who received coronary angiography catheters for coronary sinus cannulation. Results The two groups were similar in terms of the baseline characteristics of the patients. The total fluoroscopy time was less with cannulation using coronary angiography catheters. There were no differences between the two groups in terms of the amount of contrast material and the success of the operations. Conclusions Coronary sinus catheterization using coronary angiography catheters significantly reduces fluoroscopy time in patients undergoing CRT.

Evaluation of Atrial Electromechanical Delay to Predict Atrial Fibrillation in Hemodialysis Patients

Background and objective: Prevalence of atrial fibrillation is higher in hemodialysis patients as compared to the general population. Atrial electromechanical delay is known as a significant predictor of atrial fibrillation. In this study, we aimed to reveal the relationship between atrial electromechanical delay and attacks of atrial fibrillation. Materials and methods: The study included 77 hemodialysis patients over 18 years of age giving written consent to participate in the study. The patients were divided into two groups based on the results of 24-h Holter Electrocardiogram (Holter ECG) as the ones having attacks of atrial fibrillation and the others without any attack of atrial fibrillation. Standard echocardiographic measurements were taken from all patients. Additionally, atrial conduction times were measured by tissue Doppler technique and atrial electromechanical delays were calculated. Results: Intra- and interatrial electromechanical delay were found as significantly lengthened in the group of patients with attacks of atrial fibrillation (p = 0.03 and p < 0.001 respectively). The optimal cut-off time for interatrial electromechanical delay to predict atrial fibrillation was >21 ms with a specificity of 79.3% and a sensitivity of 73.7% (area under the curve 0.820; 95% confidence interval (CI), 0.716–0.898). In the multivariate logistic regression model, interatrial electromechanical delay (odds ratio = 1.230; 95% CI, 1.104–1.370; p < 0.001) and hypertension (odds ratio = 4.525; 95% CI, 1.042–19.651; p = 0.044) were also associated with atrial fibrillation after adjustment for variables found to be statistically significant in univariate analysis and correlated with interatrial electromechanical delay. Conclusions: Interatrial electromechanical delay is independently related with the attacks of atrial fibrillation detected on Holter ECG records in hemodialysis patients.

Biventricular thrombi and pulmonary embolism in a young woman with peripartum cardiomyopathy

DOI: 10.4328/JCAM.5749 Received: 02.02.2018 Accepted: 23.02.2018 Publihed Online: 25.02.2018 Printed: 01.07.2018 J Clin Anal Med 2018;9(4): 356-8 Corresponding Author: Hakan Güneş, Department of Cardiology, Kahramanmaras Sutcu Imam University School of Medicine, Kahramanmaras, Turkey. T.: +90 3443003376 F.: +90 3443003409 E-Mail: drhakangunes83@hotmail.com Abstract Postpartum cardiomyopathy (PPCM) is a rare form of left ventricular (LV) systolic dysfunction of unknown etiology that occurs in previously healthy women in the final month of pregnancy or postpartum. It is characterized by LV systolic dysfunction and congestive heart failure and is associated with thromboembolic events and LV thrombus. Here we presented a postpartum cardiomyopathy patient with biventricular thrombosis and pulmonary thromboembolism.