Halil İbrahim Erdoğan

Prognostic Value of Neutrophil to Lymphocyte Ratio in Patients with Acute Pulmonary Embolism: A Restrospective Study

BACKGROUND Acute pulmonary embolism (PE) is a serious clinical condition characterised by a high mortality rate. Previous studies showed that leukocytosis was associated with recurrences of venous thromboemboli, major bleeding and increased mortality. The aim of the present study was to investigate the prognostic value of neutrophil to lymphocyte ratio (NLR) in patients with acute PE during short term follow-up. METHOD A total of 640 patients were screened by I26 code of ICD-9 and 359 patients were included as cases of confirmed acute PE. Admission blood counts and clinical data were obtained from medical charts. The predictors of 30-day mortality were examined. RESULTS Fifty-one out of 359 patients (14.2%) included in the study died during 30 days follow-up. In multivariate Cox regression analysis systolic blood pressure (HR:0.97 (0.94-0.99 CI95%), p=0.019), diabetes mellitus (HR:3.3 (1.30-8.39 CI95%), p=0.012), CK-MB(HR:1.03 (1.01-1.06 CI95%), p=0.024) and NLR (HR:1.03 (1.01-1.06 CI95%), p=0.008) were predictors of 30-day mortality. An optimal cut-off value of NLR was determined as 9.2 by using ROC curve. Hazards ratio of NLR>9.2 was found to be 3.60 (1.44-9.18 CI95%, p=0.006). NLR>9.2 had a sensitivity, specificity, negative predictive value, and positive predictive value of 68.6%, 80.5%, 93.9% and 36.5%, respectively. CONCLUSION NLR on hospital admission may be a predictor of 30-day mortality in acute PE. Since complete blood count is a part of the routine laboratory investigation in the most hospitalised patients use and preliminary promising results of this study, NLR should be investigated in future prospective randomised trials regarding prognostic value in acute PE.

Management of right heart thrombi associated with acute pulmonary embolism: a retrospective, single-center experience

OBJECTIVE The mortality of right heart thrombi (RHT) associated with pulmonary embolism (PE) is increased about three to four times. The most devastating scenario is fragmentation of RHT and occurrence of recurrent PE. The reports regarding the management of RHT complicated with PE are very scarce in the current literature. Therefore, we report a single-center experience in this paper. METHODS From January 2006 to December 2011, data of all patients diagnosed with acute PE were analyzed retrospectively. Of the 312 acute PE cases confirmed with computed tomography, total 35 patients who were diagnosed with concomitant RHT (prevalence of 11%) by echocardiography were recruited. After excluding of six patients with metastatic malignancy a total 29 patients were accepted eligible for the analysis. In addition, catheter -induced thrombus (type B) were not included to the study. The difference between categorical variables was analyzed with Chi-square test and continuous variables were analyzed with Mann-Whitney U test. A p value of <0.05 was considered statistically significant. RESULTS Overall mortality was high (34%) in study population: among undergoing surgery-100%, therapy with thrombolytics -18%, and heparin -27%. Troponin levels were found significantly higher in died patients than that in survived patients (p=0.03). There was no significant difference regarding to clinical and echocardiographic characteristics of patients received heparin versus thrombolytic except for shock index (p=0.02). In addition, patients treated with heparin had increased duration of hospitalization compared to subjects treated with thrombolytic (median: 8 vs 3 days p<0.01). CONCLUSION Despite of the low incidence of RHT, a mortal course is still an important problem during PE. The decision on treatment modality should be performed based on the hemodynamic parameters, laboratory findings, and bleeding risk of the patients.

Therapy-resistant ventricular tachycardia caused by amiodarone-induced thyrotoxicosis: a case report of electrical storm

Electrical storm is a challenging diagnosis for the clinician and requires detailed evaluation of the patient. Amiodarone is frequently used for the cessation of ventricular tachycardia attacks. Within antiarrhythmic effects of amiodarone, there are some harmful effects of the recent drug. Thyroid gland toxicity is one of the most important adverse effects of amiodarone and is called amiodarone-induced thyrotoxicosis. Thyrotoxicosis may alter arrhythmia and lead to frequent ventricular tachycardia attacks. Herein, we report a case of electrical storm caused by amiodarone-induced thyrotoxicosis.

Differential diagnostic dilemma between pulmonary embolism and acute coronary syndrome.

Acute pulmonary embolism (PE) is a frequent life‐threatening condition in emergency departments. Careful diagnosis is important, and different diagnostic tests such as electrocardiogram (ECG), biochemical markers, echocardiogram, and computed tomography are required. Although ECG is a cheap and rapid diagnostic test for pulmonary embolism, it has some limitations in the differential diagnosis of acute coronary syndrome and acute PE. Herein, we report ECG results of a patient diagnosed with acute PE mimicking acute coronary syndrome.

Swallowing-induced atrioventricular block and syncope in a patient with achalasia.

gus characterized by increased pressure in the lower sphincter and incomplete relaxation after swallowing (1). Classical symptoms include dysphagia, regurgitation, chest pain and weight loss. Cardiovascular complications of achalasia are very rare (2). We report a patient with achalasia in whom swallowing induced bradycardia and atrioventricular (AV) complete block during ingestion of food with patient’s consent. The patient was a 47-year-old man, with an 18-year history of dysphagia and odynophagia. He was diagnosed with achalasia, and pneumatic dilatation was performed once; he had not been undergoing any medical treatment. He had three syncope attacks in the previous month, and the aetiology of his syncope was investigated by cardiologists. He was normotensive and cardiac examination yielded normal results. His resting electrocardiography (ECG) results were also normal. This was followed by transthoracic echocardiography (Philips Envisor C HD Andover, MA, ABD). No significant wall motion disorder or valve dysfunction was reported. Thoracic computed tomography (CT) revealed a noticeably dilated oesophagus (Figure 1a). We performed 24-h ambulatory ECG monitoring (SpiderView®; ELA Medical, Sorin Group, Paris,France) and, at the time of breakfast and dinner, noticed that the patient was bradycardic: there were 2:1 and 3:1 AV blocks and pauses (the longest pause was of 4.3 s; Figure 1b). During the pauses, the patient experienced dizziness. Pneumatic dilatation was performed again and pharmacotherapy [nifedipine 60 mg/day (Bayer medical, Turkey) and isosorbide dinitrate 40 mg/ day (Adeka medical, Turkey)] was initiated. The patient complained of mild dysphagia after the treatment, but he did not experience any syncope attacks again. Next, 24-h ambulatory ECG monitoring was repeated. According to his ECG holter, the patient had bradycardia, but no AV blocks were observed. Swallowing-induced syncope occurs because of AV blocks and bradycardia associated with overstimulation by vagal stimuli (1). Mechanoreceptors of the lower oesophagus play an important role in the pathophysiology of swallowingassociated cardiac arrhythmias (3), and hypersensitivity is the key feature of vagotonic reflex syncope (4). The nerves innervating the lower oesophagus can be Turk J Gastroenterol 2015; 26: 75-6

Mobile right heart thrombus as a manifestation of homozygous mutation of MTHFR 1298 A>C.

Objective: Mobile right heart thrombi (MRHT) are uncommon but the true prevalence is still unknown. Previous studies reported thay MRHT occur in 7% to 18% of patients with pulmonary embolism. Chartier et al. have reported in-hospital mortality of MRHT as 44.7%. The main manifestations of venous thromboembolism (VTE) are deep venous thrombosis (DVT) and pulmonary embolism (PE). In addition, genetic factors play an important role in pathogenesis of VTE. The relationship between common genetic mutations such as factor V Leiden, prothrombin factor II G 20210A, methylenetetrahydrofolate reductase (MTHFR), deficiencies of protein C, protein S, and antithrombin III, and VTE have been reported. Nevertheless, hyperhomocysteinemia was documented in the pathogenesis of VTE. Methods: A 34-year-old man was presented to the emergency department because of sudden onset of dyspnea. He describes loss of consciousness occurred two days before. He had no previous history of both venous thromboembolism and acute coronary syndrome. He denied any trauma, history of malignancy, recent surgery, and any drug usage. Admission physical examination was unremarkable. Examination of lower extremities was also normal. Baseline 12-lead electrocardiogram (ECG) revealed sinus rhythm and S1Q3T3 sign. Because of suspicion of PE, bedside transthoracic echocardioghraphy (TTE) was performed and revealed mobile right atrial mass. Left ventricular systolic functions were normal. Right ventricle was not enlarged and estimated systolic pulmonary arterial pressure was 28mmHg. Because of poor imaging quality with TTE, transesophageal echocardiography (TEE) was performed and two hypermobile and snake-like thrombi in the right atrium were demonstrated (Figure 1A). Duplex scan of the lower extremities was normal. Laboratory parameters were within normal limits. Homocysteine was slightly elevated: 19.6mmol/L (5.5–14mmol/L). Upon genetic testing, there were no mutations in the factor V Leiden (G1691A), factor II (G20210A), and MHFR (C677T). Only homozygous mutation of MTHFR (A1298C) was detected. Pulmonary computed tomography revealed bilateral lower lobe PE. Because of hemodynamic stability and no evidence of RV strain, anticoagulation with heparin was administered. After 10 days of hospitalization, control TEE was performed and right atrial thrombi were markedly decreased (Figure 1B). The patient was discharged with warfarin treatment for indefinite time. Results: In the present case, we postulated that the possible cause of right atrial thrombi is MTHFR A1298C homozygous mutation because no other predisposing factors were present in our patient. For the best of our knowledge, right heart thrombus as a manifestation of homozygous MTHFR mutation have not been reported previously. Figure 1. (A) Pretreatment transesophageal echocardiography showing two mobile thrombi in the right atrium. (B) Aftertreatment transesophageal echocardiography showing markedly reduced thrombi in the right atrium. RA, right atrium; RV, right ventricle; PA; pulmonary artery; Th; thrombus.

Hyperkalemia-Induced Accelerated Idioventricular Rhythm in a Patient with Acute Renal Failure

Electrolyte disorders can alter cardiac ionic currents and depending on the changes can promote proarrhythmic effects. Potassium (K+) is the most common intracellular cation related to arrhythmic disorders. Hyperkalemia is mainly seen in the setting of impaired renal function. Severe hyperkalemia may lead to rhythm disorders. Herein, we report a patient with accelerated idioventricular rhythm (AIVR) due to hyperkalemia, which was successfully treated with glucose-insulin (GI) infusion.