Turgut Karabağ

Intravenous N-acetylcysteine plus high-dose hydration versus high-dose hydration and standard hydration for the prevention of contrast-induced nephropathy: CASIS—A multicenter prospective controlled trial

BACKGROUND Contrast-induced nephropathy (CIN) is a leading cause of acute renal failure and affects mortality and morbidity. We investigated the efficacy of prophylactic intravenous (IV) N-acetylcysteine (NAC) and hydration for the prevention of CIN in patients with mild to moderate renal dysfunction who are undergoing coronary angiography and/or percutaneous coronary intervention (PCI). METHODS A total of 220 patients who had mild to moderate renal dysfunction with serum creatinine (SCr) ≥ 1.1mg/dL or creatinine clearance ≤ 60 mL/min were randomized in 3 groups: 80 patients were assigned to IV NAC plus high-dose hydration with normal saline, 80 patients to only high-dose hydration with normal saline and 60 patients to standard hydration with normal saline (control group). The primary end point was the alteration of SCr level. The secondary end point was the development of CIN after the procedure. RESULTS SCr levels changed the least in the NAC plus high-hydration group (P=0.004). The rate of the CIN in the NAC plus high-dose hydration group was also lower than the high-dose hydration group (P=0.006). No significant differences in the primary and secondary end points were found between high-dose hydration and control group. CONCLUSION The results of this study suggest that NAC plus high-dose hydration was superior to high-dose hydration alone as well as standard hydration for the protection of renal functions in patients with mild to moderate renal dysfunction who are undergoing coronary angiography and/or PCI. High-dose hydration without NAC was not better than standard hydration alone.

Atrial conduction times and left atrial mechanical functions and their relation with diastolic function in prediabetic patients

Background/Aims The aim of this study was to investigate atrial conduction times and left atrial mechanical functions, the noninvasive predictors of atrial fibrillation, in prediabetic patients with impaired fasting glucose (IFG) and impaired glucose tolerance (IGT). Methods Study included 59 patients (23 males, 36 females; mean age 52.5 ± 10.6 years) diagnosed with IFG or IGT by the American Diabetes Association criteria, and 43 healthy adults (22 males, 21 females; mean age 48.5 ± 12.1 years). Conventional and tissue Doppler echocardiography were performed. The electromechanical delay parameters were measured from the onset of the P wave on the surface electrocardiogram to the onset of the atrial systolic wave on tissue Doppler imaging from septum, lateral, and right ventricular annuli. The left atrial volumes were calculated by the disk method. Left atrial mechanical functions were calculated. Results The mitral E/A and E’/A’ ratios measured from the lateral and septal annuli were significantly lower in the prediabetics compared to the controls. The interatrial and left atrial electromechanical delay were significantly longer in prediabetic group compared to the controls. Left atrial active emptying volume (LAAEV) and fraction (LAAEF) were significantly higher in the prediabetics than the controls. LAAEV and LAAEF were significantly correlated with E/A, lateral and septal E’/A’. Conclusions In the prediabetic patients, the atrial conduction times and P wave dispersion on surface electrocardiographic were longer before the development of overt diabetes. In addition, the left atrial mechanical functions were impaired secondary to a deterioration in the diastolic functions in the prediabetic patients.

The Influence of Comorbid Conditions on Graft Stenosis in Patients with Coronary Artery Bypass Graft Operation

Mailing Address: Turgut Karabag Bulent Ecevit Universitesi İncivez Mahallesi, Üniversite Cd., Postal Code: 67100 Merkez/Zonguldak Merkez/Zonguldak Turkey E-mail: turgutkarabag@yahoo.com The Influence of Comorbid Conditions on Graft Stenosis in Patients with Coronary Artery Bypass Graft Operation Turgut Karabag, Belma Kalayci, Bahar Sahin, Elif Coskun, Mustafa Umut Somuncu, Mustafa Ozan Cakir Bulent Ecevit University, Kozlu/Zonguldak Turkey

High Serum Resistin Levels in Coronary Artery Ectasia

Introduction: The etiological and pathogenic factors responsible for coronary artery ectasia (CAE) are unclear. Therefore, we aimed to compare subjects with and without CAE with respect to resistin levels and determine whether resistin plays a role in the aetiology or pathogenesis of CAE. Patients and Methods: This study enrolled a total of 81 subjects, of whom 42 had CAE [15 female (F), mean age 60.4 ± 9.0 years] and 39 had a normal coronary anatomy (22 F, mean age 56.2 ± 10.7 years). Using coronary artery diameters of the control group as reference, subjects having coronary artery dilatation that was at least 1.5 times larger than the normal adjacent segments were considered to have CAE. Resistin levels were measured from blood samples obtained on the day of the coronary angiography. Results: Both the groups had similar baseline characteristics. Serum resistin levels were significantly higher in the CAE group [mean 703.5 ± 828.1 ng/L, median 379.5 (40-4092) ng/L] than in the control group [mean 313.5 ± 252.6 ng/L, median 256 (30-1244) ng/L] (p= 0.001). Conclusion: CAE and atherosclerosis share common histopathological and clinical characteristics. Resistin, a polypeptide with a known role in the development and clinical presentation of atherosclerosis, may also mediate the formation of CAE. There is a need for future studies with a larger sample size to better delineate the effect of resistin on the development of CAE.

Renal artery stenosis and mean platelet volume.

Objective: Increased mean platelet volume (MPV) has been reported in various atherosclerotic diseases. The aim of our study was to investigate the relationship between the atherosclerotic renal artery stenosis (ARAS) and various hematological parameters including MPV. Methods: This study was performed with a retrospective review of the angiographic images of patients who underwent renal angiography at Bülent Ecevit University catheter laboratory between January 2004 and December 2009. The patients were trichotomized into three groups based on the presence and severity of renal artery stenosis (RAS). Group 1 included patients with a critical RAS (33 patients; 18 female (F), 15 male (M); mean age 61.6±11.5 years), group 2 consisted of patients with non-critical RAS (26 patients; 15 F, 11 M; mean age 58.1±11.3 years), and group 3 was composed of patients without RAS (69 patients; 38 F, 31 M; mean age 53.5±11.9 years). Demographic data, complete blood count, and biochemical parameters were compared between the groups. Results: Comparison of the hematological parameters revealed that MPV and platelet distribution width were significantly higher in group 1 than in group 2 and 3 (8.96±0.99 fL versus 8.35±0.76 fL, 8.31±0.79 fL, respectively; p=0.001; 16.53±0.58% versus 16.19±0.56%, 16.29±0.53%, respectively; p=0.04). Conclusion: MPV levels are higher in patients with ARAS. Considering both the effect of platelets on atherosclerosis and their close association with other risk factors, MPV level may be an important factor in pathogenesis of ARAS.

Biventricular noncompaction cardiomyopathy with severe systolic and diastolic dysfunction in a systemic sclerosis patient.

Non-compaction cardiomyopathy (NCM) is a rare congenital cardiomyopathy characterized by deep increased trabeculation in one or more segments of the ventricle. The apical segment of the left ventricle is most commonly affected, but left ventricular basal segment, biventricular involvement or right ventricle predominance have also been described. While some neuromuscular anomalies and myopathies had been described in systemic sclerosis patients, coexistence of chronic inflammatory disorders and NCM is unclear. This paper presents a case of biventricular NCM with severe systolic and diastolic dysfunction in a 40-year-old female diffuse cutaneous systemic sclerosis patient.

Relationship of fetuin-A with restenosis in patients who underwent revascularization

Abstract Background: We investigated whether fetuin-A (a hepatic secretory protein that prevents arterial calcification) was related to revascularization in patients who had previously undergone coronary revascularization (percutaneous coronary intervention and/or coronary artery bypass grafting operation). Methods: This study included 71 patients who had previously undergone any revascularization procedure. All patients presented to the cardiology outpatient clinic with angina or angina equivalent and underwent coronary angiography upon findings of preliminary tests. The patients were grouped on the basis of the presence of restenosis on angiography: Group 1 consisted of 44 subjects with restenosis on angiography (30 male, 14 female; mean age 64.2±4.2 years) and group 2; 30 subjects without restenosis on angiography (20 male, 10 female; 61.2±13.1 years). In addition to routine biochemical tests and lipid panel, all patients underwent C-reactive protein, and fetuin-A measurements. Results: The groups were not significantly different with respect to age, sex, systolic and diastolic blood pressure. As compared to Group 2, Group 1 had a significantly lower fetuin-A level (383.8±76.2 vs. 416.3±49.3 ng/mL; p=0.029). There was a significantly negative correlation between fetuin-A and age; and a significantly positive correlation between fetuin-A and calcium. Conclusions: Fetuin-A levels were significantly lower in patients detected to have restenosis. Lower fetuin-A levels may contribute to restenosis by directly increasing calcium-phosphate precipitation.

Temporary pacemaker with left bundle branch block image in ECG

When we made a detailed examination with TTE, we saw that the transvenous temporary pacing was not in the jugular vein. The suprasternal view showed the lead of the pacemaker in the arcus aorta (Fig. 3A). The localization of the pacemaker lead was seen in the right ventricle by fluoroscopy in the RAO. But, we were sure the localization of lead in the left ventricle when we was seen by fluoroscopy image in LAO projection at 28°. The lead of pace was inserted via the right common carotid artery. The tip of the lead was placed in the left ventricular septum in our patient. The patient did not consent to a coronary angiography. We had inserted a permanent VDD pacemaker via the left subclavian vein. We recorded a fluoroscopy image after inserting the permanent pacemaker in the LAO projection at 26° (Fig. 3B). The day after, we removed the temporary pacemaker with cardiovascular backup in the anticoagulant treatment. There was no neurological deficit after removal of the pacemaker. The followup was uneventful until 5 days later. Because of LBBB and the image in the anterior-posterior chest radiography, we may think that the pacemaker lead was in the right ventricle. However, the fluoroscopy and echocardiography showed that the tip of the pacemaker lead was in the left ventricle. A pacemaker lead may be implanted in the left ventricle via right jugular vein presence of atrial septal defect, ventricular septal defect, and patent foramen ovale. However, suprasternal images showed the lead of pacemaker in the arcus aorta. Generally, a pacemaker is inserted by ECG guidance in the emergency room. But, some dangerous complications may occur without fluoroscopic guidance. Malposition of pacemaker leads has been described in several different locations, including the left ventricle, pulmonary outflow tract, the atria, the coronary sinus, and other cardiac veins (1). Misimplantation of a temporary pacemaker lead in the aortic sinus via the femoral artery and left subclavian vein was reported previously (2, 3). In the presence of LBBB in ECG was the main tricky situation in our patient. Likewise, the tip of the pacemaker lead was seen in the right ventricle by anterior-posterior chest radiography. Transthoracic echocardiography and fluoroscopy images helped us to determine the localization of the pacemaker lead.

Açıklanamayan Yalın Troponin Yüksekliği Olgusu

Cardiac troponins have high clinical sensitivity and specificity for the detection of myocardial injury. Elevated cardiac troponin levels may also occur in non cardiovascular conditions, leading to a misdiagnosis of acute coronary syndrome. In this paper, we report a case of unexplained isolated elevation of troponin.