X-ray-free ultrasound-guided versus fluoroscopy-guided percutaneous nephrolithotomy: a comparative study with historical control

International Urology and Nephrology - To compare the outcomes and complications of supine X-ray-free ultrasound-guided percutaneous nephrolithotomy (XG-PCNL) with fluoroscopy-guided (FG)-PCNL in...     

Increased soluble glycoprotein V concentration during the acute onset of unstable angina pectoris in association with chronic cigarette smoking

Platelet hyperactivity is important in the pathobiology of acute coronary syndromes. Glycoprotein V (GPV) is an integral membrane protein of platelets in the function of the GPIb-V-IX receptor for vWf/shear-dependent platelet adhesion in arteries. Soluble GPV is a novel marker of platelet activation. The aim of this study is to assess circulating soluble GPV levels in unstable angina pectoris (UA). Twenty-one patients (15 men, six women, aged 52+/-7 years) with UA pectoris were studied. The inclusion criteria were angina at rest lasting >20 min during the preceding 6 h, with transient ST segment depression and/or T wave inversion and no evidence of myocardial infarction detected with the use of cardiac troponin-T. Coronary artery stenosis was angiographically confirmed in all patients. Twenty age- and sex-matched healthy adults (14 men, six women, aged 48+/-7 years) served as controls. There were no significant differences among the studied groups with respect to age, sex, obesity, smoking, total cholesterol, LDL-cholesterol, HDL-cholesterol, triglyceride and platelet counts. Plasma-soluble GPV concentrations were higher in the UA patient group (126+/-46 ng/ml) than those in the healthy controls (82+/-15 ng/ml) (P=0.001). There was a significant correlation only between plasma-soluble GPV levels and smoking (r=0.526, P=0.0001). Smoker UA patients had higher levels of soluble GPV than the non-smoker patients (139+/-40 vs. 113+/-50 ng/ml, respectively, P=0.02). However, soluble GPV levels were similar in smoker and non-smoker healthy controls (P=0.2). It is concluded that soluble GPV concentrations are significantly increased during the acute clinical course of unstable angina pectoris, indicating that soluble GPV may be useful marker of platelet activation in those patients. The level of the molecule is significantly affected from smoking in those patients.     

Relation of insulin resistance and left ventricular function and structure in non-diabetic patients with essential hypertension

OBJECTIVE: Both left ventricular hypertrophy and insulin resistance (IR) have often been demonstrated in patients with essential hypertension (EH). Insulin may exert a direct growth-promoting effect on cardiomyocytes. The purpose of this study was to examine the relationship between left ventricular structure, function and IR in patients with EH. METHODS: We enrolled 73 patients (21 men, mean age 51.7 +/- 9.2 years) with untreated hypertension (BP > 140 and/or 90 mm Hg, fasting glycaemia < 110 mg/dl) and 64 healthy subjects without diabetes mellitus and hypertension (21 men, mean age 48.9 +/- 10.6 years) constituted the control group. In all subjects, transthoracic echocardiography was performed and blood samples were taken. Homeostasis model assessment (HOMA) was calculated by the formula: HOMA-index = fasting blood glucose (mg/dl) * immunoreactive insulin (microU/ml)/405 for the assessment of IR. Hypertensive patients were divided in two groups by mean HOMA index values. Each subject was examined for LV end-diastolic diameter, septal and posterior wall thickness, LV mass index (LVMI), fractional shortening (FS), mitral inflow velocity pattern, atrial filling fraction (AFF), left ventricular outflow velocity pattern and the total ejection isovolume index (TEI index). RESULTS: The HOMA index (p < 0.001), LVMI (p < 0.001), AFF (p < 0.0001), peak A velocity (p < 0.028), septal (p < 0.0001) and posterior (p < 0.0001) wall thickness were significantly higher and FS (p < 0.001), E/A ratio (p < 0.0001) were significantly lower in hypertensive patients than healthy controls. LVMI (p < 0.01) and septal wall thickness (p < 0.001) were significantly higher in those hypertensive patients with a higher HOMA index. The HOMA-index was univariately related to the TEI index (r = 0.27, p = 0.01) and septal wall thickness (IVS) (r = 0.29, p = 0.01) by Pearson correlation analysis in hypertensive patients. LVMI, FS and mitral inflow velocity pattern were not related to the HOMA index. The TEI index (R2 = 0.20, p = 0.0001) and IVS (R2 = 0.12, p = 0.002) were significantly related to the HOMA-index as an independent variable by stepwise regression analysis. CONCLUSIONS: These results demonstrated that hypertensive patients had both abnormal cardiac structure and function and higher IR index. In our study group, the effect of hypertension on cardiac structure and function was correlated with IR. Our results suggested that IR might be an important factor causing left ventricular dysfunction and wall thickness in non-diabetic patients with EH.     

Evaluation of prehospital emergency care in the field and during the ambulance drive to the hospital

This study was conducted to evaluate the appropriateness of ambulance procedures and interventions in the management of patients dispatched to 2 emergency departments (EDs) of urban hospitals in Izmir. Use of trauma boards and cervical collars, airway patency, breathing, and circulation problems were recorded in both EDs. Eighty-one patients with a mean age of 47.54±2.36 years (range, 4–89) brought into the ED via ambulances were enrolled in the study. Airway maneuvers were performed in patients with airway and breathing problems. There was no significant relationship between administration of IV fluids and the presence of circulatory impairment (P=.053). A trauma board was used in 9 of 30 trauma cases (30%) and a cervical collar in 6 of 30 (20%). It was concluded that basic procedures used in the management of patients brought into the ED via ambulances were inadequate.     

Pre-therapy Somatostatin Receptor-Based Heterogeneity Predicts Overall Survival in Pancreatic Neuroendocrine Tumor Patients Undergoing Peptide Receptor Radionuclide Therapy

Purpose

Early identification of aggressive disease could improve decision support in pancreatic neuroendocrine tumor (pNET) patients prior to peptide receptor radionuclide therapy (PRRT). The prognostic value of intratumoral textural features (TF) determined by baseline somatostatin receptor (SSTR)-positron emission tomography (PET) before PRRT was analyzed.

Procedures

Thirty-one patients with G1/G2 pNET were enrolled (G2, n?=?23/31). Prior to PRRT with [¹⁷⁷Lu]DOTATATE (mean, 3.6 cycles), baseline SSTR-PET computed tomography was performed. By segmentation of 162 (median per patient, 5) metastases, intratumoral TF were computed. The impact of conventional PET parameters (SUV_mean/max), imaging-based TF, and clinical parameters (Ki67, CgA) for prediction of both progression-free survival (PFS) and overall survival (OS) after PRRT were evaluated.

Results

Within a median follow-up of 3.7 years, tumor progression was detected in 21 patients (median, 1.5 years) and 13/31 deceased (median, 1.9 years). In ROC analysis, the TF entropy, reflecting derangement on a voxel-by-voxel level, demonstrated predictive capability for OS (cutoff?=?6.7, AUC?=?0.71, p?=?0.02). Of note, increasing entropy could predict a longer survival (>?6.7, OS?=?2.5 years, 17/31), whereas less voxel-based derangement portended inferior outcome (<?6.7, OS?=?1.9 years, 14/31). These findings were supported in a G2 subanalysis (>?6.9, OS?=?2.8 years, 9/23 vs. <?6.9, OS?=?1.9 years, 14/23). Kaplan–Meier analysis revealed a significant distinction between high- and low-risk groups using entropy (n?=?31, p?<?0.05). For those patients below the ROC-derived threshold, the relative risk of death after PRRT was 2.73 (n?=?31, p?=?0.04). Ki67 was negatively associated with PFS (p?=?0.002); however, SUV_mean/max failed in prognostication (n.s.).

Conclusions

In contrast to conventional PET parameters, assessment of intratumoral heterogeneity demonstrated superior prognostic performance in pNET patients undergoing PRRT. This novel PET-based strategy of outcome prediction prior to PRRT might be useful for patient risk stratification.

     

Endovascular repair in management of thoracic aortic aneurysms

Objective Aneurysms of the thoracic aorta are still potentially life-threatening situations. The conventional operation is still associated with morbidity. Endovascular stent graft repair offers an alternative to conventional operation for management of aortic diseases. Our aim was to report our experience with endovascular stent graft repair of thoracic aortic aneurysms. Patients and Methods Between November 2002 and October 2005, endovascular stent graft repair was performed in 26 patients: post-traumatic aortic aneurysm (n = 4), Type B dissection (n = 3) and descending thoracic aortic aneurysm (n = 19). The deployed stent graft systems were Talent-Medtronic (n = 14) and Excluder-Gore (n=12). Results Successful deployment of the stent grafts in the appropriate position was achieved in all patients. There was neither hospital mortality nor paraplegia. Late and non-procedure related death occurred in only one patient (3.8%). An average of 40% shrinkage of the aneurysmal space was observed. There was no early mortality and endoleaks. The median intensive care unit and hospital stay times were 1 and 7 days (range 4–13 days), respectively. Post-operative computed tomography scans were obtained in all patients and complete thrombosis was observed in the false lumen of dissecan aneurysms (n = 3) and sac of saccular aneurysms in 25 patients. Mean follow up time was 17.1 ± 5.4 months. Conclusions Endovascular stent graft treatment for treatment of thoracic aorta aneurysm, Type B dissection and traumatic disease of the thoracic aorta is technically feasible. Although the short and mid-term results are encouraging the long term results will determine the future of this treatment. This study was presented as an oral presentation in the 17th Annual Meeting of the Mediterranean Association of Cardiology and Cardiac Surgery, in Portorož, Slovenia, September 22–24, 2005.     

Orbital blood flow velocities in patients with rheumatoid arthritis

PURPOSE: To assess orbital blood flow changes in patients with rheumatoid arthritis using Doppler sonography. PATIENTS AND METHODS: The study comprised 35 patients who were diagnosed with RA and were treated at the Department of Physical Therapy and Rehabilitation at Duzce Medical School. A control group consisted of 35 healthy volunteers. Color Doppler imaging was used to measure peak systolic velocity (PSV) and end diastolic velocity (EDV), from which the resistance index (RI) was calculated in the ophthalmic artery (OA), central retinal artery (CRA), and posterior ciliary arteries (PCAs). RESULTS: In the OA, PSV, EDV, and RI were, respectively, 36.7 +/- 0.6 cm/sec, 9.7 +/- 0.2 cm/sec, and 0.73 in the control group versus 34.7 +/- 3.0 cm/sec, 9.1 +/- 1.1 cm/sec, and 0.74 in the patient group. In the CRA, they were, respectively, 11.8 +/- 1.7 cm/sec, 3.6 +/- 0.7 cm/sec, and 0.66 in the control group versus 11.1 +/- 1.7 cm/sec, 3.4 +/- 0.7 cm/sec, and 0.68 in the patient group. In the PCAs, they were, respectively, 13.2 +/- 1.2 cm/sec, 4.7 +/- 0.6 cm/sec, and 0.65 in the control group versus 12.4 +/- 1.2 cm/sec, 4.2 +/- 0.6 cm/sec, and 0.66 in the PCAs. PSV, EDV, and RI of the PCAs and OA and RI of the CRA were significantly different between patients and controls, whereas there was no difference in the serum levels of glucose, triglyceride, low-density lipoprotein cholesterol, and total cholesterol. In the patient group, there was a significant correlation between orbital blood flow and duration of disease. CONCLUSION: Ocular blood flow appears to be slightly lower in RA patients than in healthy controls, suggesting that RA is a systemic inflammatory disease that may also involve ocular vessels.     

Early sign of atherosclerosis in slow coronary flow and relationship with angiotensin-converting enzyme I/D polymorphism

Increase in carotid artery intima-media thickness (IMT) is an early sign of atherosclerosis. Slow coronary flow (SCF) is characterized by delay of opacification of coronary arteries in coronary angiography in the absence of any evident obstructive lesion, but its etiopathogenesis remains unclear. Genes that regulate the renin angiotensin system also play a role in developing cardiovascular system disorders. The presence of deletion (D) allele in angiotensin converting enzyme (ACE) gene polymorphism is associated with coronary artery disease. The aim of this study was to investigate the carotid artery IMT measurement, as an early sign of atherosclerosis, in patients with SCF and without SCF and also to assess the effect of the renin-angiotensin gene system on carotid IMT. Forty-four patients with angiographically proven SCF and 44 cases with normal coronary flow (NCF) pattern with similar risk profile were enrolled in the study. Coronary flow patterns of the cases were determined by thrombolysis in myocardial infarction (TIMI) frame count method. Intima-media thickness was measured by recording ultrasonographic images of both the left and right common carotid artery with a 12-MHz linear array transducer. ACE I/D polymorphism and Angiotensin II tip 1 receptor (AT1R) A/C gene polymorphism were determined by polymerase chain reaction (PCR) amplification. Demographic characteristics and coronary artery disease risk factors of SCF and NCF groups were similar. Mean TIMI frame count and carotid IMT (mm) were significantly higher in the SCF group than controls (45.9 ± 12 vs 23.3 ± 3.7, P = 0.0001; 0.75 ± 0.08 vs 0.69 ± 0.06, P = 0.0001, respectively). Mean TIMI frame count was positively correlated with IMT of carotid artery in correlation analysis (r = 0.45, P = 0.0001). When analyzed in regard to ACE genotype in all subjects, IMT values were statistically different (0.78 ± 0.06 for DD genotype, 0.72 ± 0.05 for ID genotype, and 0.64 ± 0.06 for II genotype, P = 0.0001). This difference remained significant in subgroup analyses for each genotype. No association could be observed between the AT1R A/C¹¹⁶⁶ polymorphism and IMT of carotid artery measurement (P > 0.05). Lack of association was still observed with analysis carried out when genotype effect was assumed to be inherited as additive (CC versus AA versus AC) or dominant (AA versus AC+CC). Increased IMT in patients with SCF shows that subclinical atherosclerosis may play role in this phenomenon. This increase was most marked in the presence of D allele of ACE genotype, which is associated with vascular hypertrophy.     

Aortic elastic properties in patients with coronary artery ectasia.

BACKGROUND: The purpose of the present study was to investigate the elastic characteristics of the aorta in patients with coronary ectasia (CE) and the relationship between these characteristics and echocardiographic left ventricular (LV) diastolic functions. METHODS AND RESULTS: In the first group there were 35 patients with CE, the second group consisted of 35 patients with coronary artery disease (CAD) and the third group consisted of 35 patients with normal coronary arteries. Echocardiographic investigation was carried out for the assessment of the LV diastolic functions. Aortic strain, beta index and aortic distensibility were used as aortic elasticity parameters. LV diastolic functions were impaired in both the ectasia group and the CAD group as compared with patients with normal coronary arteries. Beta index and aortic distensibility measurements were similar between the CAD and CE groups. The values obtained for aortic strain, beta index and aortic distensibility were lower in the CAD and ectasia groups when compared with the values of the normal group. On performing the stepwise linear multivariable analyses, aortic elastic parameters have been determined to possess the strongest diagnostic power for LV diastolic functions. CONCLUSIONS: The results of the current study show that stiffness parameters of aorta are impaired in the patients with CE as in the patients with CAD. The increase in aortic stiffness might be responsible for LV diastolic dysfunction.