Introduction Chronic right ventricular pacing can deteriorate cardiac function. Consequently, pacemaker system upgrades are more frequently indicated. These interventions can be hindered by venous thrombosis. In literature, it is rarely described that this problem is resolved by implanting a new lead for left ventricle (LV) stimulation on the opposite side of the previously implanted pacemaker and then subcutaneously transferring it to the old pocket. Case outline A 75-year-old male patient was hospitalized due to a planned pacemaker upgrade in December 2015. A dual-chamber pacemaker had been implanted due to sinus node dysfunction in 2011. During the previous 18 months he had been complaining about symptoms of heart failure. An upgrade to the cardiac resynchronization therapy (CRT) with a new CRT-P device was indicated due to the LV dilatation with the ejection fraction decrease, clinical deterioration, and the presence of high percentage of ventricular pacing. In October 2015, the mentioned intervention was unsuccessful due to total left subclavian vein thrombosis on the side of the previously implanted pacemaker. Anticoagulation therapy was ordinated and the reevaluation was postponed. During this hospitalization, venography confirmed total left subclavian vein thrombosis despite the anticoagulation therapy. It was decided to implant a new LV lead on the right side and then subcutaneously shift it by pre-sternal tunneling to the previous left prepectoral pocket. The intervention was uneventful. The first controls have shown stable pacemaker parameters. Conclusion This case report confirms that contralateral lead placement and subcutaneous pre-sternal tunneling of the lead is feasible and safe in patients with an implanted pacemaker, an indication for system upgrade and ipsilateral vein obstruction.

Treatment of patients with multiple sclerosis (MS) and development of new therapies have been challenging due to the disease complexity and slow progression, and the limited sensitivity of availabl ...

Introduction/Objective Pneumothorax is one of the most common complications of cardiac rhythm management (CRM) devices implantation. We aimed to assess the incidence of pneumothorax after implantation of these devices and to determine risk factors for this complication. Methods A retrospective, observational study included patients in whom CRM devices were implanted, pacing system was upgraded, or lead revision was performed during 2012 at the Pacemaker Center, Clinical Center of Serbia. We determined the connection between different variables, including sex, age, type of implanted device, prior history of chronic obstructive pulmonary disease, operator experience, venous access, the use of intravenous contrast during procedure, and the development of pneumothorax as the procedure-related complication, using multiple logistic regression. Results A total of 999 patients were included in this study. The patients’ mean age was 68.1 ± 9.2 years; 665 (66.6%) patients were male. The incidence of pneumothorax was 1.8% and an invasive treatment of this complication was required in 13 (72.2%) patients. Pneumothorax was more frequent in women (B = -2.136, p = 0.015), in patients with age > 75 years (B = 4.315, p = 0.001), venous access with subclavian vein puncture (B = 2.672, p = 0.045), and use of intravenous contrast during procedure (B = 3.155, p = 0.007). Conclusion Pneumothorax is a relatively rare complication of CRM device implantation, and for reducing its incidence, cephalic vein cut-down should be preferred to subclavian or axillary vein puncture as venous access, axillary vein puncture should not be avoided when cephalic vein cannot be found or used, and in the case of difficult vein puncture, contrast venography should be done immediately, before risky punctures.

Introduction: Diabetes mellitus (DM) is one of the most common endocrine disease of modern life. Diabetic foot (DF) is the term for a foot of a patient suffering from DM with the potential risk of a number of pathological sequels, including infection, ulceration and/or destruction of deep tissue. Goal: To determine the importance of preventive measures to prevent the development of diabetic foot. Results: The gender structure of respondents categorized by the complication of DF (yes/no) was uniform. The average age was 60.15±12.2 years. Respondents without DF, 63% had 2 visits to the doctor a month, while in the group of those with DF, 39% of them had 3 visits to a doctor and 33% four or more times. Wearing comfortable shoes and foot hygiene in relation to the development of the DF are interdependent: c2=4,409; c2 = 12.47 (p <0.0005). Also, recurrent foot injury, and slow healing of sores in comparison to the development of the DF are mutually dependent; c2=13,195; c2=14 (p <0.0005). Conclusion: We found that there is a significant statistical relationship between preventive measures and development of the DF.

Introduction: The occurrence of hyperglycemia in non-diabetics during development of acute coronary ischemia (ACI) indicates latent glucose metabolism disorder, or is a case of newly discovered diabetes mellitus (DM) as a result of stress. Acute coronary syndrome refers to a group of clinical syndromes caused by a sudden circulatory disorder in coronary arteries, resulting in the corresponding myocardial ischemia. It covers range from unstable angina and myocardial infarction (MI) without Q wave in the electrocardiogram finding (NSTEMI) up to myocardial infarction with Q wave in the electrocardiogram finding (STEMI). Goal: To determine the incidence of hyperglycemia in non-diabetics immediately after the occurrence of acute coronary ischemia and assess its risk factors. Results: The sample included 80 respondents. Men dominated with a total prevalence of 77.5%. The respondent was at mean age of 62.8±13.8 years. During the first measurement, immediately after hospital admission, 50% of respondents had increased blood glucose value and during the second measurement 62%. Hypertension as a risk factor has 54% and 56% smoking. The incidence of stress diabetes after ACI does not depend on the diagnosis of hypertension, χ2=0.050; p=0.823. The differences of mean values (median) BMI between examined persons with/without stress DM are not statistically significant p=0.402. Independent t-test showed that there was no statistically significant difference in the average values of HDL and LDL in patients with stress diabetes than in patients without diabetes stress after ACI p>0.05. For each year of age odds ratio for “stress diabetes” increases by 7% and 95% CI is 2% -12%. Conclusion: The incidence of stress diabetes ACI is not dependent on the working diagnosis (MI or angina pectoris). As risk factors we set hypertension and current smoking. There were no statistically significant associations between active smoking and hypertension as a risk factor in relation to occurrence of stress diabetes.

Covariate analysis using item response theory modelling of expanded disability status scale (EDSS) : a case study of cladribine tablets

Bordetella pertussis toxin (PTx), also known as islet-activating protein, induces insulin secretion by ADP-ribosylation of inhibitory G proteins. PTx-induced insulin secretion may result either from inactivation of Gα(o) proteins or from combined inactivation of Gα(o), Gα(i1), Gα(i2), and Gα(i3) isoforms. However, the specific role of Gα(i2) in pancreatic β-cells still remains unknown. In global (Gα(i2)(-/-)) and β-cell-specific (Gα(i2)(βcko)) gene-targeted Gα(i2) mouse models, we studied glucose homeostasis and islet functions. Insulin secretion experiments and intracellular Ca²⁺ measurements were used to characterize Gα(i2) function in vitro. Gα(i2)(-/-) and Gα(i2)(βcko) mice showed an unexpected metabolic phenotype, i.e., significantly lower plasma insulin levels upon intraperitoneal glucose challenge in Gα(i2)(-/-) and Gα(i2)(βcko) mice, whereas plasma glucose concentrations were unchanged in Gα(i2)(-/-) but significantly increased in Gα(i2)(βcko) mice. These findings indicate a novel albeit unexpected role for Gα(i2) in the expression, turnover, and/or release of insulin from islets. Detection of insulin secretion in isolated islets did not show differences in response to high (16 mM) glucose concentrations between control and β-cell-specific Gα(i2)-deficient mice. In contrast, the two- to threefold increase in insulin secretion evoked by L-arginine or L-ornithine (in the presence of 16 mM glucose) was significantly reduced in islets lacking Gα(i2). In accord with a reduced level of insulin secretion, intracellular calcium concentrations induced by the agonistic amino acid L-arginine did not reach control levels in β-cells. The presented analysis of gene-targeted mice provides novel insights in the role of β-cell Gα(i2) showing that amino acid-induced insulin-release depends on Gα(i2).

G-protein-coupled receptors (GPCRs) are the most abundant receptors in the heart and therefore are common targets for cardiovascular therapeutics. The activated GPCRs transduce their signals via heterotrimeric G-proteins. The four major families of G-proteins identified so far are specified through their α-subunit: Gαi, Gαs, Gαq and G12/13. Gαi-proteins have been reported to protect hearts from ischemia reperfusion injury. However, determining the individual impact of Gαi2 or Gαi3 on myocardial ischemia injury has not been clarified yet. Here, we first investigated expression of Gαi2 and Gαi3 on transcriptional level by quantitative PCR and on protein level by immunoblot analysis as well as by immunofluorescence in cardiac tissues of wild-type, Gαi2-, and Gαi3-deficient mice. Gαi2 was expressed at higher levels than Gαi3 in murine hearts, and irrespective of the isoform being knocked out we observed an up regulation of the remaining Gαi-protein. Myocardial ischemia promptly regulated cardiac mRNA and with a slight delay protein levels of both Gαi2 and Gαi3, indicating important roles for both Gαi isoforms. Furthermore, ischemia reperfusion injury in Gαi2- and Gαi3-deficient mice exhibited opposite outcomes. Whereas the absence of Gαi2 significantly increased the infarct size in the heart, the absence of Gαi3 or the concomitant upregulation of Gαi2 dramatically reduced cardiac infarction. In conclusion, we demonstrate for the first time that the genetic ablation of Gαi proteins has protective or deleterious effects on cardiac ischemia reperfusion injury depending on the isoform being absent.