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Introduction Theatre models in medical education have been used worldwide in order to train medical students and graduates in managing various situations. However, the literature reports little regarding its appeal to trainees. We conducted a medical seminar, entitled Emergency Cases School, which employed such techniques. Actors simulated the actions of doctors and patients involved in various emergency cases, in front of a large audience, in a specially modified theatre hall which resembled the emergency room environment. Methods A total of 303 undergraduate medical students participated in the seminar. The audience evaluated the course with the DREEM questionnaire, along with two extra questions: Q1. 'Do you think that the course will prove itself beneficial to your clinical skills?' and Q2. 'Would you suggest the course to another student?', in a 0-4 scoring scale. Of the attendees, 281 (92.7%) answered the questionnaire.Results The overall DREEM score was 140.32 (±23.39) out of 150, which is interpreted as 'More positive than negative'. The results of Q1 and Q2 were 3.07 (±0.78) and 3.65 (±0.61), respectively. Discussion The Emergency Cases School received positive feedback as a theatre educational tool, targeted to a large audience. With the advantage of the realistic setting of an emergency room, along with its low-budget needs, this course model could function as a creative alternative of the more traditional lecturing teaching techniques. [ABSTRACT FROM AUTHOR]

Purpose: To assess the difference in the prevalence of invariant Natural Killer T (iNKT) lymphocytes between hyperlipidemic and control individuals and to evaluate changes in iNKT cell levels after 6 months lipid lowering therapy. Methods: A total of 77 hyperlipidemic individuals (54 ± 5 years) were assigned to simvastatin 40 mg or ezetimibe 10 mg daily for 6 months. Fifty individuals with normal cholesterol levels were used as control. iNKT cells were measured by flow cytometry in peripheral blood. Results: Patients with hypercholesterolemia had significantly lower iNKT cell levels (percentage on the lymphocyte population) compared to control group (0.16 ± 0.04% vs 0.39 ± 0.08%, p = 0.03). iNKT cells significantly increased after 6 months treatment with simvastatin (from 0.15 ± 0.04% to 0.28 ± 0.11%, p = 0.03) but not with ezetimibe (from 0.16 ± 0.05% to 0.17 ± 0.06%, p = 0.55). Simvastatin treatment did not alter the activation status of iNKT cells as measured by HLA-DR expression. Changes of iNKT cells were independent from changes in total ( r = 0.009, p = 0.76) or LDL cholesterol ( r = 0.008, p = 0.78) reached by simvastatin. Conclusions: Hyperlipidemic patients have reduced numbers of iNKT in peripheral circulation compared to individuals with normal cholesterol levels. Their number is increasing after long term administration of simvastatin 40 mg but not after ezetimibe. [ABSTRACT FROM AUTHOR]

Purpose: Assessment of circulating levels of collagen-derived peptides has been proposed as a useful tool to monitor indirectly myocardial collagen metabolism in chronic heart failure (CHF) patients. The potential link between circulating concentrations of collagen metabolism biomarkers and health-related quality of life (HRQOL) has not been adequately evaluated. With the present study, we investigated the association between serum levels of collagen-derived peptides and HRQOL. Methods: We studied 280 consecutive outpatients (of mean age 67 ± 10 years, 180 men) with CHF. Serum concentrations of carboxy-terminal telopeptide of collagen type I (CITP)-a marker of collagen type I degradation-were measured in all patients both at baseline and during a period of 6 months follow-up. HRQOL was assessed by Minnesota living with heart failure questionnaire (MLHFQ). Results: CITP levels were significantly associated with MLHFQ scores both at baseline ( r = 0.231, P < 0.001) and at 6 months follow-up ( r = 0.145, P = 0.044). CITP levels remained significantly associated with MLHFQ score in multivariable linear regression analysis. Higher CITP levels were observed with higher MLHFQ scores (poor HRQOL) both at baseline ( P = 0.001) and at 6 months ( P = 0.041). Unadjusted analysis demonstrated a significant relationship between increasing CITP levels during 6 months follow-up and worsening HRQOL ( r = 0.204, P = 0.001). The aforementioned correlation remained significant in multivariable linear regression analysis. Conclusion: Our findings show that increased CITP levels are associated with poorer HRQOL in patients with CHF. These findings are consistent with a link between a pathophysiologic mechanism, i.e., collagen metabolism and patient self-assessed health status in CHF. [ABSTRACT FROM AUTHOR]

Background: Extracellular matrix metabolism (ECM) has an important role in left ventricular (LV) remodeling in chronic heart failure (CHF). Matrix metalloproteinases (MMPs) are involved in the regulation of extracellular matrix (ECM) metabolism. We investigated the effect of levosimendan, a novel calcium sensitizer, on serum levels of MMP-2. Methods: Our study population consisted of 60 consecutive patients with advanced heart failure who were admitted to hospital with an acute decompensation of their CHF. Patients were randomized to levosimendan ( n = 30; 18 men, aged 65 ± 3 years) or placebo ( n = 30; 15 men, aged 67 ± 4 years). Serum MMP-2 levels were assessed before and after treatment with levosimendan or placebo, using a commercially available ELISA. Results: Serum levels of MMP-2 were reduced from 427 ng/ml 95%CI 372–484 to 371 ng/ml 95%CI 329–413 in the levosimendan treated group and from 433 ng/ml 95%CI 422–444 to 425 ng/ml 95%CI 414–436 in the placebo group. Repeated measurements ANOVA showed that treatment with levosimendan significantly affected levels of MMP-2 ( p = 0.019). Conclusions: The present study showed that levosimendan may beneficially affect ECM remodeling in patients with acutely decompensated CHF. Whether these effects translate into added clinical benefits, as suggested by an improved ejection fraction in the levosimendan group, deserves further investigation. [ABSTRACT FROM AUTHOR]

It is well known that atrial fibrillation is associated with high incidence of thromboembolic events, propably due to a prothrombotic or hypercoagulable state. However, it is unclear whether or not there is any difference of this prothrombotic state in the clinical subgroups of atrial fibrillation patients, that is, in those with paroxysmal, persistent or permanent atrial fibrillation. From the other side the role of the arrhythmia duration on the changes of coagulative variables in atrial fibrillation patients is not clearly enough. The contribution of genetic and functional alterations in factors of the coagulation and fibrinolytic pathways (that is hemostatic risk factors) to the development of hypercoagulation state in atrial fibrillation requires clarification. We investigated therefore (1) if there are differences in the prothrombotic state between patients with different clinical status of the arrhythmia, (2) if the arrhythmia duration per se could be an independent determinant of the prothrombotic state in all atrial fibrillation patients and (3) if coexistent genetic alterations in haemostatic risk factors in patients with atrial fibrillation could contribute to the development of prothrombotic abnormalities. Methods: Over a period of 23 months, we studied 55 patients with chronic non-valvular atrial fibrillation. We recruited 18 consecutive patients (13 men, mean age 59 ± 10 years) with paroxysmal atrial fibrillation 17 patients (11 men, mean age 61 ± 7 years) with persistent atrial fibrillation who underwent elective successful DC and remained in sinus rhythm at the 3 month visit and 20 patients (14 men mean age 64 ± 9) with permanent atrial fibrillation. Blood results were compared to 17 age-sex- and race-matched controls. The prothrombotic state was quantified by measurement of plasma levels of fibrinogen, soluble P-selectin (an index of platelet activation) and von Willebrand factor (a marker of endothelial dysfunction). We assessed the frequencies of factor V Leiden and prothrombin variant G20210A to determine whether particular inherited haemostatic risk factors may have contribution to the development of prothrombotic state in atrial fibrillation patients. Results: Permanent atrial fibrillation was associated with significant raised levels of von Willebrand factor, fibrinogen levels and soluble P-selectin compared to matched controls (all p < 0.001) and matched patients with paroxysmal and permanent AF (all p ranged between <0.003 and <0.002). Patients with persistent atrial fibrillation had significantly elevated von Willebrand factor levels ( p = 0.0064) and fibrinogen levels ( p = 0.002), but not Soluble P-selectin ( p = 0.509). when compared to controls. Patients with paroxysmal atrial fibrillation had significantly elevated levels of P-selectin ( p = 0.005) and fibrinogen ( p = 0.003), but not von Willebrand factor ( p = .0.61) compared to controls. Stepwise multiple regression analyses demonstrated that the arrhythmia duration (approximately 3 years) was an independent predictor of abnormal von Willebrand factor, fibrinogen and soluble P-selectin levels. Restoration of sinus rhythm in paroxysmal atrial fibrillation subgroup and successful electrical cardioversion of patients with permanent fibrillation atrial fibrillation did not significantly alter levels of the affected factors. The frequency of factor V Leiden was 8.9 in all studied patients with atrial fibrillation, versus 2.4% in the control group (odds ratio {OR} 4.6 [95% confidence (CI) 1.4–17.5], p = 0.02). The frequency of the prothrombin variant G20210A was 6.4.% compared with control group 1.6% (OR 4.9 [95% confidence interval (CI) 1.2–2.9], p = 0.04). There was a trend towards an increased frequency of factor V Leiden and/or prothrombin variant G20210A in patients age <55 years and in patients living at a particular area of Thrace mountains. Conclusions: Our results showed that... [ABSTRACT FROM AUTHOR]