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Background: Remote ischemic preconditioning (RIPC) is being evaluated as a strategy to reduce cardiac injury and inflammation in patients undergoing diverse cardiac invasive and surgical procedures. However, it is unclear whether RIPC has protective effects in patients undergoing the transfemoral- transcatheter aortic valve implantation (TF-TAVΙ) procedure. Methods: Between September 2013 and September 2015, 55 random consecutive patients were prospectively assigned to receive SHAM preconditioning (SHAM, 22 patients) or Remote Ischemic Preconditioning (RIPC) (4 cycles of 5 min intermittent leg ischemia and 5 min reperfusion, 33 patients) prior to TF-TAVI. The primary endpoint was to determine the serum levels of: hs-cTn-I (necrosis), CK-18 (apoptosis), and IL-1b (inflammation). Quantification was performed using commercially available ELISA kits. Patients were sampled 1-day pre TF-TAVΙ and 24-hours post TF-TAVΙ. Secondary endpoints included: total mortality, incidence of periprocedural clinical acute myocardial infarction (AMI), acute kidney injury (AKI), and stroke. Results: 22 SHAM patients and 33 RIPC patients were finally analyzed. Our data revealed no significant difference in serum levels of hs-cTn-I and CK-18 among various groups. However, in the RIPC group, the increase in IL1b level was significantly lower for 24-h post TF-TAVΙ, (p

Transcatheter aortic valve implantation is a safe procedure even in inoperable patients with multi‐organ failure and cardiogenic shock. In such cases, the heart team should be prepared to proceed to emergent implantation for timely and successful management of the patient.

Eccentric exercise has been extensively used as a model to study the contraction-induced muscle damage and its consequent processes. This study aimed at examining molecular responses associated with tissue remodelling, inflammation and angiogenesis in skeletal muscle during the recovery period after eccentric exercise in humans. Ten healthy men performed 50 maximal eccentric muscle actions with the knee extensors and muscle biopsies were collected from the vastus lateralis before and 6 h, 48 h and 120 h post eccentric exercise. Real Time-PCR was utilized to investigate alterations in gene expression of various tissue remodelling-, inflammation- and angiogenesis-related factors: uPA, uPA-R, TGF-β1, MMP-9, TNF-α, IL-6, IL-8, VEGF, VEGFR-2, HIF-1a, Ang-1, Ang-2 and Tie-2. The uPA/uPA-R system exhibited a similar time-expression pattern increasing 6 h post exercise (p 0.05). Similarly, the expression of angiopoietin receptor Tie-2 showed an early increase only at 6 h after the completion of exercise (p

Eccentric exercise has been extensively used as a model to study the contraction-induced muscle damage and its consequent processes. This study aimed at examining molecular responses associated with tissue remodelling, inflammation and angiogenesis in skeletal muscle during the recovery period after eccentric exercise in humans. Ten healthy men performed 50 maximal eccentric muscle actions with the knee extensors and muscle biopsies were collected from the vastus lateralis before and 6 h, 48 h and 120 h post eccentric exercise. Real Time-PCR was utilized to investigate alterations in gene expression of various tissue remodelling-, inflammation- and angiogenesis-related factors: uPA, uPA-R, TGF-beta 1, MMP-9, TNF-alpha, IL-6, IL-8, VEGF, VEGFR-2, HIF-1a, Ang-1, Ang-2 and Tie-2. The uPA/uPA-R system exhibited a similar time-expression pattern increasing 6 h post exercise (p < 0.05), while the other tissue remodelling factors TGF-beta 1 and MMP-9 did not change significantly over time. Transcriptional responses of inflammatory factors TNF-alpha and IL-8 increased significantly and peaked 6 h post eccentric exercise (p < 0.05), while IL-6 exhibited a similar, though not statistically significant, expression profile (p > 0.05). Similarly, the expression of angiopoietin receptor Tie-2 showed an early increase only at 6 h after the completion of exercise (p < 0.05), while the other angiogenic factors failed to reach statistical significance due a high interindividual variability in the gene expression responses. The early transcriptional upregulation of tissue remodelling, inflammation- and angiogenesis-related factors post eccentric exercise may indicate the acute intramuscular activation of these processes functionally related to muscle damage-induced adaptation.

Eccentric exercise has been extensively used as a model to study the contraction-induced muscle damage and its consequent processes. This study aimed at examining molecular responses associated with tissue remodelling, inflammation and angiogenesis in skeletal muscle during the recovery period after eccentric exercise in humans. Ten healthy men performed 50 maximal eccentric muscle actions with the knee extensors and muscle biopsies were collected from the vastus lateralis before and 6 h, 48 h and 120 h post eccentric exercise. Real Time-PCR was utilized to investigate alterations in gene expression of various tissue remodelling-, inflammation- and angiogenesis-related factors: uPA, uPA-R, TGF-β1, MMP-9, TNF-α, IL-6, IL-8, VEGF, VEGFR-2, HIF-1a, Ang-1, Ang-2 and Tie-2. The uPA/uPA-R system exhibited a similar time-expression pattern increasing 6 h post exercise (p 0.05), while the other tissue remodelling factors TGF-β1 and MMP-9 did not change significantly over time. Transcriptional responses of inflammatory factors TNF-α and IL-8 increased significantly and peaked 6 h post eccentric exercise (p 0.05), while IL-6 exhibited a similar, though not statistically significant, expression profile (p 0.05). Similarly, the expression of angiopoietin receptor Tie-2 showed an early increase only at 6 h after the completion of exercise (p 0.05), while the other angiogenic factors failed to reach statistical significance due a high interindividual variability in the gene expression responses. The early transcriptional upregulation of tissue remodelling, inflammation- and angiogenesis-related factors post eccentric exercise may indicate the acute intramuscular activation of these processes functionally related to muscle damage-induced adaptation.

Patients with Williams syndrome often present with abnormalities of the vascular wall of the aorta and/or the pulmonary artery. Surgery may result in restenosis of the affected vessel. Herein, we report a case of an infant with multiple recurrences of aortic coarctation successfully treated with Zotarolimus drug-eluting stent.

This report presents the case of an 82-year-old man with known dextrocardia and situs inversus totalis who presented with increasing dyspnea on exertion and was diagnosed with severe aortic stenosis. Transcatheter aortic valve replacement was performed and required deviation from standard techniques for patients with normal anatomy and left-sided aortic arch. We describe two technical differences required for patients with dextrocardia and right-sided aortic arch that facilitate transcatheter aortic valve replacement in this patient group.

Background Interventional radiology (IR) is underrepresented in undergraduate medical curricula across Europe. By continuing to challenge the boundaries of IR, a rise in the demand for radiologists has been inevitable – a trend not met by a corresponding rise in the supply of radiologists. On tracing the roots of this shortage, lack of awareness of the specialty within medical trainees coupled with a global lack of IR teaching in undergraduate education seem to constitute major exacerbating factors. The purpose of this study was to identify gaps in the field of IR education and address these by implementing an international IR simulation-based course for undergraduates. Results Implementation of a multi-modality simulation-based course consisted of seven modules incorporating technical and non-technical skills, basic science and applied clinical science modules. Of all participants, 90.7% (N = 68) never had previous IR teaching experience and only 28% (N = 21) had a previous placement in an IR department. Following the course, confidence improvement was statistically significant both in IR skills (1/5, p p N = 24) reported that they would more likely consider a career in IR after completing the course. Conclusion Delivery of a tetra-core simulation course with the aim to address the gaps in undergraduate IR education has had a positive impact on students’ skills, confidence levels as well as motivation. We propose reviewing the curricula across medical schools in Europe to identify gaps and address any inadequacies; for this, we consider our simulation course an excellent starting point.

Treatment of a failing aortic bioprosthesis by transcatheter valve-in-valve (ViV) therapy has become an alternative to redo surgery. However, the ViV technique may be less effective in small surgical valves because of patient/prosthesis mismatch (PPM). Here we will discuss the bioprosthetic valve fracture/remodelling (BVF) procedure and the most important issues regarding this promising new technique.

Transcatheter aortic valve replacement (TAVI) is an established treatment for inoperable patients or patients at high surgical risk with severe aortic stenosis. Herein, we illustrate the key design features of the main new generation devices that are entering contemporary clinical practice, the labeled and off-labeled indications, the basic principles of screening process, and the clinical outcomes of the TAVI procedure. Answer questions and earn CME: https://wileyhealthlearning.com/Activity2/4193543/Activity.aspx

Coronary artery bifurcation disease is considered to be technically challenging since it is one of the most complex lesions owing to great anatomical variability. Recent data suggest the provisional approach of implanting one stent in the main vessel as the default treatment for most bifurcation lesions. However, despite the use of drug-eluting stents and different stenting techniques, coronary bifurcation stenosis continues to be a challenging lesion subset. In particular, management of the so-called ‘true coronary bifurcation lesions’, classified as B2 lesions by the Movahed bifurcation classification (B = bifurcation, 2 = both the main and side branch ostia have disease), requires a longer duration and is associated with a low procedural success rate at both short- and long-term follow-up compared with nonbifurcation lesions, presumably owing to suboptimal results in the side branch. Recently, novel dedicated bifurcation devices have been designed to facilitate the provisional approach, offering easy a...

Objectives: We assessed the role of the immunogenetic background in the development and recurrence of acute idiopathic pericarditis (AIP). Methods: Fifty-five patients with a first episode of AIP were followed for 23.8 ± 6.3 months and recurrences were recorded. The control group consisted of 246 healthy individuals. In all subjects, genomic human leukocyte antigen (HLA) typing was performed. Moreover, circulating lymphocyte subpopulations were studied in 44 randomly selected patients and in 20 controls. Results: An increased frequency of HLA-A*02, -Cw*07 and -DQB1*0202 alleles, and a decreased frequency of the -DQB1*0302 allele was detected in patients with AIP. The recurrence rate was 40% and time to recurrence was 202.8 ± 164.1 days. In patients with idiopathic recurrent pericarditis (RP), increased frequencies of HLA-A*02, -Cw*07 and -DQB1*0202 alleles were found. Notably, no patient with RP exhibited HLA-DRB1*04 and -DQB1*0302 alleles. Patients with RP exhibited lower CD4+/CD45RA+ naïve T cells (p = 0.03) than controls, and higher CD8+DR+ activated T cells (p = 0.01) than patients without recurrence and controls. Conclusions: HLA alleles may confer either susceptibility or resistance to AIP and RP. Circulating T-cell subpopulations may also predict RP. A combination of the above parameters might help to better define patients prone to recurrence.

Autophagy is a major degradative and highly conserved process in eukaryotic cells that is activated by stress signals. This self-cannibalisation is activated as a response to changing environmental conditions, cellular remodelling during development and differentiation, and maintenance of homeostasis.To review autophagy regarding its process, molecular mechanisms and regulation in mammalian cells, and its role in myocardial pathophysiology.Autophagy is a multistep process regulated by diverse, intracellular and/or extracellular signalling complexes and pathways. In the heart, normally, autophagy occurs at low basal levels, where it represents a homeostatic mechanism for the maintenance of cardiac function and morphology. However, in the diseased heart the functional role of the enhanced autophagy is unclear and studies have yielded conflicting results. Recently, it was shown that during myocardial ischemia autophagy promotes survival by maintaining energy homeostasis. Also, rapamycin was demonstrated to prevent cardiac hypertrophy. In heart failure, upregulation of autophagy acts as an adaptive response that protects cells from hemodynamic stress. In addition, sirolimus-eluting stents have been shown to lower re-stenosis rates in patients with coronary artery disease after angioplasty. Thus, this mechanism can become a major target for therapeutic intervention in heart pathophysiology.

Background: Myocarditis is defined as the inflammation of myocardium associated with cardiac dysfunction. Despite this clear-cut definition, diagnosis and etiologic treatment continue to create considerable debate. Viral infections are frequent causes of myocarditis and there is evidence that persistent viral infection is associated with poor prognosis in different subtypes of cardiomyopathy. Objective: To review methods for diagnosis of viral myocarditis and present the use of polymerase chain reaction (PCR)–based protocols for evaluating viral infection in myocarditis/cardiomyopathies. Methods: A review of published literature. Results/conclusion: There is increasing evidence that PCR-based protocols can provide reliable molecular evidence for the presence of viral infection in myocardium. Thus application of molecular techniques will allow collection and analysis of more information on the epidemiology of viral cardiomyopathies, patient risk stratification and appropriate medical treatment.

Prostate cancer shows a strong predilection to spread to the bones. Once prostate tumour cells are engrafted in the skeleton, curative therapy is no longer possible and palliative treatment becomes the only option. Herein, we review the multifactorial mechanisms and complex cellular interactions that take place inside the bone metastatic microenvironment. Emphasis is given to the detection and treatment of the micrometastatic stage of prostate cancer, as well as our recent attempts to target the bone metastasis microenvironment-related survival factors using an anti-survival factor manipulation which can increase the efficacy of anticancer therapies such as androgen ablation therapy and chemotherapy in advanced prostate cancer.