1,721,104 research outputs found
[Italian clinical trials on cardiac cell therapy: where we are and where are we going?]
In the last years translation from bench to bedside of findings regarding cardiac cell therapy is swinging between delays and accelerations. Based on experimental studies, clinical trials were started in 2001. To date in Europe more than 900 patients have been treated with cell transplantation or mobilization and new clinical trials are ongoing in many countries. Published data provide a limited idea of current Italian clinical research in this field. This investigation intends to report Italian clinical trials and projects using cell therapy in cardiology
[Cardiac cell therapy: the puzzle is waiting to be solved]
Cell therapy has been proposed as an innovative hypothesis to treat acute myocardial infarction and heart failure. However, the mechanism by which stem cells could improve cardiac function remains unclear and many controversies have been arisen in interpretation of experimental and clinical data. Answering the five "WH questions" we discuss the process that has led to consider cell therapy as a new treatment option for myocardial tissue regeneration after ischemic damage. 1) Why should we use stem cells? The rationale derives from the disclosure that apoptosis and regeneration occur at the myocardial level and stem cells migrate from bone marrow to repopulate the damaged cardiac tissue. 2) Which are the most appropriate cells, delivery methods and therapeutic purposes? Adult stem cells can be mobilized or directly transplanted in human hearts to accomplish myocardioneogenesis, neoangiogenesis and/or paracrine effects. 3) Where should we transplant these cells? The infarct border zone seems to be the best place to home and differentiate transplanted cells hampering post-ischemic cardiac remodeling. 4) When should we perform cell therapy? Cell therapy should be performed during or after an acute myocardial infarction: best setting and timing still need to be precisely addressed. 5) Who might be the suitable patient? Further multicenter randomized trials with adequate patient selection are needed to answer this crucial question
Reply: The Barcelona Bio-HF Calculator: A Contemporary Web-Based Heart Failure Risk Score
Letter regarding the article 'Heart failure with preserved ejection fraction: from mechanisms to therapies' by Lam and colleagues
T1 mapping with cardiovascular magnetic resonance: An emerging clinical biomarker
We thank Ripley and colleagues for their interest in our paper and agree that T1 mapping with CMR is an emerging imaging biomarker that is increasingly being investigated for its potential role in hypertrophic cardiomyopathy and cardiac hypertrophy in general. Convincing data have been published concerning hypertensive heart disease (Hinojar et al., 2015), hypertrophic and dilated cardiomyopathy (Puntmann et al., 2013), transthyretin amyloidosis (Fontana et al., 2014) and Anderson-Fabry disease (Pica et al., 2014). We have not found any specific published data examining the role of T1 mapping in distinguishing ventricular septal bulge in an elderly population from other etiologies of hypertrophy. We therefore decided not to include T1 mapping in our review (Canepa et al., 2016) but concur that this technique may be potentially useful in the evaluation of ventricular septal bulge
Going Beyond Counting First Authors in Author Co-citation Analysis
The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
The impossible quest to make cardiac amyloidosis diagnosis easy
Cardiac amyloidosis (CA) is an increasingly recognized myocardial infiltrative disease, causing pseudo-hypertrophy of the heart, diastolic dysfunction and heart failure. Growing efforts are ongoing to optimize screening and diagnostic algorithms for CA [1]. This is motivated by the surfacing of targeted therapies, which are supposed to be more effective the earlier the diagnosis of CA is made [2]. Echocardiography represents a fundamental methodology for the clinician to trigger the suspicion of CA [3]. Although echocardiography serves as a gatekeeper to CA diagnosis, features such as left ventricular hypertrophy (LVH) or diastolic dysfunction, which are common in CA, are frequently encountered in other more prevalent cardiovascular conditions within the ample spectrum of hypertrophic phenocopies [4,5], thus making differential diagnosis difficult. To this end, the work published by Aimo and colleagues in this issue of the European Journal of Clinical Investigation aims at simplifying the process by which a suspect of CA might be confirmed or refuted through the sole echocardiographic examination [6]. The present analysis builds on a previous recent work by the same Authors and others [7], in which two scores named "AL score" and "IWT score" were developed using differently weighted echocardiographic variables (i.e., relative wall thickness - RWT, E wave/e' wave ratio - E/e', tricuspid annular plane systolic excursion, longitudinal strain and septal longitudinal systolic apex-to-base ratio). Those scores were showed to allow a correct diagnosis of CA, respectively among patients with proven systemic light-chain amyloidosis and with unexplained LVH [7]. In the present analysis, a simplified score named "AMYLI score" is proposed, obtained by just multiplying RWT by E /e'. This new score is shown to have particularly good performance in ruling-out a diagnosis of CA when a value <2.2 is found in patients referred by hematologists and <2.36 in patients with unexplained LVH [6]. The AMYLI score is thus presented as a clinically helpful tool to this end. However, some shortcomings of the present work - and more in general, of the imaging-centric diagnostic approach to CA - should be acknowledged and deserve some discussion
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