Publications
308 results found
Cowie MR, Filippatos GS, Garcia MDLAA, et al., 2017, New medicinal products for chronic heart failure: advances in clinical trial design and efficacy assessment, European Journal of Heart Failure, Vol: 19, Pages: 718-727, ISSN: 1388-9842
Despite the availability of a number of different classes of therapeutic agents with proven efficacy in heart failure, the clinical course of heart failure patients is characterized by a reduction in life expectancy, a progressive decline in health-related quality of life and functional status, as well as a high risk of hospitalization. New approaches are needed to address the unmet medical needs of this patient population. The European Medicines Agency (EMA) is undertaking a revision of its Guideline on Clinical Investigation of Medicinal Products for the Treatment of Chronic Heart Failure. The draft version of the Guideline was released for public consultation in January 2016. The Cardiovascular Round Table of the European Society of Cardiology (ESC), in partnership with the Heart Failure Association of the ESC, convened a dedicated two-day workshop to discuss three main topic areas of major interest in the field and addressed in this draft EMA guideline: (i) assessment of efficacy (i.e. endpoint selection and statistical analysis); (ii) clinical trial design (i.e. issues pertaining to patient population, optimal medical therapy, run-in period); and (iii) research approaches for testing novel therapeutic principles (i.e. cell therapy). This paper summarizes the key outputs from the workshop, reviews areas of expert consensus, and identifies gaps that require further research or discussion. Collaboration between regulators, industry, clinical trialists, cardiologists, health technology assessment bodies, payers, and patient organizations is critical to address the ongoing challenge of heart failure and to ensure the development and market access of new therapeutics in a scientifically robust, practical and safe way.
Koulaouzidis G, Lyon AR, 2017, Proteasome Inhibitors as a Potential Cause of Heart Failure, HEART FAILURE CLINICS, Vol: 13, Pages: 289-295, ISSN: 1551-7136
Key points•Proteasome inhibitors have become an important drug class in the treatment of multiple myeloma, and currently 3 have received regulatory approval.•In addition to its role in myeloma cells, the proteasome plays a critical role in the myocardium, particularly in the context of cardiac stress.•The growing awareness of the cardiovascular toxicity of proteasome inhibitors is emerging following the phase 3 trials and the transition into real-world practice.
Patel HC, Hayward C, Keegan J, et al., 2017, Effects of renal denervation on vascular remodelling in patients with heart failure and preserved ejection fraction: A randomised control trial, JRSM Cardiovascular Disease, Vol: 6, ISSN: 2048-0040
Objective:To assess the effect of renal denervation (RDT) on micro- and macro-vascular function in patients with heartfailure with preserved ejection fraction (HFpEF).Design:A prospective, randomised, open-controlled trial with blinded end-point analysis.Setting:A single-centre London teaching hospital.Participants:Twenty-five patients with HFpEF who were recruited into the RDT-PEF trial.Main outcome measures:Macro-vascular: 24-h ambulatory pulse pressure, aorta distensibilty (from cardiac magneticresonance imaging (CMR), aorta pulse wave velocity (CMR), augmentation index (peripheral tonometry) and renal arteryblood flow indices (renal MR). Micro-vascular: endothelial function (peripheral tonometry) and urine microalbuminuria.Results:At baseline, 15 patients were normotensive, 9 were hypertensive and 1 was hypotensive. RDT did not lowerany of the blood pressure indices. Though there was evidence of abnormal vascular function at rest, RDT did not affectthese at 3 or 12 months follow-up.Conclusions:RDT did not improve markers of macro- and micro-vascular function.
Walls GM, Lyon AR, Harbinson MT, et al., 2017, Cardiotoxicity following cancer treatment, Ulster Medical Journal, Vol: 86, Pages: 3-9, ISSN: 0041-6193
More than half of those born after 1960 will develop cancer during their lifetime. Fortunately, owing to improved diagnosis and treatment, cure rates have risen steadily over the last three decades. With an increased survivorship, more will experience adverse effects of cancer therapeutics on the heart. As the oncologist's focus begins to encompass the issues of cancer survivorship, awareness of the management of cardiac toxicity would be prudent for all physicians looking after patients with cancer.
Mawad D, Mansfield C, Lauto A, et al., 2016, A conducting polymer with enhanced electronic stability applied in cardiac models, Science Advances, Vol: 2, ISSN: 2375-2548
Electrically active constructs can have a beneficial effect on electroresponsive tissues, such as the brain, heart, and nervous system. Conducting polymers (CPs) are being considered as components of these constructs because of their intrinsic electroactive and flexible nature. However, their clinical application has been largely hampered by their short operational time due to a decrease in their electronic properties. We show that, by immobilizing the dopant in the conductive scaffold, we can prevent its electric deterioration. We grew polyaniline (PANI) doped with phytic acid on the surface of a chitosan film. The strong chelation between phytic acid and chitosan led to a conductive patch with retained electroactivity, low surface resistivity (35.85 ± 9.40 kilohms per square), and oxidized form after 2 weeks of incubation in physiological medium. Ex vivo experiments revealed that the conductive nature of the patch has an immediate effect on the electrophysiology of the heart. Preliminary in vivo experiments showed that the conductive patch does not induce proarrhythmogenic activities in the heart. Our findings set the foundation for the design of electronically stable CP-based scaffolds. This provides a robust conductive system that could be used at the interface with electroresponsive tissue to better understand the interaction and effect of these materials on the electrophysiology of these tissues.
Luis Zamorano J, Lancellotti P, Rodriguez Munoz D, et al., 2016, 2016 ESC Position Paper on cancer treatments and cardiovascular toxicity developed under the auspices of the ESC Committee for Practice Guidelines, KARDIOLOGIA POLSKA, Vol: 74, Pages: 1193-1233, ISSN: 0022-9032
Chari A, Mezzi K, Zhu S, et al., 2016, Incidence and risk of hypertension in patients newly treated for multiple myeloma: a retrospective cohort study, BMC Cancer, Vol: 16, ISSN: 1471-2407
BackgroundHypertension is commonly reported in multiple myeloma (MM) patients and may be associated with older age, disease-related complications and consequences of MM treatments. This study evaluated the incidence rates of and risk factors for hypertension and malignant hypertension in newly-treated MM patients in the United States.MethodsNewly-treated adult MM patients were identified from Truven MarketScan claims database from 1/1/05 to 3/31/14. Inclusion criteria were new diagnosis of MM with start of MM treatment, ≥12 months continuous enrollment prior to diagnosis, ≥30 days of continuous enrollment following initial diagnosis, and prescription drug coverage. Non-MM patients were matched for age (within +/− 5 years), sex and distribution of index dates to MM patients. Baseline cardiovascular (CV) comorbidities, incidence rate of hypertension and malignant hypertension in the follow-up period, and risk of hypertension and malignant hypertension based on existing baseline CV comorbidities were evaluated.ResultsA total of 7895 MM patients (38% with hypertension history) and 23,685 non-MM patients (24% with hypertension history) were included in the study. Twenty-two percent of MM patients versus 3% of non-MM patients had baseline renal failure. A higher percentage of MM versus non-MM patients had baseline hypertension in combination with renal failure, congestive heart failure or both. The incidence rate of hypertension in MM and non-MM patients was 260 and 178 per 1000 person-years, respectively. There was a 30% increase in the risk of hypertension for MM versus non-MM patients: hazard ratio (HR) 1.30 (95% confidence interval [CI] 1.22, 1.37). In MM patients with a history of hypertension, the risk of malignant hypertension was significantly increased with the following comorbid conditions: cardiomyopathy, HR 2.79 (95% CI 1.20, 6.48); renal failure, HR 2.13 (95% CI 1.36, 3.34); and diabetes mellitus, HR 1.59 (95% CI 1.05, 2.39).ConclusionsThis study
Guha K, Allen CJ, Chawla S, et al., 2016, Audit of a tertiary heart failure outpatient service to assess compliance with NICE guidelines., Clinical Medicine, Vol: 16, Pages: 407-411, ISSN: 1470-2118
The National Institute for Health and Care Excellence (NICE) updated its guidelines for chronic heart failure (HF) in 2010. This re-audit assessed interim improvement as compared with an audit in 2011. Patients with HF (preserved and reduced ejection fraction) attending a tertiary cardiac centre over a 2-year period (January 2013–December 2014) were audited. The data collected included demographics, HF aetiology, medications, clinical parameters and cardiac rehabilitation. In total, 513 patients were audited. Compared with 2011, male preponderance (71%) and age (68±14 years, (Mean ± SD)) were similar. 73% of patients lived outside of London. HF aetiologies included ischaemic heart disease (37% versus 40% in 2011), dilated cardiomyopathy (26% versus 20%) primary valve disease (13% versus 12%). For patients with left ventricular systolic dysfunction (n=434, 85% of patients audited) 89% were taking beta-blockers (compared with 77% in 2011), 91% an angiotensin converting enzyme inhibitor or angiotensin receptor blocker (86% in 2011) and 56% a mineralocorticoid receptor antagonist (44% in 2011); 6% were prescribed ivabradine. All patients were reviewed at least 6-monthly. Although 100% of patients were educated about exercise, only 21 (4%) enrolled in a supervised exercise programme. This audit demonstrated high rates of documentation, follow-up and compliance with guideline-based medical therapies. A consistent finding was poor access to cardiac rehabilitation.
Sanchez-Alonso JL, Bhargava A, O'Hara T, et al., 2016, Microdomain-specific modulation of L-type calcium channels leads to triggered ventricular arrhythmia in heart failure, Circulation Research, Vol: 119, Pages: 944-955, ISSN: 1524-4571
RATIONALE: Disruption in subcellular targeting of Ca(2+) signaling complexes secondary to changes in cardiac myocyte structure may contribute to the pathophysiology of a variety of cardiac diseases, including heart failure (HF) and certain arrhythmias. OBJECTIVE: To explore microdomain-targeted remodeling of ventricular L-type Ca(2+) channels (LTCCs) in HF. METHODS AND RESULTS: Super-resolution scanning patch-clamp, confocal and fluorescence microscopy were used to explore distribution of single LTCCs in different membrane microdomains of non-failing and failing human and rat ventricular myocytes. Disruption of membrane structure in both species led to re-distribution of functional LTCCs from their canonical location in transversal tubules (T-tubules) to the non-native crest of the sarcolemma, where their open probability (Po) was dramatically increased (0.034±0.011 vs 0.154±0.027, P<0.001). High Po was linked to enhanced calcium-calmodulin kinase II (CaMKII)-mediated phosphorylation in non-native microdomains and resulted in an elevated ICa,L window current which contributed to the development of early afterdepolarizations (EADs). A novel model of LTCC function in HF was developed; following its validation with experimental data, the model was used to ascertain how HF-induced T-tubule loss led to altered LTCC function and EADs. The HF myocyte model was then implemented in a 3D left ventricle model, demonstrating that such EADs can propagate and initiate reentrant arrhythmias. CONCLUSIONS: Microdomain-targeted remodeling of LTCC properties is an important event in pathways that may contribute to ventricular arrhythmogenesis in the settings of HF-associated remodeling. This extends beyond the classical concept of electrical remodelling in HF and adds a new dimension to cardiovascular disease.
Morley-Smith AC, Lyon AR, 2016, Challenges of Chronic Cardiac Problems in Survivors of Takotsubo Syndrome, Heart Failure Clinics, Vol: 12, Pages: 551-557, ISSN: 1551-7136
A hallmark feature of the Takotsubo syndrome (TTS) is the reversible nature of the observed cardiac dysfunction. This is underlined in diagnostic criteria. However, it would appear this reversibility is a subtle process, and that myocardial catecholamine toxicity can cause lasting permanent abnormalities of myocardial physiology. A growing body of evidence suggests persisting abnormalities may predispose post-TTS patients to cardiac and noncardiac morbidity and mortality. The cardiology community needs to understand more clearly how TTS evolves, how to identify high-risk patients with incomplete resolution, and perform studies to assess which treatment(s) are effective to improve cardiac recovery and clinical outcomes.
Suzuki T, Lyon A, Saggar R, et al., 2016, Editor’s Choice-Biomarkers of acute cardiovascular and pulmonary diseases, European Heart Journal: Acute Cardiovascular Care, Vol: 5, Pages: 416-433, ISSN: 2048-8734
Acute cardiothoracic and respiratory diseases frequently remain a challenge to diagnose anddifferentiate in the emergency setting. The main diseases that manifest with chest pain includeischemic heart disease, myocarditis, acute pericarditis, aortic dissection/rupture and pulmonaryembolism (PE). Diseases that primarily present with dyspnea include heart failure (HF), acuterespiratory distress syndrome (ARDS), pneumonia, asthma exacerbations and chronic obstructivepulmonary disease. Pre-test probabilities of clinical findings play a vital part in diagnosticdecisions, and the use of a Bayesian approach to these greatly improves the ability to stratifypatients more accurately. However, blood tests (biomarkers) are increasingly used to assist in rapiddecision-making in the emergency setting in combination with imaging methods such as chestradiograph, ultrasound and increasingly computed tomography, as well as physiological tests suchas the electrocardiogram in addition to physical examination. Specific tests for ischemic heartdisease and myocarditis (cardiac troponins), HF (B-type natriuretic peptide [BNP] and NTproBNP),aortic dissection (smooth muscle markers) and PE (D-dimer) have been developed.Surfactant protein-D and interleukin-8 have been developed for ARDS. Additionally, circulatingmicroRNAs have emerged as promising biomarker candidates in cardiovascular disease. With thisincreasing array of biochemical markers to aid in the diagnosis of chest diseases presenting withchest pain and dyspnea, we herein review the clinical usefulness of these markers, in particular indifferentiating cardiac from pulmonary diseases. A symptom-oriented assessment as necessary foruse in the critical setting is described in addition to discussion of individual biomarkers.
Zamorano JL, Lancellotti P, Rodriguez Muñoz D, et al., 2016, 2016 ESC Position Paper on cancer treatments and cardiovascular toxicity developed under the auspices of the ESC Committee for Practice Guidelines: The Task Force for cancer treatments and cardiovascular toxicity of the European Society of Cardiology (ESC), European Journal of Heart Failure, Vol: 19, Pages: 9-42, ISSN: 1879-0844
Zamorano JL, Lancellotti P, Rodriguez Muñoz D, et al., 2016, 2016 ESC Position Paper on cancer treatments and cardiovascular toxicity developed under the auspices of the ESC Committee for Practice Guidelines: The Task Force for cancer treatments and cardiovascular toxicity of the European Society of Cardiology (ESC), European Heart Journal, Vol: 37, Pages: 2768-2801, ISSN: 1522-9645
Chari A, Aggarwal S, Mezzi K, et al., 2016, Risk of Hypertension (HTN) and Malignant Hypertension (mHTN) in Patients Treated for Multiple Myeloma (MM), Publisher: WILEY-BLACKWELL, Pages: 91-91, ISSN: 1053-8569
Lenihan DJ, Hartlage G, Decara J, et al., 2016, Cardio-Oncology Training: A Proposal From the International Cardioncology Society and Canadian Cardiac Oncology Network for a New Multidisciplinary Specialty, JOURNAL OF CARDIAC FAILURE, Vol: 22, Pages: 465-471, ISSN: 1071-9164
Toepfer CN, Sikkel MB, Caorsi V, et al., 2016, A post-MI power struggle: adaptations in cardiac power occur at the sarcomere level alongside MyBP-C and RLC phosphorylation., American Journal of Physiology - Heart and Circulatory Physiology, Vol: 311, Pages: H465-H475, ISSN: 0363-6135
Myocardial remodeling in response to chronic myocardial infarction (CMI) progresses through two phases, hypertrophic 'compensation' and congestive 'decompensation'. Nothing is known about the ability of un-infarcted myocardium to produce force, velocity, and power during these clinical phases, even though adaptation in these regions likely drive progression of compensation. We hypothesized that enhanced crossbridge-level contractility underlies mechanical compensation and is controlled in part by changes in the phosphorylation states of myosin regulatory proteins. We induced CMI in rats by left anterior descending coronary artery ligation. We then measured mechanical performance in permeabilized ventricular trabecula taken distant from the infarct zone and assayed myosin regulatory protein phosphorylation in each individual trabecula. During full activation, the compensated myocardium produced twice as much power and 31% greater isometric force compared to non-infarcted controls. Isometric force during submaximal activations was raised >2.4-fold, whilst power was 2-fold greater. EM and confocal microscopy demonstrated that these mechanical changes were not a result of increased density of contractile protein, and therefore not an effect of tissue hypertrophy. Hence, sarcomere-level contractile adaptations are key determinants of enhanced trabecular mechanics and of the overall cardiac compensatory response. Phosphorylation of myosin regulatory light chain (RLC) increased and remained elevated post-MI, while phosphorylation of myosin binding protein-C (MyBP-C) was initially depressed but then increased as the hearts became decompensated. These sensitivities to CMI are in accordance with phosphorylation-dependent regulatory roles for RLC and MyBP-C in crossbridge function and with compensatory adaptation in force and power that we observed in post-CMI trabeculae.
Ng FS, Kalindjian JM, Cooper SA, et al., 2016, Enhancement of Gap Junction Function During Acute Myocardial Infarction Modifies Healing and Reduces Late Ventricular Arrhythmia Susceptibility, JACC. Clinical electrophysiology, Vol: 2, Pages: 574-582, ISSN: 2405-5018
Objectives: To investigate the effects of enhancing gap junction (GJ) coupling during acute myocardial infarction (MI) on the healed infarct scar morphology and late post-MI arrhythmia susceptibility. Background: Increased heterogeneity of myocardial scarring after MI is associated with greater arrhythmia susceptibility. We hypothesized that short-term enhancement of GJ coupling during acute MI can produce more homogeneous infarct scars, reducing late susceptibility to post-MI arrhythmias. Methods: Following arrhythmic characterisation of the rat 4-week post-MI model (n=24), a further 27 Sprague-Dawley rats were randomised to receive rotigaptide to enhance GJ coupling (n=13) or saline control (n=14) by osmotic minipump immediately prior to, and for the first 7 days following surgical MI. At 4 weeks post-MI, hearts were explanted for ex vivo programmed electrical stimulation (PES) and optical mapping. Heterogeneity of infarct border zone (IBZ) scarring was quantified by histomorphometry. Results: Despite no detectable difference in infarct size at 4 weeks post-MI, rotigaptide-treated hearts had reduced arrhythmia susceptibility during PES (Inducibility score: rotigaptide 2.40.8, control 5.00.6, p=0.02) and less heterogeneous IBZ scarring (standard deviation of IBZ Complexity Score: rotigaptide 1.10.1, control 1.40.1, p=0.04), associated with an improvement in IBZ conduction velocity (rotigaptide 43.13.4 cm/s, control 34.82.0 cm/s, p=0.04). Conclusions: Enhancement of GJ coupling for only 7 days at the time of acute MI produced more homogeneous IBZ scarring and reduced arrhythmia susceptibility at 4 weeks post-MI. Short-term GJ modulation at the time of MI may represent a novel treatment strategy to modify the healed infarct scar morphology and reduce late post-MI arrhythmic risk.
Guha K, Allen C, Pryse-Hawkins H, et al., 2016, Audit of a tertiary heart failure outpatient service to assess compliance with practice guidelines, European Journal of Heart Failure, Vol: 18, Pages: 335-336, ISSN: 1879-0844
Chari A, Aggarwal S, Mezzi K, et al., 2016, Risk of hypertension (HTN) and malignant hypertension (mHTN) in patients treated for multiple myeloma (MM)., Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO), Publisher: AMER SOC CLINICAL ONCOLOGY, ISSN: 0732-183X
Morley-Smith AC, Lyon AR, 2016, Stressing the importance of cardiac assessment in pheochromocytoma, Journal of the American College of Cardiology, Vol: 67, Pages: 2375-2377, ISSN: 1558-3597
Hayward C, Patel H, Patel K, et al., 2016, The evolving landscape of oral anti-arrhythmic prescriptions for atrial fibrillation in England: 1998-2014, EUROPEAN HEART JOURNAL-CARDIOVASCULAR PHARMACOTHERAPY, Vol: 2, Pages: 90-94, ISSN: 2055-6837
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Greenberg B, Butler J, Felker GM, et al., 2016, Calcium upregulation by percutaneous administration of gene therapy in patients with cardiac disease (CUPID 2): a randomised, multinational, double-blind, placebo-controlled, phase 2b trial, Lancet, Vol: 387, Pages: 1178-1186, ISSN: 1474-547X
BACKGROUND: Sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPase (SERCA2a) activity is deficient in the failing heart. Correction of this abnormality by gene transfer might improve cardiac function. We aimed to investigate the clinical benefits and safety of gene therapy through infusion of adeno-associated virus 1 (AAV1)/SERCA2a in patients with heart failure and reduced ejection fraction. METHODS: We did this randomised, multinational, double-blind, placebo-controlled, phase 2b trial at 67 clinical centres and hospitals in the USA, Europe, and Israel. High-risk ambulatory patients with New York Heart Association class II-IV symptoms of heart failure and a left ventricular ejection fraction of 0·35 or less due to an ischaemic or non-ischaemic cause were randomly assigned (1:1), via an interactive voice and web-response system, to receive a single intracoronary infusion of 1 × 10(13) DNase-resistant particles of AAV1/SERCA2a or placebo. Randomisation was stratified by country and by 6 min walk test distance. All patients, physicians, and outcome assessors were masked to treatment assignment. The primary efficacy endpoint was time to recurrent events, defined as hospital admission because of heart failure or ambulatory treatment for worsening heart failure. Primary efficacy endpoint analyses and safety analyses were done by modified intention to treat. This trial is registered with ClinicalTrials.gov, number NCT01643330. FINDINGS: Between July 9, 2012, and Feb 5, 2014, we randomly assigned 250 patients to receive either AAV1/SERCA2a (n=123) or placebo (n=127); 243 (97%) patients comprised the modified intention-to-treat population. Patients were followed up for at least 12 months; median follow-up was 17·5 months (range 1·8-29·4 months). AAV1/SERCA2a did not improve time to recurrent events compared with placebo (104 vs 128 events; hazard ratio 0·93, 95% CI 0·53-1·65; p=0·81). No safety signals were noted. 20
Patel HC, Rosen SD, Hayward C, et al., 2016, Renal denervation in heart failure with preserved ejection fraction (RDF-PEF): a randomised controlled trial, European Journal of Heart Failure, Vol: 18, Pages: 703-712, ISSN: 1879-0844
AimHeart failure with preserved ejection fraction (HFpEF) is associated with increased sympathetic nervous system (SNS) tone. Attenuating the SNS with renal denervation (RD) might be helpful and there are no data currently in humans with HFpEF.Methods and ResultsIn this single-centre, randomised, open-controlled study we included 25 patients with HFpEF (preserved left ventricular (LV) ejection fraction, left atrial (LA) dilatation or LV hypertrophy and raised B-type natriuretic peptide (BNP) or echocardiographic assessment of filling pressures). Patients were randomised (2:1) to RD with the Symplicity™ catheter or continuing medical therapy. The primary success criterion was not met in that there were no differences between groups at 12 months for Minnesota Living with Heart Failure Questionnaire score, peak oxygen uptake (VO2) on exercise, BNP, E/e’, LA volume index or LV mass index. A greater proportion of patients improved at three months in the RD group with respect to VO2 peak (56% vs 13%, P=0.025) and E/e’ (31% vs 13%, P=0.04). Change in estimated glomerular filtration rate was comparable between groups. Two patients required plain balloon angioplasty during the RD procedure to treat renal artery wall oedema.ConclusionThis study was terminated early due to difficulties in recruitment and was underpowered to detect whether RD improved the endpoints of: quality of life, exercise function, biomarkers and left heart remodelling. The procedure was safe in patients with HFpEF though two patients did require intra-procedure renal artery dilatation.
Sikkel MB, Kumar S, Maioli V, et al., 2016, High speed sCMOS-based oblique plane microscopy applied to the study of calcium dynamics in cardiac myocytes, Journal of Biophotonics, Vol: 9, Pages: 311-323, ISSN: 1864-0648
blique plane microscopy (OPM) is a form of light sheet microscopy that uses a single high numerical aperture microscope objective for both fluorescence excitation and collection. In this paper, measurements of the relative collection efficiency of OPM are presented. An OPM system incorporating two sCMOS cameras is then introduced that enables single isolated cardiac myocytes to be studied continuously for 22 seconds in two dimensions at 667 frames per second with 960 × 200 pixels and for 30 seconds with 960 × 200 × 20 voxels at 25 volumes per second. In both cases OPM is able to record in two spectral channels, enabling intracellular calcium to be studied via the probe Fluo-4 AM simultaneously with the sarcolemma and transverse tubule network via the membrane dye Cellmask Orange. The OPM system was then applied to determine the spatial origin of spontaneous calcium waves for the first time and to measure the cell transverse tubule structure at their point of origin. Further results are presented to demonstrate that the OPM system can also be used to study calcium spark parameters depending on their relationship to the transverse tubule structure.
Vassiliou VS, Patel HC, Rosen SD, et al., 2016, Left atrial dilation in patients with heart failure and preserved ejection fraction: Insights from cardiovascular magnetic resonance, International Journal of Cardiology, Vol: 210, Pages: 158-160, ISSN: 1874-1754
Cubbon RM, Lyon AR, 2016, Cardio-oncology: concepts and practice, Indian Heart Journal, Vol: 68 Suppl 1, Pages: S77-S85, ISSN: 0019-4832
Hamo C, Bloom M, Cardinale D, et al., 2016, Cancer Therapy-Related Cardiac Dysfunction and Heart Failure:Part 2: Prevention, Treatment, Guidelines, and Future Directions, Circulation: Heart Failure, Vol: 9, ISSN: 1941-3289
Ruiz-Garcia M, Hayward C, Tang A, et al., 2016, Effects of Intramuscular Epinephrine on Cardiovascular Parameters during IgE-Mediated Allergic Reactions to Peanut, Annual Meeting of the American-Academy-of-Allergy-Asthma-and-Immunology (AAAAI), Publisher: MOSBY-ELSEVIER, Pages: AB50-AB50, ISSN: 0091-6749
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Bloom MW, Hamo CE, Cardinale D, et al., 2016, Cancer Therapy-Related Cardiac Dysfunction and Heart Failure: Part 1: Definitions, Pathophysiology, Risk Factors, and Imaging., Circulation: Heart Failure, Vol: 9, ISSN: 1941-3289
Advances in cancer therapy have resulted in significant improvement in long-term survival for many types of cancer but have also resulted in untoward side effects associated with treatment. One such complication that has become increasingly recognized is the development of cardiomyopathy and heart failure. Whether a previously healthy person from a cardiovascular perspective develops cancer therapy-related cardiac dysfunction or a high-risk cardiovascular patient requires cancer therapy, the team of oncologists and cardiologists must be better equipped with an evidence-based approach to care for these patients across the spectrum. Although the toxicities associated with various cancer therapies are well recognized, limitations to our understanding of the appropriate course of action remain. In this first of a 2-part review, we discuss the epidemiologic, pathophysiologic, risk factors, and imaging aspects of cancer therapy-related cardiac dysfunction and heart failure. In a subsequent second part, we discuss the prevention and treatment aspects, concluding with a section on evidence gap and future directions. We focus on adult patients in all stages of cancer therapy from pretreatment surveillance, to ongoing therapy, and long-term follow-up.
Morley-Smith AC, Hayward C, Harding SE, et al., 2016, Gene therapy for heart failure: The end of the beginning?, Dialogues in Cardiovascular Medicine, Vol: 21, Pages: 45-58, ISSN: 1272-9949
New therapies are required to improve myocardial function in patients with severe heart failure. Within the failing cardiomyocyte, a fundamental abnormality and potential therapeutic target is dysfunctional cellular calcium homeostasis and excitation-contraction coupling. Viral vector-mediated delivery and transduction of cardiomyocytes with a cardiac sarco(endo)plasmic reticulum Ca2+ ATPase type 2a (SERCA2a) transgene can recover electrophysiological properties and contractile function in animal models and in ex vivo human cardiomyocytes. However, a recent phase 2b study failed to show clinical benefit in heart failure patients. This article reflects on the experience to date and looks ahead to what is next in gene therapy for heart failure.
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