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Southampton, United Kingdom

Banner N.R.,Transplant Medicine and Circulatory Support | Banner N.R.,Imperial College London | Banner N.R.,Clinical Effectiveness Unit | Bonser R.S.,University of Birmingham | And 12 more authors.
Heart | Year: 2011

Patients with advanced heart failure have a dismal prognosis and poor quality of life. Heart transplantation provides an effective treatment for a subset of these patients. This article provides cardiologists with up-to-date information about referral for transplantation, the role of left ventricular assist devices prior to transplant, patient selection, waiting-list management and donor heart availability. Timing is of central importance; patients should be referred before complications (eg, cardiorenal syndrome or secondary pulmonary hypertension) have developed that will increase the risk of, or potentially contraindicate, transplantation. Issues related to heart failure aetiology, comorbidity and adherence to medical treatment are reviewed. Finally, the positive role that cardiologists can play in promoting and facilitating organ donation is discussed. Source

Chandrasekaran B.,Wessex Cardiothoracic Unit | Cowburn P.J.,Wessex Cardiothoracic Unit
Expert Review of Medical Devices | Year: 2010

Patients with heart failure die predominantly of progressive pump failure or sudden cardiac death. Therefore, it is attractive to believe that an implantable cardioverter defibrillator (ICD) will dramatically reduce mortality by reducing sudden death. However, unfortunately it is not that simple; sudden death is not the same as ICD-preventable death. While ICD prophylaxis always reduces arrhythmic death, it does not always reduce all-cause mortality due to competing risks. Importantly, an arrhythmia may be a marker for heart failure decompensation, with patients at increased risk of heart failure death following shock therapy. Randomized trials have now demonstrated the potential benefits of ICDs in selected patients with left ventricular dysfunction, yet they have also failed to demonstrate benefit in populations where one might have expected to see benefit (e.g., early post-myocardial infarction). Device therapy can offer heart failure patients much more than just a simple shock box. The addition of a left ventricular lead to allow biventricular pacing (cardiac resynchronization therapy) improves symptoms and prolongs life in selected patients with QRS prolongation. Newer technologies allow remote monitoring through the device, which offers the potential to recognize heart failure decompensation or arrhythmias early so that appropriate treatment can be instituted. However, deciding which patient should receive an ICD remains one of the most challenging questions in cardiovascular medicine. © 2010 Expert Reviews Ltd. Source

Sambu N.,Wessex Cardiothoracic Unit | Sambu N.,University of Southampton | Dent H.,University of Southampton | Englyst N.,University of Southampton | And 11 more authors.
Heart | Year: 2011

Background: The optimal duration of clopidogrel treatment, particularly following drug-eluting stent (DES) implantation, remains contentious. Previous studies have observed a clustering of adverse events following clopidogrel cessation 1 year after DES, the aetiology of which is poorly understood. Objective: To investigate, in the prospective CESSATION study, the effect of clopidogrel withdrawal at 1 year after DES implantation on (i) arachidonic acid (AA)- and adenosine diphosphate (ADP)-induced platelet aggregation, and (ii) biomarkers of vascular inflammation, including soluble CD40 ligand (sCD40L), high-sensitivity C-reactive protein (hsCRP) and interleukin 6 (IL-6). Methods and results: The prospective CESSATION study was undertaken in 33 patients receiving aspirin and due to discontinue clopidogrel 1 year after DES. Platetet reactivity was measured using short thromboelastography, and compliance with aspirin determined from serum thromboxane B2 (TXB2) levels. Venesection was performed at 4 weeks and 24 h before, and at 24 h, 48 h, 1, 2 and 4 weeks after, clopidogrel cessation. Following clopidogrel withdrawal, there was (i) a predictable increase in ADP-induced platelet aggregation (ii) an unexpected significant increase in AAinduced platelet aggregation (iii) a decline in IL-6 and hsCRP at 1 week and 4 weeks respectively; and (iv) a non-significant increase in sCD40L at 4 weeks TXB2 levels were consistently suppressed, indicating complete inhibition of cyclo-oxygenase-1 by aspirin. Conclusion: An aspirin-independent, time-dependent increase in AA-induced platelet activation following clopidogrel withdrawal in patients with a DES has been described. New insights into a potential mechanism for the observed clustering of adverse events that occur early after clopidogrel cessation have been provided. These findings raise the question as to whether AA-induced clotting is an appropriate test of aspirin sensitivity. Source

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