Publications (215)758.18 Total impact
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Article: Inflammation does not influence arterial stiffness and pulse-wave velocity in patients with coronary artery disease.
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ABSTRACT: Vascular function is an important pathophysiological factor in cardiovascular disease, and is influenced by many factors, one of the principles being hypertension. Developing evidence suggests that inflammation may be another risk factor. Vascular function and blood pressure haemodynamics can be assessed by arterial stiffness, pulse pressure and plasma markers. Testing the hypothesis of a relationship between inflammatory markers, hypertension and vascular function, we recruited 222 stable coronary artery disease outpatients, assessing inflammation with levels of high sensitivity CRP and interleukin-6 (IL-6), vascular function/arterial stiffness by pulse-wave velocity (PWV), augementation (SphygmoCor system Artcor, Sidney, Australia), aortic and brachial artery pulse pressure, Von Willebrand factor (vWf) and soluble E-selectin (both enzyme-linked immunosorbent assay). In multivariate regression analysis, PWVs, augmentation indices and pulse pressures were linked with age, blood pressure and (some) with heart rate (all P<0.01), while vWf was associated with age (P=0.01). We conclude that, in patients with stable coronary artery disease, arterial stiffness and pulse pressure are related strongly and independently with age, blood pressure and heart rate, and that any effect of inflammation is minimal.Journal of Human Hypertension advance online publication, 28 March 2013; doi:10.1038/jhh.2013.17.Journal of human hypertension 03/2013; · 2.80 Impact Factor -
Article: Does chronic kidney disease improve the predictive value of the CHADS2 and CHA2DS2-VASc stroke stratification risk scores for atrial fibrillation?
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ABSTRACT: Chronic Kidney Disease (CKD) constitutes an adverse risk factor in chronic anticoagulated atrial fibrillation (AF) patients, being related to adverse cardiovascular events, mortality and major bleeds. It is unclear if CKD adds independent prognostic information to stroke risk stratification schemes, as the risk factor components of the CHADS2 and CHA2DS2-VASc scores are themselves related to renal dysfunction. The aim of our study was to determine if CKD independently improves the predictive value of the CHADS2 and CHA2DS2-VASc stroke stratification scores in AF. We recruited consecutive patients (n=978) patients (49% male; median age 76) with permanent or paroxysmal AF on oral anticoagulants with acenocoumarol, from our out-patient anticoagulation clinic. After a median follow-up of 875 (IQR 706-1059) days, we recorded stroke/transient ischaemic attack (TIA), peripheral embolism, vascular events (acute coronary syndrome, acute heart failure and cardiac death) and all-cause mortality. During follow-up, 113 patients (4.82%/year) experienced an adverse cardiovascular event, of which 39 (1.66%/year) were strokes, 43 (1.83%/year) had an acute coronary syndrome and 32 (1.37%/year) had acute heart failure. Also, 102 patients (4.35%/year) died during the following up, 31 of them (1.32%/year) as a result of a thrombotic event. Based on c-statistics and the integrated discrimination improvement (IDI), CKD did not improve the prediction for stroke/systemic embolism, thrombotic events and all-cause mortality using the CHADS2 and CHA2DS2-VASc scores. In conclusion, evaluating renal function in AF patients is important as CKD would confer a poor overall prognosis in terms of thromboembolic events and all-cause mortality. Adding CKD to the CHADS2 and CHA2DS2-VASc stroke risk scores did not independently add predictive information.Thrombosis and Haemostasis 03/2013; 109(5). · 5.04 Impact Factor -
Article: CXCR4 positive and angiogenic monocytes in myocardial infarction.
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ABSTRACT: Limited data are available on the role of monocytes in cardiac repair. In the present study, we evaluated the dynamic alterations of monocytes with reparative and angiogenic potential in patients with myocardial infarction(MI). Reparative CXCR4+ monocytes, and CD34+ and KDR+ monocytes with angiogenic potential derived from individual monocyte subsets were quantified by flow cytometry in patients with ST-elevation MI (n=50), and stable coronary artery disease (CAD, n=40). Parameters were measured on days 1, 3, 7 and 30 post MI. Monocyte subsets were defined as CD14++CD16-CCR2+ ('classical', Mon1), CD14++CD16+CCR2+ ('intermediate', Mon2), CD14+CD16++CCR2- ('non-classical', Mon3). Plasma levels of inflammatory cytokines, fibrinolytic factors and microparticles(MPs) were assessed on day 1. CXCR4+ and KDR+ monocytes were increased following MI, being more prominently associated with Mon2 (median[IQR] of CXCR4+ Mon2 60[25-126] per μl in STEMI vs. 27[21-41] per μl in stable CAD). The counts of CXCR4+ Mon2 in STMEI significantly reduced by day 30 of follow-up (27[18-47], p<0.001). Expression of the pro-reparative scavenger receptor CD163 on Mon3 was reduced in acute MI (p=0.008), and on other subsets later during the follow-up with lowest levels at day 3 post-MI (p<0.001 for Mon1, p=0.02 for Mon2). CD204 expression on Mon1 correlated with tissue type plasminogen activator levels (r=0.46, p=0.001). Interleukin(IL)6 levels correlated with counts of Mon2-derived CXCR4+ and KDR+ cells. Interleukin-1β correlated with KDR+ Mon2 counts. IL10 correlated with CXCR4+ Mon2 levels. Low count of CXCR4+ Mon2 and low CD163 expression by Mon2 were associated with higher ejection fraction six-weeks after MI. In conclusion, the Mon2 subset has the most prominent role in the observed changes in reparative monocytes in MI. The association of reparative monocytes with inflammatory/fibrinolytic markers indicates a complex interplay of these cells in the post-MI state.Thrombosis and Haemostasis 12/2012; 109(2). · 5.04 Impact Factor -
Article: The membrane expression of P-selectin, but not monocyte-platelet aggregates, is influenced by variability in response to aspirin in patients with coronary artery disease.
Platelets 12/2012; · 1.85 Impact Factor -
Article: Cardiac troponins and the risk of stroke in atrial fibrillation. Cause or consequence?
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ABSTRACT: Atrial fibrillation (AF) is a common cardiac arrhythmia associated with an increased morbidity and mortality, and much of the AF-associated morbidity is secondary to a five-fold to six-fold increased risk of stroke and thromboembolism(1). The stroke risk in AF patients is not homogeneous, but depends on the presence of other underlying clinical conditions(2). To aid decision-making for thromboprophylaxis, several clinical risk stratification schemes have been developed using various risk factors and clinical characteristics. © 2012 International Society on Thrombosis and Haemostasis.Journal of Thrombosis and Haemostasis 09/2012; · 5.73 Impact Factor -
Article: An innovative flow cytometric approach for small-size platelet microparticles: influence of calcium.
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ABSTRACT: Microparticles (MPs) are small submicron membrane-derived vesicles shed from a variety of cells and they have been implicated in different disorders. Accordingly, understanding of physiological characteristics of MPs and improvement of methods of their quantification are important for further advance in the field. Although flow cytometry is the most widely applied technique for MP analysis, it is limited by lack of adequate standardisation. Annexin V (AnV), which binds surface phosphatidylserine (PS) with high affinity, has been long regarded as a marker of MPs, but AnV binding is Ca2+-dependent and it is unclear how [Ca2+] concentrations could affect AnV binding to MPs and its enumeration. MPs from citrated and heparinised plasma were labelled with AnV, anti-CD42b and quantified using an Apogee A50 flow cytometer. The small-size MP gate was defined with the use of size beads (from 0.1 to 0.5 μm) and confirmed with an in vitro assessment of platelet stimulation. Biotinylated anti-CD42b antibodies were then bound to streptavidin conjugated with different fluorochromes, leading to an amplified signal of platelet MPs (PMPs). Moderate increase of [Ca2+] concentrations in the annexin V staining buffer allows initial plasma recalcification and more accurate MP quantification in citrated plasma. Thrombin stimulation of platelet-free plasma containing only MPs did not produce any changes in the concentration of AnV+ MPs, but decreased the anti-CD42b binding. The results also indicate that prolonged storage and thrombin induce the release of AnV+ MPs whereas PS exposure in pre-existent MPs is not affected by thrombin. In conclusion, we present a sensitive protocol for the analysis of circulating and in vitro induced small-size PMPs that might contribute to future cardiovascular and clinical research.Thrombosis and Haemostasis 06/2012; 108(2):373-83. · 5.04 Impact Factor -
Article: High sensitivity cardiac troponin T and interleukin-6 predict adverse cardiovascular events and mortality in anticoagulated patients with atrial fibrillation.
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ABSTRACT: There are limited data on the prognostic role of biomarkers in anticoagulated patients with atrial fibrillation (AF). We evaluated the prognostic value of high sensitivity TnT (hsTnT) and high-sensitivity interleukin-6 (hsIL6) in a large cohort of AF patients taking oral anticoagulant therapy (OAC) as both biomarkers have been associated with adverse cardiovascular events. We studied 930 patients (51% male; median age 76) with permanent/ paroxysmal AF who were stabilized (for at least 6 months) on OAC (INRs 2.0-3.0). Plasma hsTnT and hsIL6 levels were quantified by electrochemiluminescense immunoassay at baseline. Patients were followed-up for up to 2 years, and adverse events (thrombotic and vascular events, mortality and major bleeding) were recorded. At follow-up, 96 patients (3.97%/year) died whilst 107 had an adverse cardiovascular event (3.14%/year). On multivariate analysis, high hsTnT and high hsIL6 remained significantly associated with prognosis even after adjusting for CHADS2 score: HR 2.21 (1.46-3.35, P<0.001) for high hsTnT and 1.97 (1.29-3.02, P=0.002) for high hsIL6, for adverse cardiovascular events. For all-cause mortality, the HRs were 1.79 (1.13-2.83, P=0.013) and 2.48 (1.60-3.85, P<0.001), respectively. The integrated discrimination index (IDI) values of clinical scores (CHADS2 and CHA2 DS2-VASc) were improved by the addition of hsTnT and/or hsIL6 (all P<0.05). In a large 'real world' cohort of anticoagulated AF patients, both hsTnT and hsIL6 levels provided prognostic information that was complementary to clinical risk scores for prediction of long-term cardiovascular events and death, suggesting that these biomarkers may potentially be used to refine clinical risk stratification in AF.Journal of Thrombosis and Haemostasis 06/2012; 10(8):1500-7. · 5.73 Impact Factor -
Article: Fibrinolytic status in acute coronary syndromes: evidence of differences in relation to clinical features and pathophysiological pathways.
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ABSTRACT: Limited data are available on the role of innate fibrinolysis in acute coronary syndromes (ACS). In the present study we evaluated the dynamic alterations of fibrinolytic markers in patients presenting with ACS. Tissue-type-(tPA) and urokinase type-(uPA) plasminogen activators, plasminogen activator inhibitor (PAI-1) antigen and activity and thrombin activatable fibrinolysis inhibitor (TAFI) were analysed in 50 patients with ST elevation myocardial infarction (STEMI), 47 non-STEMI patients (NSTEMI), 40 patients with stable coronary artery disease (CAD) and 39 controls. The parameters were measured on day 1 and days 3, 7 and 30. Counts of monocyte subsets, monocyte-platelet aggregates and plasma inflammatory cytokines were assessed on admission. On day 1, TAFI was higher in NSTEMI vs. STEMI (p<0.001) while PAI-1 activity was higher in STEMI (p<0.001). In STEMI, uPA activity levels was low on day 1 but significantly increased on day 30 (p<0.001). TAFI levels were increased in NSTEMI on day 1 and gradually reduced by day 30 (p<0.05). In STEMI, TAFI levels peaked at day 7 (p<0.05) and dropped significantly by day 30 (p<0.05). CD14++CD16+ monocytes were independently associated with PAI-1 activity in ACS (p=0.03). Monocyte-platelet aggregates rather than platelet-free monocytes were an independent determinant of tPA, PAI-1 antigen and TAFI on a multivariate analysis (p<0.05). There are significant differences in fibrinolytic activity between patients with STEMI and NSTEMI. These changes could reflect the role of these factors in post-MI myocardial healing. Monocyte-platelet interactions are independently associated with the regulation of the fibrinolytic status in ACS.Thrombosis and Haemostasis 04/2012; 108(1):32-40. · 5.04 Impact Factor -
Article: Matrix metalloproteinases and their tissue inhibitors in hypertension-related pregnancy complications.
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ABSTRACT: Matrix metalloproteinases (MMPs) are a family of endopeptidases that degrade the components of the extracellular matrix (ECM) such as collagen, and thus contribute to the remodelling and the physiological homeostasis of the ECM and its blood supply. The activities of these enzymes are regulated by endogenous tissue inhibitors of metalloproteinases (TIMPs), and it has been suggested that a balance between MMPs and TIMPs plays an important role in vascular remodelling, angiogenesis and vasodilatation in a number of physiological situations. It follows that, regarding a relationship between MMPs and TIMPs, an imbalance between these molecules may lead to pathology in a wide range of conditions, including hypertension, cancer and pulmonary disease, and in the pathophysiology of reproduction. Indeed, regarding the latter, abnormalities in the maternal peripheral vasculature have been proposed as being (partly) responsible for the effects of hypertension on pregnancy and the development of complications including pre-eclampsia and eclampsia. However, the associations between MMPs, TIMPs and disease may be simply of association, not of pathology. This brief review explores current literature on the role of abnormalities of the ECM in general, focusing on the pathogenesis of hypertension and its complications during pregnancy as a model of disordered angiogenesis and remodelling.Journal of Human Hypertension advance online publication, 15 March 2012; doi:10.1038/jhh.2012.8.Journal of human hypertension 03/2012; · 2.80 Impact Factor -
Article: Dabigatran etexilate for stroke prevention in patients with atrial fibrillation: resolving uncertainties in routine practice.
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ABSTRACT: Dabigatran etexilate is a new oral anticoagulant recently approved in Europe for the prevention of stroke or systemic embolism in adult patients with non-valvular atrial fibrillation (AF) and at least one risk factor for stroke. With a fast onset of action and a predictable anticoagulant effect obviating the need for coagulation monitoring, dabigatran etexilate offers practical advantages over vitamin K antagonists in clinical practice. However, clinicians may have questions about practical aspects of dabigatran etexilate use including monitoring anticoagulant efficacy, interruption for surgical or invasive procedures and management of bleeding. This review article aims to address these concerns and provide guidance on the use of dabigatran etexilate in special situations, such as acute coronary syndromes and cardiac revascularisation. In addition, cut-off values for different coagulation assay results associated with an increased risk of bleeding are given.Thrombosis and Haemostasis 02/2012; 107(5):838-47. · 5.04 Impact Factor -
Article: Silent cerebral embolism after catheter ablation of atrial fibrillation.
International Journal of Clinical Practice 02/2012; 66(2):118-20. · 2.41 Impact Factor -
Article: The CD14++CD16+ monocyte subset and monocyte-platelet interactions in patients with ST-elevation myocardial infarction.
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ABSTRACT: Monocytes contribute to both myocardial damage and repair by virtue of subset heterogeneity. The dynamics and functional characteristics of the three human monocyte subsets, including the unique CD14++CD16+ subset, and their contributions to monocyte platelet aggregates (MPAs) following ST-elevation myocardial infarction (STEMI) are unknown. We aimed to examine dynamic changes and relation to left ventricular ejection fraction (LVEF) of the three human monocyte subsets and their aggregates with platelets following STEMI. Three monocyte subsets, CD14++CD16-CCR2+ ('classical', Mon1), CD14++CD16+CCR2+ ('intermediate', Mon2) and CD14+CD16++CCR2- ('non-classical', Mon3), and their contribution to MPAs were analyzed by flow cytometry in 50 patients with STEMI, 40 patients with stable coronary artery disease (CAD) and 40 healthy volunteers. Study parameters were measured within 24 h of primary percutaneous coronary intervention (PCI) (day1) and on days 3, 7 and 30. Monocyte activation was assessed by measuring the nuclear factor κB (NFκB) pathway. LVEF was assessed 6 weeks after STEMI. Correlations between monocyte subsets/MPAs and plasma cytokines and troponin were assessed. We observed marked differences in subset dynamics, with a prominent increase in Mon2 (P < 0.0001) but no changes in Mon3. Significant increases in Mon2 CD14 (P = 0.002) and CCR2 (P < 0.0001) expression, and reduction in CD16 expression (P = 0.001) were seen. NFκB pathway activity increased most prominently in Mon2 (P = 0.007). Mon2 count correlated with peak troponin (r = 0.31, P = 0.04) and plasma interleukin (IL)-6 (r = 0.65, P < 0.0001) and IL-10 (r = 0.34, P = 0.017). Mon1 correlated with IL-6 (r = 0.55, P < 0.0001). Reduced Mon2 expression of CD16 on day 1 was independently predictive of higher LVEF (β = -0.37, P = 0.013). The increase in MPA count following STEMI persisted at 1 month. The Mon2 'intermediate' subset has unique dynamic and functional characteristics following STEMI and significant correlations with troponin, plasma cytokines and convalescent left ventricular function. The persistent increase in MPA count 30 days after STEMI may affect monocyte subset functional activity.Journal of Thrombosis and Haemostasis 12/2011; 10(7):1231-41. · 5.73 Impact Factor -
Article: Systolic heart failure in South Asians.
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ABSTRACT: Heart failure (HF) is a common condition leading to an unfavourable prognosis and impaired quality of life. In this review, we provide an overview of published literature on possible epidemiological and pathophysiological differences between patients with systolic HF of South Asian origin and those from other ethnic groups (mainly White). Systolic HF tends to manifest earlier among South Asians and with frequent hospital admissions. However, survival for such patients appears to be significantly better compared with the White group, which might be associated with different patterns of HF. For example, this could be attributed to a lower prevalence of left ventricular systolic dysfunction in South Asian subjects. Indeed, the high prevalence of hypertension and diabetes among South Asians may predispose to diastolic HF with preserved systolic function. In addition, because of underrepresentation of South Asians in clinical trials, there are little data on optimal management of this ethnic group.International Journal of Clinical Practice 12/2011; 65(12):1274-82. · 2.41 Impact Factor -
Article: Differences between South Asians and White Europeans in five year outcome following percutaneous coronary intervention.
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ABSTRACT: The aim of this study was to compare rates of target lesion revascularisation (TLR) and total mortality between South Asians (SAs) and White Europeans (WEs) following percutaneous coronary intervention (PCI). We followed a cohort of 293 SAs and 865 WEs patients admitted for elective or urgent PCI to de novo lesions. For each patient, baseline cardiovascular risk factors and angiographic data were obtained. Patients had long-term follow-up for all-cause mortality and TLR. Patients were followed up over a median period of 54 months (inter-quartile range: 47-65). SAs were younger (62 ± 12 years vs. 66 ± 11 years; p < 0.0001), with a higher prevalence of diabetes, greater social deprivation [Carstairs score: 10.2 (IQR 6.5-12.1) vs. 3.3 (IQR 0.9-6.5); p < 0.0001] and presented more acutely (urgent PCI procedure). During the follow-up period, a total of 119 deaths and 111 TLR [94 repeat PCI and 17 coronary artery bypass grafting (CABG)] occurred. There was no significant difference in the rate of long-term all-cause mortality between SA and WE [31 (10.6%) vs. 107 (12.4%); OR: 0.84 (0.55-1.28); p = 0.47]. However, SA ethnicity was an independent predictor of long-term TLR, after adjusting for baseline clinical and procedural characteristics [54 (18.4%) vs. 57 (6.6%); OR: 2.83 (1.87-4.29); p < 0.0001]. South Asian patients were more likely to require re-admission to treat clinical restenosis of the index lesion. There was no significant long-term difference in all-cause mortality between SA and WE patients.International Journal of Clinical Practice 12/2011; 65(12):1259-66. · 2.41 Impact Factor -
Article: Intracardiac expression of markers of endothelial damage/dysfunction, inflammation, thrombosis, and tissue remodeling, and the development of postoperative atrial fibrillation.
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ABSTRACT: Atrial fibrillation (AF) is a common complication of coronary artery bypass grafting (CABG), and may have an inflammatory and/or thrombotic etiology. We sought to determine the expression of inflammatory (interleukin [IL]-6), thrombotic (tissue factor and von Willebrand factor [VWF]) and remodeling (matrix metalloproteinase [MMP]-9 and tissue inhibitor of metalloproteinase [TIMP]-1) markers by left atrial appendage (LAA) and right atrial appendage (RAA) tissue in the prediction of postoperative AF. We determined whether the tissue expression of markers of certain different pathophysiologic mechanisms predicted the development of AF after CABG. LAA and RAA tissue was excised during CABG in 100 patients free of AF and inflammation. Tissue marker expression was quantified by immunohistochemistry and was related to 30-day postoperative AF. Overall, there were no significant differences in staining intensity of any marker between LAA tissue and RAA tissue. However, more intense expression of VWF by LAA tissue predicted the 30 patients with postoperative AF as compared with those free of AF (P = 0.006). IL-6, MMP-9 and TIMP-1 expression by RAA and LAA epicardial tissue was stronger than expression by endocardium or cardiomyocytes (all P < 0.025) but failed to predict AF. In this study, one of the largest to investigate tissue expression of pathophysiologic markers in relation to postoperative AF, we show that more intense expression of VWF by LAA tissue is a significant predictor of postoperative AF. This points towards a possible role of endothelial damage/dysfunction (as reflected by VWF changes) in the pathogenesis of postoperative AF.Journal of Thrombosis and Haemostasis 12/2011; 9(12):2345-52. · 5.73 Impact Factor -
Article: Comprehensive risk reduction in patients with atrial fibrillation: Emerging diagnostic and therapeutic options. Executive summary of the report from the 3rd AFNET/EHRA consensus conference.
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ABSTRACT: There are exciting new developments in several areas of atrial fibrillation (AF) management that carry the hope of improving outcomes in AF patients. This paper is an executive summary that summarises the proceedings from the 3rd AFNET/EHRA consensus conference on atrial fibrillation, held in Sophia Antipolis from November 7th to 9th 2010, shortly after the release of the new ESC guidelines on AF. The conference was jointly organised by the German Atrial Fibrillation competence NETwork (AFNET) and the European Heart Rhythm Association (EHRA). This executive summary report covers four sections: 1. Risk factors and risk markers for AF, 2. Pathophysiological classification of AF, 3. Relevance of monitored AF duration for AF-related outcomes, and 4. Perspectives and needs for implementing better antithrombotic therapy.Thrombosis and Haemostasis 11/2011; 106(6):1012-9. · 5.04 Impact Factor -
Article: Bleeding risk assessment and management in atrial fibrillation patients. Executive Summary of a Position Document from the European Heart Rhythm Association [EHRA], endorsed by the European Society of Cardiology [ESC] Working Group on Thrombosis.
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ABSTRACT: In this executive summary of a Consensus Document from the European Heart Rhythm Association, endorsed by the European Society of Cardiology Working Group on Thrombosis, we comprehensively review the published evidence and propose a consensus on bleeding risk assessments in atrial fibrillation (AF) patients. The main aim of the document was to summarise 'best practice' in dealing with bleeding risk in AF patients when approaching antithrombotic therapy, by addressing the epidemiology and size of the problem, and review established bleeding risk factors. We also summarise definitions of bleeding in the published literature. Patient values and preferences balancing the risk of bleeding against thromboembolism as well as the prognostic implications of bleeding are reviewed. We also provide an overview of published bleeding risk stratification and bleeding risk schema. Brief discussion of special situations (e.g. periablation, peri-devices such as implantable cardioverter defibrillators [ICD] or pacemakers, presentation with acute coronary syndromes and/or requiring percutanous coronary interventions/stents and bridging therapy) is made, as well as a discussion of the prevention of bleeds and managing bleeding complications. Finally, this document puts forwards consensus statements that may help to define evidence gaps and assist in everyday clinical practice.Thrombosis and Haemostasis 11/2011; 106(6):997-1011. · 5.04 Impact Factor -
Article: Stroke prevention in non-valvular atrial fibrillation: can warfarin do better?
Thrombosis and Haemostasis 09/2011; 106(5):753-4. · 5.04 Impact Factor -
Article: Improving the diagnosis and prognosis of atrial fibrillation in stroke: quo vadis?
European Journal of Neurology 09/2011; 19(2):187-8. · 3.69 Impact Factor -
Article: Antithrombotic therapy in patients with atrial fibrillation undergoing coronary stenting: similarities and dissimilarities between North America and Europe.
Thrombosis and Haemostasis 09/2011; 106(4):569-71. · 5.04 Impact Factor
Top co-authors
Top Journals
Institutions
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2003–2013
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University Hospitals Birmingham NHS
- Department of Medicine
Birmingham, ENG, United Kingdom
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2002–2013
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University of Birmingham
- School of Psychology
Birmingham, ENG, United Kingdom -
Birmingham City University
Birmingham, ENG, United Kingdom
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2012
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Universidad de Murcia
Murcia, Murcia, Spain
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2011
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Medical University of Vienna
Vienna, Vienna, Austria
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2005–2008
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Sandwell and West Birmingham Hospitals NHS Trust
Birmingham, ENG, United Kingdom -
Southampton University Hospitals NHS
Southampton, ENG, United Kingdom
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2004–2008
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Hospital General Universitario de Alicante
Alicante, Valencia, Spain
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