Iain A Simpson

University Hospital Southampton NHS Foundation Trust, Southampton, England, United Kingdom

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Publications (34)286.24 Total impact

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    ABSTRACT: Purpose of the study: Out-of-hospital cardiac arrest (OHCA) has a poor prognosis despite bystander resuscitation and rapid transfer to hospital. Optimal management of patients after arrival to hospital continues to be contentious, especially the timing of emergency coronary angiography±revascularisation. Robust predictors of inhospital outcome would be of clinical value for initial decision-making. Study design: A retrospective analysis of consecutive patients who presented to a university hospital following OHCA over a 70-month period (2008-2013). Patients were identified from the emergency department electronic patient registration and coding system. For those patients who underwent emergency percutaneous coronary intervention, details were crosschecked with national databases. Results: We identified 350 consecutive patients who were brought to our hospital following OHCA. Return of spontaneous circulation (ROSC) for >20 min was achieved either before arrival or inhospital in 196 individuals. From the 350 subjects, 114 (32.6%) survived to hospital discharge. When sustained ROSC was achieved, either before or inhospital, survival to discharge was 58.2% (114 of 196). Non-shockable rhythm, absence of bystander cardiopulmonary resuscitation, 'downtime' >15 min and initial pH ≤7.11 were predictors of inhospital death. 12% patients who underwent angiography in the presence of ST elevation had no acute coronary occlusion. 21% patients with acute coronary occlusion at angiography did not have ST elevation. Conclusions: In our cohort of patients with OHCA, those who achieve ROSC had a survival-to-discharge rate of 58.2%. We identified four predictors of inhospital death, which are readily available at the time of patient presentation. Reliance on ST elevation to decide about coronary angiography and revascularisation may be flawed. More data are required.
    Preview · Article · Jan 2016 · Postgraduate medical journal
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    ABSTRACT: Purpose Genome-wide association studies have identified ADAMTS7 as a risk locus for coronary artery disease (CAD) and myocardial infarction (MI). Functional studies suggest ADAMTS7 may promote cellular processes in atherosclerosis. We studied if risk variant carriers exhibit a greater burden of angiographic CAD. Methods We genotyped ADAMTS7 in the Southampton Atherosclerosis Study (SAS, n = 1359), and replicated in the Emory Genebank (Emory GB, n = 2684). Angiographic CAD was phenotyped as presence of >50% stenosis in epicardial vessel and semi-quantitative scores including the Gensini Score (GS), Sullivan Extent Score (SES) and the Duke Severity Index (DSI); and ex-vivo immunohistochemical analysis of human coronary plaques (n = 48). Results We confirmed an association between ADAMTS7 genotype and presence of CAD under an additive genotype model in SAS (p = 0.05) and Emory GB (p = 0.017), but found no associations with MI in the presence of CAD. ADAMTS genotypes were associated with all of the angiographic severity scores in SAS (GS p = 0.017, SES p = 0.045, DSI p = 0.029), and independently replicated in Emory GB (GS p < 0.001, SES p < 0.001, DSI p = 0.001). Meta-analysis demonstrated that homozygous carriers of the risk allele had greater odds of multi-vessel disease [OR 1.36 (95% CI 1.13–1.63)] and proximal stenoses [OR 1.41 (95% CI 1.15–1.72)], compared to non-risk allele carriers. Additionally, the risk genotype was associated with greater fibrous cap thickness (p = 0.013) and% area of α-actin (smooth muscle cell marker) in the intima (p = 0.029). Conclusions The ADAMTS7 risk variant is associated with multiple angiographic measures of CAD burden and plaque remodelling, further supporting the role of this protease in promoting atherosclerosis.
    No preview · Article · Jun 2015 · Heart (British Cardiac Society)
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    ABSTRACT: Background Dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 inhibitor, mostly clopidogrel, is the default therapy in both acute coronary syndrome and after intracoronary stents. It is well established that responses to antiplatelet therapy (APT), particularly clopidogrel, are subject to considerable interindividual variability.Objectives We investigated whether responses to APT in individuals vary significantly over time.Methods Simultaneous assay with VerifyNow™ and Short thrombelastography (s-TEG) was performed before and at four time points over six months following hospital discharge in 40 patients on DAPT. Serum thromboxane B2 (TXB2) levels were also measured.ResultsWhilst aspirin response units (ARU) by VerifyNow™ and serum TXB2 levels remained stable over time, arachidonic acid (AA) mediated platelet aggregation with s-TEG (i.e. AUC15AA) increased at 1 week compared to pre-discharge (p < 0.008). In addition, platelet reactivity units (PRU) by VerifyNow™ (p = 0.046) and adenosine diphosphate (ADP) mediated platelet aggregation with s-TEG (i.e. AUC15ADP) also increased at 1 week compared to pre-discharge (p = 0.026). There were no significant changes in either platelet reactivity (PR) or rates of HTPR on clopidogrel beyond 1 week.Conclusions In conclusion, this study demonstrates important variability in responses to APT within individuals between pre-discharge and 1 week but not thereafter. The use of a single early (pre-discharge) platelet function assay as an indicator of future response may therefore be flawed. The design of future strategies to assess individual responses for tailored therapy need to take this into account.This article is protected by copyright. All rights reserved.
    No preview · Article · Mar 2015 · Journal of Thrombosis and Haemostasis
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    ABSTRACT: Resistant hypertension continues to pose a major challenge to clinicians worldwide and has serious implications for patients who are at increased risk of cardiovascular morbidity and mortality with this diagnosis. Pharmacological therapy for resistant hypertension follows guidelines-based regimens although there is surprisingly scant evidence for beneficial outcomes using additional drug treatment after three antihypertensives have failed to achieve target blood pressure. Recently there has been considerable interest in the use of endoluminal renal denervation as an interventional technique to achieve renal nerve ablation and lower blood pressure. Although initial clinical trials of renal denervation in patients with resistant hypertension demonstrated encouraging office blood pressure reduction, a large randomised control trial (Symplicity HTN-3) with a sham-control limb, failed to meet its primary efficacy end point. The trial however was subject to a number of flaws which must be taken into consideration in interpreting the final results. Moreover a substantial body of evidence from non-randomised smaller trials does suggest that renal denervation may have an important role in the management of hypertension and other disease states characterised by overactivation of the sympathetic nervous system. The Joint UK Societies does not recommend the use of renal denervation for treatment of resistant hypertension in routine clinical practice but remains committed to supporting research activity in this field. A number of research strategies are identified and much that can be improved upon to ensure better design and conduct of future randomised studies.
    Full-text · Article · Jan 2015 · Heart
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    ABSTRACT: Resistant hypertension continues to pose a major challenge to clinicians worldwide and has serious implications for patients who are at increased risk of cardiovascular morbidity and mortality with this diagnosis. Pharmacological therapy for resistant hypertension follows guidelines-based regimens although there is surprisingly scant evidence for beneficial outcomes using additional drug treatment after three antihypertensives have failed to achieve target blood pressure. Recently there has been considerable interest in the use of endoluminal renal denervation as an interventional technique to achieve renal nerve ablation and lower blood pressure. Although initial clinical trials of renal denervation in patients with resistant hypertension demonstrated encouraging office blood pressure reduction, a large randomised control trial (Symplicity HTN-3) with a sham-control limb, failed to meet its primary efficacy end point. The trial however was subject to a number of flaws which must be taken into consideration in interpreting the final results. Moreover a substantial body of evidence from non-randomised smaller trials does suggest that renal denervation may have an important role in the management of hypertension and other disease states characterised by overactivation of the sympathetic nervous system. The Joint UK Societies does not recommend the use of renal denervation for treatment of resistant hypertension in routine clinical practice but remains committed to supporting research activity in this field. A number of research strategies are identified and much that can be improved upon to ensure better design and conduct of future randomised studies.
    Full-text · Article · Nov 2014 · Heart (British Cardiac Society)
  • Geraint Fuller · Iain A Simpson

    No preview · Article · Apr 2014 · BMJ (online)
  • Simon Ray · Richmond Jeremy · Rick Nishimura · Iain A Simpson

    No preview · Article · Jan 2013 · Heart (British Cardiac Society)
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    ABSTRACT: OBJECTIVES: The aim of this study was to ascertain the relationship of 9p21 locus with: 1) angiographic coronary artery disease (CAD) burden; and 2) myocardial infarction (MI) in individuals with underlying CAD. BACKGROUND: Chromosome 9p21 variants have been robustly associated with coronary heart disease, but questions remain on the mechanism of risk, specifically whether the locus contributes to coronary atheroma burden or plaque instability. METHODS: We established a collaboration of 21 studies consisting of 33,673 subjects with information on both CAD (clinical or angiographic) and MI status along with 9p21 genotype. Tabular data are provided for each cohort on the presence and burden of angiographic CAD, MI cases with underlying CAD, and the diabetic status of all subjects. RESULTS: We first confirmed an association between 9p21 and CAD with angiographically defined cases and control subjects (pooled odds ratio [OR]: 1.31, 95% confidence interval [CI]: 1.20 to 1.43). Among subjects with angiographic CAD (n = 20,987), random-effects model identified an association with multivessel CAD, compared with those with single-vessel disease (OR: 1.10, 95% CI: 1.04 to 1.17)/copy of risk allele). Genotypic models showed an OR of 1.15, 95% CI: 1.04 to 1.26 for heterozygous carrier and OR: 1.23, 95% CI: 1.08 to 1.39 for homozygous carrier. Finally, there was no significant association between 9p21 and prevalent MI when both cases (n = 17,791) and control subjects (n = 15,882) had underlying CAD (OR: 0.99, 95% CI: 0.95 to 1.03)/risk allele. CONCLUSIONS: The 9p21 locus shows convincing association with greater burden of CAD but not with MI in the presence of underlying CAD. This adds further weight to the hypothesis that 9p21 locus primarily mediates an atherosclerotic phenotype.
    Full-text · Article · Jan 2013 · Journal of the American College of Cardiology
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    ABSTRACT: Background: Giant cell myocarditis (GCM) typically causes fulminant heart failure, arrhythmias, or heart block, necessitating aggressive immunosuppression, ventricular assist device insertion, or cardiac transplantation. We describe a novel variant of GCM, primarily involving the atria, that displays distinctive clinical features and follows a more benign course than ventricular GCM. Methods and results: We identified 6 patients (median age 67.5 years, 4 male) with atrial GCM in our pathology consultation practices from 2010 to 2012. Clinical history, imaging, and pathology materials were reviewed. Clinically, 4 patients had atrial fibrillation, 1 had acute heart failure, and 1 had incidental disease at autopsy. Among the 5 living patients, echocardiography revealed severe atrial dilatation (5 cases), mitral/tricuspid regurgitation (5), atrial mural thrombus (3), atrial wall thickening (2), and atrial hypokinesis (2). Ventricular function was preserved in all 5. Histological review of surgically resected atria showed giant cell and lymphocytic infiltrates, lymphocytic myocarditis-like foci, cardiomyocyte necrosis, and cardiomyocyte hypertrophy in all cases. Other features included interstitial fibrosis (5), poorly-formed granulomas (4), eosinophils (4), neutrophils (1), and vasculitis (1). Treatment consisted of steroids and cyclosporine (1), pacemaker placement for sick sinus syndrome (1), and supportive care (3). All 5 living patients returned to baseline exercise tolerance after 6 to 16 weeks of follow-up. Conclusions: Atrial GCM represents a distinct clinicopathologic entity with a more favorable prognosis than classic ventricular GCM. This disorder should be included in the differential diagnosis of atrial dilatation, particularly when associated with atrial wall thickening. The utility of immunomodulatory therapy for this condition remains unknown.
    Full-text · Article · Nov 2012 · Circulation
  • Simon Ray · Iain Simpson

    No preview · Article · Jul 2012 · BMJ (online)
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    ABSTRACT: Previous studies have demonstrated significant heterogeneity in responses to antiplatelet therapy (APT), and high residual platelet reactivity is associated with the risk of ischaemic events, including stent thrombosis (ST). The prevalence of APT hyporesponsiveness in a 'real world' registry of ST patients and the feasibility of personalising APT are reported. 39 consecutive patients admitted to a single regional cardiothoracic centre with definite ST were prospectively evaluated. Response to aspirin and clopidogrel was measured following discharge using short thrombelastography (TEG), a rapid, well validated near patient platelet function test. Treatment modification in hyporesponders comprised an increase in aspirin dose and/or changing clopidogrel to prasugrel or ticagrelor. Short TEG was repeated following treatment modification to ensure an adequate response had been achieved. 12 (31%) patients had an adequate response to both aspirin and clopidogrel, 16 (41%) were hyporesponsive to clopidogrel alone, one (3%) was hyporesponsive to aspirin alone and 10 (26%) were hyporesponsive to both aspirin and clopidogrel. Following treatment modification, an adequate response to aspirin and P2Y12 agent was achieved in 10 (91%) and 22 (85%) patients, respectively. None has presented with a further ST episode. There is a high prevalence of hyporesponsiveness to APT in patients with ST. Improved APT efficacy can be achieved by tailored therapy. Short TEG is a plausible platelet function test that can be used to deliver point of care personalised APT.
    No preview · Article · May 2012 · Heart (British Cardiac Society)
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    ABSTRACT: To evaluate the associations of emergent genome-wide-association study-derived coronary heart disease (CHD)-associated single nucleotide polymorphisms (SNPs) with established and emerging risk factors, and the association of genome-wide-association study-derived lipid-associated SNPs with other risk factors and CHD events. Using two case-control studies, three cross-sectional, and seven prospective studies with up to 25 000 individuals and 5794 CHD events we evaluated associations of 34 genome-wide-association study-identified SNPs with CHD risk and 16 CHD-associated risk factors or biomarkers. The Ch9p21 SNPs rs1333049 (OR 1.17; 95% confidence limits 1.11-1.24) and rs10757274 (OR 1.17; 1.09-1.26), MIA3 rs17465637 (OR 1.10; 1.04-1.15), Ch2q36 rs2943634 (OR 1.08; 1.03-1.14), APC rs383830 (OR 1.10; 1.02, 1.18), MTHFD1L rs6922269 (OR 1.10; 1.03, 1.16), CXCL12 rs501120 (OR 1.12; 1.04, 1.20), and SMAD3 rs17228212 (OR 1.11; 1.05, 1.17) were all associated with CHD risk, but not with the CHD biomarkers and risk factors measured. Among the 20 blood lipid-related SNPs, LPL rs17411031 was associated with a lower risk of CHD (OR 0.91; 0.84-0.97), an increase in Apolipoprotein AI and HDL-cholesterol, and reduced triglycerides. SORT1 rs599839 was associated with CHD risk (OR 1.20; 1.15-1.26) as well as total- and LDL-cholesterol, and apolipoprotein B. ANGPTL3 rs12042319 was associated with CHD risk (OR 1.11; 1.03, 1.19), total- and LDL-cholesterol, triglycerides, and interleukin-6. Several SNPs predicting CHD events appear to involve pathways not currently indexed by the established or emerging risk factors; others involved changes in blood lipids including triglycerides or HDL-cholesterol as well as LDL-cholesterol. The overlapping association of SNPs with multiple risk factors and biomarkers supports the existence of shared points of regulation for these phenotypes.
    Full-text · Article · Jul 2011 · European Heart Journal
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    ABSTRACT: 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. 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). 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 B(2) (TXB(2)) 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 AA-induced 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 TXB(2) levels were consistently suppressed, indicating complete inhibition of cyclo-oxygenase-1 by aspirin. 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.
    No preview · Article · Jul 2011 · Heart (British Cardiac Society)
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    ABSTRACT: IntroductionA clustering of adverse events, in particular stent thrombosis (ST) has been observed following clopidogrel cessation 1-year after drug-eluting stenting (DES), the aetiology of which is poorly understood. We investigated the effect of withdrawing clopidogrel in DES patients using a simple, rapid, reproducible near-patient platelet function test known as short Thrombelastography (s-TEG) that has been developed and validated by this group.Methods33 patients on aspirin and due to stop clopidogrel at 1 year following DES were investigated. Venesection was performed at (i) 4 weeks and 24 h pre clopidogrel cessation (ii) 24 h, 48 h, 1, 2 and 4 weeks post clopidogrel cessation. At all time-points, platelet reactivity was determined using s-TEG and thromboxane (TX) B2, IL-6, CD40 ligand and high sensitivity CRP were measured.ResultsClopidogrel cessation produced (i) a predictable increase in ADP-induced platelet aggregation, and (ii) an unexpected and significant rise in AA-induced platelet aggregation. TXB2 was consistently suppressed confirming inhibition of COX by aspirin.Conclusion We have described for the first time an aspirin-independent increase in AA-induced clotting following clopidogrel withdrawal in DES patients. As well as potentially helping to explain the observed clustering of ST events early after clopidogrel withdrawal, these findings raise the question as to whether AA-induced clotting is an appropriate test of aspirin sensitivity. Our results also confirm s-TEG as a plausible candidate for near-patient platelet function testing in this field.
    No preview · Article · Jun 2011 · Heart (British Cardiac Society)
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    ABSTRACT: Whether triglyceride-mediated pathways are causally relevant to coronary heart disease is uncertain. We studied a genetic variant that regulates triglyceride concentration to help judge likelihood of causality. We assessed the -1131T>C (rs662799) promoter polymorphism of the apolipoprotein A5 (APOA5) gene in relation to triglyceride concentration, several other risk factors, and risk of coronary heart disease. We compared disease risk for genetically-raised triglyceride concentration (20,842 patients with coronary heart disease, 35,206 controls) with that recorded for equivalent differences in circulating triglyceride concentration in prospective studies (302 430 participants with no history of cardiovascular disease; 12,785 incident cases of coronary heart disease during 2.79 million person-years at risk). We analysed -1131T>C in 1795 people without a history of cardiovascular disease who had information about lipoprotein concentration and diameter obtained by nuclear magnetic resonance spectroscopy. The minor allele frequency of -1131T>C was 8% (95% CI 7-9). -1131T>C was not significantly associated with several non-lipid risk factors or LDL cholesterol, and it was modestly associated with lower HDL cholesterol (mean difference per C allele 3.5% [95% CI 2.6-4.6]; 0.053 mmol/L [0.039-0.068]), lower apolipoprotein AI (1.3% [0.3-2.3]; 0.023 g/L [0.005-0.041]), and higher apolipoprotein B (3.2% [1.3-5.1]; 0.027 g/L [0.011-0.043]). By contrast, for every C allele inherited, mean triglyceride concentration was 16.0% (95% CI 12.9-18.7), or 0.25 mmol/L (0.20-0.29), higher (p=4.4x10(-24)). The odds ratio for coronary heart disease was 1.18 (95% CI 1.11-1.26; p=2.6x10(-7)) per C allele, which was concordant with the hazard ratio of 1.10 (95% CI 1.08-1.12) per 16% higher triglyceride concentration recorded in prospective studies. -1131T>C was significantly associated with higher VLDL particle concentration (mean difference per C allele 12.2 nmol/L [95% CI 7.7-16.7]; p=9.3x10(-8)) and smaller HDL particle size (0.14 nm [0.08-0.20]; p=7.0x10(-5)), factors that could mediate the effects of triglyceride. These data are consistent with a causal association between triglyceride-mediated pathways and coronary heart disease. British Heart Foundation, UK Medical Research Council, Novartis.
    Full-text · Article · May 2010 · The Lancet
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    ABSTRACT: A-disintegrin-and-metalloproteinase-domains (ADAMs) are membrane-anchored glycoproteins involved in cell adhesion, cell migration and proteolysis. ADAM15 has been implicated in atherosclerosis, with an effect on vascular smooth muscle cell migration. We investigated whether ADAM33, which is evolutionally closely related to ADAM15, was expressed in atheromas and whether it had an effect on vascular smooth muscle migration. We also tested whether ADAM33 gene variation had an influence on the extent of atherosclerosis in patients with coronary artery disease. Immunohistochemical analyses showed that ADAM33 was expressed in smooth muscle cells in the arterial wall and that the expression was increased in smooth muscle cells in atheromas. ADAM33 immunostaining on inflammatory cells in atheromas was also observed. Primary vascular smooth muscle cells in culture were also found to express ADAM33. Boyden chamber assays showed that a neutralising antibody against ADAM33 increased the ability of arterial smooth muscle cells to migrate through a reconstituted basement membrane, suggesting that ADAM33 has an inhibitory effect on vascular smooth muscle migration. Moreover, we detected an association between ADAM33 genotype and the extent of atherosclerosis in a large cohort of coronary artery disease patients. These findings suggest that ADAM33 is implicated in the pathogenesis of atherosclerosis.
    Full-text · Article · Feb 2010 · Atherosclerosis

  • No preview · Article · Jan 2010 · Circulation Research
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    ABSTRACT: Atherosclerotic lesions express matrix metalloproteinase (MMP)8, which possesses proteolytic activity on matrix proteins particularly fibrillar collagens and on nonmatrix proteins such as angiotensin (Ang) I. We studied whether MMP8 plays a role in atherogenesis. In atherosclerosis-prone apolipoprotein E-deficient mice, inactivating MMP8 resulted in a substantial reduction in atherosclerotic lesion formation. Immunohistochemical examinations showed that atherosclerotic lesions in MMP8-deficient mice had significantly fewer macrophages but increased collagen content. In line with results of in vitro assays showing that Ang I cleavage by MMP8 generated Ang II, MMP8 knockout mice had lower Ang II levels and lower blood pressure. In addition, we found that products of Ang I cleavage by MMP8 increased vascular cell adhesion molecule (VCAM)-1 expression and that MMP8-deficient mice had reduced VCAM-1 expression in atherosclerotic lesions. Intravital microscopy analysis showed that leukocyte rolling and adhesion on vascular endothelium was reduced in MMP8 knockout mice. Furthermore, we detected an association between MMP8 gene variation and extent of coronary atherosclerosis in patients with coronary artery disease. A relationship among MMP8 gene variation, plasma VCAM-1 level, and atherosclerosis progression was also observed in a population-based, prospective study. These results indicate that MMP8 is an important player in atherosclerosis.
    Full-text · Article · Oct 2009 · Circulation Research
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    ABSTRACT: Stent thrombosis (ST) is an uncommon but serious complication of percutaneous coronary intervention (PCI), and is associated with the discontinuation of antiplatelet therapy. In a retrospective study of ST cases during a two-year period at the Wessex Regional Cardiac Unit, 3,004 (1,661 emergency and 1,343 elective) patients underwent PCI between November 2003 and October 2005. There were 25 episodes of ST occurring in 22 patients (overall incidence of ST is 0.83%). There were two (8%) cases of acute ST, eight (32%) of sub-acute ST and 15 (60%) of late or very late ST (five cases between six and 12 months and one case more than one year post-procedure). In the late and very late ST group only one patient was taking dual antiplatelet therapy. Clopidogrel had been discontinued in 14 of the 15 cases and aspirin in five. Nine of the 15 cases occurred within six months following the procedure. All of the patients had a myocardial infarction as a direct consequence of ST and one patient died. We conclude that the incidence of ST in our unit is comparable with previously published data. Late and very late ST was strongly associated with discontinuation of dual antiplatelet therapy. This risk appears to extend beyond six months. These data support the administration of dual antiplatelet therapy for at least one year post-PCI and improving education for patients and healthcare staff about the importance of maintaining antiplatelet therapy.
    No preview · Article · Sep 2007
  • Rajan Sharma · Adrian Ooi · Percy Jokhi · Geoff M Tsang · Iain A Simpson
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    ABSTRACT: Prosthetic heart valve thrombosis is a potentially life-threatening complication of low anticoagulation. We present a case of acute prosthetic mitral valve thrombosis in a patient whose anticoagulation was inadequate after phenindione was changed to low molecular weight heparin. We discuss the diagnosis and treatment of this condition and highlight the danger of long-term low molecular weight heparin use in patients with prosthetic heart valves, especially those in the mitral position. We review the current guidelines for anticoagulation of prosthetic heart valves and discuss potential treatment options if adequate anticoagulation is not achieved by oral anticoagulant alone.
    No preview · Article · Sep 2007 · Journal of the American Society of Echocardiography: official publication of the American Society of Echocardiography

Publication Stats

667 Citations
286.24 Total Impact Points

Institutions

  • 2011-2016
    • University Hospital Southampton NHS Foundation Trust
      • Wessex Cardiothoracic Centre
      Southampton, England, United Kingdom
  • 2015
    • Queen Mary, University of London
      • Barts and The London School of Medicine and Dentistry
      Londinium, England, United Kingdom
  • 1998-2015
    • University of Southampton
      • • Faculty of Medicine
      • • Developmental Origins of Health and Disease
      Southampton, England, United Kingdom
  • 2012
    • British Cardiovascular Society
      Londinium, England, United Kingdom
  • 2007
    • WWF United Kingdom
      Londinium, England, United Kingdom