John J V McMurray

British Heart Foundation, Londinium, England, United Kingdom

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Publications (804)8856.75 Total impact

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    ABSTRACT: Cardiovascular hospitalization (CVH) in patients with heart failure (HF) is associated with a high post-discharge rate of early re-admission and CV death. Eplerenone might be effective in reducing the incidence of these adverse clinical outcomes during this period. The EMPHASIS-HF trial compared eplerenone with placebo added to standard therapy in 2737 patients with New York Heart Association class II HF and left ventricular ejection fraction ≤35%. We conducted a post hoc analysis in the 2338 patients randomized within 180 days of a CVH. The interaction between the time from the qualifying CVH to randomization and the primary outcome of CV death or hospitalization for HF (HHF), as well as other secondary outcomes, was assessed in Cox survival models. Most of the qualifying CVHs were HHF (N = 1496, 64.0%), acute coronary syndromes (N = 390, 16.7%), and arrhythmias (N = 197, 7.2%). The median time of study drug initiation from qualifying CVH was 42 days. The relative rate reductions in CV death/HHF, HHF, and all-cause mortality were similar (P for interaction = 0.65, 0.44, and 0.40, respectively) whether the treatment was initiated <42 or 42+ days after qualifying CVH. Absolute rate reductions were -5.61 [-8.67, -2.55] events per 100 patient × years in the <42 days group and -3.58 [-6.37, -0.79] in the 42+ days group. The adverse effects of eplerenone were also unaffected by the time from the qualifying CVH. Eplerenone is safe, improves survival, and may prevent re-admission when initiated soon after a hospitalization for HF or acute coronary syndromes in patients with systolic HF and mild symptoms. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2015. For permissions please email: journals.permissions@oup.com.
    European Heart Journal 06/2015; DOI:10.1093/eurheartj/ehv273 · 14.72 Impact Factor
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    ABSTRACT: -The aim of our study was to investigate the relationship between coronary artery disease (CAD), angina and clinical outcomes in patients with heart failure and preserved ejection fraction (HF-PEF) enrolled in the irbesartan in patients with heart failure and preserved systolic function (I-Preserve) trial. -The mean follow-up period for the 4128 patients enrolled in I-Preserve was 49.5 months. Patients were divided into four mutually exclusive groups according to history of CAD and angina: patients with no history of CAD or angina (n=2008), patients with no history of CAD but a history of angina (n=649), patients with a history of CAD but no angina (n=468) and patients with a history of CAD and angina (n=1003); patients with no known CAD or angina were the reference group. After adjustment for other prognostic variables using Cox proportional-hazard models, patients with CAD but no angina were found to be at higher risk of all-cause mortality [HR 1.58 (1.22-2.04); p<0.01] and sudden death [HR 2.12 (1.33-3.39); p<0.01], compared with patients with no CAD or angina. Patents with CAD and angina were also at higher risk of all-cause mortality [HR 1.29 (1.05-1.59); p=0.02] and sudden death [HR 1.83 (1.24-2.69); p<0.01] compared with the same reference group and had the highest risk of unstable angina or myocardial infarction [HR 5.84 (3.43-9.95); p<0.01]. -Patients with HF-PEF and CAD are at higher risk of all-cause mortality and sudden death when compared with those without CAD. Clinical Trial Registration-URL: http://www.clinicaltrials.gov. Unique identifier: NCT00095238.
    Circulation Heart Failure 06/2015; DOI:10.1161/CIRCHEARTFAILURE.114.002024 · 5.95 Impact Factor
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    ABSTRACT: The aim of this study was to investigate N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels and recent heart failure (HF) hospitalization as predictors of future events in heart failure - preserved ejection fraction (HF-PEF). Recently, doubt has been expressed about the value of a history of HF hospitalization as a predictor of adverse cardiovascular outcomes in patients with HF and HF-PEF. We estimated rates and adjusted hazard ratios (HRs) for the composite endpoint of cardiovascular death or HF hospitalization, according to history of recent HF hospitalization and baseline NT-proBNP level in the I-PRESERVE (Irbesartan in Heart Failure with Preserved systolic function) trial. Rates of composite endpoints in patients with (n = 804) and without (n = 1,963) a recent HF hospitalization were 12.78 (95% confidence interval [CI]: 11.47 to 14.24) and 4.49 (95% CI: 4.04 to 4.99) per 100 person-years, respectively (HR: 2.71; 95% CI: 2.33 to 3.16). For patients with NT-proBNP concentrations >360 pg/ml (n = 1,299), the event rate was 11.51 (95% CI: 10.54 to 12.58) compared to 3.04 (95% CI: 2.63 to 3.52) per 100 person-years in those with a lower level of NT-proBNP (n = 1468) (HR: 3.19; 95% CI: 2.68 to 3.80). In patients with no recent HF hospitalization and NT-proBNP ≤360 pg/ml (n = 1,187), the event rate was 2.43 (95% CI: 2.03 to 2.90) compared with 17.79 (95% CI: 15.77 to 20.07) per 100 person-years when both risk predictors were present (n = 523; HR: 6.18; 95% CI: 4.96 to 7.69). Recent hospitalization for HF or an elevated level of NT-proBNP identified patients at higher risk for cardiovascular events, and this risk was increased further when both factors were present. Copyright © 2015 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
    06/2015; 3(6):478-486. DOI:10.1016/j.jchf.2015.01.014
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    ABSTRACT: The angiotensin-receptor-neprilysin inhibitor (ARNI) LCZ696 reduced cardiovascular deaths and all-cause mortality compared with enalapril in patients with chronic heart failure in the prospective comparison of ARNI with an Angiotensin-Converting Enzyme Inhibitor to Determine Impact on Global Mortality and Morbidity in Heart Failure (PARADIGM-HF) trial. To more completely understand the components of this mortality benefit, we examined the effect of LCZ696 on mode of death. PARADIGM-HF was a prospective, double-blind, randomized trial in 8399 patients with chronic heart failure, New York Heart Association Class II-IV symptoms, and left ventricular ejection fraction ≤40% receiving guideline-recommended medical therapy and followed for a median of 27 months. Mode of death was adjudicated by a blinded clinical endpoints committee. The majority of deaths were cardiovascular (80.9%), and the risk of cardiovascular death was significantly reduced by treatment with LCZ (hazard ratio, HR 0.80, 95% CI 0.72-0.89, P < 0.001). Among cardiovascular deaths, both sudden cardiac death (HR 0.80, 95% CI 0.68-0.94, P = 0.008) and death due to worsening heart failure (HR 0.79, 95% CI 0.64-0.98, P = 0.034) were reduced by treatment with LCZ696 compared with enalapril. Deaths attributed to other cardiovascular causes, including myocardial infarction and stroke, were infrequent and distributed evenly between treatment groups, as were non-cardiovascular deaths. LCZ696 was superior to enalapril in reducing both sudden cardiac deaths and deaths from worsening heart failure, which accounted for the majority of cardiovascular deaths. https://clinicaltrials.gov/, NCT01035255. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2015. For permissions please email: journals.permissions@oup.com.
    European Heart Journal 05/2015; DOI:10.1093/eurheartj/ehv186 · 14.72 Impact Factor
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    ABSTRACT: The incidence of end-stage renal disease (ESRD) has been consistently shown to be higher among blacks and Hispanics compared to whites with unmeasured risk factors and access to care as suggested explanations. In a high-risk cohort with frequent protocol-directed follow-up, we evaluated the influence of race on cardiovascular (CV) outcomes and incidence of ESRD.
    American Heart Journal 05/2015; DOI:10.1016/j.ahj.2015.05.008 · 4.56 Impact Factor
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    ABSTRACT: Acute heart failure is a fatal syndrome. Emergency physicians, cardiologists, intensivists, nurses and other health care providers have to cooperate to provide optimal benefit. However, many treatment decisions are opinion-based and few are evidenced-based. This consensus paper provides guidance to practicing physicians and nurses to manage acute heart failure in the pre-hospital and hospital setting. Criteria of hospitalization and of discharge are described. Gaps in knowledge and perspectives in the management of acute heart failure are also detailed. This consensus paper on acute heart failure might help enable contiguous practice. © 2015 The Authors European Journal of Heart Failure © 2015 European Society of Cardiology.
    European Journal of Heart Failure 05/2015; 17(6). DOI:10.1002/ejhf.289 · 6.58 Impact Factor
  • European Heart Journal 05/2015; DOI:10.1093/eurheartj/ehv066 · 14.72 Impact Factor
  • John J V McMurray
    European Heart Journal 05/2015; DOI:10.1093/eurheartj/ehv190 · 14.72 Impact Factor
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    ABSTRACT: Cardiovascular (CV) disease is the leading cause of morbidity and mortality in patients with type 2 diabetes mellitus (T2DM). Furthermore, patients with T2DM and acute coronary syndrome (ACS) have a particularly high risk of CV events. The glucagon-like peptide 1 receptor agonist, lixisenatide, improves glycemia, but its effects on CV events have not been thoroughly evaluated. ELIXA (www.clinicaltrials.gov no. NCT01147250) is a randomized, double-blind, placebo-controlled, parallel-group, multicenter study of lixisenatide in patients with T2DM and a recent ACS event. The primary aim is to evaluate the effects of lixisenatide on CV morbidity and mortality in a population at high CV risk. The primary efficacy end point is a composite of time to CV death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for unstable angina. Data are systematically collected for safety outcomes, including hypoglycemia, pancreatitis, and malignancy. Enrollment began in July 2010 and ended in August 2013; 6,068 patients from 49 countries were randomized. Of these, 69% are men and 75% are white; at baseline, the mean ± SD age was 60.3 ± 9.7 years, body mass index was 30.2 ± 5.7 kg/m(2), and duration of T2DM was 9.3 ± 8.2 years. The qualifying ACS was a myocardial infarction in 83% and unstable angina in 17%. The study will continue until the positive adjudication of the protocol-specified number of primary CV events. ELIXA will be the first trial to report the safety and efficacy of a glucagon-like peptide 1 receptor agonist in people with T2DM and high CV event risk. Copyright © 2015. Published by Elsevier Inc.
    American heart journal 05/2015; 169(5):631-638.e7. DOI:10.1016/j.ahj.2015.02.002 · 4.56 Impact Factor
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    ABSTRACT: The cause of death in patients with chronic kidney disease (CKD) varies with CKD severity, but variation has not been quantified. Retrospective analysis of prospective randomized clinical trial. We analyzed 4,038 individuals with anemia and diabetic CKD from TREAT, a randomized trial comparing darbepoetin alfa and placebo. Baseline estimated glomerular filtration rate (eGFR) and protein-creatinine ratio (PCR). Cause of death as adjudicated by a blinded committee. Median eGFR and PCR ranged from 20.6mL/min/1.73m(2) and 4.1g/g in quartile 1 (Q1) to 47.0mL/min/1.73m(2) and 0.1g/g in Q4 (P<0.01). Of 806 deaths, 441, 298, and 67 were due to cardiovascular (CV), non-CV, and unknown causes, respectively. Cumulative CV mortality at 3 years was higher with lower eGFR (Q1, 15.5%; Q2, 11.1%; Q3, 11.2%; Q4, 10.3%; P<0.001) or higher PCR (Q1, 15.2%; Q2, 12.3%; Q3, 11.7%; Q4, 9.0%; P<0.001). Similarly, non-CV mortality was higher with lower eGFR (Q1, 12.7%; Q2, 8.4%; Q3, 6.7%; Q4, 6.1%; P<0.001) or higher PCR (Q1, 10.3%; Q2, 7.9%; Q3, 9.4%; Q4, 6.4%; P=0.01). Sudden death was 1.7-fold higher with lower eGFR (P=0.04) and 2.1-fold higher with higher PCR (P<0.001). Infection-related mortality was 3.3-fold higher in the lowest eGFR quartile (P<0.001) and 2.8-fold higher in the highest PCR quartile (P<0.02). The overall proportion of CV and non-CV deaths was not significantly different across eGFR or PCR quartiles. Results may not be generalizable to nondiabetic CKD or diabetic CKD in the absence of anemia. Measured GFR was not available. In diabetic CKD, both lower baseline GFR and higher PCR are associated with higher CV and non-CV mortality rates, particularly from sudden death and infection. Efforts to improve outcomes should focus on CV disease and early diagnosis and treatment of infection. Copyright © 2015 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.
    American Journal of Kidney Diseases 04/2015; DOI:10.1053/j.ajkd.2015.02.324 · 5.76 Impact Factor
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    ABSTRACT: In patients with heart failure (HF) and reduced ejection fraction, decreases or increases in NT-proBNP levels are associated with better and worse outcomes, respectively. The association in HF and preserved ejection fraction (HF-PEF) is unknown. We examined the association between change in level of NT-proBNP and prognosis in patients with HF-PEF. We examined the association between change in NT-proBNP from baseline to 6 months and cardiovascular (CV) death or HF hospitalization in 2612 participants in the Irbesartan in Patients with Heart Failure and Preserved Systolic Function Study (I-Preserve). Change in NT-proBNP was modelled as a restricted cubic spline in a Cox model after adjusting for baseline NT-proBNP and known prognostic variables. Median change in NT-proBNP from baseline was -7 pg/mL (interquartile range -143 to +108). After adjustment, a 1000 pg/mL decrease in NT-proBNP from baseline was associated with a reduction in the risk of CV death or HF hospitalization [hazard ratio (HR) 0.73, 95% confidence interval (CI) 0.53-1.02]; a 1000 pg/mL increase was associated with an increase in risk (HR 2.01, 95% CI 1.50-2.69). Beyond a 1000 pg/mL rise or fall, there was little additional change in risk. Addition of change in NT-proBNP at 6 months to a model with only baseline NT-proBNP improved the C-statistic from 0.752 to 0.769 (P = 0.013). In HF-PEF, a rise in NT-proBNP was associated with an increase in risk of CV death or HF hospitalization and a fall was associated with a trend towards a decrease in risk. NT-proBNP may be a useful marker to monitor prognosis in this condition. © 2015 The Authors European Journal of Heart Failure © 2015 European Society of Cardiology.
    European Journal of Heart Failure 04/2015; DOI:10.1002/ejhf.274 · 6.58 Impact Factor
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    ABSTRACT: The aim of this study was to investigate prognosis in patients with heart failure (HF) with preserved ejection fraction and the causes of hospitalization and post-hospitalization mortality. Although hospitalizations in patients with HF with preserved ejection fraction are common, there are limited data from clinical trials on the causes of admission and the influence of hospitalizations on subsequent mortality risk. Patients (n = 4,128) with New York Heart Association functional class II to IV HF and left ventricular ejection fractions > 45% were enrolled in I-PRESERVE (Irbesartan in Heart Failure and Preserved Ejection Fraction). A blinded events committee adjudicated cardiovascular hospitalizations and all deaths using predefined and standardized definitions. The risk for death after HF, any-cause, or non-HF hospitalization was assessed using time-dependent Cox proportional hazard models. A total of 2,278 patients had 5,863 hospitalizations during the 49 months of follow-up, of which 3,585 (61%) were recurrent hospitalizations. For any-cause hospitalizations, 26.5% of patients died during follow-up, with an incident mortality rate of 11.1 deaths per 100 patient-years (PYs) and an adjusted hazard ratio of 5.32 (95% confidence interval: 4.21 to 6.23). Overall, 53.6% of hospitalizations were classified as cardiovascular and 43.7% as noncardiovascular, with 2.7% not classifiable. HF was the largest single cause of initial (17.6%) and overall (21.1%) hospitalizations, although, after HF hospitalization, a substantially higher proportion of readmissions were due to primary HF causes (40%). HF hospitalization occurred in 685 patients, with 41% deaths during follow-up, an incident mortality rate of 19.3 deaths per 100 PYs. The adjusted hazard ratio was 2.93 (95% confidence interval: 2.40 to 3.57) relative to patients who were not hospitalized for HF and was greater in those with longer durations of hospitalization. There were 1,593 patients with only non-HF hospitalizations, 21% of whom died during follow-up, with an incident mortality rate of 8.7 deaths per 100 PYs and an adjusted hazard ratio of 4.25 (95% confidence interval: 3.27 to 5.32). The risk for death was highest in the first 30 days and declined over time for all hospitalization categories. Patients not hospitalized for HF or for any cause had observed incident mortality rates of 3.8 and 1.3 deaths per 100 PYs, respectively. In I-PRESERVE, HFpEF patients hospitalized for any reason, and especially for HF, were at high risk for subsequent death, particularly early. The findings support the need for careful attention in the post-discharge time period including attention to comorbid conditions. Among those hospitalized for HF, the high mortality rate and increased proportion of readmissions due to HF (highest during the first 30 days), suggest that this group would be an appropriate target for investigation of new interventions. Copyright © 2015 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
    04/2015; 3(6). DOI:10.1016/j.jchf.2014.12.017
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    ABSTRACT: Renin-angiotensin-aldosterone system (RAAS) inhibition is 1 of the most effective strategies for the management of heart failure with reduced systolic function. However, trials that included patients with preserved systolic function have not shown a clear beneficial effect. Pooling evidence from several heart failure trials provides the opportunity to better assess the differential effects of RAAS inhibition across the continuum of systolic function. The authors searched MEDLINE for large-scale trials published from 1966 to March 2014 that compared RAAS inhibitors against placebos. Studies were eligible for inclusion if they were conducted in heart failure populations with either clinical signs of heart failure or reduced ejection fractions. Inverse variance-weighted fixed-effects meta-analysis was used to pool outcomes of interest, with metaregression used to test for trends. In 16 trials with 54,621 randomized heart failure participants, RAAS inhibition reduced the risks for hospitalization for heart failure by 20% (relative risk [RR] 0.80, 95% confidence interval [CI] 0.77 to 0.83), cardiovascular mortality by 14% (RR 0.86, 95% CI 0.83 to 0.90), and all-cause mortality by 11% (RR 0.89, 95% CI 0.85 to 0.92). However, proportional effects decreased with increasing mean left ventricular ejection fraction (LVEF) for all outcomes (p for trend <0.01). Although there was no significant proportional effect on cardiovascular and all-cause mortality in trials with a mean LVEF >50%, RAAS inhibition was still found to decrease the risk for heart failure hospitalization in patients with preserved LVEFs (RR 0.88, 95% CI 0.80 to 0.97). In conclusion, the relative beneficial effects of RAAS inhibition in heart failure decreases with increasing left ventricular systolic function. Nonetheless, RAAS inhibition significantly reduces the risks for all-cause mortality and cardiovascular mortality in patients with moderately reduced LVEFs and the incidence of hospitalization in patients with preserved left ventricular function. Copyright © 2015 Elsevier Inc. All rights reserved.
    The American journal of cardiology 04/2015; 116(1). DOI:10.1016/j.amjcard.2015.03.052 · 3.43 Impact Factor
  • American Heart Journal 04/2015; DOI:10.1016/j.ahj.2015.04.006 · 4.56 Impact Factor
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    ABSTRACT: Pulse pressure (PP) remains an elusive cardiovascular risk factor with inconsistent findings. We clarified the prognostic value in patients with type 2 diabetes, chronic kidney disease (CKD) and anemia in the Trial to Reduce cardiovascular Events with Aranesp (darbepoetin alfa) Therapy. In 4038 type 2 diabetes patients, darbepoetin alfa treatment did not affect the primary outcome. Risk related to PP at randomization was evaluated in a multivariable model including age, gender, kidney function, cardiovascular disease (CVD) and other conventional risk factors. End points were myocardial infarction (MI), stroke, end stage renal disease (ESRD) and the composite of cardiovascular death, MI or hospitalization for myocardial ischemia, heart failure or stroke (CVD composite). Median (interquartile range) age, gender, eGFR and PP was 68 (60-75) years, 57.3% women, 33 (27-42) ml min(-1) per 1.73 m(2) and 60 (50-74) mm Hg. During 29.1 months (median) follow-up, the number of events for composite CVD, MI, stroke and ESRD was 1010, 253, 154 and 668. In unadjusted analyses, higher quartiles of PP were associated with higher rates per 100 years of follow-up of all end points (P⩽0.04), except stroke (P=0.52). Adjusted hazard ratios (95% confidence interval) per one quartile increase in PP were 1.06 (0.99-1.26) for MI, 0.96 (0.83-1.11) for stroke, 1.01 (0.94-1.09) for ESRD and 1.01 (0.96-1.07) for CVD composite. Results were similar in continuous analyses of PP (per 10 mm Hg). In patients with type 2 diabetes, CKD and anemia, PP did not independently predict cardiovascular events or ESRD. This may reflect confounding by aggressive antihypertensive treatment, or PP may be too rough a risk marker in these high-risk patients.Journal of Human Hypertension advance online publication, 26 March 2015; doi:10.1038/jhh.2015.22.
    Journal of human hypertension 03/2015; DOI:10.1038/jhh.2015.22 · 2.69 Impact Factor
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    ABSTRACT: -Our aim was to describe the incidence and predictors of stroke in heart failure (HF) patients without atrial fibrillation (AF). -We pooled two contemporary HF trials, the Controlled Rosuvastatin in Multinational Trial Heart Failure (CORONA) and the Gruppo Italiano per lo Studio della Sopravvivenza nell'Insufficienza cardiac- Heart Failure trial (GISSI-HF). Of the 9585 total patients, 6054 did not have AF. Stroke occurred in 165 patients (4.7%) with and in 206 patients (3.4%) without AF (rates 16.8 per 1000 patient-years and 11.1 per 1000 patient-years, respectively). Using Cox proportional-hazards models, we identified the following independent predictors of stroke in patients without AF (ranked by chi-square value): age (hazard ratio [HR] 1.34, 95% CI 1.18-1.63 per 10 years), NYHA class (1.60, 1.21-2124 class III/IV vs II), diabetes treated with insulin (1.87, 1.22-2.88), body mass index (0.74, 0.60-0.91 per 5kg/m(2) up to 30) and previous stroke (1.81, 1.19-2.74). N-terminal pro B-type natriuretic peptide (NT-proBNP, available in 2,632 patients) was also an independent predictor of stroke (HR 1.31, 1.11-1.57 per log unit) when added to this model. Using a risk-score formulated from these predictors, we found that patients in the upper third of risk had a rate of stroke that approximated to the risk in patients with AF. -A small number of demographic and clinical variables identified a subset of HF patients without AF at high risk of stroke.
    Circulation 03/2015; DOI:10.1161/CIRCULATIONAHA.114.013760 · 14.95 Impact Factor
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    ABSTRACT: The effect of statins on risk of heart failure (HF) hospitalization and HF death remains uncertain. We aimed to establish whether statins reduce major HF events. We searched Medline, EMBASE, and the Cochrane Central Register of Controlled Trials for randomized controlled endpoint statin trials from 1994 to 2014. Collaborating trialists provided unpublished data from adverse event reports. We included primary- and secondary-prevention statin trials with >1000 participants followed for >1 year. Outcomes consisted of first non-fatal HF hospitalization, HF death and a composite of first non-fatal HF hospitalization or HF death. HF events occurring <30 days after within-trial myocardial infarction (MI) were excluded. We calculated risk ratios (RR) with fixed-effects meta-analyses. In up to 17 trials with 132 538 participants conducted over 4.3 [weighted standard deviation (SD) 1.4] years, statin therapy reduced LDL-cholesterol by 0.97 mmol/L (weighted SD 0.38 mmol/L). Statins reduced the numbers of patients experiencing non-fatal HF hospitalization (1344/66 238 vs. 1498/66 330; RR 0.90, 95% confidence interval, CI 0.84-0.97) and the composite HF outcome (1234/57 734 vs. 1344/57 836; RR 0.92, 95% CI 0.85-0.99) but not HF death (213/57 734 vs. 220/57 836; RR 0.97, 95% CI 0.80-1.17). The effect of statins on first non-fatal HF hospitalization was similar whether this was preceded by MI (RR 0.87, 95% CI 0.68-1.11) or not (RR 0.91, 95% CI 0.84-0.98). In primary- and secondary-prevention trials, statins modestly reduced the risks of non-fatal HF hospitalization and a composite of non-fatal HF hospitalization and HF death with no demonstrable difference in risk reduction between those who suffered an MI or not. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2015. For permissions please email: journals.permissions@oup.com.
    European Heart Journal 03/2015; DOI:10.1093/eurheartj/ehv072 · 14.72 Impact Factor
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    ABSTRACT: Aims We compared clinical outcomes in patients with AF with and without diabetes in the Apixaban for Reduction in Stroke and Other Thromboembolic Events in Atrial Fibrillation trial.
    03/2015; 1(2):86-94. DOI:10.1093/ehjcvp/pvu024
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    ABSTRACT: To determine and compare the diagnostic accuracy of serum natriuretic peptide levels (B type natriuretic peptide, N terminal probrain natriuretic peptide (NTproBNP), and mid-regional proatrial natriuretic peptide (MRproANP)) in people presenting with acute heart failure to acute care settings using thresholds recommended in the 2012 European Society of Cardiology guidelines for heart failure. Systematic review and diagnostic meta-analysis. Medline, Embase, Cochrane central register of controlled trials, Cochrane database of systematic reviews, database of abstracts of reviews of effects, NHS economic evaluation database, and Health Technology Assessment up to 28 January 2014, using combinations of subject headings and terms relating to heart failure and natriuretic peptides. Eligible studies evaluated one or more natriuretic peptides (B type natriuretic peptide, NTproBNP, or MRproANP) in the diagnosis of acute heart failure against an acceptable reference standard in consecutive or randomly selected adults in an acute care setting. Studies were excluded if they did not present sufficient data to extract or calculate true positives, false positives, false negatives, and true negatives, or report age independent natriuretic peptide thresholds. Studies not available in English were also excluded. 37 unique study cohorts described in 42 study reports were included, with a total of 48 test evaluations reporting 15 263 test results. At the lower recommended thresholds of 100 ng/L for B type natriuretic peptide and 300 ng/L for NTproBNP, the natriuretic peptides have sensitivities of 0.95 (95% confidence interval 0.93 to 0.96) and 0.99 (0.97 to 1.00) and negative predictive values of 0.94 (0.90 to 0.96) and 0.98 (0.89 to 1.0), respectively, for a diagnosis of acute heart failure. At the lower recommended threshold of 120 pmol/L, MRproANP has a sensitivity ranging from 0.95 (range 0.90-0.98) to 0.97 (0.95-0.98) and a negative predictive value ranging from 0.90 (0.80-0.96) to 0.97 (0.96-0.98). At higher thresholds the sensitivity declined progressively and specificity remained variable across the range of values. There was no statistically significant difference in diagnostic accuracy between plasma B type natriuretic peptide and NTproBNP. At the rule-out thresholds recommended in the 2012 European Society of Cardiology guidelines for heart failure, plasma B type natriuretic peptide, NTproBNP, and MRproANP have excellent ability to exclude acute heart failure. Specificity is variable, and so imaging to confirm a diagnosis of heart failure is required. There is no statistical difference between the diagnostic accuracy of plasma B type natriuretic peptide and NTproBNP. Introduction of natriuretic peptide measurement in the investigation of patients with suspected acute heart failure has the potential to allow rapid and accurate exclusion of the diagnosis. © Roberts et al 2015.
    BMJ Clinical Research 03/2015; 350(mar04 22):h910. DOI:10.1136/bmj.h910 · 14.09 Impact Factor
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    ABSTRACT: AimTo investigate whether previous physical activity levels are associated with blood glucose levels in individuals with impaired glucose tolerance in the context of an international pharmaceutical trial.Methods Data were analysed from the NAVIGATOR trial, which involved 9306 individuals with impaired glucose tolerance and high cardiovascular risk from 40 different countries, recruited in the period 2002–2004. Fasting glucose, 2-h post-challenge glucose and physical activity (pedometer) were assessed annually. A longitudinal regression analysis was used to determine whether physical activity levels 2 years (t-2) and 1 year (t-1) previously were associated with levels of glucose, after adjusting for previous glucose levels and other patient characteristics. Those participants with four consecutive annual measures of glucose and two consecutive measures of physical activity were included in the analysis.ResultsThe analysis included 3964 individuals. Change in physical activity from t-2 to t-1 and activity levels at t-2 were both associated with 2-h glucose levels after adjustment for previous glucose levels and baseline characteristics; however, the associations were weak: a 100% increase in physical activity was associated with a 0.9% reduction in 2-h glucose levels. In addition, previous physical activity only explained an additional 0.05% of the variance in 2-h glucose over the variance explained by the history of 2-h glucose alone (R2=0.3473 vs. 0.3468). There was no association with fasting glucose.Conclusions In the context of a large international clinical trial, previous physical activity levels did not meaningfully influence glucose levels in those with a high risk of chronic disease, after taking into account participants’ previous trajectory of glucose control.This article is protected by copyright. All rights reserved.
    Diabetic Medicine 03/2015; DOI:10.1111/dme.12762 · 3.06 Impact Factor

Publication Stats

52k Citations
8,856.75 Total Impact Points

Institutions

  • 2010–2015
    • British Heart Foundation
      Londinium, England, United Kingdom
    • Georgetown University
      Washington, Washington, D.C., United States
    • Stavanger University Hospital
      Stavenger, Rogaland, Norway
    • Hamilton Health Sciences
      Hamilton, Ontario, Canada
  • 1996–2015
    • University of Glasgow
      • • Institute of Cardiovascular and Medical Sciences
      • • BHF Glasgow Cardiovascular Research Centre
      Glasgow, Scotland, United Kingdom
  • 2005–2014
    • Brigham and Women's Hospital
      • Department of Medicine
      Boston, Massachusetts, United States
    • University of Massachusetts Boston
      Boston, Massachusetts, United States
  • 2003–2014
    • Duke University Medical Center
      • • Duke Clinical Research Institute
      • • Division of Cardiology
      Durham, North Carolina, United States
    • University of Gothenburg
      Goeteborg, Västra Götaland, Sweden
    • Karolinska University Hospital
      Tukholma, Stockholm, Sweden
  • 2013
    • Mario Negri Institute for Pharmacological Research
      • Department of Cardiovascular Research
      Milano, Lombardy, Italy
    • London School of Hygiene and Tropical Medicine
      • Department of Medical Statistics
      London, ENG, United Kingdom
    • Uppsala University
      • UCR-Uppsala Clinical Research center
      Uppsala, Uppsala, Sweden
  • 2012–2013
    • Oslo University Hospital
      • • Research Institute of Internal Medicine
      • • Department of Cardiology
      Oslo, Oslo, Norway
    • Harvard Medical School
      • Department of Medicine
      Boston, Massachusetts, United States
  • 2005–2012
    • University of Groningen
      • Department of Clinical Pharmacology
      Groningen, Groningen, Netherlands
  • 2011
    • Golden Jubilee National Hospital
      Clydebank, Scotland, United Kingdom
    • Harvard University
      Cambridge, Massachusetts, United States
    • NHS Greater Glasgow and Clyde
      Glasgow, Scotland, United Kingdom
  • 2002–2011
    • Columbia University
      • • Division of Cardiology
      • • College of Physicians and Surgeons
      New York City, NY, United States
  • 2009
    • Maastricht University
      Maestricht, Limburg, Netherlands
    • Aintree University Hospital NHS Foundation Trust
      Liverpool, England, United Kingdom
  • 2008
    • University of Bergen
      • Section of Cardiology
      Bergen, Hordaland, Norway
  • 2007
    • Odense University Hospital
      Odense, South Denmark, Denmark
    • University of Oslo
      • Department of Cardiology
      Oslo, Oslo, Norway
  • 2004–2007
    • Duke University
      Durham, North Carolina, United States
    • University of Lodz
      Łódź, Łódź Voivodeship, Poland
    • University of Alberta
      • Department of Medicine
      Edmonton, Alberta, Canada
    • Hospital General Universitario Gregorio Marañón
      Madrid, Madrid, Spain
    • Charles University in Prague
      Praha, Praha, Czech Republic
  • 2000–2007
    • University of Stirling
      Stirling, Scotland, United Kingdom
    • North Carolina Clinical Research
      Raleigh, North Carolina, United States
  • 2006
    • Dokuz Eylul University
      Ismir, İzmir, Turkey
    • University of Aberdeen
      Aberdeen, Scotland, United Kingdom
    • University of Cincinnati
      Cincinnati, Ohio, United States
    • University of Liverpool
      • Department of Public Health and Policy
      Liverpool, ENG, United Kingdom
  • 2004–2005
    • McMaster University
      Hamilton, Ontario, Canada
  • 1999–2005
    • WWF United Kingdom
      Londinium, England, United Kingdom
  • 2001–2002
    • Glasgow Caledonian University
      • Division of Biomedical Sciences
      Glasgow, Scotland, United Kingdom
    • The Queen Elizabeth Hospital
      • Department of Cardiology
      Adelaide, South Australia, Australia
  • 1994–2000
    • Western General Hospital
      Edinburgh, Scotland, United Kingdom