ORCID Profile
0000-0002-5194-8550
Current Organisation
University of Oxford
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Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 05-03-2013
DOI: 10.1161/CIRCULATIONAHA.112.000908
Abstract: We aimed to determine the prevalence of silent myocardial infarction (SMI) in people with newly diagnosed type 2 diabetes mellitus and its relationships to future myocardial infarction (MI) and all-cause mortality. We examined data from the 5102 patients in the 30-year UK Prospective Diabetes Study (UKPDS) and used Cox proportional hazards regression to examine outcomes by SMI status. Of 1967 patients with complete baseline data, 326 (16.6%) had ECG evidence of SMI (Minnesota codes 1.1 or 1.2) at enrollment. Those with SMI were more likely to be older, female, sedentary, and nonsmokers compared with those without SMI. Their mean blood pressure was greater despite more intensive antihypertensive treatment they were more likely to be taking aspirin and lipid-lowering therapy and they had a greater prevalence of microangiopathy. Fully adjusted hazard ratios for those with versus those without SMI in multivariate models that included UKPDS Risk Engine variables were 1.58 (95% confidence interval, 1.22–2.05) for fatal MI and 1.31 (95% confidence interval, 1.10–1.56) for all-cause mortality. Hazard ratios for first fatal or nonfatal MI and for first nonfatal MI were nonsignificant. The net reclassification index showed no improvement when SMI was added to these models, and the integrated discrimination index showed that SMI marginally improved the prediction of fatal MI and all-cause mortality. About 1 in 6 UKPDS patients with newly diagnosed type 2 diabetes mellitus had evidence of SMI, which was independently associated with an increased risk of fatal MI and all-cause mortality. However, identification of SMI does not add substantively to current UKPDS Risk Engine predictive variables. URL: www.controlled-trials.com . Identifier: ISRCTN number 75451837.
Publisher: Elsevier BV
Date: 06-2017
Publisher: American Medical Association (AMA)
Date: 10-2017
Publisher: American Diabetes Association
Date: 05-2009
DOI: 10.2337/DC09-0183
Publisher: American College of Physicians
Date: 2021
DOI: 10.7326/M20-4298
Publisher: Elsevier BV
Date: 08-2017
Publisher: American Diabetes Association
Date: 06-2007
DOI: 10.2337/DC07-9919
Abstract: Computer simulation models are mathematical equations combined in a structured framework to represent some real or hypothetical system. One of their uses is to allow the projection of short-term data from clinical trials to evaluate clinical outcomes and costs over a long-term period. This technology is becoming increasingly important to assist decision making in modern medicine in situations where there is a paucity of long-term clinical trial data, as recently acknowledged in the American Diabetes Association Consensus Panel Guidelines for Computer Modeling of Diabetes and its Complications. The Mount Hood Challenge Meetings provide a forum for computer modelers of diabetes to discuss and compare models and identify key areas of future development to advance the field. The Fourth Mount Hood Challenge in 2004 was the first meeting of its kind to ask modelers to perform simulations of outcomes for patients in published clinical trials, allowing comparison against “real life” data. Eight modeling groups participated in the challenge. Each group was given three of the following challenges: to simulate a trial of type 2 diabetes (CARDS [Collaborative Atorvastatin Diabetes Study]) to simulate a trial of type 1 diabetes (DCCT [Diabetes Control and Complications Trial]) and to calculate outcomes for a hypothetical, precisely specified patient (cross-model validation). The results of the models varied from each other and for methodological reasons, in some cases, from the published trial data in important ways. This approach of performing systematic comparisons and validation exercises has enabled the identification of key differences among the models, as well as their possible causes and directions for improvement in the future.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 30-05-2023
DOI: 10.1161/CIRCULATIONAHA.122.062021
Abstract: Sodium–glucose co-transporter 2 inhibitors (SGLT2i) have emerged as a paramount treatment for patients with heart failure (HF), irrespective of underlying reduced or preserved ejection fraction. However, a definite cardiac mechanism of action remains elusive. Derangements in myocardial energy metabolism are detectable in all HF phenotypes, and it was proposed that SGLT2i may improve energy production. The authors aimed to investigate whether treatment with empagliflozin leads to changes in myocardial energetics, serum metabolomics, and cardiorespiratory fitness. EMPA-VISION (Assessment of Cardiac Energy Metabolism, Function and Physiology in Patients With Heart Failure Taking Empagliflozin) is a prospective, randomized, double-blind, placebo-controlled, mechanistic trial that enrolled 72 symptomatic patients with chronic HF with reduced ejection fraction (HFrEF n=36 left ventricular ejection fraction ≤40% New York Heart Association class ≥II NT-proBNP [N-terminal pro-B-type natriuretic peptide] ≥125 pg/mL) and HF with preserved ejection fraction (HFpEF n=36 left ventricular ejection fraction ≥50% New York Heart Association class ≥II NT-proBNP ≥125 pg/mL). Patients were stratified into respective cohorts (HFrEF versus HFpEF) and randomly assigned to empagliflozin (10 mg n=35: 17 HFrEF and 18 HFpEF) or placebo (n=37: 19 HFrEF and 18 HFpEF) once daily for 12 weeks. The primary end point was a change in the cardiac phosphocreatine:ATP ratio (PCr/ATP) from baseline to week 12, determined by phosphorus magnetic resonance spectroscopy at rest and during peak dobutamine stress (65% of age-maximum heart rate). Mass spectrometry on a targeted set of 19 metabolites was performed at baseline and after treatment. Other exploratory end points were investigated. Empagliflozin treatment did not change cardiac energetics (ie, PCr/ATP) at rest in HFrEF (adjusted mean treatment difference [empagliflozin – placebo], –0.25 [95% CI, –0.58 to 0.09] P =0.14) or HFpEF (adjusted mean treatment difference, –0.16 [95% CI, –0.60 to 0.29] P =0.47]. Likewise, there were no changes in PCr/ATP during dobutamine stress in HFrEF (adjusted mean treatment difference, –0.13 [95% CI, –0.35 to 0.09] P =0.23) or HFpEF (adjusted mean treatment difference, –0.22 [95% CI, –0.66 to 0.23] P =0.32). No changes in serum metabolomics or levels of circulating ketone bodies were observed. In patients with either HFrEF or HFpEF, treatment with 10 mg of empagliflozin once daily for 12 weeks did not improve cardiac energetics or change circulating serum metabolites associated with energy metabolism when compared with placebo. Based on our results, it is unlikely that enhancing cardiac energy metabolism mediates the beneficial effects of SGLT2i in HF. URL: www.clinicaltrials.gov Unique identifier: NCT03332212.
Publisher: Wiley
Date: 22-11-2013
DOI: 10.1111/DME.12353
Abstract: Evidence of ethnic differences in vascular complications of diabetes has been inconsistent. The aim of this study was to examine the relationship between ethnicity and long-term outcome in a large s le of in iduals with newly diagnosed Type 2 diabetes. In a prospective observational study of 4273 UK Prospective Diabetes Study participants followed for a median of 18 years, 3543 (83%) were White Caucasian, 312 (7%) Afro-Caribbean and 418 (10%) Asian Indian. Relative risks for predefined outcomes were assessed comparing Afro-Caribbean and Asian Indian with White Caucasian using accelerated failure time models, with adjustment for cardiovascular risk factors and other potentially confounding variables. During follow-up, 2468 (58%) participants had any diabetes-related end point, 1037 (24%) a myocardial infarction and 401 (9%) a stroke, and 1782 (42%) died. Asian Indian were at greater risk (relative risk, 95% confidence interval) for any diabetes-related end point (1.18, 1.07-1.29), but at lower risk of all-cause mortality (0.89, 0.80-0.97) and peripheral vascular disease (0.43, 0.23-0.82), vs. White Caucasian. Afro-Caribbean participants were at lower risk for all-cause mortality (0.84, 0.76-0.93), diabetes-related death (0.75, 0.64-0.88), myocardial infarction (0.55, 0.43-0.71) and peripheral vascular disease (0.55, 0.33-0.93) vs. White Caucasian. No ethnicity-related associations were found for stroke or microangiopathy. Asian Indian ethnicity is associated with the greatest burden of disease, but not with an increased risk of major vascular complications or death. Afro-Caribbean ethnicity is associated with reduced risk of all-cause and diabetes-related death, myocardial infarction and peripheral vascular disease, suggesting an ethnicity-specific protective mechanism.
Publisher: Springer Science and Business Media LLC
Date: 26-12-2010
DOI: 10.1038/NG.735
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Ruth Coleman.