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Patel N.,Royal Infirmary | Patel N.,Leicester NIHR Cardiovascular Biomedical Research Unit | Horsfield M.A.,Royal Infirmary | Horsfield M.A.,University of Leicester | And 9 more authors.
Stroke | Year: 2015

Background and Purpose: Brain injury after cardiac surgery is a serious concern for patients and their families. The purpose of this study was to use 3-T fluid attenuated inversion recovery MRI to characterize new and preexisting cerebral ischemic lesions in patients undergoing cardiac surgery and to test whether the accumulation of new ischemic lesions adversely affects cognition. Methods: Digital comparison of before and after fluid attenuated inversion recovery MRI images was performed for 77 cardiac surgery patients. The burden of preexisting versus new ischemic lesions was quantified and compared with the results of baseline and postoperative neuropsychological testing. Results: After surgery, new lesions were identified in 31% of patients, averaging 0.5 lesions per patient (67 mm3 [0.004%] of brain tissue). Patients with preexisting lesions were 10× more likely to receive new lesions after surgery than patients without preexisting lesions. Preexisting ischemic lesions were observed in 64% of patients, averaging 19.4 lesions (1542 mm3 [0.1%] of brain tissue). New lesions in the left hemisphere were significantly smaller and more numerous (29 lesions; median volume, 44 mm3; volume range, 5-404 mm3) than those on the right (10 lesions; median volume, 128 mm3; volume range, 13-1383 mm3), which is consistent with a cardioembolic source of particulate emboli. Overall, the incidence of postoperative cognitive decline was 46% and was independent of whether new lesions were present. Conclusions: New lesions after cardiac surgery added a small (≈4%) contribution to the burden of preexisting cerebrovascular disease and did not seem to affect cognitive function. © 2015 American Heart Association, Inc. Source

Saratzis A.,Leicester NIHR Cardiovascular Biomedical Research Unit | Bath M.F.,Leicester NIHR Cardiovascular Biomedical Research Unit | Harrison S.,Leicester NIHR Cardiovascular Biomedical Research Unit | Sayers R.D.,Leicester NIHR Cardiovascular Biomedical Research Unit | And 3 more authors.
Clinical Journal of the American Society of Nephrology | Year: 2015

Background and objectives Endovascular repair (EVAR) is a common treatment for abdominal aortic aneurysm (AAA). However, its long-term effects on renal function remain unclear. We aimed to assess long-term renal dysfunction after EVAR using a contemporary estimate of GFR and to compare long-term renal outcomes in patients after EVAR with open aneurysm repair (OAR) and in patients without an AAA. Design, settings, participants, & measurements We performed a nested case-matched analysis of 726 patients (using a prospectively maintained database for repairs that took place between January 2000 and May 2010 in a tertiary center): 121 patients undergoing OAR (with data at baseline and 5 years postrepair) were case matched (age, sex, smoking, diabetes, baseline eGFR) to patients undergoing suprarenal and infrarenal fixation EVAR (242 in each group) and to 121 patients undergoing carotid endarterectomy (CEA) without AAA. Changes in eGFR were compared (1 and 5 years). Results The OAR patients lost an average of 7.4 ml/min per 1.73 m2at 5 years (95% confidence interval [95% CI], 4.8 to 10.6), compared with 8.2 ml/min per 1.73 m2(95% CI, 6.5 to 10.8; P<0.001) for infrarenal-fixation EVAR, 16.9 ml/min per 1.73m2(95% CI, 13.0 to 21.9, P<0.001) for suprarenal-fixation EVAR, and 5.4ml/min per 1.73m2(95%CI, 1.7 to 7.5; P<0.001) for CEA. The decrease in eGFRwas steeper during the first postoperative year, with each group losing 22.2 ml/min per 1.73 m2(infrarenal-fixation EVAR), 210.7 ml/min per 1.73 m2(suprarenalfixation EVAR), and 24.6 ml/min per 1.73 m2(OAR), compared with 21.9 ml/min per 1.73 m2for CEA. Conclusions Elective EVAR is associated with a significant decline in eGFR after 5 years, which is steeper in the first postoperative year and more pronounced compared with a similar population with atherosclerotic disease. © 2015 by the American Society of Nephrology. Source

Zachariah D.,Portsmouth Hospitals NHS Trust | Brown R.,University of Hull | Kanagala P.,University of Leicester | Kanagala P.,Leicester NIHR Cardiovascular Biomedical Research Unit | And 11 more authors.
QJM | Year: 2014

Objective: Historical data suggest elderly patients and those with chronic kidney disease (CKD) receive suboptimal secondary prevention following myocardial infarction (MI). We evaluated the impact of age and CKD on secondary prevention following primary percutaneous coronary intervention (PPCI) in a contemporary unselected cohort.Design: We studied 1169 consecutive patients from five UK centres receiving PPCI for ST elevation MI, with use of evidence-based secondary prevention at discharge assessed by age (<60, 60-75 and >75 years) and estimated glomerular filtration rate (eGFR). Follow-up prescribing practice was assessed in 567 patients.Results: One-fifth of patients receiving PPCI were >75 years. This group received fewer secondary prevention drugs at discharge compared to younger patients (P < 0.01 for β-blockers, angiotensin-converting enzyme (ACE) inhibitors/angiotensin receptor blockers (ARB) and statins). By 6 weeks post-PPCI, there was a small drop-off in evidence-based therapy; β-blocker and statin use in those >75 years fell from 90% to 86% and 96% to 93%, respectively. CKD (eGFR<60 ml/min/1.73 m2) was seen in 17.6%. Declining renal function was associated with age, female sex and lower use of ACE inhibitor/ARB. At discharge 83.5% of patients with eGFR<60 ml/min/1.73 m2 were receiving ACE inhibitors/ARB, dropping to 77.5% at 6 weeks (compared with 95% and 92%, respectively, in patients with eGFR >60 ml/min/1.73 m2).Conclusions: The uptake of secondary prevention medication is high following PPCI in the UK, even in the elderly and in those with renal dysfunction. A focus on strategies to improve up-titration and continuation of drugs following discharge is required. © The Author 2013. Published by Oxford University Press on behalf of the Association of Physicians. All rights reserved. Source

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