Dataset Information

Prestroke physical activity and outcomes after intracerebral haemorrhage in comparison to ischaemic stroke: protocol for a matched cohort study (part of PAPSIGOT).

ABSTRACT:

Introduction

Piling evidence suggests that a higher level of prestroke physical activity can decrease stroke severity, and reduce the risk of poststroke mortality. However, prior studies have only included ischaemic stroke cases, or a majority of such. We aim to investigate how premorbid physical activity influences admission stroke severity and poststroke mortality in patients with intracerebral haemorrhage, compared with ischaemic stroke. A prespecified analysis plan counteract some inherent biases in observational studies, and promotes transparency.

Methods and analysis

This is a statistical analysis protocol for a matched cohort study, including all adult patients with intracerebral haemorrhage, and matched ischaemic stroke controls, treated at Sahlgrenska University Hospital in Sweden between 1 November 2014 and 30 June 2019. All patients have been identified in the Väststroke register, and the data file has been sent for merging with national registries. The follow-up of time for survival will be approximately 2-7 years. The sample size calculation indicates that a minimum of 628 patients with intracerebral haemorrhage is needed for power of 80% at an alpha level of 0.01. Multiple imputation by chained equations will be used to handle missing data. The entire cohort of patients with intracerebral haemorrhage will be matched with consecutive ischaemic stroke controls (1:3 ratio) using nearest neighbour propensity score matching. The association between prestroke physical activity and admission stroke severity will be evaluated using multivariable ordinal regression models, and risk for all-cause mortality will be analysed using multivariable Cox proportional-hazards models. Potential confounders include age, ethnicity, income, educational level, comorbidity, medical treatments, alcohol-related disorders, drug abuse and smoking.

Ethics

Data collection for the Physical Activity Pre-Stroke In GOThenburg project was approved by the Regional Ethical Board on 4 May 2016. An additional application was approved by the National Ethical Review Authority on 7 July 2021.

SUBMITTER: Viktorisson A

PROVIDER: S-EPMC8606775 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:Aim: Since tissue inhibitors of matrix metalloproteinase 3 (TIMP-3) was reported to be a potential risk factor of atherosclerosis, aneurysm, hypertension, and post-ischaemic neuronal injury, it may also be a candidate risk factor of stress. Therefore, this study was designed to explore the causal role of TIMP-3 in the risk of ischaemic stroke (IS) and intracerebral haemorrhage (ICH), which are the two main causes of stress via this Mendelian Randomisation (MR) study. Methods: The summarised data of TIMP-3 level in circulation was acquired from the Cooperative Health Research in the Region of Augsburg public database and the outcome of IS and ICH was obtained from genome-wide association studies conducted by MEGASTROKE and the International Stroke Genetics Consortium, respectively. Five statistical methods including inverse-variance weighting, weighted-median analysis, MR-Egger regression, MR Pleiotropy RESidual Sum and Outlier test, and MR-Robust Adjusted Profile Score were applied to evaluate the causal role of TIMP-3 in the occurrence of IS and ICH. Inverse-variance weighting was applied for assessing causality. Furthermore, heterogeneity and pleiotropic tests were utilised to confirm the reliability of this study. Results: We found that TIMP-3 could be a positively causal relationship with the incidence of IS (OR = 1.026, 95% CI: 1.007-1.046, p = 0.0067), especially for the occurrence of small vessel stroke (SVS; OR = 1.045, 95% CI: 1.016-1.076, p = 0.0024). However, the causal effects of TIMP-3 on another IS subtype cardioembolic stroke (CES; OR = 1.049, 95% CI: 1.006-1.094, p = 0.024), large artery stroke (LAS; OR = 1.0027, 95% CI: 0.9755-1.0306, p = 0.849) and ICH (OR = 0.9900, 95% CI: 0.9403-1.0423, p = 0.701), as well as ICH subtypes were not observed after Bonferroni corrections (p = 0.00714). Conclusion: Our results revealed that high levels of circulating TIMP-3 causally increased the risk of developing IS and SVS, but not CES, LAS, ICH, and all ICH subtypes. Further investigation is required to elucidate the underlying mechanism.

Project description:BackgroundIt is often assumed that blood pressure increases acutely after major stroke, resulting in so-called post-stroke hypertension. In view of evidence that the risks and benefits of blood pressure-lowering treatment in acute stroke might differ between patients with major ischaemic stroke and those with primary intracerebral haemorrhage, we compared acute-phase and premorbid blood pressure levels in these two disorders.MethodsIn a population-based study in Oxfordshire, UK, we recruited all patients presenting with stroke between April 1, 2002, and March 31, 2012. We compared all acute-phase post-event blood pressure readings with premorbid readings from 10-year primary care records in all patients with acute major ischaemic stroke (National Institutes of Health Stroke Scale >3) versus those with acute intracerebral haemorrhage.FindingsOf 653 consecutive eligible patients, premorbid and acute-phase blood pressure readings were available for 636 (97%) individuals. Premorbid blood pressure (total readings 13,244) had been measured on a median of 17 separate occasions per patient (IQR 8-31). In patients with ischaemic stroke, the first acute-phase systolic blood pressure was much lower than after intracerebral haemorrhage (158·5 mm Hg [SD 30·1] vs 189·8 mm Hg [38·5], p<0·0001; for patients not on antihypertensive treatment 159·2 mm Hg [27·8] vs 193·4 mm Hg [37·4], p<0·0001), was little higher than premorbid levels (increase of 10·6 mm Hg vs 10-year mean premorbid level), and decreased only slightly during the first 24 h (mean decrease from <90 min to 24 h 13·6 mm Hg). By contrast with findings in ischaemic stroke, the mean first systolic blood pressure after intracerebral haemorrhage was substantially higher than premorbid levels (mean increase of 40·7 mm Hg, p<0·0001) and fell substantially in the first 24 h (mean decrease of 41·1 mm Hg; p=0·0007 for difference from decrease in ischaemic stroke). Mean systolic blood pressure also increased steeply in the days and weeks before intracerebral haemorrhage (regression p<0·0001) but not before ischaemic stroke. Consequently, the first acute-phase blood pressure reading after primary intracerebral haemorrhage was more likely than after ischaemic stroke to be the highest ever recorded (OR 3·4, 95% CI 2·3-5·2, p<0·0001). In patients with intracerebral haemorrhage seen within 90 min, the highest systolic blood pressure within 3 h of onset was 50 mm Hg higher, on average, than the maximum premorbid level whereas that after ischaemic stroke was 5·2 mm Hg lower (p<0·0001).InterpretationOur findings suggest that systolic blood pressure is substantially raised compared with usual premorbid levels after intracerebral haemorrhage, whereas acute-phase systolic blood pressure after major ischaemic stroke is much closer to the accustomed long-term premorbid level, providing a potential explanation for why the risks and benefits of lowering blood pressure acutely after stroke might be expected to differ.FundingWellcome Trust, Wolfson Foundation, UK Medical Research Council, Stroke Association, British Heart Foundation, National Institute for Health Research.