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Background: Data on long-term outcomes following an acute stroke are sparse. We assessed survival, risk of recurrent stroke and loss in life expectancy following an acute stroke using population-wide data from Australia and New Zealand. Methods: We included all adults with the first stroke hospitalization during 2008 and 2017 at all public and most private hospitals. Patients were followed up to 10 years after the stroke by linkage to each region’s Registry of Deaths and subsequent hospitalizations. Flexible parametric survival modeling was used to estimate all-cause mortality, stroke recurrence, and loss in life expectancy. Competing risk model was used when estimating the risk of stroke recurrence. Results: Three hundred thirteen thousand one hundred sixty-two patients were included (mean age 73.0±14.6 y, 52.0% males) with ischemic stroke (175 547, 56.1%) being the most common, followed by hemorrhagic stroke (77 940, 24.9%) and unspecified stroke (59 675, 19.1%). The overall survival probability was 79.4% at 3 months, 73.0% at 1 year, 52.8% at 5 years, and 36.4% at 10 years. Cumulative incidence of stroke recurrence was 7.8% at 3 months, 11.0% at 1 year, 19.8% at 5 years, and 26.8% at 10 years. Hemorrhagic stroke was associated with greater mortality (hazard ratio, 2.02 [95% CI, 1.99–2.04]) and recurrent stroke (hazard ratio, 1.63 [95% CI, 1.59–1.67]) compared with ischemic stroke. Female sex (hazard ratio, 1.10 [95% CI, 1.09–1.11]) and increasing age (≥85 years versus 18–54 years: hazard ratio, 7.36 [95% CI, 7.15–7.57]) were also associated with increased mortality. Several risk factors including atherosclerotic coronary and noncoronary vascular disease, cardiac arrhythmia, and diabetes were associated with increased risk of mortality and recurrent stroke. Compared with the general population, an acute stroke was associated with a loss of 5.5 years of life expectancy, or 32.7% of the predicted life expectancy, and was pronounced in patients with a hemorrhagic stroke (7.4 years and 38.5% of predicted life expectancy lost). Conclusions: In this population-wide study, death and recurrence of stroke were common after an acute stroke and an acute stroke was associated with considerable loss in life expectancy. Further improvements in treatment and secondary prevention of stroke are needed to reduce these risks.

Thoracic aortic calcium(TAC) is an important marker of extra-coronary atherosclerosis with established predictive value for all-cause mortality. We sought to explore the predictive value of TAC for stroke mortality, independent of the more established coronary artery calcium(CAC) score. The CAC Consortium is a retrospectively assembled database of 66,636 patients aged ≥18 years with no prior history of cardiovascular disease, baseline CAC scans for risk stratification, and follow-up for 12±4 years. CAC scans capture the adjacent thoracic aorta, enabling assessment of TAC from the same images. TAC was available in 41,066 (62%), and was primarily analyzed as present or not present. To account for competing risks for non-stroke death, we utilized multivariable-adjusted Fine and Gray competing risk regression models adjusted for traditional cardiovascular risk factors and CAC score. The mean age of participants was 53.8±10.3 years, with 34.4% female. There were 110 stroke deaths during follow-up. The unadjusted sub-distribution hazard ratio(SHR) for stroke mortality among those who had TAC present compared to those who did not was 8.80(95%CI:5.97,12.98). After adjusting for traditional risk factors and CAC score, the SHR was 2.21(95%CI:1.39,3.49). In sex-stratified analyses, the fully adjusted SHR for females was 3.42(95%CI:1.74,6.73) while for males it was 1.55(95%CI:0.83,2.90). TAC was associated with stroke mortality independent of CAC and traditional risk factors, more so in women. The presence of TAC appears to be an independent risk marker for stroke mortality.

Aspiration risk, especially with propofol sedation, remains a concern after split-dose bowel preparation of up to 1 L polyethylene glycol for the procedure. We aimed to identify the ideal timing of bowel preparation to achieve optimal colon cleansing with no increased risk of aspiration.A total of 892 consecutive patients undergoing simultaneous esophagogastroduodenoscopy (EGD) and colonoscopy were prospectively recruited. Residual gastric volume (RGV) and pH of gastric contents were measured at EGD, and patients' characteristics, runway time (duration between completion of the final liter of bowel preparation and colonoscopy commencement), and cleansing quality were recorded.A shorter runway time resulted in better colon cleansing (r = -0.124, P0.001). No correlation between runway time and RGV or pH was found (r = -0.017, P = 0.62 and r = -0.030, P = 0.47, respectively). RGV and pH did not differ significantly with runway time of 4 or 5 h. RGV with runway time ≤3 h was 35.9 ± 11.8 mL and 17.4 ± 0.6 mL after runway time3 h (P0.001). No aspiration pneumonia occurred. The only factors independently related to higher RGV were younger age and male sex.The consumption of bowel preparation agent within 3-4 h before propofol sedation resulted in a similar RGV and pH as those achieved by more prolonged fasting, with no increased risk of aspiration even in patients perceived to be at high risk.

Background Cardiac Troponin I (cTnI) is frequently measured in patients presenting with symptomatic atrial fibrillation (AF). The significance of elevated cTnI levels in this patient cohort is unclear. We investigated the value of cTnI elevation in this setting and whether it is predictive for significant coronary artery disease (sCAD). Methods We conducted a retrospective, single-center, case–control study of 231 patients who presented with symptomatic AF to The Prince Charles Hospital emergency department, Brisbane, Australia between 2006 and 2014. Patients who underwent serial cTnI testing and assessment for CAD were included. Clinical variables that are known to predict CAD and could potentially predict cTnI elevation were collected. Binary logistic regression was performed to identify predictors of sCAD and cTnI elevation. Results Cardiac Troponin I elevation above standard cut off was not predictive for sCAD after adjustment for other predictors (OR 1.62, 95% CI 0.79–3.32. p=0.19). However, the highest cTnI concentration value (cTnI peak) was predictive for sCAD (OR 2.02, 95% CI 1.02–3.97, p=0.04). Dyspnea on presentation (OR 4.52, 95% CI 1.87–10.91, p=0.001), known coronary artery disease (OR 3.44, 95% CI 1.42–8.32, p=0.006), and ST depression on the initial electrocardiogram (OR 2.57, 95% CI 1.11–5.97, p=0.028) predicted sCAD in our cohort, while heart rate on initial presentation was inversely correlated with sCAD (OR 0.99, 95% CI 0.971–1.00, p=0.034). Conclusion Troponin elevation is common in patients presenting to hospital with acute symptomatic AF and it is not a reliable indicator for underlying sCAD in this patient cohort. However, cTnI peak was a predictor of significant coronary artery disease.