We examined the accuracy of International Classification of Disease 10th iteration (ICD-10) diagnosis codes within Canadian administrative data in identifying cerebral venous thrombosis (CVT). Of 289 confirmed cases of CVT admitted to our comprehensive stroke center between 2008 and 2018, 239/289 were new diagnoses and 204/239 were acute events with only 75/204 representing symptomatic CVTs not provoked by trauma or structural processes. Using ICD-10 codes in any position, sensitivity was 39.1% and positive predictive value was 94.2% for patients with a current or history of CVT and 84.0% and 52.5% for acute and symptomatic CVTs not provoked by trauma or structural processes.

Arterial wall thickening, stimulated by low-grade systemic inflammation, underlies many cardiovascular events. As diet is a significant moderator of systemic inflammation, the dietary inflammatory index (DIITM) has recently been devised to assess the overall inflammatory potential of an individual’s diet. The primary objective of this study was to assess the association of the DII with common carotid artery–intima-media thickness (CCA–IMT) and carotid plaques. To substantiate the clinical importance of these findings we assessed the relationship of DII score with atherosclerotic vascular disease (ASVD)-related mortality, ischaemic cerebrovascular disease (CVA)-related mortality and ischaemic heart disease (IHD)-related mortality more. The study was conducted in Western Australian women aged over 70 years (n 1304). Dietary data derived from a validated FFQ (completed at baseline) were used to calculate a DII score for each individual. In multivariable-adjusted models, DII scores were associated with sub-clinical atherosclerosis: a 1 sd (2·13 units) higher DII score was associated with a 0·013-mm higher mean CCA–IMT (P=0·016) and a 0·016-mm higher maximum CCA–IMT (P=0·008), measured at 36 months. No relationship was seen between DII score and carotid plaque severity. There were 269 deaths during follow-up. High DII scores were positively associated with ASVD-related death (per sd, hazard ratio (HR): 1·36; 95 % CI 1·15, 1·60), CVA-related death (per sd, HR: 1·30; 95 % CI 1·00, 1·69) and IHD-related death (per sd, HR: 1·40; 95 % CI 1·13, 1·75). These results support the hypothesis that a pro-inflammatory diet increases systemic inflammation leading to development and progression of atherosclerosis and eventual ASVD-related death.

Given the importance of prevention of complications in type 2 diabetes (T2D), we aimed to examine changes over time in consumption of fruits, vegetables and juice among men who were diagnosed with T2D in comparison with men without diabetes. The prospective Cohort of Swedish Men, aged 45–79 years in 1997, was used to examine changes in diet after diagnosis of T2D. Dietary intake was assessed using FFQ in 1997 and 2009. In all, 23 953 men who were diabetes free at baseline (1997) and completed both FFQ were eligible to participate in the study. Diagnosis of T2D was reported by subjects and ascertained through registers. Multivariable linear mixed models were used to examine changes in mean servings/week over time. In total, 1741 men developed T2D during the study period. Increased consumption of vegetables and fruits was observed among those who developed T2D (equivalent to 1·6 servings/week, 95 % CI 1·08, 2·03) and men who remained diabetes free (0·7 servings/week, 95 % CI 0·54, 0·84). Consumption of juice decreased by 0·6 servings/week (95 % CI −0·71, −0·39) among those who developed T2D and increased by 0·1 servings/week (95 % CI 0·05, 0·15) in those who were diabetes free. Changes over time and between groups were statistically significant. Although improvements in diet were observed, only 36 % of those with T2D and 35 % of those without diabetes consumed ≥5 servings of fruits and vegetables/d in 2009.