Halvor Naess

Introduction: Age, sex and family history of cardiovascular disease (CVD) are non-modifiable risk factors of CVD in offspring. Our aim was to relate parental CVD (pCVD) to artery vessel-wall measurements in offspring. Patients and methods: Offspring consisted of acute ischaemic stroke patients (15-60 years) and their partners. Young offspring was defined as ≤45 years old. Arterial wall changes were assessed as intima-media thickness of carotid and femoral arteries (cIMT/fIMT), abdominal aortic plaques (AAP), and ankle-arm index (AAI). Any offspring reported parental coronary artery disease (pCAD) and parental peripheral artery disease (pPAD). In addition, pCAD and pPAD were also verified by standardized questionnaires for living parents, or by medical records for deceased parents. Results: Reported vs. verified pCVD was present for around 90% vs. 50% of parents. Reported pCAD/pPAD was positive for 227/67 offspring and verified pCAD/pPAD was positive for 148/36 offspring, respectively. Reported and verified pCAD and pPAD were related to higher cIMT and fIMT. Reported and verified pCAD was also related to AAP and reported pPAD to AAI. The effect attenuated after adjusting for age, hypertension, dyslipidemia, diabetes mellitus and smoking. Among young offspring, reported pCAD was associated with higher cIMT and fIMT, even though the total number of young offspring was 4-fold lower compared to middle-aged offspring. Conclusions: Parental CVD is related to artery wall changes in offspring, particularly in young offspring. Regarding CVD risk assessment, extensive parental verification of CVD might not be necessary as many young patients and partners seem to be well-orientated about their parental CVD. Primary prevention from young age should get more attention.

Objective: This study is aimed at examining the prevalence of cognitive impairment following minor stroke and its associations with stroke subtype, location, and pre‐existing vascular pathology. Material and Methods: We included 305 patients from stroke units at the Central Norway Health Trust and from Haukeland University Hospital. MRI was performed using 1.5‐T scanners as part of the routine stroke protocol during hospitalization at stroke units at baseline. Minor stroke was classified according to NIHSS 0–7 and mRS 0–2. We registered left versus right hemispheric location as well as Fazekas classification of pre‐existing white matter hyperintensities (WMHs). Study patients underwent cognitive assessment 3 months after the stroke using a wide range of neuropsychological tests. Cognitive impairment was defined as performance 1.5 SD below the norm‐based average on ≥ 2 tests. Chi‐square and regression analyses were conducted to consider the associations between cognitive impairment and WMH and infarction subtype and location. Results: 78.4% of participants had impaired results on at least one test, and 62% had impaired results on ≥ 2 tests. WMH and several infarction locations were associated with impaired cognitive performance in the initial analyses, but only the association between supratentorial infarctions and impaired memory recall remained significant after Benjamini–Hochberg correction. Higher education was associated with lower risk of impaired cognitive performance. Conclusions: Our findings showed a high prevalence of cognitive impairment 3 months after minor stroke in a younger cohort, largely irrespective of stroke location and subtype. Such substantial cognitive burden should be taken into consideration during clinical stroke assessment, while also accounting for demographic variables such as education. In future research, longer follow‐up periods may provide a more nuanced understanding of the trajectory of cognitive impairment after minor stroke.

04.09.2025: Kronikk - Språklig forståelse oppstår ikke ved direkte overføring og kopiering av informasjon, men som cerebral modellbygging etter bayesiansk mønster.

Background: Studies in young patients with stroke identified coronary artery disease (CAD) as a main contributor to mortality. In the present NOR‐SYS (Norwegian Stroke in the Young Study), we aimed to investigate the prevalence of CAD, and the impact on new vascular events and mortality. Methods: A total of 385 patients with ischemic stroke, aged ≤60 years, were included. CAD was defined as a history of CAD or positive coronary imaging (computed tomography or coronary angiography). Results: Mean age was 49.6 years, and 68.1% were men. The prevalence of CAD was 25.2% (n=97) (nonobstructive, 9.6% [n=37]; and obstructive, 15.6% [n=60]). In the subsample of patients without clinical CAD but with femoral plaque on ultrasound (n=58) who underwent cardiac computed tomography, 46% (n=27) had nonobstructive CAD and 28% (n=16) had obstructive CAD. During a median follow‐up of 10.1 years, 36 patients (9.4%) died, 84 (21.8%) reached a composite end point of new stroke, myocardial infarction, or death, whereas 64 (16.6%) had a composite end point of new stroke or death. Event‐free survival was significantly lower in patients with obstructive CAD versus no CAD or nonobstructive CAD (log‐rank P P =0.037) and the composite end point of death or recurrent ischemic stroke (HR, 3.24 [95% CI, 1.46–7.20]; P =0.004). Conclusions: In young and middle‐aged ischemic stroke survivors, a quarter of patients had CAD. CAD was an independent predictor of recurrent stroke and mortality. In patients without previous CAD, but femoral plaque on ultrasound, nearly a half had nonobstructive and one‐fourth had obstructive CAD. Systematic screening with cardiac computed tomography may identify high‐risk patients after ischemic stroke. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT01597453.

Background The optimal dose of tenecteplase in acute ischaemic stroke remains to be defined. We present a pooled analysis of the two NOR-TEST trials exploring the efficacy and safety of tenecteplase 0.4 mg/kg in acute ischemic stroke. Methods We retrospectively reviewed two multi-center PROBE trials, NOR-TEST and NOR-TEST 2A, conducted in Norway. The patients were randomized to either 0.4 mg/kg single bolus tenecteplase or standard 0.9 mg/kg alteplase. The primary endpoint was favorable functional outcome at three months (mRS 0-1) or return to baseline if pre-stroke mRS was 2. The secondary endpoints included favorable functional outcome at three months (Modified Rankin Scale 0-2), major neurological improvement and safety data. The pooling project includes a pooled analysis of patients with moderate to severe stroke (NIHSS ≥6) from both trials and an additional post-hoc analysis of patients with mild stroke (NIHSS ≤5) from NOR-TEST. Results The per-protocol analysis contains 483 patients, of which 235 were assigned to tenecteplase and 248 to alteplase. In per-protocol analysis, functional outcome was better in the alteplase arm with cut-off mRS 2 (OR 0.52, 95% CI 0.33-0.80, p=0.003) and expressed by ordinal shift analysis (OR 1.64, 95% CI 1.17-2.28, p=0.004). Mortality at 3 months was higher in the tenecteplase arm (OR 2.48, 95% CI 1.20-5.10, p=0.014). Mortality and intracranial hemorrhage rates were higher in the severe stroke group randomized to tenecteplase, whereas these rates were similar for alteplase and tenecteplase in moderate and mild stroke. High age was not associated with either higher mortality or intracranial hemorrhage rates. Conclusions Tenecteplase 0.4 mg/kg is unsafe in moderate and severe stroke and the risk of death and intracranial hemorrhage probably increases with stroke severity. A lower tenecteplase dose should be tested in future trials. Trial Registration ClinicalTrials.gov Identifiers: NCT01949948, NCT03854500 https://clinicaltrials.gov/ct2/show/NCT01949948 https://clinicaltrials.gov/ct2/show/NCT03854500

Background: Inflammation is proposed to be involved in the pathogenesis of poststroke cognitive impairment. The aim of this study was to investigate associations between concentrations of systemic inflammatory biomarkers after ischemic stroke and poststroke cognitive impairment. Methods: The Nor-COAST study (Norwegian Cognitive Impairment After Stroke) is a prospective observational multicenter cohort study, including patients hospitalized with acute stroke between 2015 and 2017. Inflammatory biomarkers, including the TCC (terminal C5b-9 complement complex) and 20 cytokines, were analyzed in plasma, collected at baseline, 3-, and 18 months poststroke, using ELISA and a multiplex assay. Global cognitive outcome was assessed with the Montreal Cognitive Assessment (MoCA) scale. We investigated the associations between plasma inflammatory biomarkers at baseline and MoCA score at 3-, 18-, and 36-month follow-ups; the associations between inflammatory biomarkers at 3 months and MoCA score at 18- and 36-month follow-ups; and the association between these biomarkers at 18 months and MoCA score at 36-month follow-up. We used mixed linear regression adjusted for age and sex. Results: We included 455 survivors of ischemic stroke. Higher concentrations of 7 baseline biomarkers were significantly associated with lower MoCA score at 36 months; TCC, IL (interleukin)-6, and MIP (macrophage inflammatory protein)-1α were associated with MoCA at 3, 18, and 36 months ( P P P <0.01). Conclusions: Higher concentrations of plasma inflammatory biomarkers were associated with lower MoCA scores up to 36 months poststroke. This was most pronounced for inflammatory biomarkers measured in the acute phase following stroke. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT02650531.

Introduction. Nonmodifiable cardiovascular risk factors, like age and sex, are easily quantifiable. Due to immense technical progress in diagnostics and medical data storage, the aim of this study was to quantify, verify, and to compare parental cardiovascular events (CVE) as an additional nonmodifiable risk factor for young and middle-aged ischaemic stroke patients and controls. Methods. Information about parental CVE was first obtained by standardized questionnaires answered by 385 acute ischaemic stroke patients (15-60 years of age) and 260 controls. After consent to contact living and include deceased parents, patients and controls provided necessary personal identification of their parents. Thereafter, CVE were verified by standardized questionnaires answered by parents or medical records in case of deceased parents. Results. One hundred-and-nine (14.2) of 770 patient parents vs. 128 (24.6) of 520 control parents were not available for verification. Active participation was obtained for 229 (73.9) of 310 patient parents vs.113 (58.2) of 194 control parents. Medical record verification was obtained for 192 (54.7) of 351 deceased patient parents, vs.103 (52.0) of 198 deceased control parents. This study showed highest death rates of fathers (65.3 patient fathers and 57.6 control fathers) and highest numbers of CVE, especially myocardial infarction among patient fathers of patients aged 50-60 years. Discussion and Conclusion. Obtaining verified parental CVE as a nonmodifiable risk factor is still challenging, despite widely available digital medical information. To attain more accurate information on parental CVE, we recommend active involvement of family members in addition to medical record verification, especially for patients aged 50 years. Trial Registration. This trial is registered with NCT01597453

All stroke patients should receive timely admission to a stroke unit (SU). Consequently, most patients with suspected strokes – including stroke mimics (SM) are admitted. The aim of this study was to estimate the current total demand for SU bed capacity today and give estimates for future (2020–2040) demand. Time trend estimates for stroke incidence and time constant estimates for length of stay (LOS) were estimated from the Norwegian Patient Registry (2010–2015). Incidence and LOS models for SMs were based on data from Haukeland University Hospital (2008–2017) and Akershus University Hospital (2020), respectively. The incidence and LOS models were combined with scenarios from Statistic Norway’s population predictions to estimate SU demands for each health region. A telephone survey collected data on the number of currently available SU beds. In 2020, 361 SU beds are available, while demand was estimated to 302. The models predict a reduction in stroke incidence, which offsets projected demographic shifts. Still, the estimated demand for 2040 rose to 316, due to an increase in SMs. A variation of this reference scenario, where stroke incidence was frozen at the 2020-level, gave a 2040-demand of 480 beds. While the stroke incidence is likely to continue to fall, this appears to be balanced by an increase in SMs. An important uncertainty is how long the trend of decreasing stroke incidence can be expected to continue. Since the most important uncertainty factors point toward a potential increase, which may be as large as 50%, we would recommend that the health authorities plan for a potential increase in the demand for SU bed capacity.