Background Among asymptomatic patients with severe carotid artery stenosis but no recent stroke or transient cerebral ischaemia, either carotid artery stenting (CAS) or carotid endarterectomy (CEA) can restore patency and reduce long-term stroke risks. However, from recent national registry data, each option causes about 1% procedural risk of disabling stroke or death. Comparison of their long-term protective effects requires large-scale randomised evidence.Methods ACST-2 is an international multicentre randomised trial of CAS versus CEA among asymptomatic patients with severe stenosis thought to require intervention, interpreted with all other relevant trials. Patients were eligible if they had severe unilateral or bilateral carotid artery stenosis and both doctor and patient agreed that a carotid procedure should be undertaken, but they were substantially uncertain which one to choose. Patients were randomly allocated to CAS or CEA and followed up at 1 month and then annually, for a mean 5 years. Procedural events were those within 30 days of the intervention. Intention-to-treat analyses are provided. Analyses including procedural hazards use tabular methods. Analyses and meta-analyses of non-procedural strokes use Kaplan-Meier and log-rank methods. The trial is registered with the ISRCTN registry, ISRCTN21144362.

Abstract Aims As large population-based studies of aortic dissection are lacking, the incidence numbers and knowledge about time-trends and sex differences are uncertain. The objective was to describe incidence, temporal trends and outcome of aortic dissection with particular emphasis on sex differences. Methods and results During the study period 2002–2016, 8057 patients in Sweden were diagnosed with aortic dissection, identified from the National Patient Register and the Cause of Death Register. A total of 5757 (71%) patients were hospitalized, whereas 2300 (29%) patients were deceased without concurrent hospital stay. The annual incidence was 7.2 per 100 000 (9.1 in men and 5.4 in women), decreasing over time in men (P = 0.005). Mean age in the hospitalized patients was 68 years (SD 13), 2080 (36%) were women. Within the first 14 days after onset, 1807 patients (32%) underwent surgical repair. The proportion of surgically treated increased from the 5-year period 2002–2006 to 2012–2016 [27% vs. 35%, odds ratio (OR) 1.61, 95% confidence interval (CI) 1.39–1.86; P < 0.001]. In hospitalized patients, 30-day mortality decreased between the same periods (26% vs. 21%, OR 0.68, 95% CI 0.59–0.80; P < 0.001). Long-term mortality decreased as well (hazard ratio 0.74, 95% CI 0.67–0.82; P < 0.001). Women had higher 30-day mortality than men after acute repair, a sex difference that remained after age adjustment (17% vs. 12%, OR 1.38, 95% CI 1.04–1.82; P = 0.006). Conclusion This population-based study detected a higher incidence of aortic dissection than prior reports, but a decreasing incidence in men. Surgical therapy was increasingly used and with more favourable outcome but was less frequently offered to elderly patients. The sustained sex differences regarding both incidence and outcome require further attention.

In patients with acute complicated type B aortic dissection, TEVAR can be performed with excellent early and long-term survival, whereas morbidity and long-term durability must be further elucidated.

Enzyme elevation after CABG implied an increased risk of both early and late death. The long-term effect persisted many years after surgery.

Elevated biochemical markers after CABG correspond to the amount of peri-operatively infarcted myocardium.

BackgroundAtherosclerosis is characterized by the presence of activated immune‐competent cells including dendritic cells (DCs) and T cells, dead cells, and oxidized low‐density lipoprotein. HSP60 (Heat shock protein 60) has been implicated in atherosclerosis. A plasma protein, Annexin A5, has atheroprotective properties.Methods and ResultsHuman DCs differentiated from peripheral blood monocytes were treated with human HSP60 or HSP90 and autologous T cells were cocultured with these pretreated DCs (mDCs). HSP60 induced mDCs and T‐cell activation as determined by FACScan (Fluorescence associated cell scan), gene‐activation, and cytokine production. HSP60‐induced T‐cell activation was partly major histocompatibility complex class II–dependent. T cells exposed to HSP60‐treated mDCs produced interferon‐γ, interleukin‐17, but not transforming growth factor‐β. HSP60 did not promote expression of Toll‐like receptors 2 or 4. HSP90 promoted mDCs maturation but had no effect on T‐cell activation. Annexin A5 inhibited HSP60‐proinflammatory Th1/Th17 effects on mDCs and T cells, and partly bound HSP60. Further, Annexin A5 inhibited HSP‐induced activation of mDCs and also oxidized low‐density lipoprotein–induced HSP‐production from mDCs. Experiments on mDCs and T cells derived from carotid atherosclerotic plaques from patients with symptomatic carotid disease gave similar results as from blood donors.Conclusions HSP60 induces mDCs activation and partly major histocompatibility complex class II–dependent activation of blood‐ and plaque‐derived T cells, which is mostly of Th1/Th17 type. HSP60 could thus be an important T‐cell antigen in plaques, and also mediate oxidized low‐density lipoproteins immunogenic effects on DC‐T‐cell activation, promoting plaque rupture and clinical manifestations of cardiovascular disease. Annexin A5 inhibits both oxidized low‐density lipoprotein–induced HSP60, and HSP60‐mediated immune activation, which suggests a potential therapeutic role.

TEVAR allows rapid and effective therapy in trauma patients with blunt aortic injury. The outcome is dependent on the severity of the concomitant injuries. The treatment is durable during the first decade after the procedure, but even longer follow up is needed to determine the impact of TEVAR in young patients on the degenerative changes that take place in the aging aorta.

No abstract