Young patients with psoriasis have increased arterial stiffness but not microvascular dysfunction compared with healthy controls. More importantly, hs-CRP positively correlated with, and independently predicted, arterial stiffness. This suggests that systemic inflammation in patients with psoriasis is associated with premature atherosclerosis.

Recent studies suggest that reductions in circulating endothelial progenitor cells (EPCs) may contribute to the development of atherosclerosis. However, whether reduced circulating EPCs contribute to cerebrovascular disease remains undefined. We tested the hypothesis that reduced circulating EPCs was associated with an increased burden of carotid atherosclerosis. The level of circulating CD34 þ /KDR þ EPCs and the extent of carotid atherosclerosis were determined in 30 patients with a history of atherothrombotic ischaemic stroke and 30 age-and sex-matched controls (mean age: 6372 years; 63% men). Stroke patients, compared with controls, had significantly higher carotid mean maximum intima-media thickness (mmIMT) (1.0870.05 versus 0.9070.02 mm, P ¼ 0.002), prevalence of carotid plaque (60.0 versus 23.3%, P ¼ 0.004) and a lower number of circulating CD34 þ /KDR þ EPCs (235.7745.5 versus 400.4756.8 cells/ll, P ¼ 0.027). The circulating CD34 þ /KDR þ EPC count correlated negatively with carotid mmIMT (r ¼ À0.50, Po0.001), and was an independent risk factor for increased carotid mmIMT41 mm (odds ratio (OR): 7.71; 95% confidence interval (CI): 1.62-36.74, P ¼ 0.010) and the presence of carotid plaque (OR: 7.04; 95% CI: 1.95-25.43, P ¼ 0.003). Furthermore, stroke patients with low (o25th percentile of controls) as compared to those with normal CD34 þ /KDR þ EPC count had a significantly greater carotid mmIMT (1.217 0.07 versus 0.9370.05 mm, P ¼ 0.005) and a significantly higher prevalence of carotid plaque (87.5% versus 28.6%; P ¼ 0.001). Our observations suggested that reduced circulating EPC may contribute to the progression of carotid atherosclerosis. Circulating EPC count may provide a novel marker for the burden of carotid atherosclerosis.

Hypertension is one of the most important risk factors associated with atrial fibrillation (AF) and increased the risk of cardiovascular events in patients with AF. However, the pathophysiological link between hypertension and AF is unclear. Nevertheless, this can be explained by the hemodynamic changes of the left atrium secondary to long standing hypertension, resulting in elevated left atrium pressure and subsequently left atrial enlargement. Moreover, the activation of renin --angiotensin --aldosterone system (RAAS) activation in patients with hypertension induces left atrial fibrosis and conduction block in the left atrium, resulting in the development of AF. Accordingly, recent studies have shown that effective blockage of RAAS by angiotensin converting enzyme inhibitors or angiotensin receptor antagonist may be effective in both primary and secondary prevention of AF in patients with hypertension, although with controversies. In addition, optimal antithrombotic therapy, blood pressure control as well as rate control for AF are key to the management of patients with AF. 1,2 Both hypertension 3 and AF 4 have increased frequency with the ageing population worldwide, and are associated with increased cardiovascular events. They are important risk factors for stroke, heart failure and overall mortality. 5 --7 On the other hand, hypertension is one of the important risk factors for the occurrence of AF, 8 and increased the risk of stroke and cardiovascular mortality in patients with AF.9,10 Compare with other risk factors for AF, hypertension appears to be responsible for more AF than any other risk factor because of its high prevalence. However, the pathophysiological link between AF and hypertension remains unclear. Moreover, it is also unclear whether treatment of hypertension prevents AF or reduces the risk of AF related complications. The purpose of this article is to review the epidemiology, underlying mechanisms and therapeutic implications of AF in hypertensive patients. A systematic literature search for full-text papers in the English language was performed using MEDLINE, Embase and the Cochrane library through to July 2011. In the search phrases used, the following terms were used: 'atrial fibrillation', 'hypertension', 'epidemiology', 'pathophysiology' and 'treatment'. Papers selected and cited in this review were based on the authors' view on the relevance to the manuscript. In addition, abstracts from international cardiovascular meetings were studied to identify unpublished studies.