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Elevated High-Sensitive C-Reactive Protein, Large Arterial Stiffness and Atherosclerosis: a Relationship Between Inflammation and Hypertension?

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Elevated High-Sensitive C-Reactive Protein, Large Arterial Stiffness and Atherosclerosis: a Relationship Between Inflammation and Hypertension? Journal of Human Hypertension (2005) 19, 511–513 & 2005 Nature Publishing Group All rights reserved 0950-9240/05 $30.00 www.nature.com/jhh COMMENTARY Elevated high-sensitive C-reactive protein, large arterial stiffness and atherosclerosis: a relationship between inflammation and hypertension? CJ Boos and GYH Lip Haemostasis, Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, UK Journal of Human Hypertension (2005) 19, 511–513. doi:10.1038/sj.jhh.1001858 Published online 19 May 2005 Cardiovascular disease (CVD) is currently the lead- pneumoniae, and is synthesized primarily by the ing cause of death and disability in the developed liver in response to IL-6 and IL-1b. As a risk world, and will soon overtake infectious disease as assessment tool, it has several good points — it is the pre-eminent cause of death worldwide.1 Athero- very stable, with very little difference in values sclerosis is the most important contributor to this between fresh or frozen plasma and has a long half- substantial disease burden. Whereas previously life of up to 20 h.5 It normally circulates at very low considered a bland process, our current under- levels, but acute inflammatory processes induce standing of atherosclerosis suggests that it is a marked hepatic synthesis of hsCRP, which can dynamic and progressive disease arising from a induce a 100-fold serum increase.6 combination of endothelial damage/dysfunction, Evidence has shown that, even in apparently thrombosis and inflammation.2,3 healthy subjects, there is good and consistent A substantial body of evidence has suggested that significant relationship (in all populations) between four modifiable risk factors — smoking, diabetes, baseline hsCRP levels and risk of future cardio- hypertension and hyperlipidaemia — account for a vascular events (stroke, peripheral vascular disease, significant proportion of CVD, and that reduction of sudden cardiac death and myocardial infarction).7 these risk factors leads to improved morbidity and In those with existing CVD, it has been shown to mortality. However, these traditional risk factors are predict future cardiovascular events including re- not present in up to half of patients presenting with a current ischaemia, atrial fibrillation, death, stroke clinical manifestation of CVD.4 Hence, there has been and percutaneous coronary intervention.8,9 Elevated enormous interest in the identification of other CRP also appears to correlate with softer plaques measurable CVD risk factors in persons without overt that are more prone to rupture,10 and early data disease. This would allow for the introduction of suggest that it may be useful in targeting ‘high-risk’ targeted pre-emptive preventive measures to prevent patients who would most benefit from aggressive future cardiovascular events. Several novel candidate CVD prevention therapies, such as aspirin, statins markers of potential use have been identified and and angiotensin-converting enzyme inhibitors.11,12 It include high-sensitivity C-reactive protein (hsCRP), is likely that CRP is more than simply an inflam- lipoprotein (a), homocysteine and fibrinogen. matory marker of increased CVD risk, as deposits of HsCRP has emerged as a strong, robust and CRP have been demonstrated, on immunohisto- independent risk factor for CVD that appears to chemical staining, in the vascular wall of athero- have significant clinical utility. It is a circulating sclerotic plaques, where it is colocalized with the acute phase reactant named initially for its capacity terminal complement complex and appears to be to bind to the c-polysaccharide of Streptococcus involved in foam cell formation.13 Of note, the investigation of arterial stiffness has gathered pace in recent years with the development Correspondence: Professor GYH Lip, Haemostasis, Thrombosis of readily available noninvasive assessment techni- and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham B18 7QH, UK. ques. Previous studies have shown increased E-mail: [email protected] large artery stiffness to be an additional predictor Published online 19 May 2005 of both atherosclerosis and cardiovascular risk.14,15 Elevated high-sensitive C-reactive protein CJ Boos and GYH Lip 512 A number of methods for assessing arterial stiffness Indeed, some data on interventions on inflamma- have evolved and include arterial pulse wave tion do exist. Schram et al,22 recently investigated velocity (the speed at which the forward pressure the effects of aggressive antihypertensive therapy is transmitted from the aorta through the vascular (hydrochlorothiazide, candesartan or lisinopril) on tree), ultrasound or arterial waveform analysis urinary albumin excretion, endothelial function and (either by systolic or diastolic pulse contour analy- inflammatory activity in hypertensive type II dia- sis).16 Arterial pulse pressure has also been used, but betic individuals. They found that urinary albumin is less accurate. excretion and levels of soluble vascular cell adhe- In this edition of the Journal of Human Hyper- sion molecule-1 and intercellular adhesion mole- tension, two complementary studies are introduced, cule-1 (in part related to inflammation) decreased, which together further supports the value of CRP as but flow-mediated vasodilation and levels of von a surrogate marker for atherosclerosis. In the first Willebrand factor (both measures of endothelial article, Duprez et al17 add to an increasing body damage/dysfunction) and CRP did not change. of evidence18,19 demonstrating a significant relation- Thus, aggressive antihypertensive therapy appears ship between CRP and stiffness of large arteries (as to improve urinary albumin excretion, endothelial an early marker of atherosclerosis). In this study, function and inflammatory activity in hypertensive radial artery pulse wave activity was studied in 391 type II diabetic individuals, irrespective of type of asymptomatic, apparently low-risk patients (mean antihypertensive therapy used. age 50.9 years, only 10% smokers and 16% on Nonetheless, it would be hard to imagine that hypertensive treatment) undergoing primary pre- atherogenesis is simply a ‘yes/no’ phenomenon. The vention screening. In the second much smaller process of atherogenesis starts in early childhood study of 83 higher risk hypertensive patients, and hypertension is simply one associated risk Hommels et al20 have shown a modest correlation factor. It is therefore possible that inflammatory between CRP and atherosclerosis of the abdominal parameters are abnormal in essential hypertension aorta and renal arterial tree. Taken together, these and may simply indicate subclinical or early two papers lend further support to the hypothesis vascular disease or atherosclerosis. Many recent that inflammation within the arterial wall of large studies have suggested a direct relationship between arteries (as manifested by increased levels of hsCRP) hsCRP and hypertension.23–28 Importantly, the stu- exerts its vascular effects by decreasing large artery dies by Duprez et al17 and Hommels20 challenge elasticity and increasing its stiffness, both markers previous work, and would support hsCRP as a of developing atherosclerosis. marker of vascular inflammation, which itself How does inflammation relate to hypertension decreases large artery vascular stiffness and leads as a disorder? It is possible that inflammation may to atherosclerosis and vascular disease, rather than be involved in the initiation as well as develop- be a consequence of hypertension per se. Rather ment of hypertension, with the exertion of proin- than debate a ‘chicken or egg’ question, it is more flammatory actions through several mediators, likely that the inflammation remains one part of the including adhesion molecules, chemokines, growth complex pathophysiology linking hypertension to factors, heat shock proteins, endothelin-1 and vascular disease. This would help our understand- angiotensin. Indeed, even a persistent low-grade ing and management of hypertension, which con- inflammatory state could result in a high but within tinues to be a major disease risk factor and burden the ‘normal range’ concentrations of inflamma- on our healthcare resources.29,30 tory cytokines. Certainly, low-grade inflamma- tion has been associated with other components of the metabolic syndrome, and endothelial damage/ dysfunction. Is a proinflammatory state relevant in hyperten- References sion? By impairing the capacity of the endothelium 1 Murray CJ, Lopez AD. Global mortality, disability, and to generate vasodilating factors, particularly nitric the contribution of risk factors: Global Burden of oxide (NO), elevated cytokines may cause endo- Disease Study. Lancet 1997; 349: 1436–1442. thelial dysfunction, chronic impaired vasodilation 2 Szmitko PE et al. New markers of inflammation and and hypertension.21 Inflammation is also intimately endothelial cell activation: Part I. Circulation 2003; related to thrombogenesis, which is of relevance 108: 1917–1923. since the main complications of hypertension 3 Szmitko PE et al. Biomarkers of vascular disease (stroke, myocardial infarction) are mainly thrombo- linking inflammation to endothelial activation: Part sis-related. The possibility that hypertension may be II. Circulation 2003; 108: 2041–2048. an inflammatory disease may have implications for 4 Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive novel therapeutic strategies to decrease
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