Keeping Your Arteries Young: Vascular Health

Abstract

quoted saying ‘‘you’re only as old as your arteries.’’ 4 At a pathobiological level, aortic wall stiffness has been associated with processes involving wall matrix, inflammation, and mechanical stress. Increased collagen content and extracellular matrix (arteriosclerosis) is commonly seen in hypertension and aging. In contrast, atherosclerosis relates to endovascular inflammation, increased cellular oxidative stress, and plaque formation; however, both processes can lead to increased vascular stiffness. 5 Patients with increased aortic stiffness have increased aortic pulse wave velocity and reduced arterial compliance. 6 The clinical implication of increased aortic stiffness results in increased afterload on the left ventricle; alteration in coronary perfusion, which affects cardiac diastolic relaxation; and increased myocardial oxygen consumption. Moreover, these surrogates have been tested in multiple trials with important CV outcomes data. Based on the studies so far, it is evident that increased aortic pulse wave velocity is a strong independent predictor of CV risk, regardless of whether it plays a causative role in CV risk or merely serves as a marker of CV disease already present. One example is found in the Strong Heart Study, 7 which evaluated 2405 patients without CV disease at entry with a 5-year follow-up. During this period, 344 patients had CV events that were significantly associated with high central pulse pressure, thus associating high central pulse pressure with increased arterial stiffness. 1 Another study, the Conduit Artery Function Evaluation (CAFE) trial 8 substudy (on behalf of the Anglo-Scandinavian Cardiac Outcomes Trial [ASCOT] Investigators), evaluated the differential impact of BPlowering drugs on central aortic pressure and clinical outcomes. The study enrolled 2073 patients from 5 ASCOT centers after being on treatment for about 1 year. A total of 19,257 patients were enrolled in the ASCOT trial. All patients had hypertension and 3 additional risk factors. They were randomized in a 2 2 factorial design to receive 1 of 2 antihypertensive regimens: amlodipine (5 ⁄10 mg) with or without perindopril (4 ⁄8 mg) or atenolol (50 ⁄100 mg) with or without a diuretic. Despite similar brachial arm systolic BPs in the two treatment arms, there was a significant decrease in both central aortic pulse pressure and central aortic systolic pressure in the angiotensin-converting enzyme (ACE) inhibitor ⁄calcium channel blocker (CCB) arm vs the b-blocker ⁄diuretic arm. This study suggested that ACE inhibitor ⁄CCB treatment was significantly better. In addition, using the Cox proportional hazards modeling, they determined that central aortic pulse pressure was significantly associated with a post hoc‐defined composite outcome of total CV events (unadjusted P<.0001; P<.05 after adjustment for baseline variables). Based on these data, it can be inferred that arterial stiffness and its components do affect CV outcomes. The vascular etiologies of these vessel wall changes require a closer look.