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Statins and Renin-Angiotensin System Inhibitor Combination Treatment To Circulation Journal REVIEW Official Journal of the Japanese Circulation Society http://www.j-circ.or.jp Statins and Renin-Angiotensin System Inhibitor Combination Treatment to Prevent Cardiovascular Disease Hae-Young Lee, MD, PhD; Ichiro Sakuma, MD, PhD; Sang-Hyun Ihm, MD, PhD; Choong-Won Goh, MD; Kwang Kon Koh, MD, PhD Hypercholesterolemia and hypertension are common risk factors for cardiovascular disease (CVD). Updated guide- lines emphasize target reductions of overall cardiovascular risks. Experimental studies have shown reciprocal rela- tionships between insulin resistance (IR) and endothelial dysfunction. Hypercholesterolemia and hypertension have a synergistic deleterious effect on IR and endothelial dysfunction. Unregulated renin-angiotensin system (RAS) is important in the pathogenesis of atherosclerosis and hypertension. Various strategies with different classes of anti- hypertensive medications to reach target goals have failed to reduce residual CVD risk further. Of interest, treating moderate cholesterol elevations with low-dose statins in hypertensive patients reduced CVD risk by 35–40% further. Therefore, statins are important in reducing CVD risk. Unfortunately, statin therapy causes IR and increases the risk of type 2 diabetes mellitus. RAS inhibitors improve both endothelial dysfunction and IR. Further, cross-talk between hypercholesterolemia and RAS exists at multiple steps of IR and endothelial dysfunction. In this regard, combined therapy with statins and RAS inhibitors demonstrates additive/synergistic effects on endothelial dysfunction and IR in addition to lowering cholesterol levels and blood pressure when compared with either monotherapy in patients. This is mediated by both distinct and interrelated mechanisms. Therefore, combined therapy with statins and RAS inhibitors may be important in developing optimal management strategies in patients with hypertension, hypercho- lesterolemia, diabetes, metabolic syndrome, or obesity to prevent CVD. (Circ J 2014; 78: 281 – 287) Key Words: Cardiovascular disease; Hypercholesterolemia; Hypertension; Renin-angiotensin system inhibitors; Statins n the past, the goal of treating patients with hypertension proximately 26%; however, this prevalence doubles in the or hypercholesterolemia was merely to control numerical hypertensive population, reaching nearly 60%.6 Although it is I factors such as blood pressure (BP) or serum cholesterol not possible to provide a definite pathogenesis of hypertension- level alone; nowadays, it has changed. The updated guidelines hypercholesterolemia/dyslipidemia clustering, it is gaining target reductions in overall cardiovascular risk.1,2 Hypercholes- consensus that IR and endothelial dysfunction might play terolemia and hypertension are both associated with endothe- major roles.7,8 lial dysfunction and insulin resistance (IR) and their coexis- From 1988–1994 to 2005–2010, control of concomitant tence is a vicious cycle associated with an increased incidence hypertension and the low-density lipoprotein-cholesterol of cardiovascular events. Moreover, both risk factors are fre- (LDL-C) level rose from 5.0% to 30.7%. By multivariable lo- quently prevail together.3,4 Indeed, more than 60% of hyper- gistic regression, factors associated with concomitant hyper- tensive patients were consistently hypercholesterolemic in the tension, LDL-C, and non-high-density lipoprotein-cholesterol United States National Health and Nutrition Examination Sur- control were statin therapy (10.7) and antihypertensive (3.32) veys 1988–2010.5 More importantly, the prevalence of dyslip- medications, and ≥2 healthcare visits/year (1.90), whereas age idemia increased parallel to BP. In the prehypertensive range, (0.77/10-year increase), black race (0.59), Hispanic ethnicity prevalence was similar to that of the general population, ap- (0.62), cardiovascular disease (CVD) (0.44), and diabetes mel- Received December 9, 2013; accepted December 12, 2013; released online January 8, 2014 Division of Cardiology, Seoul National University College of Medicine, Seoul (H.-Y.L.); Division of Cardiology, College of Medicine, The Catholic University of Korea, Seoul (S.-H.I.); Department of Cardiology, Sanggyepaik Hospital, Inje University, Seoul (C.-W.G.); Division of Cardiology, Gachon University Gil Hospital, Incheon (K.K.K.); Gachon Cardiovascular Research Institute, Incheon (K.K.K.), Korea; and Cardiovascular Medicine, Hokko Memorial Clinic, Sapporo (I.S.), Japan We presented part of this work at the American Heart Association 2012 Scientific Session, November 4, 2012, Los Angeles, CA, USA Mailing address: Kwang Kon Koh, MD, PhD, FACC, Professor of Medicine, Director, Vascular Medicine and Atherosclerosis Unit, Division of Cardiology, Gachon University Gil Hospital, 1198 Kuwol-dong, Namdong-gu, Incheon 405-760, South Korea. E-mail: kwangk@ gilhospital.com ISSN-1346-9843 doi: 10.1253/circj.CJ-13-1494 All rights are reserved to the Japanese Circulation Society. For permissions, please e-mail: [email protected] Circulation Journal Vol.78, February 2014 282 LEE HY et al. Figure 1. Differential effects of antihypertensive medication on insulin sensitivity. Ramipril and candesartan therapies signifi- cantly increased adiponectin levels to a greater extent than atenolol or thiazide. Amlodipine therapy significantly increased adi- ponectin levels to a greater extent than atenolol. Ramipril and candesartan therapies significantly increased insulin sensitivity [as assessed by the Quantitative Insulin-Sensitivity Check Index (QUICKI)] to a greater extent than atenolol or thiazide. Standard error of the mean is identified by the bars. Pl, placebo; At, atenolol; Am, amlodipine; Th, thiazide; Ra, ramipril; Ca, candesartan. (Re- produced with permission from Koh et al.24) litus (DM) (0.54) were inhibiting factors. Interestingly, 69.3% comes,15 recently published hypertension guidelines state that of hypertensive hypercholesterolemic patients failed to be con- diuretics, β-blockers, calcium antagonists, angiotensin-con- comitantly controlled in 2005–2010.5 Various strategies to verting enzyme inhibitors (ACEIs) and angiotensin-receptor reduce residual CVD risk in hypertensive patients include blockers (ARBs) are equally recommendable for the initiation treating BP to lower target goals and using different classes of and maintenance of antihypertensive treatment.16 However, it antihypertensive medications; however still considerable re- is also widely accepted that there are substantial differing ef- sidual risks remains. In contrast, controlling hypercholesterol- fects on insulin sensitivity among the various classes of anti- emia in hypertensive patients by statins is very effective in hypertensive agents. The Antihypertensive and Lipid-Lower- reducing residual CVD risk by 35–40%.1 Therefore, statins are ing Treatment to Prevent Heart Attack Trial (ALLHAT), a of paramount importance in reducing CVD risk.2 clinical outcome trial in 42,418 high-risk patients with hyper- However, IR and the risk of type 2 DM have recently be- tension, which compared 3 classes of antihypertensive agents come problematic with statin therapy.9 In contrast, statin-based as initial therapy of hypertension, showed an increased inci- combination treatment with renin-angiotensin-aldosterone sys- dence of DM among diuretic-treated patients.17 Diuretic treat- tem (RAS) blockade has additive effects to control BP, lipid ment resulted in 4–6 mg/dl higher fasting plasma glucose lev- profiles, endothelial dysfunction and IR by both distinct and els, causing 17% increased incidence of DM compared with interrelated mechanisms,10–12 which may explain positive out- other agents.18 Hypokalemia associated with thiazide diuretics comes of recent clinical trials. Here, we review the role of IR is suggested to be the main mechanism of IR.19 β-blockers tend in hypertension-hypercholesterolemia/dyslipidemia clustering to increase body weight and cause IR, facilitating new-onset and suggest a strategy for achieving maximal additive effect DM.20 It is still unclear why β-blockers impair insulin sensi- with statin-based combination treatment to prevent CVD and tivity; however, peripheral vasoconstriction by traditional DM. β-blockers such as atenolol might limit glucose transportation to muscle, a major glucose-utilizing organ, thus causing de- 21 Insulin Resistance Associated With creased glucose metabolism. In contrast, new vasodilating β-blockers such as nebivolol and carvedilol are associated with Antihypertensive Drugs more favorable effects on glucose and lipid profiles than non- IR plays a pivotal role in hypertension, hypercholesterolemia/ vasodilating β-blockers.22,23 dyslipidemia, and atherosclerosis, and thus is present in most In contrast, RAS inhibitors such as ACEIs and ARBs po- patients with these diseases. Approximately half of hyperten- tentially improve insulin sensitivity in hypertensive patients.24 sive individuals are in the hyperinsulinemic category,13 and up The RAS also has multiple effects in the central nervous sys- to three-quarters of people with type 2 DM have hypertension.14 tem, skeletal muscle, liver, and adipose tissue that may inter- The prevalence of dyslipidemia is more than double in hyper- fere with insulin action. Thus, RAS dysregulation may con- tensive patients compared with the normotensive population.6 tribute to the evolution of IR, and conversely, RAS blockade Although meta-analyses occasionally suggest superiority of may potentially help prevent new-onset DM. RAS blockade 1 class of
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