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Effects of Fluvastatin on Insulin Resistance and Cardiac Morphology in Hypertensive Patients

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Effects of Fluvastatin on Insulin Resistance and Cardiac Morphology in Hypertensive Patients Journal of Human Hypertension (2011) 25, 492–499 & 2011 Macmillan Publishers Limited All rights reserved 0950-9240/11 www.nature.com/jhh ORIGINAL ARTICLE Effects of fluvastatin on insulin resistance and cardiac morphology in hypertensive patients AA Teixeira, A Buffani, A Tavares, AB Ribeiro, MT Zanella, O Kohlmann Jr and MC Batista Division of Nephrology, Hypertension and Cardiovascular Metabology Center, Kidney and Hypertension Hospital, Federal University of Sa˜o Paulo, Sa˜o Paulo, Brazil Among hypertensive patients, cardiovascular disease resting systolic blood pressure. However, maximum morbidity is common, even in those who are adequately systolic EBP was lower in the treatment group than in treated. New pharmacological strategies to mitigate the the placebo group (175±18 vs 192±23 mm Hg, Po0.05), burden of arterial hypertension are needed. This 12- as was left ventricular mass index (LVMI; 82±15 vs month, randomized, double-blind placebo-controlled 100±23, Po0.05), and HOMA-IR index was lower after study investigated the effect of statin (fluvastatin) fluvastatin treatment (2.77±1.46 vs 3.33±1.73, Po0.05). treatment on ambulatory blood pressure (ABP), exercise Changes in lipid profile were not correlated with blood blood pressure (EBP), myocardial structure, endothelial pressure, endothelial function, LVMI or HOMA-IR data. function and insulin resistance in 50 hypertensive In hypertensive patients, fluvastatin can improve max- patients. At baseline, the groups were comparable in imum systolic EBP, myocardial remodelling and insulin terms of demographic characteristics, ABP, EBP, en- resistance, independently of lipid profile variations and dothelial function and homeostasis model assessment endothelial function. of insulin resistance (HOMA-IR). At the end of the study, Journal of Human Hypertension (2011) 25, 492–499; there was no difference between groups in terms of doi:10.1038/jhh.2010.87; published online 9 September 2010 Keywords: endothelium/drug effects; pleiotropism; hydroxymethylglutaryl-CoA reductase inhibitors; insulin resistance; hypertrophy; left ventricular Introduction one of the potential mechanisms linking cholesterol with cardiovascular disease. In that context, insulin The risk of adverse cardiovascular events increases resistance and progressive endothelial dysfunction dramatically when dyslipidaemia and hypertension 1,2 have a role in the pathogenesis of hypertension and co-exist, and the simultaneous prescription of atherosclerosis.11 Recent studies have demonstrated antihypertensive and hypolipidaemic agents is that the so-called pleiotropic effects of statins can common. Addition of hypolipidaemic agents to prevent cardiovascular remodelling in experimental hypertension treatment regimens can be beneficial, models of human disease.12,13 Dechend et al.,14 lessening target organ lesions and possibly reducing 3 studying transgenic rats, found that, in addition to the number of cardiovascular events. The 3-hydro- the known lipid-lowering effect, statin treatment xyl-3–methylglutaryl-coenzyme A (HMG-CoA) re- reduced hypertension, myocardial hypertrophy and ductase inhibitors, or statins, are the most effective vascular fibrosis. Other experimental studies, of low-density lipoprotein cholesterol-lowering drugs, rosuvastatin and pravastatin, have shown that with significant benefits in the prevention of 4–9 statins slow the development of cardiovascular primary and secondary cardiovascular disease. hypertrophy, inflammation and glucose intoler- Endothelial dysfunction is an event that occurs 13,15,16 10 ance. Although these experimental results early in atherosclerosis and in hypertension. It is suggest that statins act simultaneously on endothe- lial function, insulin resistance and myocardial Correspondence: Dr AA Teixeira, Division of Nephrology, structure, efforts to translate such findings to the Hypertension and Cardiovascular Metabology Center, Kidney clinical setting have been unsuccessful. and Hypertension Hospital, Federal University of Sa˜o Paulo, This study investigated the effect of fluvastatin Rua Benedita Alves Funchal, 81, Apto 303—Jardim Guanabara, treatment on ambulatory blood pressure (ABP), Pouso Alegre, Minas Gerais, CEP 37550-000, Brazil. exercise blood pressure (EBP), myocardial structure, E-mail: [email protected] Received 20 January 2010; revised 30 May 2010; accepted 12 July endothelial function and insulin resistance in a 2010; published online 9 September 2010 group of patients under treatment for hypertension. Effects of fluvastatin in hypertensive patients AA Teixeira et al 493 Materials and methods according to the American Diabetes Association criteria:18 Symptoms of diabetes plus casual plasma We conducted a randomized, double-blind study glucose concentration X200 mg dlÀ1 without regard comparing fluvastatin (20 mg) with placebo in to time since last meal or fasting plasma glucose patients with primary hypertension that was classi- concentration X126 mg dlÀ1 (fasting defined as no fied as stage 1 hypertension, as defined in The caloric intake for 8 h) or 2-h post-load glucose Seventh Report of the Joint National Committee on X200 mg dlÀ1 during oral glucose tolerance test. At Prevention, Detection, Evaluation, and Treatment of 17 months 0 and 12, pregnancy tests were carried out. High Blood Pressure (JNC 7). A total of 50 patients At months 0, 6 and 12, albuminuria was measured were enrolled in the study. The study was divided by 12-h nocturnal immunoturbidimetry, and ABP into two phases, the selection/washout phase was measured on the same day. At months 0 and 12, (3 weeks) and the randomized treatment phase (12 insulin resistance was calculated by the homeostasis months). During the selection/washout phase (visits model assessment of insulin resistance model 1 and 2, V1 and V2), patients received only placebo assessment of insulin resistance (HOMA-IR) index,19 and were taken off any antihypertensive or hypo- calculated according to the following equation: lipidaemic agents. Patients entering the randomized treatment phase then received either placebo or HOMA-IR ¼ [fasting insulin (mUlÀ1) Â fasting fluvastatin throughout the 12-month study period, glucose (mmol lÀ1)]/22.5 with evaluations every 2 months (visits V3–V8). The ABP was measured during a 24-h period at All patients, regardless of group assignment, were months 0, 6 and 12 using an automatic monitor treated for hypertension with enalapril. If necessary, (Model 90207; Spacelabs Healthcare, Issaquah, WA, the dose was increased or hydrochlorothiazide was USA) fitted on the non-dominant arm. A percentage added as follows: step 1—enalapril, 10 mg b.i.d.; of successful readings greater than 80% was con- step 2—enalapril, 20 mg b.i.d.; step 3—enalapril sidered adequate. At months 0, 6 and 12, treadmill (20 mg b.i.d.) þ hydrochlorothiazide (12.5 mg per exercise stress tests were carried out using compu- day). With regard to previous therapies, both groups terized equipment (Challenger 5.0; Ecafix Indu´ stria were comparable in terms of exposition to anti- e Come´rcio Ltda, Sa˜o Paulo, Brazil) including an hypertensive agents, before the wash-out period, electrocardiograph and cardiac monitor for contin- with a median 62% use of thiazide diuretics and uous observation. To evaluate maximum systolic 54% use of renin–angiotensin system blockers in blood pressure during exercise (ExSBPmax), we both groups, in comparable proportions. measured blood pressure before the stress test and The inclusion criteria were being between 18 and once per minute thereafter, during treadmill activity, 65 years of age and having primary hypertension using the Ellestad protocol. that was classified as stage 1. Exclusion criteria were At months 0, 6 and 12, patients underwent as follows: stage 2 hypertension or any form of echocardiography (Model SIM 5000; Escote Biome- secondary hypertension; secondary dyslipidaemia; dica, Florence, Italy) in order to determine the left prior cardiovascular disease; endocrinopathy (in- ventricular mass index (LVMI), calculated in accor- cluding diabetes mellitus); pneumopathy or nephro- dance with the American Society of Echocardio- pathy of any origin; any pathology of the locomotor graphy guidelines. system that could interfere with the treadmill test; At months 0, 6 and 12, endothelial function was known hypersensitivity to fluvastatin; positive evaluated by two independent, experienced radio- pregnancy test and breastfeeding. Written informed logists. Measurements of the endothelium-depen- consent was obtained from all patients. dent and endothelium-independent vasodilator ca- pacity of the brachial artery were made using Doppler B-mode ultrasound.20 Evaluations were Clinical evaluation made in separate tests: The primary demographic and anthropometric data Endothelium-dependent phase: Patients were put collected were age (years), weight (kg), height (m) at rest, in the horizontal decubitus position, for and body mass index (kg mÀ2). During all visits, 10 min. Intima–media thickness was measured in blood pressure was calculated as the mean of three the right brachial artery, at 2–15 cm above the crook measurements taken while the patients were seated, of the arm. Subsequently, a pneumatic cuff was in accordance with JNC 7 recommendations.17 inflated to 290 mm Hg for 5 min on the same arm, resulting in total interruption of regional blood flow. Fifteen seconds after deflating the cuff the max- Clinical and biochemical parameters imum blood flow was measured during reactive At months 0, 2,
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