Beneficial pleiotropic vascular effects of rosuvastatin in two hypertensive models

Sušić, Dinko; Varagić, Jasmina; Ahn, Jeong‐Ah; Slama, Michael; Fröhlich, Edward D.

doi:10.1016/s0735-1097(03)00926-4

Cited by 74 publications

(74 citation statements)

References 27 publications

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“…25 These authors found a greater reduction in MAP from baseline among statin recipients (1872 vs 1271%, Po0.05), resulting in a 7 mm Hg difference in MAP between groups after 16 weeks despite equivalent MAP at baseline. These data are consistent with experimental data and retrospective studies in humans suggesting that statin use may reduce blood pressure, [13][14][15][16][17]25,26 possibly independent of their effects on serum cholesterol. 27 However, three previous blinded, randomized studies that included a total of 480 patients found no significant effect of statins on blood pressure, 18,28,29 although the confidence limits for the individual studies did not exclude a moderate antihypertensive effect of statin treatment.…”

Section: Discussionsupporting

confidence: 90%

“…[7][8][9][10][11][12][13][14] What this study adds Pravastatin 40 mg daily did not reduce blood pressure or pulse pressure at any time point in 4126 survivors of myocardial infarction who were followed for more than 5 years.…”

mentioning

confidence: 72%

“…11,12 Several previous experimental and retrospective studies suggest that statins reduce blood pressure in animals and humans with and without hypertension. [13][14][15][16] However, randomized trials have reached conflicting results. 17,18 We analysed blood pressure data from a previously conducted randomized trial, which examined the cardiovascular benefits of pravastatin 40 mg daily compared with placebo.…”

Section: Introductionmentioning

confidence: 99%

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Effect of pravastatin on blood pressure in people with cardiovascular disease

et al. 2006

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Experimental evidence and several small studies in humans suggest that HMG-CoA (3-hydroxy 3-methylglutaryl coenzyme A) reductase inhibitors (statins) reduce blood pressure, perhaps through effects on endothelial function or by reducing inflammation. We tested the hypothesis that pravastatin would reduce blood pressure at 3 months and the risk of developing new hypertension over a follow-up period of 5 years. This was a post hoc subgroup analysis of a randomized double-blind placebo-controlled trial of pravastatin 40 mg daily vs placebo in 4159 participants with previous myocardial infarction and total plasma cholesterol o240 mg/dl (6.2 mmol/l). The primary outcome was the unadjusted change in mean arterial pressure (MAP) from baseline to 3 months. We also considered systolic and diastolic blood pressure (SBP and DBP) and pulse pressure. Analysis of covariance was used to calculate the adjusted effect of treatment on change in these outcomes at 3, 6, 12 and 24 months postrandomization, after controlling for potential confounders. Logistic regression was used to calculate the adjusted effect of treatment on incident hypertension (blood pressure X140/90 in those without known hypertension at baseline). This analysis included 4126/4159 (99.2%) participants for whom blood pressure was measured at baseline and during at least one follow-up visit. Median duration of follow-up was 57.8 months. The unadjusted and adjusted change in MAP, SBP, DBP or pulse pressure from baseline was not significantly different for pravastatin or placebo recipients at 3, 6, 12 or 24 months after randomization, or at last follow-up. Pravastatin did not reduce the adjusted risk of incident systolic hypertension (odds ratio 0.99, 95% CI 0.80-1.23), or incident diastolic hypertension (odds ratio 0.97, 95% CI 0.73-1.27). In summary, pravastatin 40 mg daily did not reduce blood pressure in survivors of myocardial infarction without overt hypercholesterolaemia.

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Section: Discussionsupporting

confidence: 90%

mentioning

confidence: 72%

Section: Introductionmentioning

confidence: 99%

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Effect of pravastatin on blood pressure in people with cardiovascular disease

et al. 2006

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“…This so-called 'sympatho-inhibitory effect' may be mediated by an increase in NO production, with the upregulation of eNOS expression in the brain. 42 In another study, Susic et al 43 evaluated the effects of rosuvastatin on systemic and regional haemodynamics in two hypertensive rat models (one genetically determined, and the other hypertensive-induced via inhibition of NO synthesis). Rosuvastatin reduced arterial BP in SHR rats and decreased total peripheral resistance.…”

Section: Do Lipid Abnormalities Predict the Risk For Hypertension?mentioning

confidence: 99%

Statins: another class of antihypertensive agents?

et al. 2006

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The assessment of global cardiovascular risk is an essential step in the management of atherosclerotic disease prevention. Among the risk factors to be addressed are hypertension and hyperlipidaemia; these commonly coexist. A neutral or lipid-friendly antihypertensive agent is probably useful in the presence of lipid abnormalities. Similarly, statins have been shown to decrease cardiovascular risk in hypertensive patients. There is also experimental and clinical evidence that statins have blood pressure (BP)-lowering effects. In this review, we discuss the beneficial effects of statins on BP, and provide an overview of the underlying pathophysiology. We also consider the evidence justifying the use of statins in the management of hypertensive patients.

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“…These experimental subgroups were as follows: HF group (untreated group), HF-R10 group (high-fat plus rosuvastatin 10 mg), HF-R20 group (high-fat plus rosuvastatin 20 mg), and HF-R40 (highfat plus rosuvastatin 40 mg). The dose of 20 mg/kg/day of rosuvastatin used in the present study is known to produce beneficial effects upon endothelial dysfunction and systemic and regional hemodynamic and has been used previously [22,23]. The doses of 10 mg/kg/day and 40 mg/kg/day of rosuvastatin have to aim to examine whether the beneficial effects of rosuvastatin are dose-dependent.…”

Section: Animals and Dietmentioning

confidence: 99%

Beneficial Effects of Rosuvastatin in Heart of C57Bl/6 Mice with Diet- Induced Metabolic Syndrome - A Preliminary Study

Carvalho¹

2014

Endocrinol Metab Synd

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Background: There is a significant association between the prevalence of cardiovascular disease and metabolic syndrome. Evidence shows that obesity is associated with structural and functional changes in the heart. Estatin drugs can reduce the endogenous synthesis of cholesterol and possess properties that are independent of their effects on lipids, the so-called pleiotropic effects. The present work aims to study the effects of rosuvastatin on the heart of mice with diet-induced metabolic syndrome, such as tissue remodeling and ultrastructural changes.

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Beneficial pleiotropic vascular effects of rosuvastatin in two hypertensive models

Cited by 74 publications

References 27 publications

Effect of pravastatin on blood pressure in people with cardiovascular disease

Effect of pravastatin on blood pressure in people with cardiovascular disease

Statins: another class of antihypertensive agents?

Beneficial Effects of Rosuvastatin in Heart of C57Bl/6 Mice with Diet- Induced Metabolic Syndrome - A Preliminary Study

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