Improvement of endothelial function by pitavastatin: a meta-analysis

Katsiki, Niki; Reiner, Željko; Reiner, Eugenia Tedeschi; Al-Rasadi, Khalid; Pirro, Matteo; Mikhailidis, Dimitri P.; Sahebkar, Amirhossein

doi:10.1080/14656566.2018.1428560

Cited by 31 publications

(17 citation statements)

References 62 publications

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“…Therefore, the consequence of impaired endothelium-mediated dilatation in the resistance vessels would be the elevation of SVR. Twelve month treatment with statins improved flow-mediated dilatation in the brachial artery [25], while a meta-analysis reported increased flow-mediated dilatation following treatment with pitavastatin [26].…”

Section: Discussionmentioning

confidence: 98%

“…As the deleterious effect of LDL-C on endothelial dysfunction can be reversed by statins, this provides a potential explanation for the beneficial effects of these agents on BP [20,[24][25][26]. Experimental evidence suggests that LDL-C can increase the angiotensin II type 1 receptor density in the arterial wall [15,17], while statin treatment in vivo can reduce the vasoconstrictor responses elicited by angiotensin II in isolated human internal thoracic artery segments in vitro [47].…”

Section: Discussionmentioning

confidence: 99%

“…LDL-C can reduce nitric oxide bioavailability and blunt the vasodilator response to acetylcholine [4,[14][15][16][17], and the resulting endothelial dysfunction could be manifested as increased BP. Following treatment with statins, several trials have shown moderate but statistically significant lowering effect on BP [18][19][20][21][22][23], reduction of arterial stiffness [19,20,24], and improved endothelial function [25,26].…”

Section: Introductionmentioning

confidence: 99%

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LDL cholesterol is associated with systemic vascular resistance and wave reflection in subjects naive to cardiovascular drugs

et al. 2018

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Background and aim: Low density lipoprotein cholesterol (LDL-C) is a primary risk factor for atherosclerosis, but it is also associated with elevated blood pressure (BP) and future development of hypertension. We examined the relationship between LDL-C and haemodynamic variables in normotensive and never-treated hypertensive subjects. Methods: We recruited 615 volunteers (19-72 years) without lipid-lowering and BP-lowering medication. Supine haemodynamics were recorded using continuous radial pulse wave analysis, wholebody impedance cardiography, and single channel electrocardiogram. The haemodynamic relations of LDL-C were examined using linear regression analyses with age, sex, body mass index (BMI) (or height and weight as appropriate), smoking status, alcohol use, and plasma C-reactive protein, sodium, uric acid, high density lipoprotein cholesterol (HDL-C), triglycerides, estimated glomerular filtration rate, and quantitative insulin sensitivity check index as the other included variables. Results: The mean (SD) characteristics of the subjects were: age 45 (12) years, BMI 27 (4) kg/m 2 , office BP 141/89 (21/13) mmHg, creatinine 74 (14) µmol/l, total cholesterol 5.2 (1.0), LDL-C 3.1 (0.6), triglycerides 1.2 (0.8), and HDL-C 1.6 (0.4) mmol/l. LDL-C was an independent explanatory factor for aortic systolic and diastolic BP, augmentation index, pulse wave velocity (PWV), and systemic vascular resistance index (p<0.05 for all). When central BP was included in the model for PWV, LDL-C was no longer an explanatory factor for PWV. Conclusions: LDL-C is independently associated with BP via systemic vascular resistance and wave reflection. These results suggest that LDL-C may play a role in the pathogenesis of primary hypertension.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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LDL cholesterol is associated with systemic vascular resistance and wave reflection in subjects naive to cardiovascular drugs

et al. 2018

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“…Therefore, as well as immunomodulation, COVID-19 treatment should also target reduction of inflammation. In this context, statins have been consistently reported to exert immunomodulatory and anti-inflammatory properties [20][21][22][23][24][25][26][27][28][29][30]. Also, it was previously suggested that statins could enhance host defence and suppress inflammation, thus representing a practical and inexpensive adjunctive or alternative host-directed treatment for infections by viruses, fungi, protozoa, and bacteria [31].…”

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confidence: 99%

Lipid-lowering therapy and renin-angiotensin-aldosterone system inhibitors in the era of the COVID-19 pandemic

Katsiki¹,

Banach²,

Mikhailidis³

2020

aoms

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“…FMD has been shown to be impaired in patients with traditional coronary risk factors, including hypertension, dyslipidemia, diabetes mellitus, and smoking, and it has been considered to be a cause of atherosclerosis [14]. Statins improve endothelial function as assessed by FMD [15,16]. In addition, hypertriglyceridemia is independently associated with endothelial dysfunction as assessed by FMD in patients with CHD during statin therapy [17].…”

Section: Introductionmentioning

confidence: 99%

Combination Therapy with Pemafibrate (K-877) and Pitavastatin Improves Vascular Endothelial Dysfunction in Dahl/Salt-sensitive Rats Fed a High-salt and High-fat Diet

Yoshida

Nakamura

Miyoshi

et al. 2020

Preprint

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Background Statins suppress the progression of atherosclerosis by reducing low-density lipoprotein (LDL) cholesterol levels. Pemafibrate (K-877), a novel selective peroxisome proliferator-activated receptor α modulator, is expected to reduce residual risk factors including high triglycerides (TGs) and low high-density lipoprotein (HDL) cholesterol during statin treatment. However, it is not known if statin therapy with add-on pemafibrate improves the progression of atherosclerosis. The aim of this study was to assess the effect of combination therapy with pitavastatin and pemafibrate on lipid profiles and endothelial dysfunction in hypertension and hyperlipidemia model rats. Methods Seven-week-old male Dahl salt-sensitive (DS) rats were divided into the following five treatment groups (normal diet (ND) plus vehicle, high-salt and high-fat diet (HD) plus vehicle, HD plus pitavastatin (0.3 mg/kg), HD plus pemafibrate (K-877) (0.5 mg/kg), and HD plus combination of pitavastatin and pemafibrate) and treated for 12 weeks. At 19 weeks, endothelium-dependent relaxation of the thoracic aorta in response to acetylcholine was evaluated. Results After feeding for 12 weeks, systolic blood pressure and plasma levels of total cholesterol were significantly higher in the HD-vehicle group compared with the ND-vehicle group. Combination therapy with pitavastatin and pemafibrate significantly reduced systolic blood pressure, TG levels, including total, chylomicron (CM), very LDL (VLDL), HDL-TG, and cholesterol levels, including total, CM, VLDL, and LDL-cholesterol, compared with vehicle treatment. Acetylcholine caused concentration-dependent relaxation of thoracic aorta rings that were pre-contracted with phenylephrine in all rats. Relaxation rates in the HD-vehicle group were significantly lower compared with the ND-vehicle group. Relaxation rates in the HD-combination of pitavastatin and pemafibrate group significantly increased compared with the HD-vehicle group, although neither medication alone ameliorated relaxation rates significantly. Western blotting experiments showed increased phosphorylated endothelial nitric oxide synthase protein expression in aortas from rats in the HD-combination group compared with the HD-vehicle group. However, the expression levels did not respond significantly to either medication alone. Conclusions Combination therapy with pitavastatin and pemafibrate improved lipid profiles and endothelial dysfunction in hypertension and hyperlipidemia model rats. Pemafibrate as an add-on strategy to statins may be useful for preventing atherosclerosis progression.

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Improvement of endothelial function by pitavastatin: a meta-analysis

Abstract: This meta-analysis of all available clinical trials revealed a significant increase of FMD induced by pitavastatin.

Cited by 31 publications

References 62 publications

LDL cholesterol is associated with systemic vascular resistance and wave reflection in subjects naive to cardiovascular drugs

LDL cholesterol is associated with systemic vascular resistance and wave reflection in subjects naive to cardiovascular drugs

Lipid-lowering therapy and renin-angiotensin-aldosterone system inhibitors in the era of the COVID-19 pandemic

Combination Therapy with Pemafibrate (K-877) and Pitavastatin Improves Vascular Endothelial Dysfunction in Dahl/Salt-sensitive Rats Fed a High-salt and High-fat Diet

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Improvement of endothelial function by pitavastatin: a meta-analysis

Abstract: This meta-analysis of all available clinical trials revealed a significant increase of FMD induced by pitavastatin.

Cited by 31 publications

References 62 publications

LDL cholesterol is associated with systemic vascular resistance and wave reflection in subjects naive to cardiovascular drugs

LDL cholesterol is associated with systemic vascular resistance and wave reflection in subjects naive to cardiovascular drugs

Lipid-lowering therapy and renin-angiotensin-aldosterone system inhibitors in the era of the COVID-19 pandemic

Combination Therapy with Pemafibrate (K-877) and Pitavastatin Improves Vascular Endothelial Dysfunction in Dahl/Salt-sensitive Rats Fed a High-salt and High-fat Diet​

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Combination Therapy with Pemafibrate (K-877) and Pitavastatin Improves Vascular Endothelial Dysfunction in Dahl/Salt-sensitive Rats Fed a High-salt and High-fat Diet