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Angiotensin Receptor Blockers Versus Angiotensin Converting Enzyme Inhibitors for the Treatment of Arterial Hypertension and the Role of Olmesartan.
Omboni, S, Volpe, M
Advances in therapy. 2019;(2):278-297
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Abstract
Blood pressure lowering by all classes of antihypertensive drugs is accompanied by significant reductions of stroke and major cardiovascular (CV) events. Drugs acting on the renin-angiotensin-aldosterone system, such as angiotensin converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs), showed similar benefit on major CV events to other antihypertensive medications. In real-world practice, ARBs reduced by 10% the incidence of CV mortality, non-fatal myocardial infarction, non-fatal stroke and provided superior protection against CV events than ACEIs in high-risk patients. Despite similar antihypertensive properties and a favourable safety profile for both ACEIs and ARBs, evidence indicates that patients treated with ARBs have lower rates of withdrawal for adverse events and greater persistence to therapy than those treated with ACEIs. Among ARBs, olmesartan is one of the latest generation compounds introduced in clinical practice for treating hypertension: head-to-head comparative trials suggest that the efficacy of olmesartan is superior to that of commonly prescribed ACEIs (ramipril and perindopril). The drug, administered as a monotherapy or in combination with a dihydropyridine calcium channel blocker or a thiazide diuretic, has proved to be effective in maintaining blood pressure stability over 24 h, with a favourable safety profile and low discontinuation rates. These properties are pivotal for considering olmesartan as a useful antihypertensive agent especially for high-risk patients (e.g. elderly, diabetics, patients with metabolic syndrome).Funding: Article preparation and open access fee were funded by Menarini International Operations Luxembourg S.A. (M.I.O.L.).
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Metabolic parameters in the short- and long-term treatment of schizophrenia with sertindole or risperidone.
De Hert, M, Mittoux, A, He, Y, Peuskens, J
European archives of psychiatry and clinical neuroscience. 2011;(4):231-9
Abstract
The presence of the metabolic syndrome is an important risk factor for cardiovascular disease and diabetes. The short- and long-term metabolic safety of sertindole was compared to that of risperidone in a subset of patients enrolled in the sertindole cohort prospective (SCoP) study, an open randomized study. In 261 randomized patients, there were moderate increases in mean weight, BMI, and waist circumference during treatment with either sertindole or risperidone; after 12 weeks, the increase in weight was 1.3 and 1.1 kg, respectively, and after 36 weeks, it was 2.2 and 2.0 kg, respectively. From baseline to last assessment (up to 60 weeks), weight gains of 1.8 and 1.7 kg for sertindole and risperidone, respectively, were observed. Similar proportions of patients (sertindole: 17% versus risperidone: 16%) had weight increases ≥7% from baseline to last assessment. The mean changes from baseline in triglycerides, total cholesterol, HDL-cholesterol, LDL-cholesterol, plasma glucose and blood pressure were small and not clinically relevant in both treatment groups. No patient in either of the groups developed type 2 diabetes during the study. At last assessment, the prevalence of metabolic syndrome (International Diabetes Federation) was 17% in the sertindole group and 26% in the risperidone group and the incidence of metabolic syndrome was 7% in the sertindole group and 10% in the risperidone group. Treatment with either sertindole or risperidone did not appear to be associated with an increased comparative risk of developing metabolic syndrome. In general, the metabolic effects of sertindole and risperidone were similar.
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Treatment of hypertension in metabolic syndrome subjects with amlodipine and olmesartan-effects on oxidized non-esterified free fatty acids and cytokine production.
Rosenson, RS
Cardiovascular drugs and therapy. 2009;(4):289-94
Abstract
PURPOSE Angiotensin II increases activation of oxidative signaling and vascular inflammatory gene expression, and interruption of the renin-angiotensin system has been considered more vasculoprotective than use of calcium channel antagonists and other anti-hypertensive therapies. Despite these putative mechanisms, amlodipine is equally efficacious as other therapies in reducing cardiovascular events. METHODS Double-blind, controlled trial, designed to investigate the effects of 2-months treatment with amlodipine and olmesartan on oxidized non-esterified fatty acids (ox-NEFA), and lipopolysaccharide-stimulated cytokine production in whole blood among 23 hypertensive subjects with the metabolic syndrome. RESULTS Treatment with olmesartan was no different than amlodipine in changing concentrations of total oxidized fatty acids (p = 0.37), total ox-NEFA (p = 0.43) and 9, 10, 11, 12, 13, 14, 15 and 16 ox-NEFA concentrations. In contrast, 8 ox-NEFA increased (median [interquartile ranges] by 45.2% [5.3 to 50.0] in olmesartan-treated subjects) compared with a decrease of 18.4% (-45.1-13.9) in amlodipine-treated subjects (p = 0.03). Lipopolysaccharide-stimulated cytokine production and levels of soluble cellular adhesion molecules did not change with either treatment. CONCLUSION Despite experimental data that demonstrates that angiotensin receptor antagonists reduce cellular oxidant stress and inflammation, olmesartan was not different than amlodipine in changing ox-NEFA and inflammatory markers in hypertensive subjects with the metabolic syndrome.
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Moxonidine improves glycaemic control in mildly hypertensive, overweight patients: a comparison with metformin.
Chazova, I, Almazov, VA, Shlyakhto, E
Diabetes, obesity & metabolism. 2006;(4):456-65
Abstract
AIM: To compare the effects of moxonidine and metformin on glycaemic control in patients with impaired glucose tolerance and signs of the metabolic syndrome. METHODS A multicentre, prospective, randomized, open-label study design was adopted with blinded endpoint evaluation. Patients > or =40 years old, with impaired glucose tolerance (or diabetes mellitus treated with diet alone) and a body mass index (BMI) of at least 27 kg/m2 were treated twice daily with moxonidine 0.2 mg or metformin 500 mg for 16 weeks. Oral glucose tolerance test (OGTT) was performed at baseline and end-of-study; plasma insulin and plasma glucose levels were measured at 0, 60, 120 and 180 min after administration. RESULTS With regard to effects on insulin [mean area under the curve (AUC) for insulin], the primary efficacy endpoint of the study, both drugs did not show equivalence. On the contrary, in the per protocol (PP) population, moxonidine statistically significantly (p = 0.025) decreased the AUC for insulin from baseline in the PP population; for metformin, the treatment effect on insulin was a small, net increase resulting in a statistically significant between-group difference of 16.2% (95% CI = 0.1-35.0). The change in mean insulin AUC was most marked in the subgroup of patients with higher sympathetic activity (heart rate >80 bpm). Mean fasting plasma glucose (FPG) levels and HbA1c levels were largely unchanged by moxonidine treatment but significantly decreased by metformin treatment. The difference between the groups was 14.7% (p = 0.0523) in the intent-to-treat (ITT) sample. By study end, both treatments had significantly increased the Matsuda Insulin Sensitivity Index (ISI) from baseline to a comparable extent: moxonidine by reducing plasma insulin after a glucose challenge, metformin by reducing FPG. BMI fell significantly in both groups and blood pressure normalized; both drugs were well tolerated. CONCLUSIONS Moxonidine improved insulin sensitivity in response to glucose challenge in patients with evidence of metabolic syndrome. This improvement resulted from a reduction in plasma insulin levels and was most marked in patients with high sympathetic drive at baseline. By enhancing insulin sensitivity, moxonidine treatment may help prevent the development of diabetes and thereby ameliorate the risk for cardiovascular disease.
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The effect of moxonidine on endothelial dysfunction in metabolic syndrome.
Topal, E, Cikim, AS, Cikim, K, Temel, I, Ozdemir, R
American journal of cardiovascular drugs : drugs, devices, and other interventions. 2006;(5):343-8
Abstract
BACKGROUND Endothelial dysfunction has been reported in patients with type 2 diabetes mellitus and even in healthy obese individuals with a normal metabolic profile. Sympathetic activity commonly is increased in obese hypertensive patients, and moxonidine is effective in lowering BP and improving insulin sensitivity. OBJECTIVE To evaluate the effect of moxonidine on endothelial dysfunction in patients with metabolic syndrome. METHODS Twenty-six patients with mild hypertension were treated with moxonidine and a hypocaloric diet for 3 months, while a second normotensive group (n = 26) were followed-up with calorie restriction alone. Anthropometric (body mass index, waist and hip circumferences, and waist-to-hip ratio) and metabolic features (fasting plasma glucose and insulin, aminotransferases, gamma-glutamyl transpeptidase, triglycerides, and cholesterol levels) and flow-mediated dilatation (FMD) were evaluated. Insulin resistance was calculated by using the homeostasis model assessment formula. Insulin sensitivity was calculated according to the quantitative insulin-sensitivity check index (QUICKI). RESULTS SBP and DBP (both p < 0.001) and waist circumference (p = 0.02) were higher, and QUICKI (p = 0.043) and FMD (p = 0.01) were lower in the hypertensive group at baseline. After 3 months, nearly all the study parameters improved in both treatment groups. The decrease in BP, increase in FMD, and improvements in metabolic and anthropometric parameters were significantly greater in the moxonidine-treated group than in those treated with diet alone. CONCLUSION Moxonidine is proposed as a valuable option for treating mild-to-moderate hypertension in obese and insulin-resistant patients with metabolic syndrome as it appears to improve endothelial dysfunction in these patients.