Fibrinolysis and insulin sensitivity in imidapril and candesartan (FISIC study) recipients with hypertension

Fogari, Roberto; Zoppi, Annalisa; Salvadeo, Sibilla A T; Mugellini, Amedeo; Lazzari, Pierangelo; Santoro, Tara; Derosa, Giuseppe

doi:10.1038/hr.2010.260

Cited by 15 publications

(20 citation statements)

References 61 publications

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“…In addition, results of multiple intervention studies indicated that lifestyle modification 39,40 and pharmacologic treatment for hypertension, 41,42 such as the angiotensin converting enzyme inhibitor, imidapril or the angiotensin II type 1 receptor antagonist, irbesartan, not only reduced BP values but also improved insulin sensitivity and endothelial function. Therefore, weight management or drug therapy may be necessary for hypertensive patients to reduce incidence of cardiovascular events.…”

Section: Discussionmentioning

confidence: 99%

Co-effect of insulin resistance and biomarkers of inflammation and endothelial dysfunction on hypertension

Zhu

Wang

et al. 2012

Hypertens Res

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To explore the co-effects of inflammation and endothelial dysfunction and insulin resistance (IR) on hypertension in a large Asian population. Data on demographic characteristics, blood pressure and other variables were collected; additionally, fasting plasma glucose, insulin and biomarkers, including C-reactive protein (CRP), soluble intercellular cell adhesion molecule-1 (sICAM-1), soluble E-selectin (sE-selectin) and angiotensin II were examined among 2553 Mongolian adults aged X20 years. IR was assessed using the homeostasis model. The co-effects of elevated biomarkers of inflammation and endothelial dysfunction and IR on hypertension were analyzed. A total of 953 subjects were diagnosed with hypertension. Among hypertensive subjects, the levels of CRP (11.0 vs. 6.7 mg l À1 ), sICAM-1 (348.3 vs. 335.9 ng ml À1 ), sE-selectin (20.9 vs. 18.5 ng ml À1 ) and angiotensin II (61.3 vs. 50.0 pg ml À1 ) were significantly higher among subjects with IR than those without IR; among normotensives, levels of CRP (6.3 vs. 5.2 mg l À1 ) and sE-selectin (20.1 vs. 17.8 ng ml À1 ) were higher among IR subjects than those without IR. The prevalence of hypertension was significantly higher among subjects with IR and 2 elevated biomarkers (69.0%) and those with IR and X3 elevated biomarkers (79.3%) than among those with IR and no elevated biomarkers (45.9%) and those with IR and 1 elevated biomarker (50.6%). After adjusting for multivariate, the risk of hypertension was significantly associated with the coexistence of IR and any two or three elevated biomarkers (odds ratios (OR) (95% confidence intervals (CIs))¼2.55 (1.60-4.06) and 3.19 (1.15-8.86), respectively). In this Mongolian population, IR and elevated biomarkers of inflammation and endothelial dysfunction were related to hypertension and the coexistence of IR and elevated biomarkers of inflammation and endothelial dysfunction increased the risk of hypertension.

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Section: Discussionmentioning

confidence: 99%

Co-effect of insulin resistance and biomarkers of inflammation and endothelial dysfunction on hypertension

Zhu

Wang

et al. 2012

Hypertens Res

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“…2,49,50 Although in the present study we did not evaluate changes in tPA levels, data from previous studies by ourselves and other authors indicated that ARB, which do not affect the metabolism of bradykinin, do not influence or even decrease plasma tPA. 1,25,28,29 Coronary release of tPA from the endothelium is an important defense against coronary heart disease. The recently published results of the Shiga Plasminogen Activator In Coronary Circulation study 51 have demonstrated that ACE inhibition increased coronary release of tPA, although only in women.…”

Section: Discussionmentioning

confidence: 99%

“…21,22 Accordingly, most, although not all, 23,24 direct comparative studies on the effects of ACE-Is and ARBs on the fibrinolytic balance observed a decrease in PAI-1 plasma levels with ACE-Is, but not with ARBs. [25][26][27][28][29] One possible reason for such a dissimilar effect might be the different effect of the two drug classes on plasma Ang II. Unlike ACE-Is, which inhibit ACE-dependent production of Ang II, thus decreasing its plasma levels, treatment with ARBs is known to elevate markedly circulating Ang II.…”

Section: Introductionmentioning

confidence: 99%

Role of angiotensin II in plasma PAI-1 changes induced by imidapril or candesartan in hypertensive patients with metabolic syndrome

et al. 2011

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To evaluate the relationship between plasma plasminogen activator inhibitor-1 (PAI-1) and angiotensin II (Ang II) changes during treatment with imidapril and candesartan in hypertensive patients with metabolic syndrome. A total of 84 hypertensive patients with metabolic syndrome were randomized to imidapril 10 mg or candesartan 16 mg for 16 weeks. At weeks 4 and 8, there was a dose titration to imidapril 20 mg and candesartan 32 mg in nonresponders (systolic blood pressure (SBP) 4140 and/or diastolic blood pressure (DBP) 490 mm Hg). We evaluated, at baseline and after 2, 4, 8, 12 and 16 weeks, clinic blood pressure, Ang II and PAI-1 antigen. Both imidapril and candesartan induced a similar SBP/DBP reduction (À19.4/16.8 and À19.5/16.3 mm Hg, respectively, Po0.001 vs. baseline). Both drugs decreased PAI-1 antigen after 4 weeks of treatment, but only the PAI-1 lowering effect of imidapril was sustained throughout the 16 weeks (À9.3 ng ml À1 , Po0.01 vs. baseline), whereas candesartan increased PAI-1 (+6.5 ng ml À1 , Po0.05 vs. baseline and Po0.01 vs. imidapril). Imidapril significantly decreased Ang II levels (À14.6 pg ml À1 at week 16, Po0.05 vs. baseline), whereas candesartan increased them (+24.2 pg ml À1 , Po0.01 vs. baseline and vs. imidapril). In both groups there was a positive correlation between Ang II and PAI-1 changes (r¼0.61, Po0.001 at week 16 for imidapril, and r¼0.37, Po0.005 at week 16 for candesartan). Imidapril reduced plasma PAI-1 and Ang II levels, whereas candesartan increased them. This suggests that the different effect of angiotensin-converting enzyme inhibitors and Ang II blockers on Ang II production has a role in their different influence on fibrinolysis.

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“…6,7 In a homogenous population of normoweight (BMIo25 kgm À2 ) hypertensive patients, the effects of ARB on fibrinolysis and insulin sensitivity in comparison with the effects of ACE-I have not yet been determined. Fogari et al 8 compared the effects of 12-week treatment with the ACE-I imidapril and the ARB candesartan on plasma PAI-1 antigen and its activity, and on plasma t-PA activity in normoweight hypertensive patients. In this study, despite similar blood pressure reduction, imidapril but not candesartan improved the fibrinolytic balance, possibly through bradykinin-mediated effects on insulin sensitivity and endothelial function.…”

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confidence: 99%

Angiotensin-converting enzyme inhibition and fibrinolytic balance

Matsumoto

Horie

2011

Hypertens Res

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F ibrinolytic activity is primarily determined by the balance between the levels of tissue plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1). 1 Impaired fibrinolytic function, characterized by increased PAI-1 level and decreased t-PA activity, has been found in patients with hypertension. The t-PA antigen concentration reflects both active t-PA and inactive t-PA complexed with PAI-1. The t-PA antigen concentration is determined in part by increased PAI-1 level. Free and unbound t-PA is physiologically active and leads to endogenous fibrinolysis.Data from the literature indicate that different antihypertensive drugs may vary in their influence on fibrinolysis. Blood pressure reduction itself could improve the capacity for pharmacologically stimulated t-PA release. 2 There is a growing body of evidence that angiotensin-converting enzyme inhibitors (ACE-I) and angiotensin receptor blockers (ARB) improve endothelial dysfunction. Previous comparative studies have shown that ACE-I and ARB differ in their effects on fibrinolysis. 3,4 ACE-I have generally been shown to improve the fibrinolytic balance by reducing plasma PAI-1 level, and ARB seem to be neutral in their effect. The positive effect of ACE-I on the fibrinolytic system is related to (1) a decrease in the release of angiotensin II-mediated PAI-1; (2) an increase in the release of bradykinin-induced t-PA and (

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Fibrinolysis and insulin sensitivity in imidapril and candesartan (FISIC study) recipients with hypertension

Cited by 15 publications

References 61 publications

Co-effect of insulin resistance and biomarkers of inflammation and endothelial dysfunction on hypertension

Co-effect of insulin resistance and biomarkers of inflammation and endothelial dysfunction on hypertension

Role of angiotensin II in plasma PAI-1 changes induced by imidapril or candesartan in hypertensive patients with metabolic syndrome

Angiotensin-converting enzyme inhibition and fibrinolytic balance

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