Angiotensin II type 1 receptor antagonist decreases plasma levels of tumor necrosis factor alpha, interleukin-6 and soluble adhesion molecules in patients with chronic heart failure

Tsutamoto, Takayoshi; Wada, Atsuyuki; Maeda, Keiko; Mabuchi, Naoko; Hayashi, Meiso; Tsutsui, Takashi; Ohnishi, Masato; Sawaki, Masahide; Fujii, Masazumi; Matsumoto, Takehiro; Kinoshita, Masahiko

doi:10.1016/s0735-1097(99)00594-x

Cited by 172 publications

(94 citation statements)

References 40 publications

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“…sICAM-1 is considered as a pro-inflammatory factor and thus as a possible marker of inflammatory events (Witkowska and Borawska, 2004). Indeed, sICAM-1 levels could be lowered in HF patients by decreasing the cytokines TNF-alpha and IL-6 (Tsutamoto et al, 2000). Thus, our preliminary findings may suggest that sICAM-1 as a pre-clinical indicator of vascular inflammation may predict future depressive symptoms in vulnerable HF patients, which is consistent with a recent review by Dantzer et al (2008).…”

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confidence: 90%

Response regarding inflammation as a predictor of depression in heart failure

Wirtz¹,

Redwine²,

Mills³

2010

Brain, Behavior, and Immunity

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Response regarding inflammation as a predictor of depression in heart failureThe main criticisms by Glover and colleagues of our ''Short Report" (Wirtz et al., 2009) relate primarily to the fact that our study was exploratory, which is fully acknowledged in the paper. However, the point of publishing an exploratory paper is to allow other researchers to view provocative preliminary findings in order to gain insight into promising avenues of investigation. We reported that the circulating inflammatory biomarker sICAM-1 independently predicted depression severity (as assessed by the Beck Depression Inventory (BDI)) in a prospective design at both 12 and 18 months later in 30 heart failure (HF) patients. We controlled for cardiovascular risk factors, indicators of HF severity, and medication intake. This finding potentially suggests that vascular inflammation precedes depression in HF patients. Glover et al. have apparently misunderstood that our findings are limited to HF patients since they attempted negate our findings by using examples from other populations.In the following we will provide a point-by-point-reply to each of the authors' points of contention.

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supporting

confidence: 90%

Response regarding inflammation as a predictor of depression in heart failure

Wirtz¹,

Redwine²,

Mills³

2010

Brain, Behavior, and Immunity

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“…These data are in line with what already observed by other research groups patients affected by hypertension 35 or chronic heart failure. 36 Before the treatment with candesartan, the OFL determined a significantly lower increase in Tg (+17.7 vs. +50.5%) and Hs-CRP (+62.5 vs. +75.0%) in diabetics than in nondiabetic patients. Six months of treatment with candesartan prevented the OFL-related changes in Tg and sICAM-1 level in non-diabetic patients, whereas it was associated to a reduced increase in IL-6 (+28.6 vs. +47.4%) and Hs-CRP (+62.5 vs. +75.0%).…”

Section: Discussionmentioning

confidence: 85%

Candesartan effect on inflammation in hypertension

et al. 2010

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The aim of this study was to evaluate the effect of candesartan on inflammatory biomarkers in hypertensive patients with and without type 2 diabetes mellitus after a standardized oral fat load (OFL). A total of 219 patients were enrolled: 106 patients were assigned to the non-diabetic hypertensive (NH) group, and 113 to the diabetic hypertensive (DH) group. All patients received candesartan therapy for 6 months and underwent a standardized OFL at baseline and after 6 months of therapy. We evaluated systolic blood pressure (SBP) and diastolic blood pressure (DBP), blood glucose (BG), triglycerides (Tg), soluble intercellular adhesion molecule-1 (sICAM-1), interleukin-6 (IL-6) and high-sensitivity C reactive protein (Hs-CRP). At baseline, glycated hemoglobin, homeostasis model assessment insulin resistance index, BG, fasting plasma insulin, Tg, sICAM-1, IL-6 and Hs-CRP in the DH group were significantly higher, whereas high-density lipoprotein-cholesterol value was significantly lower compared to NH group. After 6 months of candesartan therapy, sICAM-1, IL-6 and Hs-CRP were significantly lower compared to baseline in both groups; furthermore, there was a significant decrease of SBP and DBP values in both groups. After the OFL administered at baseline, there was an increase of Tg, sICAM-1, IL-6 and Hs-CRP in both groups. After the OFL administered after 6 months of therapy, instead, there was no significant variation of BG, Tg or sICAM-1 value in both groups, whereas there was an increase of IL-6 and Hs-CRP compared to time 0. We observed that candesartan treatment attenuated the inflammatory answer in both groups of patients, even if more efficiently in nondiabetic ones.

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“…The plasma levels of PRC, Ang II and ALD were measured using commercial radioimmunoassay kits as previously reported. 15,17 Samples for the assay of plasma BNP concentrations were transferred to chilled disposable tubes containing aprotinin (500 kallikrein inactivator units ml À1 ). The blood samples were immediately placed on ice and centrifuged at 4 1C, and then the plasma was frozen in aliquots and stored at À30 1C until assay.…”

Section: Measurement Of Neurohumoral Factorsmentioning

confidence: 99%

“…15 Therefore, we hypothesize that there is a difference in chronic effect on Ang II between candesartan and olmesartan in patients with essential hypertension. In this study, we compared the chronic effects of olmesartan on Ang II in comparison with those of candesartan, as well as the long-term effects of olmesartan on left ventricular mass index (LVMI) in comparison with those of candesartan.…”

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confidence: 99%

Comparison of the long-term effects of candesartan and olmesartan on plasma angiotensin II and left ventricular mass index in patients with hypertension

et al. 2009

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In general, treatment with most angiotensin receptor blockers (ARBs) increases plasma angiotensin II (Ang II) level because of a lack of negative feedback on renin activity. Olmesartan is a potential ARB inducing activation of angiotensin-converting enzyme 2 (ACE2) that hydrolyzes Ang II to Ang 1-7, and has shown a beneficial effect on ventricular remodeling. Indeed, a previous study reported that olmesartan treatment resulted in decreased plasma levels of Ang II and aldosterone. However, there has not yet been a study showing the relationship of chronic effects of olmesartan on Ang II and the left ventricular mass index (LVMI) in comparison with those of other ARB. A total of 50 stable outpatients with essential hypertension who had received candesartan for more than 1 year were randomized into two groups: control group (n¼25): continuous candesartan treatment at a stable dose; and olmesartan group (n¼25): candesartan (8 mg day À1 ) was changed to olmesartan given at a dose of 20 mg day À1 . There was no difference in the baseline characteristics between the two groups. In the control group, there were no significant changes in blood pressure, LVMI or biomarkers during 12 months of study. In the olmesartan group, blood pressure did not change and plasma levels of Ang II decreased during 12 months of study, whereas LVMI was significantly decreased after 12 months (135 ± 36 vs. 123 ± 29 g m À2 ; Po0.01). These findings indicate that replacing candesartan with olmesartan decreased LVMI in association with a sustained decrease of plasma Ang II over a 12-month period without changing blood pressure or plasma aldosterone in patients with essential hypertension.

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Angiotensin II type 1 receptor antagonist decreases plasma levels of tumor necrosis factor alpha, interleukin-6 and soluble adhesion molecules in patients with chronic heart failure

Cited by 172 publications

References 40 publications

Response regarding inflammation as a predictor of depression in heart failure

Response regarding inflammation as a predictor of depression in heart failure

Candesartan effect on inflammation in hypertension

Comparison of the long-term effects of candesartan and olmesartan on plasma angiotensin II and left ventricular mass index in patients with hypertension

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