Effect of Direct Renin Inhibitor, Aliskiren, on Peripheral Blood Monocyte Subsets and Myocardial Salvage in Patients With Primary Acute Myocardial Infarction

Ozaki, Yuichi; Imanishi, Toshio; Tanimoto, Takashi; Kashiwagi, Manabu; Tsujioka, Hiroto; Sougawa, Hiromichi; Orii, Makoto; Shiono, Yasutsugu; Shimamura, Kazuo; Ishibashi, Keiichiro; Komukai, Kenichi; Ino, Yasushi; Kitabata, Hironori

doi:10.1253/circj.cj-12-0006

Cited by 7 publications

(3 citation statements)

References 24 publications

(9 reference statements)

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“…It appears that the healing process may be controlled by the use of direct renin inhibitor (aliskiren) in addition to angiotensin‐converting enzyme inhibitors or angiotensin II type 1 receptor blockers. This therapy improved the extent of myocardial salvage after AMI, probably through decrease in numbers of CD14+CD16‐ monocytes .…”

Section: Monocytes In Acssmentioning

confidence: 95%

The Role of Different Monocyte Subsets in the Pathogenesis of Atherosclerosis and Acute Coronary Syndromes

et al. 2015

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The inflammation underlying both atherosclerosis and acute coronary syndromes is strongly related to monocyte-related actions. However, different monocyte subsets can play differential roles in the formation and destabilization of atherosclerotic plaque as well as healing of damaged myocardial tissue. Monocytes are currently being divided into three functionally distinct subsets with different levels of CD14 (cluster of differentiation 14) and CD16 expression. Thus, there are classical CD14++CD16-, intermediate CD14++CD16+ and nonclassical CD14+CD16++ monocytes. Here, we summarize the current knowledge on complex activities of different monocyte subsets in atherosclerosis and acute coronary syndromes. Moreover, we discuss which monocyte subsets can serve either as predictive biomarkers of cardiovascular risk or as potential targets used in atherosclerosis and its complications.

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Section: Monocytes In Acssmentioning

confidence: 95%

The Role of Different Monocyte Subsets in the Pathogenesis of Atherosclerosis and Acute Coronary Syndromes

et al. 2015

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“…11) We previously reported that both PRA and aldosterone levels were reduced by direct renin inhibitor (DRI) treatment in addition to ACEI or ARB therapy in primary AMI patients. 12) Based on these fi ndings, we hypothesized that adding a DRI to conventional ACEI or ARB treatment could be benefi cial in controlling the PRA and aldosterone levels in AMI patients, leading to an improvement in LVR in the chronic phase. The aim of this study was to examine whether DRI treatment has an additive effect on LVR in patients with primary AMI receiving conventional therapy including ACEIs or ARBs.…”

Section: Eft Ventricular Remodeling (Lvr) Occurs In Response Tomentioning

confidence: 99%

Effect of Direct Renin Inhibitor on Left Ventricular Remodeling in Patients With Primary Acute Myocardial Infarction

et al. 2014

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SummarySome patients with acute myocardial infarction (AMI) have a poor prognosis due to left ventricular remodeling (LVR), resulting in the recurrence of congestive heart failure even when therapy with angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin II type 1 receptor blockers (ARBs) has been initiated. We investigated the effect of early administration of the direct renin inhibitor (DRI) aliskiren in combination with an ACEI or an ARB on LVR using cardiac magnetic resonance (CMR) imaging in patients with AMI.Twenty-one consecutive patients were treated with an ACEI or an ARB (non-DRI group), and another 21 consecutive patients received aliskiren 150 mg/day combined with an ACEI or an ARB (DRI group). CMR imaging was performed 7 days after AMI and 10 months later.CMR imaging revealed no signifi cant changes in LV end-systolic volume, LV end-diastolic volume, or LV ejection fraction between the patients with and without DRI aliskiren. In the DRI group, plasma renin activity was signifi cantly lower in both the acute and chronic phases; however, aldosterone levels were signifi cantly lower in the acute but not the chronic phase.A low dose of aliskiren may be insuffi cient to maintain suppression of aldosterone under current standard therapies with an ACEI or an ARB and β-blocker in patients with primary AMI, and results in no attenuation of LVR. (Int Heart J 2014; 55: 17-21) Key words: Magnetic resonance imaging L eft ventricular remodeling (LVR) occurs in response to myocardial damage 1) and is a strong predictor of both heart failure and cardiovascular death after myocardial infarction (MI).2) Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II type 1 receptor blockers (ARBs) are common therapies for preventing LVR after MI and have generally obtained a consensus.3-6) Furthermore, early treatment with ACEIs or ARBs is effective for preventing LVR after MI. 7) However, some patients show a poor prognosis due to LVR resulting in recurrence of congestive heart failure, even when ACEI or ARB therapy has been initiated. Interpreting the progression of LVR can be partly achieved by evaluating the aldosterone escape phenomenon in patients who receive ACEIs 8,9) or by the elevation of plasma renin activity (PRA) due to negative feedback. Moreover, extracted aldosterone plays an important role in modulating post-infarct LVR, 10) and suppression of aldosterone levels improved LVR after acute MI (AMI). 11)We previously reported that both PRA and aldosterone levels were reduced by direct renin inhibitor (DRI) treatment in addition to ACEI or ARB therapy in primary AMI patients.12) Based on these fi ndings, we hypothesized that adding a DRI to conventional ACEI or ARB treatment could be benefi cial in controlling the PRA and aldosterone levels in AMI patients, leading to an improvement in LVR in the chronic phase. The aim of this study was to examine whether DRI treatment has an additive effect on LVR in patients with primary AMI receiving conventional therapy including ACEIs or ARBs. Met...

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“…Furthermore, addition of the renin inhibitor aliskiren suppresses circulating numbers of classical monocytes and increases myocardial salvage after acute MI. 41 A direct role for monocytes in the progression of coronary artery disease was recently observed in a prospective, placebo-controlled phase II clinical trial assessing the effects of intravenous administration of liposomal alendronat (LABR-312, Biorest) on percutaneous coronary intervention and stenting. Monocytes and macrophages are transiently depleted after the uptake of LABR-312 liposomes as a result of intracellular accumulation of toxic levels of bisphosphonates and the induction of apoptosis.…”

mentioning

confidence: 98%

Monocyte Fate in Atherosclerosis

Hilgendorf

Świrski

Robbins

2015

ATVB

167

122

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Abstract-Monocytes and their descendant macrophages are essential to the development and exacerbation of atherosclerosis, a lipid-driven inflammatory disease. Lipid-laden macrophages, known as foam cells, reside in early lesions and advanced atheromata. Our understanding of how monocytes accumulate in the growing lesion, differentiate, ingest lipids, and contribute to disease has advanced substantially over the last several years. These cells' remarkable phenotypic and functional complexity is a therapeutic opportunity: in the future, treatment and prevention of cardiovascular disease and its complications may involve specific targeting of atherogenic monocytes/macrophages and their products.

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Effect of Direct Renin Inhibitor, Aliskiren, on Peripheral Blood Monocyte Subsets and Myocardial Salvage in Patients With Primary Acute Myocardial Infarction

Cited by 7 publications

References 24 publications

The Role of Different Monocyte Subsets in the Pathogenesis of Atherosclerosis and Acute Coronary Syndromes

The Role of Different Monocyte Subsets in the Pathogenesis of Atherosclerosis and Acute Coronary Syndromes

Effect of Direct Renin Inhibitor on Left Ventricular Remodeling in Patients With Primary Acute Myocardial Infarction

Monocyte Fate in Atherosclerosis

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