Effect of a hydrophilic and a hydrophobic statin on cardiac salvage after ST-elevated acute myocardial infarction – A pilot study

Chitose, Tadasuke; Sugiyama, Seigo; Sakamoto, Kenji; Shimomura, Hideki; Yamashita, Takuro; Hokamaki, Jun; Tsunoda, Ryusuke; Shiraishi, Shinya; Yamashita, Yasuyuki; Ogawa, Hisao

doi:10.1016/j.atherosclerosis.2014.08.053

Cited by 19 publications

(15 citation statements)

References 40 publications

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“…A standard echocardiography was performed at 72 h, with apical four-and two-chamber views (11). The researchers who later analyzed echocardiographic images were blinded to information of MACE.…”

Section: Echocardiography Of Patients With MImentioning

confidence: 99%

Association of serum HMGB2 level with MACE at 1 mo of myocardial infarction: Aggravation of myocardial ischemic injury in rats by HMGB2 via ROS

Liu¹,

Dai²,

Ding³

et al. 2017

American Journal of Physiology-Heart and Circulatory Physiology

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High-mobility group box (HMGB) family is related to inflammatory diseases. We investigated whether serum HMGB2 levels are related to myocardial infarction (MI) severity and major adverse cardiac events (MACE) during MI. We included 432 consecutive patients with ST-segment elevation myocardial infarction and 312 controls. Serum HMGB2 levels were significantly higher in MI patients than in controls. Increased HMGB2 levels were associated with MACE and negatively with ejection fraction in MI patients. HMGB2 was an independent determinant of MACE in logistic regression analysis. HMGB2 protein (10 μg) or saline was injected intramyocardially in MI rats, with or without coadministration of the NADPH oxidase inhibitor apocynin. After 72 h, pathological, echocardiographic, and hemodynamic examinations showed that HMGB2 increased infarct size and worsened cardiac function in MI rats. Moreover, HMGB2 administration enhanced reactive oxygen species (ROS) production, cell apoptosis, inflammation, and autophagosome clearance impairment, which were attenuated by coadministration of apocynin or knock down of receptor for advanced glycation end products (RAGE). In conclusion, increased serum HMGB2 levels are associated with MI severity and MACE at 1 mo. HMGB2 promotes myocardial ischemic injury in rats and hypoxic H9C2 cell damage via ROS provoked by RAGE. We demonstrate that serum high-mobility group box 2 is associated with major adverse cardiac events at 1 mo in myocardial infarction patients. Mechanistically, high-mobility group box 2 promotes reactive oxygen species production via receptor for advanced glycation end products signaling in ischemic myocardium, thereby aggravating cell apoptosis, inflammation, and autophagosome clearance impairment. This study reveals that high-mobility group box 2 is a novel factor enhancing ischemic injury in myocardial infarction.

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Section: Echocardiography Of Patients With MImentioning

confidence: 99%

Association of serum HMGB2 level with MACE at 1 mo of myocardial infarction: Aggravation of myocardial ischemic injury in rats by HMGB2 via ROS

Liu¹,

Dai²,

Ding³

et al. 2017

American Journal of Physiology-Heart and Circulatory Physiology

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“…Angiotensin-converting enzyme (ACE)2 is the only homologue of ACE that has been identified to date; it exhibits 42% homologous sequences with ACE (3). ACE2 is an inner membrane carboxypeptidase that can hydrolyze angiotensin 1 (Ang-1) into Ang- (1)(2)(3)(4)(5)(6)(7)(8)(9), and this may be further hydrolyzed by ACE into Ang-(1-7) (4). ACE2 can also remove the terminal tryptophan of Ang-II, thus directly hydrolyzing Ang-II to Ang-(1-7).…”

Section: Introductionmentioning

confidence: 99%

“…Diabetic cardiomyopathy (DCM) is a chronic and complex pathological process that can alter cell metabolism, resulting in damage to the endoplasmic reticulum, mitochondria and other organelles, and ultimately result in myocardial hypertrophy and increased apoptosis (9). Furthermore, apoptosis resulting from altered energy metabolism of the cell serves an additional role in the pathology of DCM; large scale apoptosis can aggravate myocardial remodeling and cause further tissue dysfunction, thus creating a destructive pathogenic cycle (10,11).…”

Section: Introductionmentioning

confidence: 99%

Puerarin reduces ischemia/reperfusion-induced myocardial injury in diabetic rats via upregulation of vascular endothelial growth factor A/angiotensin-1 and suppression of apoptosis

Guo

Xiao

et al. 2018

Mol Med Report

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Puerarin is an active ingredient of pueraria, which has been developed for puerarin injections, used in the treatment of cardiovascular diseases including arrhythmia, myocardial ischemia and hypertension. However, the molecular mechanisms of puerarin on ischemia/reperfusion (I/R)‑induced myocardial apoptosis in diabetic rats are not fully understood. The present study aimed to investigate whether puerarin can attenuate I/R‑induced myocardial apoptosis in diabetic rats, and to investigate the underlying mechanism. A hemodynamic analyzing system was employed to analyze the left ventricular developed pressure (LVDP), the left ventricular end‑systolic interior dimension (LVIDs) and the left ventricular end diastolic interior dimension (LVIDd). ELISA kits were used to analyze malondialdehyde (MDA), superoxide dismutase (SOD), tumor necrosis factor‑α (TNF‑α) and interleukin (IL)‑6 levels, NO production and caspase‑3 activity. Nuclear factor (NF)‑κB, ascular endothelial growth factor A (VEGFA), angiotensin (Ang)‑I, phosphorylated (p)‑endothelial nitric oxide synthase protein expression was analyzed using western blot analysis. Puerarin significantly reduced the myocardial infarct area, and increased left ventricular developed pressure in diabetic rats with myocardial I/R. Oxidative stress, inflammation and nuclear factor‑κB protein expression were significantly reduced by puerarin. Furthermore, puerarin activated the protein expression levels of VEGFA and Ang‑I, and increased nitric oxide production, phosphorylated‑endothelial nitric oxide synthase protein expression and caspase‑3 activity. These results demonstrated that the myocardial protective effect of puerarin serves to reduce myocardial I/R injury, via upregulation of VEGFA/Ang‑1 and suppression of apoptosis, in diabetic rats with myocardial I/R.

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“…A major limitation in almost all studies thus far is the large heterogeneity of AMD disease (more than 100 at-risk genes and several phenotypes) ( Miller, 2013 , Fritsche et al, 2015 ) and lack of standardization in statin dosage ( Gehlbach and Li, 2009 , Gehlbach et al, 2015 ) or lipophilicity ( Wu et al, 2010 , Chitose et al, 2014 , Fong, 2014 ). There is clear evidence from the cardiovascular literature that statin dose does matter ( Cannon et al, 2004 , Pitt et al, 1999 ).…”

Section: Introductionmentioning

confidence: 99%

Regression of Some High-risk Features of Age-related Macular Degeneration (AMD) in Patients Receiving Intensive Statin Treatment

Vavvas¹,

Daniels²,

Kapsala³

et al. 2016

EBioMedicine

128

104

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ImportanceAge-related macular degeneration (AMD) remains the leading cause of blindness in developed countries, and affects more than 150 million worldwide. Despite effective anti-angiogenic therapies for the less prevalent neovascular form of AMD, treatments are lacking for the more prevalent dry form. Similarities in risk factors and pathogenesis between AMD and atherosclerosis have led investigators to study the effects of statins on AMD incidence and progression with mixed results. A limitation of these studies has been the heterogeneity of AMD disease and the lack of standardization in statin dosage.ObjectiveWe were interested in studying the effects of high-dose statins, similar to those showing regression of atherosclerotic plaques, in AMD.DesignPilot multicenter open-label prospective clinical study of 26 patients with diagnosis of AMD and the presence of many large, soft drusenoid deposits. Patients received 80 mg of atorvastatin daily and were monitored at baseline and every 3 months with complete ophthalmologic exam, best corrected visual acuity (VA), fundus photographs, optical coherence tomography (OCT), and blood work (AST, ALT, CPK, total cholesterol, TSH, creatinine, as well as a pregnancy test for premenopausal women).ResultsTwenty-three subjects completed a minimum follow-up of 12 months. High-dose atorvastatin resulted in regression of drusen deposits associated with vision gain (+ 3.3 letters, p = 0.06) in 10 patients. No subjects progressed to advanced neovascular AMD.ConclusionsHigh-dose statins may result in resolution of drusenoid pigment epithelial detachments (PEDs) and improvement in VA, without atrophy or neovascularization in a high-risk subgroup of AMD patients. Confirmation from larger studies is warranted.

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Effect of a hydrophilic and a hydrophobic statin on cardiac salvage after ST-elevated acute myocardial infarction – A pilot study

Cited by 19 publications

References 40 publications

Association of serum HMGB2 level with MACE at 1 mo of myocardial infarction: Aggravation of myocardial ischemic injury in rats by HMGB2 via ROS

Association of serum HMGB2 level with MACE at 1 mo of myocardial infarction: Aggravation of myocardial ischemic injury in rats by HMGB2 via ROS

Puerarin reduces ischemia/reperfusion-induced myocardial injury in diabetic rats via upregulation of vascular endothelial growth factor A/angiotensin-1 and suppression of apoptosis

Regression of Some High-risk Features of Age-related Macular Degeneration (AMD) in Patients Receiving Intensive Statin Treatment

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