Journal of Cardiovascular Pharmacology and Therapeutics Impact Factor & Information

Publisher: Hindawi Publishing Corporation, SAGE Publications

Journal description

Every informative issue of the Journal of Cardiovascular Pharmacology and Therapeutics (JCPT) offers cardiologists, clinical pharmacologists and researchers involved in disease relevant clinical and experimental investigations of newer cardiovascular drugs and other therapeutic options.

Current impact factor: 2.09

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 2.094
2013 Impact Factor 3.072
2012 Impact Factor 2.38
2011 Impact Factor 1.753
2010 Impact Factor 1.969
2009 Impact Factor 1.871
2008 Impact Factor 1.672
2007 Impact Factor 1.485
2006 Impact Factor 1

Impact factor over time

Impact factor

Additional details

5-year impact 1.99
Cited half-life 3.90
Immediacy index 1.13
Eigenfactor 0.00
Article influence 0.59
Website Journal of Cardiovascular Pharmacology and Therapeutics website
ISSN 1940-4034
OCLC 321528431
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

SAGE Publications

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Authors retain copyright
    • Pre-print on any website
    • Author's post-print on author's personal website, departmental website, institutional website or institutional repository
    • On other repositories including PubMed Central after 12 months embargo
    • Publisher copyright and source must be acknowledged
    • Publisher's version/PDF cannot be used
    • Post-print version with changes from referees comments can be used
    • "as published" final version with layout and copy-editing changes cannot be archived but can be used on secure institutional intranet
    • Must link to publisher version with DOI
    • Publisher last reviewed on 29/07/2015
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: The effect of oral beta-blocker therapy on long-term mortality in patients with ST-segment elevation myocardial infarction (STEMI) who are treated with primary percutaneous coronary intervention (PCI) and who have preserved left ventricular ejection fraction (LVEF) remains unclear. Methods: We searched MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials for studies evaluating the effect of oral beta-blocker therapy in patients with STEMI who underwent primary PCI and who had preserved LVEF. The primary outcome was all-cause mortality. Randomized controlled trials and the observational studies that reported an adjusted hazard ratio (or hazard ratio in the propensity score-matched patients) with follow-up duration equal to or more than 6 months were included. Pooled hazard ratio with 95% confidence interval (CI) was calculated using a random effect model. Results: No randomized controlled trials met the inclusion criteria. Seven observational studies totaling 10 857 patients met the inclusion criteria. Follow-up duration ranged from 6 months to 5.2 years. Preserved LVEF was defined as 40% in 4 studies and 50% in 3 studies. Based on the pooled estimate, oral beta-blocker therapy was associated with a reduction in all-cause mortality (combined hazard ratio 0.79, 95% CI 0.65-0.97). Conclusion: This meta-analysis demonstrates that oral beta-blocker therapy is associated with decreased all-cause mortality in patients with STEMI who are treated with primary PCI and who have preserved LVEF. This supports the current American College of Cardiology Foundation/American Heart Association 2013 Guideline for the Management of STEMI.
    Journal of Cardiovascular Pharmacology and Therapeutics 10/2015; DOI:10.1177/1074248415608011
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    ABSTRACT: Background: A highly efficient approach to select microRNA (miRNA) targets is a key to develop a miRNA-based therapeutic approach to cardiac ischemia-reperfusion (I/R). To reverse the change induced by disease, I/R in this case, is the traditional strategy to develop therapeutic drugs. However, examples show that it will not always serve the purpose. In this study, we demonstrate an additional approach of selecting miRNA targets with therapeutic potential following cues from cardioprotection-induced changes rather than by reversing disease-induced changes in cardiac I/R. Methods: Isolated perfused rat hearts subjected to I/R were treated with 50 μmol/L sodium hydrosulfide (NaHS) or 10 nmol/L urocortin 2 (UCN2). Cardiac miRNA regulations were determined by miRNA array. Functional screening of selected miRNA mimics, assessed by WST (2-(4-Iodophenyl)-3-(4-nitrophenyl)-5-(2,4-disulfophenyl)-2H-tetrazolium, monosodium salt) activity and lactate dehydrogenase (LDH) release, was performed in H9c2 and neonatal rat ventricular myocytes (NRVMs) with hypoxia/reoxygenation. RNA-induced silencing complex (RISC)-loaded miRNAs caused by mimic transfection were quantified following argonaute-2 immunoprecipitation. Gene regulations of 1 selected miRNA were determined by quantitative polymerase chain reaction and Western blot. Results: Treatment with NaHS and UCN2 significantly improved cardiac function and reduced LDH release. The miRNA array indicated a panel of commonly up- and downregulated miRNAs. Among them, 10 upregulated miRNAs with antiapoptotic and antiautophagy potentials were selected for further screening. Mimics of miRNA-221, -150, and -206 were protective in both H9c2 and NRVM. RISC-loaded miRNAs were up by ∼20-fold above. To further prove the feasibility of this approach, miRNA-221 was studied. It reduced I/R-induced caspase 3/7 activity and LC3-II (microtubule-associated protein 1 light chain 3). Measuring genes predicted to regulate apoptosis and autophagy, miRNA-221 mimic decreased Ddit4, TP53inp1, and p27 at both messenger RNA (mRNA) and protein levels, and reduced mRNA of Bak1 and Puma and proteins of Bim and Bmf. Conclusion: Mimicking miRNA changes caused by cardioprotective agents, combined with functional screening, enables investigators to efficiently identify novel miRNAs with therapeutic potential in cardiac I/R.
    Journal of Cardiovascular Pharmacology and Therapeutics 09/2015; DOI:10.1177/1074248415604463
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    ABSTRACT: Introduction: The Langendorff perfused isolated mouse heart model is commonly used to assess the efficacy of cardioprotective therapies, although the duration of ischemia and reperfusion vary considerably between different laboratories. We aimed to provide a thorough characterization of the model with different durations of ischemia and reperfusion by means of 2 different end points-infarct size (IS) using triphenyltetrazolium staining and lactate dehydrogenase (LDH) release. Methods: C57/BL6 mice hearts were retrograde perfused on a Langendorff apparatus and allocated into 9 groups in a 3 × 3 factorial design-3 ischemic durations (25, 35, and 45 minutes) matched by 3 reperfusion durations (60, 120, and 180 minutes). A protocol of ischemic preconditioning (IPC) was applied to investigate IS and LDH kinetics with different ischemic durations. Results: Infarct size progressively increased with the duration of both ischemia and reperfusion and was found to be independently associated with both determinants. In terms of LDH release kinetics, a peak was observed within the first 10 to 15 minutes of reperfusion and steadily declined thereafter, although a second smaller peak was observed in the 25-minute ischemia group. Only LDH peak release was associated with the ischemia length, with area under the curve (AUC) failing to follow ischemic duration. Interestingly, while IPC reduced IS in all ischemic durations investigated, a significant attenuation of LDH AUC was only observed in the 25-minute index ischemia group. Only a moderately positive correlation was observed between IS and LDH peak (R = .547, P = .006) and AUC (R = .664, P < .001). Conclusion: Myocardial IS measured by triphenyltetrazolium staining depends on both the duration of ischemia and the length of the reperfusion period. The LDH assessment may not be the most reliable tool to assess IS and/or to examine cardioprotective effectiveness at various times of ischemia.
    Journal of Cardiovascular Pharmacology and Therapeutics 09/2015; DOI:10.1177/1074248415604462
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    ABSTRACT: Acute medical illnesses are associated with a prolonged elevation in inflammatory markers that predisposes patients to thrombosis beyond the duration of their hospital stay. In parallel, both observational and randomized data have demonstrated a rate of postdischarge venous thromboembolic events that often exceeds that observed in the hospital setting. Despite this significant residual risk of venous thromboembolic events following discharge among acute medically ill patients, no therapeutic strategies have been recommended to address this unmet need. Available randomized trials have demonstrated the efficacy of extending the duration of thromboprophylaxis with available anticoagulants; however, the efficacy is offset, at least in part, by an increase in bleeding events. Identification of the optimal therapeutic strategies, treatment duration, and risk assessment tools that reconcile both efficacy and safety of extended-duration thromboprophylaxis among acute medically ill patients is an area of ongoing investigation. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 09/2015; DOI:10.1177/1074248415601894
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    ABSTRACT: Statin therapy has been thought to improve outcomes in cardiac surgeries. We aimed to determine the statin effects on the development of postoperative atrial fibrillation (AF), hospital length of stay (LOS), and inflammatory status in patients undergoing cardiac surgeries. A systematic literature search in databases was performed, until January 2015. Randomized clinical trial (RCT) studies evaluating statin effect on statin-naive patients with sinus rhythm undergoing cardiac surgeries were eligible to be analyzed. Twelve RCTs involving 1116 patients, 559 receiving statin and 557 receiving control regimen, were analyzed. Postoperative AF occurred in 17.9% and 36.1% of patients in the statin and control groups, respectively. The statin therapy was associated with decreases in the postoperative AF (risk ratio [RR] 0.50, 95% confidence interval [CI] 0.41-0.61, P < .000010), hospital LOS (mean difference in days, RR -0.44, 95% CI -0.67 to -0.20, P = .0002), and postoperative C-reactive protein (CRP) compared with control (mean difference in mg/L, RR -12.37, 95% CI -23.87 to -0.87, P = .04). The beneficial effects on AF and CRP were more marked in patients receiving atorvastatin compared to other statins. Decrease in postoperative AF was greater in coronary artery bypass graft surgery compared to that in isolated valvular surgery. Perioperative statin therapy in statin-naive patients with sinus rhythm undergoing cardiac surgeries was associated with decreases in the development of postoperative AF, the hospital LOS, and the CRP level. However, there were insufficient data to provide evidences regarding statin impacts in patients undergoing isolated valvular surgery. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 09/2015; DOI:10.1177/1074248415602557
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    ABSTRACT: Cardiomyocyte apoptosis by coronary microembolization (CME) contributes to myocardial dysfunction, in which mitochondrial pathway and death receptor pathway are activated. Lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1) is a membrane protein involved in apoptosis. The study aimed to explore the role of LOX-1 in the activation of these 2 major apoptotic pathways. Twenty Bama miniature swine were randomized into 4 groups (n = 5 per group). The groups were Sham, CME, LOX-1 small-interfering RNA (siRNA), and control siRNA. Microspheres were injected into the left anterior descending artery of swine to establish CME model. Twelve hours after operation, cardiac function, serum c-troponin I level, microinfarct, and apoptotic index were examined. The levels of LOX-1, Bcl-2, Bax, cytochrome c as well as cleaved caspase 9, -8, and -3 were detected. Myocardial dysfunction, enhanced serum c-troponin I, microinfarct, and apoptosis were induced following CME. Moreover, CME induced increased expression of LOX-1, Bax, cytochrome c, cleaved caspase 9, -8, and -3 as well as decreased Bcl-2 expression levels. The LOX-1 siRNA reversed these effects by CME except cleaved caspase 8 expression, while the control siRNA had no effect. Coronary microembolization induces cardiomyocyte apoptosis via the LOX-1-dependent mitochondrial pathway and caspase 8-dependent pathway. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 08/2015; DOI:10.1177/1074248415599265
  • Journal of Cardiovascular Pharmacology and Therapeutics 08/2015; DOI:10.1177/1074248415599266
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    ABSTRACT: Supplemental oxygen has been used in the setting of acute myocardial infarction (AMI). Once an official recommendation in the guidelines for the management of acute ST-segment elevation myocardial infarction, it is now mentioned as an intervention to be considered. Data for the use of supplemental oxygen or AMI are limited, and some data have suggested associated harm. We performed a systematic review of the literature and a subsequent meta-analysis of the data to determine the effect of high concentration oxygen versus titrated oxygen or room air in the setting of AMI. The following end points were studied: in-hospital mortality, opiate use, percentage of infarcted myocardium by magnetic resonance imaging (MRI), and mass of infarcted myocardium by MRI. No significant difference was noted with end points when comparing those randomized to high-concentration oxygen versus those randomized to titrated oxygen or room air in the setting of AMI. No significant publication bias was identified although this could not be assessed for all end points. High-concentration oxygen may not offer any benefit when compared to titrated oxygen or room air. A large, randomized trial is warranted to further delineate these differences with respect to multiple end points. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 08/2015; DOI:10.1177/1074248415598004
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    ABSTRACT: Gingerol inhibits growth of cancerous cells; however, its role in vascular smooth muscle cell (VSMC) proliferation is not known. The present study investigated the effect of gingerol on VSMC proliferation in cell culture and during neointima formation after balloon injury. Rat VSMCs or carotid arteries were harvested at 15 minutes, 30 minutes, 1, 6, 12, and 24 hours of fetal bovine serum (FBS; 10%) stimulation or balloon injury, respectively. Gingerol prevented FBS (10%)-induced proliferation of VSMCs in a dose-dependent manner (50 μmol/L-400 μmol/L). The FBS-induced proliferating cell nuclear antigen (PCNA) upregulation and p27(Kip1) downregulation were also attenuated in gingerol (200 μmol/L) pretreated cells. Fetal bovine serum-induced p38 mitogen-activated protein kinase (MAPK) activation, PCNA upregulation, and p27(Kip1) downregulation were abrogated in gingerol (200 μmol/L) and p38 MAPK inhibitor (SB203580, 10 μmol/L) pretreated cells. Balloon injury induced time-dependent p38 MAPK activation in the carotid artery. Pretreatment with gingerol (200 μmol/L) significantly attenuated injury-induced p38 MAPK activation, PCNA upregulation, and p27(Kip1) downregulation. After 14 days of balloon injury, intimal thickening, neointimal proliferation, and endothelial dysfunction were significantly prevented in gingerol pretreated arteries. In isolated organ bath studies, gingerol (30 nmol/L-300 μmol/L) inhibited phenylephrine-induced contractions and induced dose-dependent relaxation of rat thoracic aortic rings in a partially endothelium-dependent manner. Gingerol prevented FBS-induced VSMC proliferation and balloon injury-induced neointima formation by regulating p38 MAPK. Vasodilator effect of gingerol observed in the thoracic aorta was partially endothelium dependent. Gingerol is thus proposed as an attractive agent for modulating VSMC proliferation, vascular reactivity, and progression of vascular proliferative diseases. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 08/2015; DOI:10.1177/1074248415598003
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    ABSTRACT: Atrial fibrillation (AF) is associated with an increased risk of thromboembolic events. Many patients with AF receive chronic anticoagulation, either with vitamin K antagonists (VKAs) or with non-VKA oral anticoagulants (NOACs). We sought to analyze variables associated with prescription of NOAC. Patients with AF under anticoagulation treatment were prospectively recruited in this observational registry. The sample comprised 1290 patients under chronic anticoagulation for AF, 994 received VKA (77.1%) and 296 NOAC (22.9%). Univariate and multivariate analyses were performed to identify variables associated with use of NOAC. Mean age was 73.8 ± 9.4 years, and 42.5% of the patients were women. The CHA2DS2-VASc score was 0 in 4.9% of the population, 1 in 24.1%, and ≥2 in 71% (median = 4, interquartile range = 2). Variables associated with NOAC treatment were major bleeding (odds ratio [OR] = 3.36; confidence interval [CI] 95%: 1.73-6.51; P < .001), hemorrhagic stroke (OR = 3.19; CI 95% 1.00-10.15, P = .049), university education (OR = 2.44; CI 95%: 1.55-3.84; P < .001), high diastolic blood pressure (OR = 1.02; CI 95%: 1.00-1.03; P = .006), and higher glomerular filtration rate (OR 1.01, CI 95% 1.00-1.01; P = .01). And variables associated with VKA use were history of cancer (OR = 0.46; CI 95%: 0.25-0.85; P = .013) and bradyarrhythmia (OR = 0.40; CI 95% 0.19-0.85; P = .020). Medical and social variables were associated with prescription of NOAC. Major bleeding, hemorrhagic stroke, university education, and higher glomerular filtration rate were more frequent among patients under NOAC. On the contrary, patients with history of cancer or bradyarrhythmias more frequently received VKA. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 07/2015; DOI:10.1177/1074248415596426
  • Journal of Cardiovascular Pharmacology and Therapeutics 07/2015; 38(supplement 1):110.
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    ABSTRACT: During ischemia/reperfusion (I/R), ribosomal S6 kinase (RSK) activates Na(+)/H(+) exchanger 1 (NHE1) by phosphorylating NHE1 at serine 703 (pS703-NHE1), which promotes cardiomyocyte death and injury. Pharmacologic inhibition of NHE1 effectively protects animal hearts from I/R. However, clinical trials using NHE1 inhibitors failed to show benefit in patients with acute myocardial infarction (MI). One possible explanation is those inhibitors block both agonist-stimulated activity (increasing I/R injury) and basal NHE1 activity (necessary for cell survival). We previously showed that dominant-negative RSK (DN-RSK) selectively blocked agonist-stimulated NHE1 activity. Therefore, we hypothesized that a novel RSK inhibitor (BIX02565) would blunt agonist-stimulated NHE1 and protect hearts from I/R. Serum/angiotensin II-stimulated pS703-NHE1 was significantly decreased by BIX02565 in cultured cells. Intracellular pH recovery assay showed that BIX02565 selectively inhibited serum-stimulated NHE1 activity. Ischemia/reperfusion decreased left ventricular-developed pressure (LVDP; inhibited) to 8.7% of the basal level in non-transgenic littermate control (NLC) mouse hearts, which was significantly improved (44.6%) by BIX02565. Similar protection was observed in vehicle-treated, cardiac-specific DN-RSK-Tg mice (43%). No additional protective effect was seen in BIX02565-treated DN-RSK-Tg hearts. BIX02565 also improved LVDP in cardiac-specific wild-type (WT)-RSK-Tg mouse hearts (7.4%-40.9%, P < .01). Finally, Western Blotting results confirmed DN-RSK and BIX02565 significantly decreased I/R-induced pS703-NHE1. The RSK plays a crucial role in I/R-induced activation of NHE1 and cardiac injury. The RSK inhibition may provide an alternative target for patients with MI. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 06/2015; DOI:10.1177/1074248415591700
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    ABSTRACT: The development of heart failure is associated with changes in the size, shape, and structure of the heart that has a negative impact on cardiac function. These pathological changes involve excessive extracellular matrix deposition within the myocardial interstitium and myocyte hypertrophy. Alterations in fibroblast phenotype and myocyte activity are associated with reprogramming of gene transcriptional profiles that likely requires epigenetic alterations in chromatin structure. The aim of our work was to investigate the potential of a currently licensed anticancer epigenetic modifier as a treatment option for cardiac diseases associated with hypertension-induced cardiac hypertrophy and fibrosis. The effects of DNA methylation inhibition with 5-azacytidine (5-aza) were examined in a human primary fibroblast cell line and in a spontaneously hypertensive rat (SHR) model. The results from this work allude to novel in vivo antifibrotic and antihypertrophic actions of 5-aza. Administration of the DNA methylation inhibitor significantly improved several echocardiographic parameters associated with hypertrophy and diastolic dysfunction. Myocardial collagen levels and myocyte size were reduced in 5-aza-treated SHRs. These findings are supported by beneficial in vitro effects in cardiac fibroblasts. Collagen I, collagen III, and α-smooth muscle actin were reduced in a human ventricular cardiac fibroblast cell line treated with 5-aza. These findings suggest a role for epigenetic modifications in contributing to the profibrotic and hypertrophic changes evident during disease progression. Therapeutic intervention with 5-aza demonstrated favorable effects highlighting the potential use of this epigenetic modifier as a treatment option for cardiac pathologies associated with hypertrophy and fibrosis. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 06/2015; DOI:10.1177/1074248415591698
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    ABSTRACT: The β3-adrenoceptor (β3-AR) is implicated in cardiac remodeling. Since metabolic dysfunction due to loss of mitochondria plays an important role in heart diseases, we examined the effects of β3-AR on mitochondrial biogenesis and energy metabolism in atrial fibrillation (AF). Atrial fibrillation was created by rapid atrial pacing in adult rabbits. Rabbits were randomly divided into 4 groups: control, pacing (P7), β3-AR antagonist (L748337), and β3-AR agonist (BRL37344) groups. Atrial effective refractory period (AERP) and AF induction rate were measured. Atrial concentrations of adenine nucleotides and phosphocreatine were quantified through high-performance liquid chromatography. Mitochondrial DNA content was determined. Real-time polymerase chain reaction and Western blot were used to examine the expression levels of signaling intermediates related to mitochondrial biogenesis. After pacing for 7 days, β3-AR was significantly upregulated, AERP was reduced, and the AF induction rate was increased. The total adenine nucleotides pool was significantly reduced due to the decrease in adenosine triphosphate (ATP). The P7 group showed decreased activity of F0F1-ATPase. Mitochondrial DNA content was decreased and mitochondrial respiratory chain subunits were downregulated after pacing. Furthermore, expression of transcription factors involved in mitochondrial biogenesis, including peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), nuclear respiratory factor 1 (NRF-1), and mitochondrial transcription factor A (Tfam), was lower in the P7 group in response to β3-AR activation. Further stimulation of β3-AR with BRL37344 exacerbated these effects, together with a significant decrease in the levels of phosphocreatine. In contrast, inhibition of β3-AR with L748337 partially restored mitochondrial biogenesis and energy metabolism of atria in the paced rabbits. The activation of β3-AR contributes to atrial metabolic remodeling via transcriptional downregulation of PGC-1α/NRF-1/Tfam pathway that are involved in mitochondrial biogenesis, which ultimately perturbs mitochondrial function in rapid pacing-induced AF. The β3-AR is therefore a potential novel therapeutic target for the treatment or prevention of AF. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 06/2015; DOI:10.1177/1074248415590440
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    ABSTRACT: It is uncertain whether remote ischemic conditioning (RIC) has a protective effect on contrast-induced acute kidney injury (CI-AKI) after percutaneous coronary intervention (PCI)/coronary artery angiography (CAG). We performed a meta-analysis of randomized controlled trials (RCTs) to assess the effect of RIC on CI-AKI in such patients. PubMed, MEDLINE, EMBASE,, and the Cochrane Central Register of Controlled Trials databases were searched for RCTs that assessed the effect of RIC on CI-AKI in patients undergoing PCI/CAG. Ten RCTs with 1389 patients (RIC group, 757 and control, 632) were included. The RIC group significantly exerted a lower risk of CI-AKI compared to the controls (odds ratio [OR] = 0.52, 95% confidence interval [CI] = 0.34-0.77, P = .001), and they had the similar effect on major adverse cardiovascular events within 1 year (OR = 0.36, 95% CI = 0.20-0.66, P < .001). The RIC reduced the rates of death within 30 days, but this was not significant (OR = 0.16, 95% CI = 0.02-1.34, P = .091). The RIC was associated with a significantly lower incidence of CI-AKI in patients following elective PCI/CAG (OR = 0.54, 95% CI = 0.33-0.87, P = .011). The RIC before not after the intervention was effective in reducing the occurrence of CI-AKI (OR: 0.37 vs 1.05, P = .022). The RIC of the upper arm has statistically significant effect on protecting CI-AKI but not that of the lower limb (OR: 0.41 vs 1.41, P = .004). The effect of RIC on CI-AKI was similar between patients with a mean estimated glomerular filtration rate <60 mL/min/1.73 m(2) and those with mean rates ≥60 (OR: 0.23 vs 0.41, P = .333). The RIC reduced the incidence of CI-AKI in those receiving PCI/CAG. And RIC of the upper arm significantly reduced the risk of CI-AKI but not RIC of the lower limb in patients undergoing PCI/CAG. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 06/2015; DOI:10.1177/1074248415590197
  • Journal of Cardiovascular Pharmacology and Therapeutics 06/2015; DOI:10.1177/1074248415591699
  • Journal of Cardiovascular Pharmacology and Therapeutics 06/2015; DOI:10.1177/1074248415591701