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: 3.07

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 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 1.97
Cited half-life 4.00
Immediacy index 0.54
Eigenfactor 0.00
Article influence 0.63
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
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    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
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    ABSTRACT: Current clinical cardiovascular practice requires a clinician to have a strong foundation in multiple aspects of pharmacology. Modern cardiovascular regimens are complex, and optimal management, application of evolving guidelines, and adoption of new therapies build off a more basic understanding of pharmacokinetics and pharmacodynamics. In addition, it is likely time to add a third pillar into this discussion, the expanding field of pharmacogenomics referring to the genetic influences on drug response. This field has increasing applications in medicine and clearly holds significant promise for cardiovascular disease management. Awareness of pharmacogenomic advances and the fundamentals of pharmacokinetics and pharmacodynamics can help the clinician more easily deliver great care. Here we attempt to briefly summarize and simplify key concepts of pharmacokinetics, pharmacodynamics, and pharmacogenomics relevant to the cardiovascular disease practitioner. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 06/2015; DOI:10.1177/1074248415590196
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    ABSTRACT: Direct vasodilators and sympatholytic agents were some of the first antihypertensive medications discovered and utilized in the past century. However, side effect profiles and the advent of newer antihypertensive drug classes have reduced the use of these agents in recent decades. Outcome data and large randomized trials supporting the efficacy of these medications are limited; however, in general the blood pressure-lowering effect of these agents has repeatedly been shown to be comparable to other more contemporary drug classes. Nevertheless, a landmark hypertension trial found a negative outcome with a doxazosin-based regimen compared to a chlorthalidone-based regimen, leading to the removal of α-1 adrenergic receptor blockers as first-line monotherapy from the hypertension guidelines. In contemporary practice, direct vasodilators and sympatholytic agents, particularly hydralazine and clonidine, are often utilized in refractory hypertension. Hydralazine and minoxidil may also be useful alternatives for patients with renal dysfunction, and both hydralazine and methyldopa are considered first line for the treatment of hypertension in pregnancy. Hydralazine has also found widespread use for the treatment of systolic heart failure in combination with isosorbide dinitrate (ISDN). The data to support use of this combination in African Americans with heart failure are particularly robust. Hydralazine with ISDN may also serve as an alternative for patients with an intolerance to angiotensin antagonists. Given these niche indications, vasodilators and sympatholytics are still useful in clinical practice; therefore, it is prudent to understand the existing data regarding efficacy and the safe use of these medications. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 06/2015; DOI:10.1177/1074248415587969
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    ABSTRACT: Testosterone is an anabolic steroid hormone, which is the major circulating androgen hormone in males. Testosterone levels decreasing below the normal physiological levels lead to a status known as androgen deficiency. Androgen deficiency has been shown to be a major risk factor in the development of several disorders, including obesity, metabolic syndrome, and ischemic heart disease. In the past decades, although several studies from animal models as well as clinical studies demonstrated that testosterone exerted cardioprotection, particularly during ischemia-reperfusion (I/R) injury, other preclinical and clinical studies have shown an inverse relationship between testosterone levels and cardioprotective effects. As a result, the effects of testosterone replacement on the heart remain controversial. In this review, reports regarding the roles of testosterone replacement in the heart following I/R injury are comprehensively summarized and discussed. At present, it may be concluded that chronic testosterone replacement at a physiological dose demonstrated cardioprotective effects, whereas acute testosterone replacement can cause adverse effects in the I/R heart. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 05/2015; DOI:10.1177/1074248415587977
  • Journal of Cardiovascular Pharmacology and Therapeutics 05/2015; 20(3):346-7. DOI:10.1177/1074248414560967
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    ABSTRACT: Little is known about ivabradine in cardiac rehabilitation in patients with coronary artery bypass graft (CABG). In this prospective, randomized study, suitable patients admitted for cardiac rehabilitation after recent CABG were randomized to ivabradine 5 mg twice a day + standard medical therapy including bisoprolol 1.25 mg once daily (group I-BB, n = 38) or standard medical therapy including bisoprolol 2.5 to 3.75 mg once daily (group BB, n = 43). Patients were evaluated at admission, discharge, and 3 months. The primary end point was improvement in functional status, and other end points were improvement in diastolic function and recovery of systolic function. End points were assessed by distance covered in 6-minute walking test (6MWT), percentage with normal diastolic function, and percentage increase in left ventricular ejection fraction (LVEF). Cardiac rehabilitation improved functional capacity in both groups. In group BB, distances covered in the 6MWT at admission, discharge, and 3 months were 215 ± 53, 314 ± 32, and 347 ± 42 m, respectively. Corresponding distances in group I-BB were 180 ± 91, 311 ± 58, and 370 ± 55 m. Normal diastolic function was restored in I-BB patients, increasing from 24% at admission to 50% and 79% at discharge and 3 months; in BB patients, it decreased from 23% to 19% and 16%. The LVEF improved in I-BB patients, from 57% ± 3% at admission to 62% ± 4% at discharge and 66% ± 3% at 3 months, while remaining unchanged in BB patients (57% ± 3%, 59% ± 4%, and 59% ± 3%). Adding ivabradine to low-dose bisoprolol during cardiac rehabilitation in patients with CABG improved functional capacity, enhanced recovery of systolic function, and reduced diastolic dysfunction. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 04/2015; DOI:10.1177/1074248415575963
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    ABSTRACT: Intestinal barrier dysfunction would lead to a rigorous inflammatory reaction due to the translocation of intestinal lumen-derived bacteria and endotoxins. The aim of the present study was to investigate whether intestinal barrier dysfunction occurs in patients with acute Stanford type A aortic dissection (ATAAD) and to determine its potential relationship with the plasma levels of several inflammatory biomarkers in the progression of ATAAD. Serum samples from a total of 46 patients with ATAAD and 36 healthy volunteers were prospectively collected and analyzed. The serum levels of diamine oxidase (DAO), lactate dehydrogenase (LDH), interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), and C-reactive protein (CRP) were measured using colorimetric assay, enzyme-linked immunosorbent assay, and immunoturbidimetric assay. Serum levels of DAO, LDH, IL-6, TNF-α, and CRP in patients with ATAAD were significantly higher than those in healthy participants. A significantly positive correlation between DAO activity and IL-6 (r = .56, P < .001), TNF-α (r = .63, P < .001), and CRP (r = .53, P < .001) was observed. Moreover, the activity of DAO correlated negatively with the Pao 2/fraction of inspired oxygen (Fio 2) ratio (r = -.39, P = .007). Intestinal barrier dysfunction, reflected by an increased level of serum DAO, may play an important role in the development of systemic inflammatory responses in patients with ATAAD. Therefore, strategies of preserving a normal intestinal barrier function may open new horizons in the treatment of inflammation-related adverse events in the setting of ATAAD. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 04/2015; DOI:10.1177/1074248415581176
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    ABSTRACT: Atherosclerosis is recognized as a chronic inflammatory disease. The aim of this study was to examine the role of urinary trypsin inhibitor (UTI) in inflammation response induced by hyperlipidemia in rabbits. Thirty rabbits after injury of the right iliac artery endothelium were randomly divided into 3 groups: control group, model group, and UTI group. Iliac arteries were isolated and histology was performed on arterial regions that were injured by balloon after 8 weeks. Neointimal thickness (NT) and neointimal to media radio (N/M) were measured. Blood lipids, interleukin 6, and tumor necrosis factor-α were evaluated. Macrophages were evaluated by immunohistochemical analysis. MicroRNA-181b (miR-181b) was measured by reverse transcriptase-polymerase chain reaction. Urinary trypsin inhibitor therapy decreased serum inflammatory factor levels without significant changes in blood lipids. Compared with model group, UTI reduced macrophage infiltration of iliac artery (13.91 ± 2.03% vs 24.21 ± 8.94%, P < .01). Hyperlipidemia reduced the expression of miR-181b and increased NT and N/M ratio. Systemic administration of UTI rescued miR-181b expression and inhibited neointimal formation. Urinary trypsin inhibitor could reduce neointimal hyperplasia by inhibiting inflammatory response induced by hyperlipidemia and may become a potential antiatherosclerosis supplement. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 04/2015; DOI:10.1177/1074248415578907
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    ABSTRACT: Myocardial ischemia has become one of the main causes of sudden cardiac death worldwide. Autophagy has been demonstrated to protect cardiomyocytes from ischemia/reperfusion (I/R)-induced damage. A novel small molecule compound 2-Chloro-5-[[5-[[5-(4,5-Dimethyl-2-nitrophenyl)-2-furanyl]methylene]-4,5-dihydro-4-oxo-2-thiazolyl]amino]benzoic acid (PT1) has been previously shown to specifically activate 5'-adenosine monophosphate-activated protein kinase (AMPK). Because AMPK activation effectively induces autophagy, we tested the protective efficacy of PT1 on cardiomyocytes after oxygen glucose deprivation/reoxygenation (OGD/R) in vitro. Mouse neonatal cardiomyocytes were treated with PT1 after OGD/R. 3-[4-(1,3-benzodioxol-5-yl)-2-oxo-3-buten-1-yl]-3-hydroxy-1,3-dihydro-2H-indol-2-one (3HOI-BA-01), a novel small compound showing potent inhibitory effect on mammalian target of rapamycin (mTOR) activation, was also tested for its cardioprotective effect, based on the established relationship between mTOR signaling and autophagy. Cell survival and autophagy-related signal pathways were examined after treatment with these agents. Our data indicate that both PT1 and 3HOI-BA-01 enhance cell survival after OGD/R. As expected, both PT1 and 3HOI-BA-01 induced autophagy in cardiomyocytes through activating AMPK pathway and inhibiting mTOR signaling, respectively. Induction of autophagy by PT1 and 3HOI-BA-01 was responsible for their cardioprotective effect, since inhibition of autophagy abolished the protective efficacy. Furthermore, simultaneous administration of PT1 and 3HOI-BA-01 profoundly upregulated autophagy after OGD/R and significantly promoted survival of cardiomyocytes. In vivo administration of PT1 and 3HOI-BA-01 in a murine myocardial (I/R injury model remarkably reduced infarct size and induced autophagy. Taken together, our research suggests that PT1 and 3HOI-BA-01 could be promising therapeutic agents for myocardial ischemia. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 04/2015; DOI:10.1177/1074248415581177
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    ABSTRACT: Pregnane X receptor (PXR) is a transcriptional regulator of many drug-metabolizing enzymes including cytochrome P450 (CYP) 2C9. The objective of this study was to assess the possible association between PXR single-nucleotide polymorphisms (SNPs) and stable warfarin doses. A total of 201 patients with stable warfarin doses from the EwhA-Severance Treatment (EAST) Group of Warfarin were included in this study. The influence of genetic polymorphisms on stable warfarin doses was investigated by genotyping 11 SNPs, that is, vitamin K epoxide reductase complex 1 (VKORC1) rs9934438, CYP2C9 rs1057910, CYP4F2 rs2108622, constitutive androstane receptor (CAR) rs2501873, hepatocyte nuclear factor 4α (HNF4α) rs3212198, and PXR (rs3814055, rs1403526, rs3732357, rs3732360, rs2276707 and rs2472682). Subgroup analysis was conducted on CYP2C9 wild-type homozygote allele (AA) carriers. One PXR SNP of rs2472682 (A>C) exhibited significant association with stable warfarin doses in study population and the subgroup; variant homozygote carriers required significantly lower daily doses of warfarin than those carrying wild allele by about 0.8 mg. Approximate 43.7% of overall interindividual variability in warfarin dose requirement was explained by multivariate regression model. VKORC1, CYP2C9, age, CYP4F2, PXR rs2472682, and CAR/HNF4α rs2501873/rs3212198 accounted for 29.6%, 5.9%, 3.7%, 2.3%, 1.3%, and 0.9% of the variability, respectively. PXR SNP of rs2472682 remained a significant factor in CYP2C9 wild-type homozygote carriers based on univariate and multivariate analyses. The combination of CAR/HNF4α/PXR SNPs of rs2501873/rs3212198/rs2472682 showed about 1 mg dose difference between grouped genotypes in study population and subgroup. Our results revealed that PXR could be a determinant of stable warfarin doses. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 04/2015; DOI:10.1177/1074248415578906
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    ABSTRACT: Statin nonadherence is a major challenge to optimal management. Patients nonadherent to statin therapy do not receive the expected benefit relative to the degree of low-density lipoprotein cholesterol (LDL-C) lowering obtained. This is important because new evidence guidelines recommend statins as the first-line therapy for those in high-risk groups (secondary prevention, patients with diabetes 40-75 years of age, and LDL-C ≥ 190 mg/dL) and in selected primary prevention patients. Statin assignment in the latter group occurs only in those with an estimated ≥7.5% 10-year atherosclerotic cardiovascular disease risk after shared decision making in a clinician-patient risk discussion. However, in numerous studies, statin nonadherence shows little or no benefit in reducing cardiovascular events or mortality compared to placebo, effectively negating the risk reduction expected from statin use and concomitantly increasing the total cost of health care. The causes and solutions for nonadherence are multifactorial and include patient, clinician, and health system factors. We believe that a clinician-patient partnership that facilitates patients' understanding of the potential for optimal benefit with the least adverse effects is an important first step toward improving adherence. A transtheoretical model of stages of behavior change helps clinicians address many of the common factors limiting adherence to statins. We conclude with a teaching tool emphasizing a structured approach to statin therapy with patient-centered risk discussions. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 03/2015; DOI:10.1177/1074248415578170
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    ABSTRACT: Patients who undergo catheter ablation for atrial fibrillation (AF) are at increased risk of developing thromboembolic and bleeding complications periprocedurally. Many patients are now on newer oral anticoagulants (NOACs), but data regarding their safety and efficacy during AF ablation are limited. This article reviews the literature in PubMed from 1998 to 2014 and includes clinical trials and meta-analysis that analyzed the safety and efficacy of NOACs during AF catheter ablation. Dabigatran seems to be as effective and safe as warfarin, although most data are from single-center studies, with small samples and very low overall bleeding and thromboembolic complications. Periprocedural anticoagulation protocols also vary greatly between studies. Some recent meta-analysis has shown that warfarin could still be a safer and more effective alternative. There are fewer studies with rivaroxaban in AF ablation, and there have been no meta-analysis yet comparing rivaroxaban to warfarin or dabigatran. There seems to be no significant differences in safety or efficacy of rivaroxaban compared to warfarin. Interestingly, there are no available data for apixaban in AF ablation yet. There are no consensus guidelines regarding the use of NOACs during AF ablation. Dabigatran and rivaroxaban seem as safe and effective as warfarin, although larger studies with standardized protocols are needed, as available studies may be underpowered to detect small differences in bleeding and thromboembolic rates. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 03/2015; DOI:10.1177/1074248415576193
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    ABSTRACT: Renalase is a protein that can regulate sympathetic nerve activity by metabolizing catecholamines, while redundant catecholamines are thought to contribute to atherosclerosis (As). Catecholamine release can be facilitated by angiotensin (Ang) II by binding to Ang II type 1 (AT1) receptors. Valsartan, a special AT1 antagonist, can dilate blood vessels and reduce blood pressure, but it remained unclear whether valsartan can promote the stability of atherosclerotic plaque by affecting renalase. This study examined the tissue distribution of renalase in ApoE(-/-) mice fed with a high-fat diet and the effect of valsartan on expression of renalase. ApoE(-/-) mice were fed with a high-fat diet for 13 or 26 weeks. As a control, 10 C57BL mice were fed with a standard chow diet. After 13 weeks on the high-fat diet, the ApoE(-/-) mice were randomized (10 mice/group) and treated with valsartan, simvastatin, or distilled water (control group) for an additional 13 weeks accompanied by a high-fat diet. Knockout of ApoE caused a dramatic increase in expression of renalase in mice adipose tissue. With the disturbance of lipid metabolism induced by a high-fat diet, renalase expression decreased in the liver. Renalase can be expressed in smooth muscle cells and M2 macrophages in atherosclerotic plaque, and its expression gradually decreases in the fibrous cap during the transition from stable to vulnerable atherosclerotic plaque. Valsartan, an AT1 receptor antagonist, promotes the stabilization of atherosclerotic plaque by increasing the levels of renalase in serum and the expression of renalase in the fibrous cap of atherosclerotic plaque. It also reduces triglyceride levels in serum and increases the expression of renalase in the liver. Renalase may be a potential-related gene of lipid metabolism and As, and it may be the possible molecular target of valsartan to help stabilize atherosclerotic plaque. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 03/2015; DOI:10.1177/1074248415575967