Journal of Cardiovascular Pharmacology and Therapeutics (J CARDIOVASC PHARM T)

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

2016 Impact Factor Available summer 2017
2014 / 2015 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

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: Impact of atrial fibrillation on clinical outcomes is well recognized, and application of renin-angiotensin-aldosterone system (RAAS) blockers for the prevention of atrial fibrillation (AF) is a theoretically appealing concept. However, clinical trials have yielded inconsistent results. Methods: A pooled study of 26 randomized controlled trials (RCTs) assessing the efficacy of RAAS blockers on AF prophylaxis was performed. Results: A total of 28 reports from 26 randomized controlled trials enrolled 165 387 patients, with an overall 24% reduction in the incidence of AF (odds ratio [OR]: 0.76, 95% confidence interval [CI]: 0.68-0.85], P = .000). Forty-nine percent reduction in the incidence of AF (OR: 0.51, 95% CI: 0.30-0.85, P = .010) in systolic heart failure was observed, whereas no significant effect was observed in patients with diastolic heart failure, postmyocardial infarction, and high cardiovascular disease risk. There was a 19% (OR: 0.81, 95% CI: 0.67-1.00, P = .037) reduction in new-onset and 54% (OR: 0.46, 95% CI: 0.33-0.62, P = .000) reduction in recurrent AF in hypertensive patients with 39% (OR: 0.61, 95% CI: 0.44-0.84, P = .003) risk reduction against calcium blockers and 41% (OR: 0.59, 95% CI: 0.44-0.80, P = .001) risk reduction against β blockers. Angiotensin-receptor blocker appeared marginally superior to angiotensin-converting enzyme inhibitor in primary and secondary prevention. Conclusion: This study suggests that RAAS blockade effectively suppresses AF in systolic heart failure, and hypertensives derive greater benefit against new-onset and recurrent AF compared to β blockers, calcium channel blockers, and diuretics.
    No preview · Article · Jan 2016 · Journal of Cardiovascular Pharmacology and Therapeutics
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    ABSTRACT: This editorial describes benefits and limitations of remote ischemic conditioning. Remote ischemic conditioning was shown to reduce myocardial intact size in at least 4 sizeable clinical trials of acute myocardial infarction. It was not effective in recent studies of cardiac surgery. Reasons for these differences are discussed.
    No preview · Article · Jan 2016 · Journal of Cardiovascular Pharmacology and Therapeutics
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    ABSTRACT: Apolipoprotein A-1 (Apo A-I) Milano, a naturally occurring Arg173 to Cys mutant of Apo A-1, has been shown to reduce atherosclerosis in animal models and in a small phase 2 human trial. We have shown the superior atheroprotective effects of Apo A-I Milano (Apo A-IM) gene compared to wild-type Apo A-I gene using transplantation of retrovirally transduced bone marrow in Apo A-I/Apo E null mice. In this study, we compared the effect of dietary lipid lowering versus lipid lowering plus Apo A-IM gene transfer using recombinant adeno-associated virus (rAAV) 8 as vectors on atherosclerosis regression in Apo A-I/Apo E null mice. All mice were fed a high-cholesterol diet from age of 6 weeks until week 20, and at 20 weeks, 10 mice were euthanized to determine the extent of atherosclerosis. After 20 weeks, an additional 20 mice were placed on either a low-cholesterol diet plus empty rAAV (n = 10) to serve as controls or low-cholesterol diet plus 1 single intravenous injection of 1.2 × 10(12) vector genomes of adeno-associated virus (AAV) 8 vectors expressing Apo A-IM (n = 10). At the 40 week time point, intravenous AAV8 Apo A-IM recipients showed a significant regression of atherosclerosis in the whole aorta (P < .01), aortic sinuses (P < .05), and brachiocephalic arteries (P < .05) compared to 20-week-old mice, whereas low-cholesterol diet plus empty vector control group showed no significant regression in lesion size. Immunostaining showed that compared to the 20-week-old mice, there was a significantly reduced macrophage content in the brachiocephalic (P < .05) and aortic sinus plaques (P < .05) of AAV8 Apo A-IM recipients. These data show that although dietary-mediated cholesterol lowering halts progression of atherosclerosis, it does not induce regression, whereas combination of low-cholesterol diet and AAV8 mediated Apo A-I Milano gene therapy induces rapid and significant regression of atherosclerosis in mice. These data provide support for the potential feasibility of this approach for atherosclerosis regression.
    No preview · Article · Oct 2015 · Journal of Cardiovascular Pharmacology and Therapeutics
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    ABSTRACT: Background: Published clinical practice guidelines have addressed antihypertensive therapy and sexual dysfunction (SD) in many different ways. Objective: In this systematic review, we evaluated guidelines that address antihypertensive drug-associated SD, guideline recommendations, and recent guideline trends. Methods: Thirty sets of guidelines for hypertension management in adults that had been published in the English language since 2000 were reviewed. The primary outcome measure was antihypertensive-associated SD potential, which was independently evaluated using specific questions by 2 authors in a nonblinded standardized manner. Results: Sexual dysfunctions associated with thiazide-class diuretics, β-blockers, and centrally acting sympathoplegics were addressed by half of the guidelines reviewed. There is no clarity on β-blockers and thiazide-class diuretics because one-third of the guidelines are vague about individual β-blockers and diuretics, and there is no statement on third-generation β-blockers and thiazide-like diuretics that can improve erectile function. The revised guidelines never use terms such as loss of libido, ejaculatory dysfunction, lack of orgasm, and priapism. Summary versions of guidelines are inadequate to reflect the key interpretation of the primary guidelines on SD associated with antihypertensives, even in the major guidelines that were updated recently. Therapeutic issues such as exploring SD in clinical history, assessing SD prior to and during treatment with antihypertensives, substituting the offending agents with alternatives that possess a better safety profile, intervening with phosphodiesterase-5 inhibitors, and avoiding the concomitant use of nitrovasodilators are superficially addressed by most guidelines, with the exception of 2013 European Society of Hypertension/European Society of Cardiology and Seventh Joint National Committee recommendations. Conclusion: Future guideline revisions, including both full and summary reports, should provide a balanced perspective on antihypertensive-related SD issues to improve the impact of hypertension treatment guidelines on patient care and quality of life.
    No preview · Article · Oct 2015 · Journal of Cardiovascular Pharmacology and Therapeutics
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    ABSTRACT: Background: A superficial abdominal surgical incision elicits cardioprotection against cardiac ischemia-reperfusion (I/R) injury in mice. This process, called remote preconditioning of trauma (RPCT), has both an early and a late phase. Previous investigations have demonstrated that early RPCT reduces cardiac infarct size by 80% to 85%. We evaluated the cardioprotective and molecular mechanisms of late-phase RPCT in a murine I/R injury model. Methods: Wild-type mice, bradykinin (BK) 2 receptor knockout mice, 3M transgenic mice (nuclear factor κB [NF-Kb] repressor inhibitor of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha [IκBα((S32A, S36A, Y42F))]), and inducible nitric oxide synthase (iNOS) knockout mice were analyzed using a previously established I/R injury model. A noninvasive abdominal surgical incision was made 24 hours prior to I/R injury and the infarct size was determined at 24 hours post-I/R injury. Results: The results indicated that a strong cardioprotective effect occurred during late-phase RPCT (58.42% ± 1.89% sham vs 29.41% ± 4.00% late RPCT, mean area of the infarct divided by the mean area of the risk region; P ≤ .05; n = 10). Furthermore, pharmacological intervention revealed the involvement of neurogenic signaling in the beneficial effects of late RPCT via sensory and sympathetic thoracic nerves. Pharmacological experiments in transgenic mice-implicated BK receptors, β-adrenergic receptors, protein kinase C, and NF-κB but not iNOS signaling in the cardioprotective effects of late RPCT. Conclusion: Late RPCT significantly decreased myocardial infarct size via neurogenic transmission and various other signaling pathways. This protective mechanism differentiates late and early RPCT. This study describes a new cardiac I/R injury prevention method and refines the concept of RPCT.
    No preview · Article · Oct 2015 · Journal of Cardiovascular Pharmacology and Therapeutics
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    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.
    No preview · Article · Oct 2015 · Journal of Cardiovascular Pharmacology and Therapeutics
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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.
    No preview · Article · Sep 2015 · Journal of Cardiovascular Pharmacology and Therapeutics
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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.
    No preview · Article · Sep 2015 · Journal of Cardiovascular Pharmacology and Therapeutics
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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.
    No preview · Article · Sep 2015 · Journal of Cardiovascular Pharmacology and Therapeutics
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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.
    No preview · Article · Sep 2015 · Journal of Cardiovascular Pharmacology and Therapeutics
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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.
    No preview · Article · Aug 2015 · Journal of Cardiovascular Pharmacology and Therapeutics

  • No preview · Article · Aug 2015 · Journal of Cardiovascular Pharmacology and Therapeutics
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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.
    No preview · Article · Aug 2015 · Journal of Cardiovascular Pharmacology and Therapeutics
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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.
    No preview · Article · Aug 2015 · Journal of Cardiovascular Pharmacology and Therapeutics
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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.
    No preview · Article · Jul 2015 · Journal of Cardiovascular Pharmacology and Therapeutics