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

Publisher: Hindawi Publishing Corporation, SAGE Publications

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.

Impact factor 3.07

  • Hide impact factor history
     
    Impact factor
  • 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: Dantrolene, which is primarily used to treat malignant hyperthermia, has recently been suggested for the prevention of arrhythmogenesis in various animal models. In this study, the effects of dantrolene treatment on electrophysiological properties and ventricular arrhythmias (VAs) in rats with chronic β-adrenergic receptor (β-AR) activation were investigated. Rats were randomized to treatment with saline (control group), isoproterenol (ISO; ISO group), or ISO + dantrolene (ID group) for 2 weeks. An electrophysiological study was performed to assess action potential duration restitution (APDR) and induce action potential duration (APD) alternans or VA in vitro. The protein levels of Cav1.2, sarcoplasmic reticulum Ca(2+)-ATPase (SERCA2a), and ryanodine receptor 2 (RyR2) were detected by Western blot. Compared with the control group, chronic administration of ISO significantly increased APD, the maximum slope (Smax) of APDR curve, and the spatial dispersions of Smax and APD (all P < .01), and all effects were attenuated by dantrolene treatment (all P < .05). Additionally, chronic ISO administration significantly reduced the protein levels of SERCA2 and RyR2, but increased the Cav1.2 protein expression (all P < .05). However, compared with the ISO group, dantrolene treatment preserved SERCA2a and RyR2 protein levels and decreased Cav1.2 protein levels in the ID group (all P < .05). The intracellular Ca(2+) ([Ca(2+)]i) levels measured by incubating isolated cardiomyocytes with Fluo-3/alveolar macrophages were significantly increased in the ISO group compared with the control group (P < .01). Dantrolene treatment markedly reduced the rise of [Ca(2+)]i levels caused by chronic administration of ISO (P < .05). Dantrolene treatment also prevented the reductions in the APD alternans and VA thresholds induced by chronic ISO stimulation (all P < .05). These data suggest that dantrolene stabilizes ventricular electrophysiological characteristics and increases the expression of key sarcoplasmic reticulum calcium cycling proteins to reduce vulnerability to VA in rats with chronic β-AR activation. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 01/2015;
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    ABSTRACT: Combination therapy is commonly used for pulmonary arterial hypertension (PAH) treatment. We aimed to identify factors that may predict the need for future combination therapy. We conducted a retrospective chart review of consecutive patients with PAH in an aim to describe baseline clinical, echocardiogram, and hemodynamic characteristics of patients who eventually required combination therapy during the course of their disease and compared them to the ones who were maintained on monotherapy. The monotherapy group was followed for an average of 31.8 ± 18.8 months and the combination therapy group was followed for an average of 28.7 ± 13.6 months. Among the 71 patients analyzed, a significantly higher number of patients who eventually required combination therapy belonged to World Health Organization functional class 3 (45% vs 37%) and 4 (23% vs 0) at baseline, compared with those on monotherapy (P < .05). Combination group also had a higher Registry to Evaluate Early And Long-term PAH Disease Management (REVEAL) PAH risk score at presentation. End of 6-minute walk test (6MWT), oxygen saturation (Spo 2) was also lower in the combination therapy group, 86% ± 8% versus 91% ± 7% (P < .05). Patients who eventually required combination therapy were more frequently noticed to have right ventricular enlargement, right atrial enlargement, and had a higher resting estimated right ventricular systolic pressure (RVSP). Right heart catheterization-derived hemodynamics data at baseline showed that the combination therapy group had a higher mean pulmonary artery (PA) pressure, lower pulmonary capillary wedge pressure, lower cardiac output, and higher pulmonary vascular resistance (PVR). On univariate analysis, only PVR ≥300 dyne·s/cm(5), mean PA pressure of ≥40 mm Hg, estimated RVSP ≥ 60 mm Hg, PAH risk score ≥ 10, and end of 6MWT saturation of ≤ 90% were of significance. Patients with PAH who require combination therapy in the course of their disease have worse hemodynamics, PAH risk score, functional class, and end of 6MWT oxygen saturation at the time of presentation compared to patients maintained on monotherapy. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 01/2015;
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    ABSTRACT: Atorvastatin has been demonstrated to reduce the incidence of postoperative atrial fibrillation (POAF) in patients undergoing cardiac surgery, but its effect on isolated heart valve surgery is unknown. In a randomized, double-blinded, placebo-controlled trial, 58 patients who underwent isolated heart valve surgery supported by on-pump cardiopulmonary bypass were randomly assigned to receive either placebo (n = 29) or 40 mg of atorvastatin once daily starting 3 days preoperatively and continuing within 5 days postoperatively (n = 29). A continuous monitoring tool and an electrocardiographic Holter monitoring were used for detecting the POAF (Clinical Trial Registration: www.clinicaltrials.gov; Unique Identifier: NTC02084069). The patients' median age was 49 years, and 67% were female. In all, 6 (21%) and 13 (45%) cases of POAF were observed in the atorvastatin and placebo groups, respectively (P = .050). The duration of AF before re-establishment of sinus rhythm was significantly lower in the atorvastatin group than in the placebo group (median of 70 vs 132 minutes, P = .026). The lengths of intensive care unit and hospital stay were comparable between the groups. The increase in postoperative white blood cell count was significantly lower in the atorvastatin group than in the placebo group (median of 1.5 vs 2.3 × 10(3)/µL, respectively, P = .019). After adjustment, the atorvastatin treatment was associated with a decrease in the risk of developing POAF (odds ratio 0.122, 95% confidence interval 0.027-0.548, P = .006). Perioperative treatment with 40 mg of atorvastatin is useful to decrease the incidence of POAF in the statin-naive patients undergoing isolated heart valve surgery. © The Author(s) 2014.
    Journal of Cardiovascular Pharmacology and Therapeutics 12/2014;
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    ABSTRACT: To investigate whether slight variations in core temperature prior to cardiac arrest (CA) influence short-term outcomes and mitochondrial functions. Three groups of New Zealand White rabbits (n = 12/group) were submitted to 15 minutes of CA at 38°C (T-38 group), 39°C (T-39), or 40°C (T 40) and 120 minutes of reperfusion. A Sham-operated group (n = 6) underwent only surgery. Restoration of spontaneous circulation (ROSC), survival, hemodynamics, and pupillary reactivity were recorded. Animals surviving to the end of the observation period were euthanized to assess fresh brain and heart mitochondrial functions (permeability transition and oxidative phosphorylation). Markers of brain and heart damages were also measured. The duration of asphyxia required to induce CA was significantly lower in the T-40 group when compared to the T-38 group (P < .05). The rate of ROSC was >80% in all groups (P = nonsignificant [ns]). Survival significantly differed among the T-38, T-39, and T-40 groups: 10 (83%) of 12, 7 (58%) of 12, and 4 (33%) of 12, respectively (log-rank test, P = .027). At the end of the protocol, none of the animals in the T-40 group had pupillary reflexes compared to 8 (67%) of 12 in the T-38 group (P < .05). Troponin and protein S100B were significantly higher in the T-40 versus T-38 group (P < .05). Cardiac arrest significantly impaired both inner mitochondrial membrane integrity and oxidative phosphorylation in all groups. Brain mitochondria disorders were significantly more severe in the T-40 group compared to the T-38 group (P < .05). Small changes in body temperature prior to asphyxial CA significantly influence brain mitochondrial functions and short-term outcomes in rabbits. © The Author(s) 2014.
    Journal of Cardiovascular Pharmacology and Therapeutics 12/2014;
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    ABSTRACT: Antiplatelet (AP) therapy is well established for the secondary prevention of acute coronary events. However, patients may discontinue treatment, often owing to gastrointestinal (GI) complications, leaving them at elevated risk of recurrent cardiovascular events. This descriptive retrospective study assessed trends in prescription of AP agents and coprescription of gastroprotective therapy, after an acute coronary event. Discontinuation of AP therapy within 2 years of an event and factors predicting discontinuation were investigated. The study was conducted in a UK primary care setting from 2000 to 2008; a total of 27 351 patients aged 50 to 84 years were included in the analysis. Main outcome measures were exposures to low-dose acetylsalicylic acid (ASA), clopidogrel, and proton pump inhibitors (PPIs). At 90 days after an acute coronary event, 85.9% of patients had been prescribed some form of AP therapy and 33.6% of patients who were issued at least 1 ASA prescription in this period were also issued a PPI prescription. The use of dual antiplatelet therapy (DAT) 90 days after an event increased from 2% in 2000 to over 50% in 2008. An estimated 15.1% of patients on ASA monotherapy and 37.5% on DAT discontinued treatment within 1 year. A bleeding event during follow-up, including upper GI bleeding or hemorrhagic stroke, was the strongest predictor of discontinuation. Although most patients were prescribed AP therapy in the 90 days following an acute coronary event, a substantial proportion discontinued DAT or ASA monotherapy within 1 year. It is essential that physicians consider strategies to reduce the risk of discontinuation of AP therapy. © The Author(s) 2014.
    Journal of Cardiovascular Pharmacology and Therapeutics 12/2014;
  • Journal of Cardiovascular Pharmacology and Therapeutics 12/2014;
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    ABSTRACT: This paper summarizes the pharmacologic properties of vasoactive medications used in the treatment of shock, including the inotropes and vasopressors. The clinical application of these therapies is discussed and recent studies describing their use and associated outcomes are also reported. Comprehension of hemodynamic principles and adrenergic and non-adrenergic receptor mechanisms are salient to the appropriate therapeutic utility of vasoactive medications for shock. Vasoactive medications can be classified based on their direct effects on vascular tone (vasoconstriction or vasodilation) and on the heart (presence or absence of positive inotropic effects). This classification highlights key similarities and differences with respect to pharmacology and hemodynamic effects. Vasopressors include pure vasoconstrictors (phenylephrine and vasopressin) and inoconstrictors (dopamine, norepinephrine, and epinephrine). Each of these medications acts as vasopressors to increase mean arterial pressure by augmenting vascular tone. Inotropes include inodilators (dobutamine and milrinone) and the aforementioned inoconstrictors. These medications act as inotropes by enhancing cardiac output through enhanced contractility. The inodilators also reduce afterload from systemic vasodilation. The relative hemodynamic effect of each agent varies depending on the dose administered, but is particularly apparent with dopamine. Recent large-scale clinical trials have evaluated vasopressors and determined that norepinephrine may be preferred as a first-line therapy for a broad range of shock states, most notably septic shock. Consequently, careful selection of vasoactive medications based on desired pharmacologic effects that are matched to the patient's underlying pathophysiology of shock may optimize hemodynamics while reducing the potential for adverse effects. © The Author(s) 2014.
    Journal of Cardiovascular Pharmacology and Therapeutics 11/2014;
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    ABSTRACT: The objective of this study is to examine whether carbon monoxide-releasing molecules (CORMs) can decrease the generation of excessive reactive oxygen species (ROS) in cardiac mitochondria, thereby protecting against postresuscitation myocardial injury and cardiac mitochondrial dysfunction after resuscitation in a rat model of ventricular fibrillation (VF), and further investigated the underlying mechanism. Rats suffered 8 minutes of untreated VF and resuscitation and were randomized into the control group with vehicle infusion and the CORM group with CO-releasing molecule 2 (CORM2) treatment. Animals in the Sham group were instrumented without induced VF and resuscitation. Effects of CORM2 on cardiac function, myocardial oxidative stress, cardiac mitochondrial function, and mitochondrial ROS generation were assessed. Moreover, to further evaluate the direct effect of CORM2 on cardiac mitochondria isolated from resuscitated rats, we measured mitochondrial function and ROS generation when isolated cardiac mitochondria were directly incubated with different concentrations of (CORM2). Compared with the Sham group, the control and CORM groups demonstrated impaired cardiac function, increased myocardial injury, and aggravated mitochondrial damage. CORM2 improved cardiac performance and attenuated myocardial damage and oxidative stress in resuscitated rats. Additionally, animals with CORM2 treatment showed the decreased generation of cardiac mitochondrial ROS, alleviated mitochondrial injury, and preserved mitochondrial function and complex activities when compared with the control group. In isolated cardiac mitochondria incubated with CORM2, low concentrations of CORM2 (20 μmol/L) mildly uncoupled mitochondrial respiration, leading to reduced mitochondrial ROS production. In contrast, high concentrations of CORM2 (60 μmol/L) resulted in the reverse effect presumably due to its excessive uncoupling action. These findings suggest that CORM2 attenuates oxidative stress of the heart and improves cardiac function after resuscitation. The mechanism was probably that CO, the product of CORM2, reduces the production of cardiac mitochondrial ROS and thereby attenuates mitochondrial injury and dysfunction during the postresuscitation period, due to the transient uncoupling of mitochondrial respiration. © The Author(s) 2014.
    Journal of Cardiovascular Pharmacology and Therapeutics 11/2014;
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    ABSTRACT: Antibody-coated stents to capture circulating endothelial progenitor cells (EPCs) for re-endothelialization appear to be a novel therapeutic option for the treatment of atherosclerotic disease. Hydroxybutyl chitosan (HBC), a linear polysaccharide made from shrimps and other crustacean shells, is biocompatible, nontoxic, and hydrophilic, making it ideal for biomedical applications. In this study, HBC was explored for the immobilization of anti-CD133 antibodies. We demonstrated that CD133 antibodies mediated by HBC were successfully coated on cobalt-chromium alloy discs and metal stents. The coating was homogeneous and smooth as shown by electronic microscopy analysis. Balloon expansion of coated stents did not cause cracking or peeling. The HBC discs promoted CD133+ EPCs and human umbilical vein endothelial cell growth in vitro. The CD133 antibody-coated but not bare discs bound CD133+ EPCs in vitro. Implantation of CD133 antibody-coated stents significantly inhibited intimal hyperplasia and reduced restenosis compared with implantation of bare stents in a porcine model of atherosclerosis. These findings suggest HBC is a valuable anchoring agent that can be applied for bioactive coating of stents and that CD133 antibody-coated stents might be a potential therapeutic alternative for the treatment of atherosclerotic disease. © The Author(s) 2014.
    Journal of Cardiovascular Pharmacology and Therapeutics 11/2014;
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    ABSTRACT: Recent clinical studies have reported the potential benefit of an early mineralocorticoid receptor (MR) blockade with potassium canrenoate (PC) on ventricular arrhythmias (VAs) occurrence in patients experiencing an ST-segment elevation myocardial infarction (STEMI). However, most of the electrophysiological properties of PC demonstrated to date have been investigated in normoxic conditions, and therefore, in vitro experiments during an acute myocardial ischemia-reperfusion were lacking.
    Journal of Cardiovascular Pharmacology and Therapeutics 11/2014;
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    ABSTRACT: This study investigated the effect of 6-week supplementation of a probiotic strain Lactobacillus salivarius UBL S22 with or without prebiotic fructo-oligosaccharide (FOS) on serum lipid profiles, immune responses, insulin sensitivity, and gut lactobacilli in 45 healthy young individuals. The patients were divided into 3 groups (15/group), that is, placebo, probiotic, and synbiotic. After 6 weeks, a significant reduction (P < .05) in total cholesterol, low-density lipoprotein (LDL) cholesterol, and triglycerides and increase in high-density lipoprotein cholesterol was observed in the probiotic as well as in the synbiotic group when compared to placebo; however, the results of total cholesterol and LDL-cholesterol were more pronounced in the synbiotic group. Similarly, when compared to the placebo group, the serum concentrations of inflammatory markers such as high sensitivity C-reactive protein, interleukin (IL) 6, IL-1β, and tumor necrosis factor α were significantly (P < .05) reduced in both the experimental groups, but again the reduction in the synbiotic group was more pronounced. Also, an increase (P < .05) in the fecal counts of total lactobacilli and a decrease (P < .05) in coliforms and Escherichia coli was observed in both the experimental groups after 6 weeks of ingestion. Overall, the combination of L salivarius with FOS was observed to be more beneficial than L salivarius alone, thereby advocating that such synbiotic combinations could be therapeutically exploited for improved health and quality of life.
    Journal of Cardiovascular Pharmacology and Therapeutics 10/2014;
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    ABSTRACT: Cardiovascular diseases are one of the most common causes of death in humans and are responsible for billions of dollars in health care expenditures. As the molecular basis of cardiac diseases continues to be explored, there remains the hope for identification of more effective therapeutics. MicroRNAs (miRNAs) are recognized as important regulators of numerous biological pathways and stress responses, including those found in cardiovascular diseases. MicroRNA signatures of cardiovascular diseases can provide targets for miRNA adjustment and offer the possibility of changing gene and protein expression to treat certain pathologies. These adjustments can be conferred using advances in oligonucleotide delivery methods, which can target single miRNAs, families of miRNAs, and certain tissue types. In this review, we will discuss the use of miRNAs in vivo and recent advances in their use for cardiovascular disease in mammalian models.
    Journal of Cardiovascular Pharmacology and Therapeutics 09/2014;
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    ABSTRACT: Antiplatelet therapy is invariably prescribed for patients with peripheral arterial disease and critical limb ischemia, and numerous major society guidelines espouse their use, but high-quality data in this high-risk and challenging patient population are often lacking. This article summarizes the major guidelines for antiplatelet therapy, reviews the major studies of antiplatelet therapy in peripheral arterial disease (including data for aspirin, clopidogrel, dipyridamole, cilostazol, and prostanoids), and offers perspective on the potential benefits of ticagrelor, vorapaxar, and rivaroxaban. The review concludes with a discussion of the relative lack of efficacy that antiplatelet therapy has shown in regard to peripheral vascular outcomes.
    Journal of Cardiovascular Pharmacology and Therapeutics 07/2014;
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    ABSTRACT: Dyslipidaemia is a critical risk factor for the development of cardiovascular complications such as ischemic heart disease and stroke. Although statins are effective anti-dyslipidemic drugs, their usage is fraught with issues such as failure of adequate lipid control in 30% of cases and intolerance in select patients. The limited potential of other alternatives such as fibrates, bile acid sequestrants and niacin has spurred the search for novel drug molecules with better efficacy and safety. CETP inhibitors such as evacetrapib and anacetrapib have shown promise in raising HDL besides LDL lowering property. Microsomal triglyceride transfer protein (MTP) inhibitors such as lomitapide and Apo CIII inhibitors such as mipomersen have recently been approved in Familial Hypercholesterolemia but experience in the non-familial setting is pretty much limited. One of the novel anti-dyslipidemic drugs which is greatly anticipated to make a mark in LDL-C control is the PCSK9 inhibitors. Some of the anti-dyslipidemic drugs which work by PCSK9 inhibition include evolocumab, alirocumab and ALN-PCS. Other approaches that are being given due consideration include farnesoid X receptor modulation and Lp-PLA2 inhibition. While it may not be an easy proposition to dismantle statins from their current position as a cholesterol reducing agent and as a drug to reduce coronary and cerebro-vascular atherosclerosis, our improved understanding of the disease and appropriate harnessing of resources using sound and robust technology could make rapid in-roads in our pursuit of the ideal anti-dyslipidemic drug.
    Journal of Cardiovascular Pharmacology and Therapeutics 07/2014;
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    ABSTRACT: To determine the efficacy and safety of erythropoiesis-stimulating agents (ESAs) for the treatment of anemia in patients with systolic heart failure.
    Journal of Cardiovascular Pharmacology and Therapeutics 07/2014;
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    ABSTRACT: In patients with acute ST-segment elevation myocardial infarction, early, successful, and durable reperfusion therapy optimizes the likelihood of favorable outcomes. Fibrinolysis and primary percutaneous coronary intervention improve survival compared to no reperfusion therapy in large part by reducing infarct size (IS) and preserving left ventricular ejection fraction. There is direct correlation between IS and clinical outcomes. In this article, we will review some of the more promising pharmacological agents geared toward reduction in IS, discuss the major pathways that can lead to this desirable outcome, and evaluate the results of clinical trials performed with these and other compounds.
    Journal of Cardiovascular Pharmacology and Therapeutics 07/2014;
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    ABSTRACT: Toll-like receptor 4 participates in the process of acute heart injury. The underlying mechanisms of its protection are multifactorial, but we hypothesized that toll-like receptor-mediated autophagy control plays a vital role. The purpose of this study was to clarify the effect of autophagy on cardiac fibrosis.
    Journal of Cardiovascular Pharmacology and Therapeutics 06/2014;
  • Journal of Cardiovascular Pharmacology and Therapeutics 06/2014; 19(4):329.