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
  • 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 cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • On author website, repository and PubMed Central
    • On author's personal web site
    • 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
    • If funding agency rules apply, authors may use SAGE open to comply
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    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;
  • [Show abstract] [Hide abstract]
    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;
  • [Show abstract] [Hide abstract]
    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;
  • [Show abstract] [Hide abstract]
    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.
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    ABSTRACT: While triglycerides (TGs) and diabetes increase the risk of cardiovascular disease (CVD), their combined effects have not been quantified. We explored the combined effect of elevated TGs and glucose on CVD in a post hoc analysis of the large-scale Management of Elevated Cholesterol in the Primary Prevention Group of Adult Japanese (MEGA) Study. Material and Methods: In the MEGA Study, 8214 patients with mild to moderate hypercholesterolemia were randomly allocated to the diet alone group or diet plus pravastatin group and followed for 5 years. Of those, 7832 patients included in the intention-to-treat analysis were stratified into 4 groups: abnormal fasting glucose (AFG) plus high TGs, high TGs alone, AFG alone, and normal fasting glucose plus normal TGs (reference). Cox proportional hazard models were used to compare the incidence of and mortality from CVD in the 4 groups.
    Journal of Cardiovascular Pharmacology and Therapeutics 06/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Qiliqiangxin (QL), a traditional Chinese medicine, has been shown to be beneficial for chronic heart failure. However, whether QL can also improve endothelial cell function in diabetic rats remains unknown. Here, we investigated the effect of QL treatment on endothelial dysfunction by comparing the effect of QL to that of benazepril (Ben) in diabetic Sprague-Dawley rats for 8 weeks. Cardiac function was evaluated by echocardiography and catheterization. Assays for acetylcholine-induced, endothelium-dependent relaxation (EDR), sodium nitroprusside-induced endothelium-independent relaxation, serum nitric oxide (NO), and nitric oxide synthase (NOS) as well as histological analyses were performed to assess endothelial function. Diabetic rats showed significantly inhibited cardiac function and EDR, decreased expression of serum NO and phosphorylation at Ser(1177) on endothelial NOS (eNOS), and impaired endothelial integrity after 8 weeks. Chronic treatment for 8 weeks with either QL or Ben prevented the inhibition of cardiac function and EDR and the decrease in serum NO and eNOS phosphorylation caused by diabetes. Moreover, either QL or Ben suppressed inducible NOS (iNOS) protein levels as well as endothelial necrosis compared with the diabetic rats. Additionally, QL prevented the increase in angiotensin-converting enzyme 1 and angiotensin II receptor type 1 in diabetes. Thus, chronic administration of QL improved serum NO production, EDR, and endothelial integrity in diabetic rat aortas, possibly through balancing eNOS and iNOS activity and decreasing renin-angiotensin system expression.
    Journal of Cardiovascular Pharmacology and Therapeutics 06/2014;
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    ABSTRACT: This paper summarizes the pharmacological properties of calcium channel blockers (CCBs), their established therapeutic uses for cardiovascular disorders and the current improvement of their clinical effects through drug combinations. Their identification resulted from study of small molecules including coronary dilators, which were named calcium antagonists. Further experiments showed that they reduced contraction of arteries by inhibiting calcium entry and by interacting with binding sites identified on voltage-dependent calcium channels. This led to the denomination calcium channel blockers. In short-term studies, by decreasing total peripheral resistance, CCBs lower arterial pressure. By unloading the heart and increasing coronary blood flow, CCBs improve myocardial oxygenation. In long-term treatment, the decrease in blood pressure is more pronounced in hypertensive than in normotensive patients. A controversy on the safety of CCBs ended after a large antihypertensive trial (ALLHAT) sponsored by the National Heart, Lung, and Blood Institute. There are two main types of CCBs: dihydopyridine and non-dihydropyridine; the first type is vascular selective. Dihydropyrines are indicated for hypertension, chronic, stable and vasospastic angina. Non-dihydropyridines have the same indications plus antiarrythmic effects in atrial fibrillation or flutter and paroxysmal supraventricular tachycardia. In addition, CCBs reduced newly formed coronary lesions in atherosclerosis. In order to reach recommended blood pressure goals, there is a recent therapeutic move by combination of CCBs with other antihypertensive agents particularly with inhibitors acting at the level of the renin-angiotensin system. They are also combined with statins. Prevention of dementia has been reported in hypertensive patients treated with nitrendipine, opening a way for further studies on CCBs' beneficial effect in cognitive deterioration associated with aging.
    Journal of Cardiovascular Pharmacology and Therapeutics 05/2014;
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    ABSTRACT: Cannabidiol (CBD) is a nonpsychoactive phytocannabinoid with anti-inflammatory activity mediated by enhancing adenosine signaling. As the adenosine A1 receptor activation confers protection against ischemia/reperfusion (I/R)-induced ventricular arrhythmias, we hypothesized that CBD may have antiarrhythmic effect through the activation of adenosine A1 receptor. Cannabidiol has recently been shown to suppress ischemia-induced ventricular arrhythmias. We aimed to research the effect of CBD on the incidence and the duration of I/R-induced ventricular arrhythmias and to investigate the role of adenosine A1 receptor activation in the possible antiarrhythmic effect of CBD. Myocardial ischemia and reperfusion was induced in anesthetized male rats by ligating the left anterior descending coronary artery for 6 minutes and by loosening the bond at the coronary artery, respectively. Cannabidiol alone was given in a dose of 50 µg/kg, 10 minutes prior to coronary artery occlusion and coadministrated with adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) in a dose of 100 µg/kg, 15 minutes prior to coronary artery occlusion to investigate whether the antiarrhythmic effect of CBD is modified by the activation of adenosine A1 receptors. The experimental groups were as follows: (1) vehicle control (n = 10), (2) CBD (n = 9), (3) DPCPX (n = 7), and (4) CBD + DPCPX group (n = 7). Cannabidiol treatment significantly decreased the incidence and the duration of ventricular tachycardia, total length of arrhythmias, and the arrhythmia scores compared to control during the reperfusion period. The DPCPX treatment alone did not affect the incidence and the duration of any type of arrhythmias. However, DPCPX aborted the antiarrhythmic effect of CBD when it was combined with it. The present results demonstrated that CBD has an antiarrhythmic effect against I/R-induced arrhythmias, and the antiarrhythmic effect of CBD may be mediated through the activation of adenosine A1 receptor.
    Journal of Cardiovascular Pharmacology and Therapeutics 05/2014;
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    ABSTRACT: In the adult heart, catalase (CAT) activity increases appropriately with increasing levels of hydrogen peroxide, conferring cardioprotection. This mechanism is absent in the newborn for unknown reasons. In the present study, we examined how the posttranslational modification of CAT contributes to its activation during hypoxia/ischemia and the role of c-Abl tyrosine kinase in this process. Hypoxia studies were carried out using primary cardiomyocytes from adult (>8 weeks) and newborn rats. Following hypoxia, the ratio of phosphorylated to total CAT and c-Abl in isolated newborn rat myocytes did not increase and were significantly lower (1.3- and 4.2-fold, respectively; P < .05) than their adult counterparts. Similarly, there was a significant association (P < .0005) between c-Abl and CAT in adult cells following hypoxia (30.9 ± 8.2 to 70.7 ± 13.1 au) that was absent in newborn myocytes. Although ubiquitination of CAT was higher in newborns compared to adults following hypoxia, inhibition of this did not improve CAT activity. When a c-Abl activator (5-(1,3-diaryl-1H-pyrazol-4-yl)hydantoin [DPH], 200 µmol/L) was administered prior to hypoxia, not only CAT activity was significantly increased (P < .05) but also phosphorylation levels were also significantly improved (P < .01) in these newborn myocytes. Additionally, ischemia-reperfusion (IR) studies were performed using newborn (4-5 days) rabbit hearts perfused in a Langendorff method. The DPH given as an intracardiac injection into the right ventricle of newborn rabbit resulted in a significant improvement (P < .002) in the recovery of developed pressure after IR, a key indicator of cardiac function (from 74.6% ± 6.6% to 118.7% ± 10.9%). In addition, CAT activity was increased 3.92-fold (P < .02) in the same DPH-treated hearts. Addition of DPH to adult rabbits in contrast had no significant effect (from 71.3% ± 10.7% to 59.4% ± 12.1%). Therefore, in the newborn, decreased phosphorylation of CAT by c-Abl potentially mediates IR-induced dysfunction, and activation of c-Abl may be a strategy to prevent ischemic injury associated with surgical procedures.
    Journal of Cardiovascular Pharmacology and Therapeutics 05/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Although it is recognized that a systolic blood pressure (SBP) increase ≥2 mm Hg or a diastolic blood pressure (DBP) increase ≥1 mm Hg increases the risk of heart attacks and strokes in middle-aged adults, the Food and Drug Administration (FDA) lacks an adequate policy for regulating medications that increase blood pressure (BP). Some FDA reviewers consider a clinically significant increase in BP to occur only if a drug raises SBP ≥20 mm Hg or if a drug raises DBP ≥10 to 15 mm Hg. In recent years, numerous drugs have been regulated or taken off the market due to cardiovascular safety concerns. The list includes rofecoxib (Vioxx), valdecoxib (Bextra), nonselective nonsteroidal anti-inflammatory drugs, sibutramine (Meridia), and phenylpropanolamine. It is probable that the hypertensive effect of these drugs explains why they increase the risk of adverse cardiovascular events. Other drugs, notably serotonin-norepinephrine reuptake inhibitors and drugs used to treat attention deficit hyperactivity disorder, were approved without cardiovascular safety data despite the fact that they raise BP comparable to valdecoxib and sibutramine. It is the responsibility of the FDA to ensure that drugs are properly labeled regarding risk. Even if a drug raises BP only modestly, FDA guidelines for new drug approvals should include a requirement for cardiovascular safety data. However, such guidelines will not address the problem of how to obtain cardiovascular safety data for the many already approved drugs that increase BP. The FDA should play a role in obtaining cardiovascular safety data for such drugs.
    Journal of Cardiovascular Pharmacology and Therapeutics 05/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Hypertension is the most important cardiovascular risk factor. We have witnessed a significant improvement in hypertension treatment and control and an impressive growth in the pharmacologic options available to clinicians and hypertension specialists. With up to a third of patients with hypertension not at the recommended goal blood pressures, it is critically important to develop novel therapeutic approaches to better treat hypertension. This review will explore the ever-expanding horizon of antihypertensive treatment and will focus on 2 major areas of drug development. First, we will review novel targets for pharmacologic treatment and novel molecules and classes of drugs in various phases of development and recognize the limitations we face in their transition from research and development to clinical practice. Then, we will discuss an expanding array of combination strategies to better treat hypertension with the goal of minimizing the burden of cardiovascular and renal complications of hypertension.
    Journal of Cardiovascular Pharmacology and Therapeutics 05/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: With the release of the 2013 American College of Cardiology/American Heart Association (ACC/AHA) Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults, emphasis has been placed on using evidence-based intensity of therapy to reduce atherosclerotic cardiovascular disease (ASCVD) risk, rather than focusing on goal cholesterol levels. Before initiating therapy, however, it is critical that physicians and patients discuss 4 key topics: (1) the benefit of ASCVD risk reduction, (2) medication adverse effects, (3) drug-drug interactions, and (4) patient preferences. To facilitate discussion of statin adverse effects, we present here an evidence-based review of the 5 Ms of statin adverse effects: metabolism, muscle, medication interactions, major organ effects, and memory. "Metabolism" represents the small risk of new-onset diabetes that comes with statins, which is highest in those with diabetes risk factors. "Muscle" requires discussion of the wide range of muscle symptoms that occur with statins but emphasizes that these have been no more prevalent than those experienced with placebo in randomized controlled trials (RCTs). "Medication interactions" emphasize that statins interact with numerous medications. Interaction profiles vary widely between statins, and patients should be made aware of the most common interactions with their prescription. "Major organ effects" prompt the physician to review the possibility of a transient transaminitis as well as the recent observation of rare acute kidney injury with statin use. Both are rare and do not require routine monitoring. Finally, "memory" references the recent observational data suggesting statins may contribute to memory loss and confusion, both of which have not been observed in RCTs and resolve with drug cessation. Reviewing these common effects has the possibility to strengthen the doctor-patient relationship and boost both medication adherence and patient satisfaction.
    Journal of Cardiovascular Pharmacology and Therapeutics 04/2014;
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    ABSTRACT: Myocardial infarction results from a blockage of a major coronary artery that shuts the delivery of oxygen and nutrients to a region of the myocardium, leading to massive cardiomyocytes death and regression of microvasculature. Growth factor and cell delivery methods have been attempted to revascularize the ischemic myocardium and prevent further cell death. Implantable cardiac tissue patches were engineered to directly revascularize as well as remuscularize the affected muscle. However, inadequate vascularization in vitro and in vivo limits the efficacy of these new treatment options. Breakthroughs in cardiac tissue vascularization will profoundly impact ischemic heart therapies. In this review, we discuss the full spectrum of vascularization approaches ranging from biological angiogenesis to microfluidic blood vessels as related to cardiac tissue engineering.
    Journal of Cardiovascular Pharmacology and Therapeutics 04/2014;
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    ABSTRACT: Ischemic cardiac disease is the leading cause of death in the developed world. The inability of the adult mammalian heart to adequately repair itself has motivated stem cell researchers to explore various strategies to regenerate cardiomyocytes after myocardial infarction. Over the past century, progressive gains in our knowledge about the cellular mechanisms governing fate determination have led to recent advances in cellular reprogramming. The identification of specific factors capable of inducing pluripotent phenotype in somatic cells as well as factors that can directly reprogram somatic cells into cardiomyocytes suggests the potential for these approaches to translate into clinical therapies in the future. Although conceptually appealing, the field of cell lineage reprogramming is in its infancy, and further research will be needed to improve the efficiency of the reprogramming process and the fidelity of the reprogrammed cells to their in vivo counterpart.
    Journal of Cardiovascular Pharmacology and Therapeutics 04/2014;
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    ABSTRACT: Efforts to use gene therapy to create a biological pacemaker as an adjunct or replacement of electronic pacemakers have been ongoing for about 15 years. For the past decade, most of these efforts have focused on the hyperpolarization-activated cyclic nucleotide gated-(HCN) gene family of channels alone or in combination with other genes. The HCN gene family is the molecular correlate of the cardiac pacemaker current, If. It is a suitable basis for a biological pacemaker because it generates a depolarizing inward current primarily during diastole and is directly regulated by cyclic adenosine monophosphate (cAMP), thereby incorporating autonomic responsiveness. However, biological pacemakers based either on native HCN channels or on mutated HCN channels designed to optimize biophysical characteristics have failed to attain the desired basal and maximal physiological heart rates in large animals. More recent work has explored dual gene therapy approaches, combining an HCN variant with another gene to reduce outward current, increase an additional inward current, or enhance cAMP synthesis. Several of these dual gene therapy approaches have demonstrated appropriate basal and maximal heart rates with little or no reliance on a backup electronic pacemaker during the period of study. Future research, besides examining the efficacy of other gene combinations, will need to consider the additional issues of safety and persistence of the viral vectors often used to deliver these genes to a specific cardiac region.
    Journal of Cardiovascular Pharmacology and Therapeutics 04/2014;

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