Progress in Cardiovascular Diseases (PROG CARDIOVASC DIS )

Publisher: Elsevier

Description

Each issue of Progress in Cardiovascular Diseases comprehensively covers a single topic in the understanding and treatment of disorders of the heart and circulation. Some issues contain special articles, definitive reviews that capture the state-of-the-art in the management of particular clinical problems in cardiology. Also appearing at least twice per volume is a feature article comparing clinical trials of a single therapeutic problem of interest to cardiologists and internal medicine physicians.

  • Impact factor
    4.00
    Show impact factor history
     
    Impact factor
  • 5-year impact
    4.64
  • Cited half-life
    6.40
  • Immediacy index
    0.17
  • Eigenfactor
    0.01
  • Article influence
    1.66
  • Website
    Progress in Cardiovascular Diseases website
  • Other titles
    Progress in cardiovascular diseases
  • ISSN
    0033-0620
  • OCLC
    1624043
  • Material type
    Periodical, Internet resource
  • Document type
    Journal / Magazine / Newspaper, Internet Resource

Publisher details

Elsevier

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Voluntary deposit by author of pre-print allowed on Institutions open scholarly website and pre-print servers
    • Voluntary deposit by author of authors post-print allowed on institutions open scholarly website including Institutional Repository
    • Deposit due to Funding Body, Institutional and Governmental mandate only allowed where separate agreement between repository and publisher exists
    • Set statement to accompany deposit
    • Published source must be acknowledged
    • Must link to journal home page or articles' DOI
    • Publisher's version/PDF cannot be used
    • Articles in some journals can be made Open Access on payment of additional charge
    • NIH Authors articles will be submitted to PMC after 12 months
    • Authors who are required to deposit in subject repositories may also use Sponsorship Option
    • Pre-print can not be deposited for The Lancet
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Author's personal copy ECG Patch Monitors for Assessment of Cardiac Rhythm Abnormalities S. Suave Lobodzinski ⁎ Department of Electrical and Biomedical Engineering, California State University, Long Beach, CA, USA ARTICLE INFO ABSTRACT The primary goal of long-term monitoring is the improvement of diagnostic yield. Despite the clear utility of Holter monitoring in clinical cardiology, issues of relatively low diagnostic yield, cost and inconvenience have motivated the development of ultra- portable devices referred to as ECG patch monitors. Although the “ gold standard ” for assessing cardiac rhythm abnormalities remains a 12-lead Holter, there is an increasing interest in portable monitoring devices that provide the opportunity for evaluating cardiac rhythm in real-world environments such as the workplace or home. To facilitate patient acceptance these monitors underwent a radical miniaturization and redesign to include wireless communication, water proofing and a patch carrier for attaching devices directly to the skin. We review recent developments in the field of “ patch ” devices primarily designed for very long-term monitoring of cardiac arrhythmic events. As the body of supporting clinical validation data grows, these devices hold promise for a variety of cardiac monitoring applications. From a clinical and research standpoint, the capacity to obtain longitudinal cardiac activity data by patch devices may have significant implications for device selection, monitoring duration, and care pathways for arrhythmia evaluation and atrial fibrillation surveillance. From a research standpoint, the new devices may allow for the development of novel diagnostic algorithms with the goal of finding patterns and correlations with exercise and drug regimens.
    Progress in Cardiovascular Diseases 09/2013; 56(2):224-229.
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    ABSTRACT: The patient with abdominal aortic aneurysm (AAA) commonly is a nondiabetic, white man with a history of smoking. Moreover, AAA represents a leading cause of death in elderly men in Western countries. The purpose of this manuscript is to review current evidence as to the pathobiology of AAA as well as potential future drug targets to prevent progression of AAA.
    Progress in Cardiovascular Diseases 01/2007; 50(3):209-17.
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    ABSTRACT: Emotional triggers of acute coronary syndromes include population-level events such as earthquakes and terrorist attacks, and individual experiences of acute anger, stress and depression. The methodology of studying emotional triggers has developed markedly over recent years, though limitations remain. The biological processes underlying triggering include acute autonomic dysregulation, neuroendocrine activation, hemostatic and inflammatory responses which, when associated with plaque disruption, promote myocardial ischemia, cardiac dysrhythmia and thrombosis formation. Prevention and management strategies for ameliorating emotional triggering remain to be effectively developed.
    Progress in Cardiovascular Diseases 01/2007; 49(5):353-65.
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    ABSTRACT: The human immunodeficiency virus (HIV) epidemic has been associated with an increase in all forms of extrapulmonary tuberculosis including tuberculous pericarditis. Tuberculosis is responsible for approximately 70% of cases of large pericardial effusion and most cases of constrictive pericarditis in developing countries, where most of the world's population live. However, in industrialized countries, tuberculosis accounts for only 4% of cases of pericardial effusion and an even smaller proportion of instances of constrictive pericarditis. Tuberculous pericarditis is a dangerous disease with a mortality of 17% to 40%; constriction occurs in a similar proportion of cases after tuberculous pericardial effusion. Early diagnosis and institution of appropriate therapy are critical to prevent mortality. A definite or proven diagnosis is based on demonstration of tubercle bacilli in pericardial fluid or on histologic section of the pericardium. A probable or presumed diagnosis is based on proof of tuberculosis elsewhere in a patient with otherwise unexplained pericarditis, a lymphocytic pericardial exudate with elevated biomarkers of tuberculous infection, and/or appropriate response to a trial of antituberculosis chemotherapy. Treatment consists of 4-drug therapy (isoniazid, rifampicin, pyrazinamide, and ethambutol) for 2 months followed by 2 drugs (isoniazid and rifampicin) for 4 months regardless of HIV status. It is uncertain whether adjunctive corticosteroids are effective in reducing mortality or pericardial constriction, and their safety in HIV-infected patients has not been established conclusively. Surgical resection of the pericardium is indicated for those with calcific constrictive pericarditis or with persistent signs of constriction after a 6 to 8 week trial of antituberculosis treatment in patients with noncalcific constrictive pericarditis.
    Progress in Cardiovascular Diseases 01/2007; 50(3):218-36.
  • Progress in Cardiovascular Diseases 01/2007; 50(2):126-35.
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    ABSTRACT: Whatever the pathogenesis of syncope is, the ultimate common cause leading to loss of consciousness is insufficient cerebral perfusion with a critical reduction of blood flow to the reticular activating system. Brain circulation has an autoregulation system that keeps cerebral blood flow constant over a wide range of systemic blood pressures. Normally, if blood pressure decreases, autoregulation reacts with a reduction in cerebral vascular resistance, in an attempt to prevent cerebral hypoperfusion. However, in some cases, particularly in neurally mediated syncope, it can also be harmful, being actively implicated in a paradox reflex that induces an increase in cerebrovascular resistance and contributes to the critical reduction of cerebral blood flow. This review outlines the anatomic structures involved in cerebral autoregulation, its mechanisms, in normal and pathologic conditions, and the noninvasive neuroimaging techniques used in the study of cerebral circulation and autoregulation. An emphasis is placed on the description of autoregulation pathophysiology in orthostatic and neurally mediated syncope.
    Progress in Cardiovascular Diseases 01/2007; 50(1):49-80.
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    ABSTRACT: Cell transplantation is emerging as a new treatment designed to improve the poor outcome of patients with cardiac failure. Its rationale is that implantation of contractile cells into postinfarction scars could functionally rejuvenate these areas. Primarily for practical reasons, autologous skeletal myoblasts have been the first to be considered for a clinical use. A large number of experimental studies have consistently documented a robust engraftment of myoblasts, their in-scar differentiation into myotubes, and an associated improvement in left ventricular function. The early results of phase I clinical trials have then established both the feasibility and safety of this procedure with the caveat of arrhythmic events. Efficacy data are equally encouraging but definitely need to be validated by large prospective placebo-controlled, double-blind randomized trials such as the Myoblast Autologous Grafting in Ischemic Cardiomyopathy (MAGIC) study, the results of which are now pending. In addition to assessing the effect of myoblast transplantation on regional and global heart function, these results will also provide comprehensive safety data and thus allow a more objective assessment of the risk-benefit ratio. However, it is already apparent that the outcome of myoblast transfer could most likely be improved by optimizing the purity of the cell yield (by selecting muscle-derived progenitors less lineage-committed than the myoblasts), the mode of delivery (by increasing the accuracy of cell injections while decreasing their invasiveness), and the survival of the engrafted cells (by concomitant graft vascularization and incorporation of cells in three-dimensional matrices). Most, if not all, of these changes will have to be incorporated before skeletal myoblasts can acquire the status of therapeutic agents. Furthermore, there is increasing evidence that myoblasts may act by attenuating left ventricular remodeling or paracrinally affecting the surrounding myocardium but not by generating new cardiomyocytes because of their strict commitment to a myogenic lineage. Thus, improvement of function is not tantamount of myocardial regeneration, and if such a regeneration remains the primary objective, it is worth considering alternate cell types able to generate new cardiac cells that will be electromechanically coupled with the host cardiomyocytes. In the setting of this second generation of cells, human cardiac-specified embryonic stem cells may hold the greatest promise.
    Progress in Cardiovascular Diseases 01/2007; 50(1):7-17.
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    ABSTRACT: Acute stroke therapy took a major step forward in 1996 after the approval of Intravenous (IV) tissue plasminogen activator (t-PA) by the US Food and Drug Administration for patients presenting within 3 hours of the onset of stroke symptoms. Since that time, there have been considerable advances in imaging techniques as well as the advent of devices to help in the management of acute stroke patients. As a result, the arsenal to treat acute stroke has grown, and the field of stroke as a subspecialty of neurology has emerged. Despite these advances, only 3% to 8% of eligible patients with acute stroke in the United States are administered thrombolytics.(1) We herein review the use of thrombolytics in stroke and provide an overview of the imaging advances, new devices, and recent trials that are shaping modern stroke therapy. Finally, we provide a practical approach to the management of acute stroke, specifically for the practicing cardiologist, who may encounter stroke during cardiac catheterization, post myocardial infarction (MI), and in a variety of other settings.
    Progress in Cardiovascular Diseases 01/2007; 49(6):430-8.
  • Source
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    ABSTRACT: In the past few years it has been established that the heart contains a reservoir of stem and progenitor cells. These cells are positive for various stem/progenitor cell markers (Kit, Sca-1, Isl-1, and Side Population (SP) properties). The relationship between the various cardiac stem cells (CSC) and progenitor cells described awaits clarification. Furthermore, they may open a new therapeutic strategies of cardiac repair based on the regeneration potential of cardiac stem cells. Currently, cellular cardiomyoplasty is actively explored as means of regenerating damaged myocardium using several different cell types. CSCs seem a logical cell source to exploit for cardiac regeneration therapy. Their presence into the heart, the frequent co-expression of early cardiac progenitor transcription factors, and the capability for ex vivo and in vivo differentiation toward the cardiac lineages offer promise of enhanced cardiogenicity compared to other cell sources. CSCs, when isolated from various animal models by selection based on c-Kit, Sca-1, and/or MDR1, have shown cardiac regeneration potential in vivo following injection in the infracted myocardium. Recently, we have successfully isolated CSCs from small biopsies of human myocardium and expanded them ex vivo by many folds without losing differentiation potential into cardiomyocytes and vascular cells, bringing autologous transplantation of CSCs closer to clinical evaluation. These cells are spontaneously shed from human surgical specimens and murine heart samples in primary culture. This heterogeneous population of cells forms multi-cellular clusters, dubbed cardiospheres (CSs), in suspension culture. CSs are composed of clonally-derived cells, consist of proliferating c-Kit positive cells primarily in their core and differentiating cells expressing cardiac and endothelial cell markers on their periphery. Although the intracardiac origin of adult myocytes has been unequivocally documented, the potential of an extracardiac source of cells, able to repopulate the lost CSCs in pathological conditions (infarct) cannot be excluded and will be discussed in this review. The delivery of human CSs or of CSs-derived cells into the injured heart of the SCID mouse resulted in engraftment, migration, myocardial regeneration and improvement of left ventricular function. Our method for ex vivo expansion of resident CSCs for subsequent autologous transplantation back into the heart, may give these cell populations, the resident and the transplanted one, the combined ability to mediate myocardial regeneration to an appreciable degree, and may change the way in which cardiovascular disease will be approached in the future.
    Progress in Cardiovascular Diseases 01/2007; 50(1):31-48.
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    ABSTRACT: First isolated in the early 1960s, doxorubicin (DOX) remains among the most effective anticancer drug ever developed. However, this drug has proven to be a double-edged sword because it also causes a cardiomyopathy that leads to a form of congestive heart failure that is usually refractory to common medications. It is hoped that a better understanding of the mechanisms underlying DOX's cardiotoxicity will enable development of therapies with which to prevent and/or treat the heart failure it causes. Suggested contributors to DOX-induced cardiomyopathy include formation of reactive oxygen species, apoptosis, inhibited expression of cardiomyocyte-specific genes, and altered molecular signaling. And taking these various contributors into consideration, a variety of approaches aimed at preventing or mitigating the cardiotoxicity of DOX have been tried, but so far, the ability of these treatments to protect the heart from damage has been limited. That said, one recent approach that shows promise is adjuvant therapy with a combination of hematopoietic cytokines, including erythropoietin, granulocyte colony-stimulating factor, and thrombopoietin. We suggest this approach to preventing DOX-induced cardiomyopathy is worthy of serious consideration for clinical use.
    Progress in Cardiovascular Diseases 01/2007; 49(5):330-52.
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    ABSTRACT: Traditional explanations for the symptoms of fatigue and breathlessness experienced by patients with chronic heart failure (CHF) focus on how reduced cardiac output on exercise leads to impaired skeletal muscle blood supply, thus causing fatigue, and on how the requirement for a raised left ventricular filling pressure to maintain cardiac output results in reduced pulmonary diffusion owing to interstitial edema, thus causing breathlessness. However, indices of left ventricular function relate poorly to exercise capacity and symptoms, suggesting that the origin of symptoms may lie elsewhere. There is a specific heart failure myopathy that is present early in the condition which may contribute largely to the sensation of fatigue. Receptors present in skeletal muscle sensitive to work (ergoreceptors) are overactive in patients with CHF, presumably as a consequence of the myopathy, and their activity is related both to the ventilatory response to exercise and breathlessness, and to the sympathetic overactivity of CHF. In the present paper, we review the systemic consequences of left ventricular dysfunction to understand how they relate to the symptoms of heart failure.
    Progress in Cardiovascular Diseases 01/2007; 49(5):366-84.
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    ABSTRACT: Infective endocarditis is an evolving disease that presents as a great a problem to physicians, cardiologists, microbiologists, and cardiac surgeons in both the developed and developing world now as at any time over the past 3 decades. This article provides the reader with an up-to-date review of epidemiology, etiology, pathogenesis, presentation, diagnosis, and treatment. A major area of ongoing work is an approach to the culture-negative patient resulting in expanding diagnostic techniques. Limitations of current diagnostic strategies are detailed with focus on the use of the polymerase chain reaction to aid diagnosis. The technique offers several advantages, including extreme sensitivity and the opportunity for early diagnosis. Three general circumstances exist in which molecular approaches may be used: (1) identification of agents in cases of culture-negative infective endocarditis; (2) characterization of cultured agent(s) to determine clinical significance; (3) determination of antibiotic resistance. It should be recognized that there are limitations and certain quality assurance measures that should be implemented for optimal use of such methods. However, when executed properly and interpreted in the correct clinical and laboratory context, the incorporation of molecular diagnostics as a major Duke diagnostic criterion has been proposed with widespread support, although it is unlikely to supersede blood cultures as a primary diagnostic tool.
    Progress in Cardiovascular Diseases 01/2007; 50(3):181-97.
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    ABSTRACT: As research on stem cell therapeutics for the treatment of cardiovascular diseases in adults is being planned and conducted it is essential to address the ethical issues associated with it. The considerable attention that is currently focused on the ethical issues associated with stem cell research as well as the acute clinical situations sometimes encountered when treating cardiovascular disease, underscore the need for explicit attention to the ethical aspects of this research. In this article, I survey some of the key ethical considerations regarding research involving stem cell therapeutics for cardiovascular diseases including: (1) the standard ethical considerations for translational and clinical research and mechanisms of ethical oversight of them; (2) additional oversight related to stem cell research; (3) considerations for obtaining informed consent for this research and in selecting individual human subjects to participate in it; (4) concerns related to justice that may manifest themselves with respect to which research endeavors move forward and (5) conflicts of interest in research and their potential relationship to research integrity.
    Progress in Cardiovascular Diseases 01/2007; 50(1):1-6.

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