Esomeprazole and aspirin fixed combination for the prevention of cardiovascular events

Low dose aspirin therapy plays a fundamental role in both the primary and secondary prevention of cardiovascular events. Although the evidence using low dose aspirin for secondary prevention is well-established, the decision to use aspirin for primary prevention is based on an evaluation of the patient’s risk of cardiovascular events compared to their risk of adverse events, such as bleeding. In addition to the risk of bleeding associated with long term aspirin administration, upper gastrointestinal side effects, such as dyspepsia often lead to discontinuation of therapy, which places patients at an increased risk for cardiovascular events. One option to mitigate adverse events and increase adherence is the addition of esomeprazole to the medication regimen. This review article provides an evaluation of the literature on the concomitant use of aspirin and esomeprazole available through February 2013. The efficacy, safety, tolerability, cost effectiveness, and patient quality of life of this regimen is discussed. A summary of the pharmacokinetic and pharmacodynamic interactions between aspirin and esomeprazole, as well as other commonly used cardiovascular medications are also reviewed. The addition of esomeprazole to low dose aspirin therapy in patients at high risk of developing gastric ulcers for the prevention of cardiovascular disease, significantly reduced their risk of ulcer development. Pharmacokinetic and pharmacodynamic studies suggested that esomeprazole did not affect the pharmacokinetic parameters or the antiplatelet effects of aspirin. Therefore, for those patients who are at a high risk of developing a gastrointestinal ulcer, the benefit of adding esomeprazole likely outweighs the risks of longer term proton pump inhibitor use, and the combination can be recommended. Administering the two agents separately may also be more economical. On the other hand, for those patients at lower risk of developing a gastrointestinal ulcer, both the additional risk and cost make the inclusion of a proton pump inhibitor unwarranted

Right heart failure: toward a common language

Abstract In this guideline, the International Right Heart Foundation Working Group moves a step forward to develop a common language to describe the development and defects that exemplify the common syndrome of right heart failure. We first propose fundamental definitions of the distinctive components of the right heart circulation and provide consensus on a universal definition of right heart failure. These definitions will form the foundation for describing a uniform nomenclature for right heart circulatory failure with a view to foster collaborative research initiatives and conjoint education in an effort to provide insight into mechanisms of disease unique to the right heart

Sources, Fate, and Impact of Microplastics in Aquatic Environment

Over the past decade, enhanced scientific interest has produced an expanding knowledge base for microplastics. The highest abundance of microplastics is typically associated with coastlines and oceans but the fate of these microplastics is elusive. Microplastics sink following fragmentation which is further ingested by marine biota thus imposes threat to them. Thus, the present review focuses on properties and sources of microplastics, its impact on environment, the bioaccumulation and trophic transfer of microplastics and its impact on living biota. This study would be helpful for the development and implementation of risk management strategies for managing the disposal of microplastics

Advanced cancer is also a heart failure syndrome: a hypothesis

We present the hypothesis that advanced stage cancer is also a heart failure syndrome. It can develop independently of or in addition to cardiotoxic effects of anti-cancer therapies. This includes an increased risk of ventricular arrhythmias. We suggest the pathophysiologic link for these developments includes generalized muscle wasting (i.e. sarcopenia) due to tissue homeostasis changes leading to cardiac wasting associated cardiomyopathy. Cardiac wasting with thinning of the ventricular wall increases ventricular wall stress, even in the absence of ventricular dilatation. In addition, arrhythmias may be facilitated by cellular wasting processes affecting structure and function of electrical cells and conduction pathways. We submit that in some patients with advanced cancer (but not terminal cancer), heart failure therapy or defibrillators may be relevant treatment options. The key points in selecting patients for such therapies may be the predicted life expectancy, quality of life at intervention time, symptomatic burden, and consequences for further anti-cancer therapies. The cause of death in advanced cancer is difficult to ascertain and consensus on event definitions in cancer is not established yet. Clinical investigations on this are called for. Broader ethical considerations must be taken into account when aiming to target cardiovascular problems in cancer patients. We suggest that focused attention to evaluating cardiac wasting and arrhythmias in cancer will herald a further evolution in the rapidly expanding field of cardio-oncology

901-25 The Paradox of Donor Stimulation of Endothelial-induced Smooth Muscle Growth

Cardiac allograft vasculopathy (CAV) is the major cause of long-term morbidity and mortality in cardiac transplant recipients. It appears to be related to immune damage to the coronary endothelial cells, resulting in intimal proliferation. In order to delineate the mechanisms by which CAY can occur, a co-culture model of human endothelial cells (EC) and smooth muscle cells (SMC) obtained from the donor at the time of organ procurement was utilized. These cells were separated by collagenase digestion, and cultured for four passages. EC and SMC were then grown to confluence in the separate chambers of a co-culture plate separated by a 0.45 micron Millipore filter. Preserved lymphocytes (LYMPH) obtained from the donor and pooled blood lymphocytes from the recipient 3-4 weeks following transplant were added to the EC well so as to cause an immunologic stimulation of the EC. None of the recipients were exposed to monoclonal or polyclonal antibodies to lymphocytes. All cultures and assays were done in triplicate. Results are as follows:Patient#% Increase in donor lymph H3thymidinep ValueDonor 1+510.04Donor 2+450.05Donor 3+1040.05Donor 4+250.01Donor 5-19NSThe donor EC/donor LYMPH co-culture stimulated SMC growth measured by H3thymidine incorporation in 4 of 5 patients. The donor EC/recipient LYMPH co-culture did not result in significant SMC H3thymidine incorporation.ConclusionThese paradoxical findings of a lack in significant SMC proliferation in the recipient stimulated donor cells continue to raise questions in relation to the effects of circulating lymphocytes on the development of cardiac allograft vasculopathy