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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

ACE (angiotensin converting enzyme) inhibitors are revolutionizing the management of heart failure and are now earning themselves a place in the early treatment of post myocardial infarction (MI) patients who have evidence of left ventricular (LV) dysfunction or, more modestly, evidence of infarct expansion. The aims of ACE inhibitor therapy are to control symptoms, if any, and to improve prognosis. For these indications, they are impressive. Nonetheless, they are not a panacea. Post MI patients face a variety of threats, not least from progression of their underlying ischemic disease, and they should not be denied prognostically advantageous interventions, such as beta-blockers and aspirin. Moreover, ACE inhibitor monotherapy may not be the best management for heart failure itself. The role of other additive agents should not be dismissed.
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PMID:Post infarct heart failure: what to do in addition to ACE inhibition. 791 1

Cardiovascular disease is the leading cause of death in developed countries (40% of all causes of mortality). Heart disease is common in the working age population and thus it contributes to a decline in employees' fitness for work. In Israel about 80% of patients recuperating from myocardial infarction (MI) return to work. However, long term employment may be as low as 50% and its patterns are associated predominantly with patient age and job characteristics, as compared to measures of illness severity or the method of coronary revascularization. The need for clinical guidelines in the management of return to work after myocardial infarction has recently led to the initiation of a joint committee of the Israeli National Heart and Occupational Societies. These clinical guidelines have been published and are summarized in this issue. For most common cardiac disease, including heart failure, valve disease and angina, patients can exert themselves up to onset of symptoms. Therefore, patients with functional capacity I and II, as estimated by New York Heart Association (NYHA) criteria, can return to their previous work. Timing of return to work for patients with asymptomatic uncomplicated cardiac disease: Post MI within 4 weeks, CABG within 4-8 weeks and percutaneous interventions within 1 week. For patients with a strenuous job or in NYHA functional capacity III or IV, a few weeks of delay and exercise or other functional testing may be needed. There are a few exceptions including patients with strenuous work or specific cardiac diseases as hypertrophic cardiomyopathy, severe aortic stenosis and Marfan's syndrome. In such cases, cardiological and occupational specialist advice should be sought.
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PMID:[Return to work with heart disease]. 1735 80

In cardiovascular disorders including advanced atherosclerosis and myocardial infarction (MI), increased cell death and tissue destabilization is associated with recruitment of inflammatory monocyte subsets that give rise to differentiated macrophages. These phagocytic cells clear necrotic and apoptotic bodies and promote inflammation resolution and tissue remodeling. The capacity of macrophages for phagocytosis of apoptotic cells (efferocytosis), clearance of necrotic cell debris, and repair of damaged tissue are challenged and modulated by local cell stressors that include increased protease activity, oxidative stress, and hypoxia. The effectiveness, or lack thereof, of phagocyte-mediated clearance, in turn is linked to active inflammation resolution signaling pathways, susceptibility to atherothrombosis and potentially, adverse post MI cardiac remodeling leading to heart failure. Previous reports indicate that in advanced atherosclerosis, defective efferocytosis is associated with atherosclerotic plaque destabilization. Post MI, the role of phagocytes and clearance in the heart is less appreciated. Herein we contrast the roles of efferocytosis in atherosclerosis and post MI and focus on how targeted modulation of clearance and accompanying resolution and reparative signaling may be a strategy to prevent heart failure post MI.
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PMID:Contrasting Inflammation Resolution during Atherosclerosis and Post Myocardial Infarction at the Level of Monocyte/Macrophage Phagocytic Clearance. 2256 22

In response to myocardial infarction (MI), time-dependent leukocyte infiltration is critical to program the acute inflammatory response. Post-MI leukocyte density, residence time in the infarcted area, and exit from the infarcted injury predict resolving or nonresolving inflammation. Overactive or unresolved inflammation is the primary determinant in heart failure pathology post-MI. Here, our review describes supporting evidence that the acute inflammatory response also guides the generation of healing and regenerative mediators after cardiac damage. Time-dependent leukocyte density and diversity and the magnitude of myocardial injury is responsible for the resolving and nonresolving pathway in myocardial healing. Post MI, the diversity of leukocytes, such as neutrophils, macrophages, and lymphocytes, has been explored that regulate the clearance of deceased cardiomyocytes by using the classic and reparative pathways. Among the innovative factors and intermediates that have been recognized as essential in acute the self-healing and clearance mechanism, we highlight specialized proresolving mediators as the emerging factor for post-MI reparative mechanisms-translational leukocyte modifiers, such as aging, the source of leukocytes, and the milieu around the leukocytes. In the clinical setting, it is possible that leukocyte diversity is more prominent as a result of risk factors, such as obesity, diabetes, and hypertension. Pharmacologic agents are critical modifiers of leukocyte diversity in healing mechanisms that may impair or stimulate the clearance mechanism. Future research is needed, with a focused approach to understand the molecular targets, cellular effectors, and receptors. A clear understanding of resolving and nonresolving inflammation in myocardial healing will help to develop novel targets with major emphasis on the resolution of inflammation in heart failure pathology.-Tourki, B., Halade, G. Leukocyte diversity in resolving and nonresolving mechanisms of cardiac remodeling.
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PMID:Leukocyte diversity in resolving and nonresolving mechanisms of cardiac remodeling. 2864 28