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Myocarditis
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
George Lazaros, Emilia Lazarou, Dimitris Tousoulis
In acute myocarditis with left ventricular dysfunction, the term “infective cardiomyopathy” is reserved for cases attributed to infection.2–4 In this context, the term “viral cardiomyopathy” is used in cases of persistent cardiotropic viral genome in endomyocardial biopsy (EMB) samples, detected with polymerase chain reaction, and accompanied by inflammation. In contrast, the term “viral heart disease” denotes the presence of ongoing lytic viral infection without concurrent inflammation.2–5 “Inflammatory cardiomyopathy” is used in cases of dilated cardiomyopathy due to biopsy-proven non-infectious myocarditis, demonstrated by the presence of inflammation in the absence of infectious microorganisms.2–5 When neither viral genome nor inflammation is demonstrated in a patient with dilated cardiomyopathy, then the term “idiopathic dilated cardiomyopathy” is used in the absence of a pathogenic gene mutation (see Chapter 31).5 This nomenclature is useful for clinical and research purposes and has contributed to overcoming the confusion created by different definitions in this setting.
Exercise and Infection
Published in Ronald R. Watson, Marianne Eisinger, Exercise and Disease, 2020
David C. Nieman, Sandra L. Nehlsen-Cannarella
It has been known for several decades that many types of viral infections can produce myocarditis and/or pericarditis.81 Respiratory infections, including the “common cold” and “flu” syndromes are all potentially serious; the patient may be prone to develop cardiac damage and sudden death through acute arrhythmias. Patients who develop viral cardiomyopathy are usually previously healthy, young people who have stressed themselves with vigorous, prolonged physical exercise during the height of a viral infection, or soon thereafter. Furthermore, these subjects usually have continued with stressful exercise, while ignoring the early onset of dyspnea, palpitation, weakness, fatigability, and general ill feeling — all symptoms and signs also observed in persons suffering cardiac damage. It is recommended that strenuous physical stress be avoided for at least two weeks post-infection.81
Copper deficiency myeloneuropathy with a history of malabsorption: a tale of two cases
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Anum Qureshi, Emily Bergbower, Janki Patel
We present the case of a 69-year-old female who presented with the complaints of recurrent nausea and vomiting. Her medical history is significant for stage IV colon cancer status post (s/p) resection and colostomy placement, viral cardiomyopathy, ventricular tachycardia s/p AICD placement, malnutrition, hypoalbuminemia, and multiple small bowel obstructions. She was initially assessed at her nursing home where an x-ray of the abdomen showed small bowel obstruction. On admission, a CT scan showed was suggestive of small bowel obstruction with marked dilatation of the stomach and proximal small bowel loops, decompressed distal small bowel, and a transition point within the midline of the pelvis. She was evaluated by colorectal surgery who recommended conservative management and nasogastric (NG) tube placement.
NRG1 PLGA MP locally induce macrophage polarisation toward a regenerative phenotype in the heart after acute myocardial infarction
Published in Journal of Drug Targeting, 2019
S. Pascual-Gil, G. Abizanda, E. Iglesias, E. Garbayo, F. Prósper, M. J. Blanco-Prieto
As a consequence, the ideal treatment for AMI should address inflammation, enhancing the reparative over the inflammatory response and inducing positive heart tissue remodelling and repair. Among the new treatments currently under development for AMI, protein therapy is probably the most promising [13–16]. Protein therapy consists of the administration of growth factors (GF) into the heart. Several GF have been tested so far for tissue repair in the cardiovascular field [17]. Among these, neuregulin-1 (NRG1) holds huge potential for cardiac repair in mammals, since it promotes cardiomyocyte proliferation, angiogenesis, arteriogenesis, embryonic stem cell differentiation into cardiac lineage and stem cell survival [12,18,19]. Importantly, NRG1 is not only effective in the early development of the heart, but also prevents severe dysfunction of the adult heart and improves cardiac performance in rodent models of ischaemic, dilated and viral cardiomyopathy [20], making NRG1 a broad-spectrum therapeutic agent for the treatment of heart failure. In addition, our group has shown NRG1 efficacy in a large pre-clinical model of AMI in pigs [21]. Nevertheless, the effects NRG1 may have on inflammatory response remain unknown. Moreover, NRG1 is a labile molecule with an extremely short circulating half-life of 30 min [22]. Therefore, it is encapsulated into delivery systems such as poly (lactic-co-glycolic acid) microparticles (PLGA MP) to protect it against in vivo degradation and to improve its bioavailability [17,23]. It is worth noting that although PLGA is a biodegradable and biocompatible polymer approved by the Food and Drug Administration for use in humans, inflammatory responses associated with PLGA administration were reported in some cases [24]. In particular, predicting the behaviour of the phagocytic cells after particle uptake may be challenging, and is extremely important to evaluate the contributions of both polymer and GF to the inflammatory response [25]. Finally, inflammation in adult mammals is a progressive process in which macrophage populations evolve dramatically over time [26]. piMac and aiMac have different genotypes and functions and may respond differently to the presence of NRG1 PLGA MP. As a consequence, the time of treatment administration could affect polarisation and resolution of inflammation, which could condition final heart repair. Taking all this into account, the objective of this paper is to assess the relationship between NRG1 PLGA MP and the heart inflammatory response after AMI.