Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A cytomegalovirus-associated heart failure in a young infant with atrial and ventricular septal defects is reported in this case report. The patient recovered by an anti-congestive and anti-viral therapy with an extra percutaneous transcatheter treatment strategy. In the context of bi-ventricular predominant right heart failure associated with supra-systemic pulmonary hypertension, the already closed arterial duct was re-opened and stented to unload the right ventricle and thereby augment the systemic blood flow. Either the left-to-right shunting atrial septal defect or bi-directional shunting ventricular septal defect was involved in the disease process and was not able to avoid global heart failure. After clinical improvement, the stented duct was shunted left-to-right and was occluded with an ADO-II-AS. During the same procedure the atrial septal defect was closed with an Amplatzer-ASD occluder, while the peri-membranous ventricular septal defect was closed with an ADO-II occluder 2 months later.
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PMID:Fulminant cytomegalovirus myocarditis in an infant with concomitant large atrial and ventricular septal defects: medical intervention strategy for functional cardiac regeneration. 3057 76

Cytomegalovirus (CMV) seropositivity in adults has been linked to increased cardiovascular disease burden. Phenotypically, CMV infection leads to an inflated CD8 T-lymphocyte compartment. We employed a 8-colour flow cytometric protocol to analyse circulating T cells in 597 octogenarians from the same birth cohort together with NT-proBNP measurements and followed all participants over 7 years. We found that, independent of CMV serostatus, a high number of CD27-CD28+ CD8 EMRA T-lymphocytes (TEMRA) protected from all-cause death after adjusting for known risk factors, such as heart failure, frailty or cancer (Hazard ratio 0.66 for highest vs lowest tertile; confidence interval 0.51-0.86). In addition, CD27-CD28+ CD8 EMRA T-lymphocytes protected from both, non-cardiovascular (hazard ratio 0.59) and cardiovascular death (hazard ratio 0.65). In aged mice treated with the senolytic navitoclax, in which we have previously shown a rejuvenated cardiac phenotype, CD8 effector memory cells are decreased, further indicating that alterations in T cell subpopulations are associated with cardiovascular ageing. Future studies are required to show whether targeting immunosenescence will lead to enhanced life- or healthspan.
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PMID:CMV-independent increase in CD27-CD28+ CD8+ EMRA T cells is inversely related to mortality in octogenarians. 3199 14

Coronavirus disease 2019 (COVID-19) has been reported as the possible cause of acute myocarditis. Myocarditis is an inflammatory heart disease mostly caused by viral infections. Cytomegalovirus (CMV) primary infection is often not suspected as a cause of myocarditis in immune-competent adults. We report the case of a 37-year-old male admitted with fever, cough and dyspnea. Chest CT showed typical ground-glass changes indicative of viral pneumonia. He was tested negative for COVID-19 but had biological markers that made us still suspect it. He had elevated troponin I level (up to 111.5 ng/mL) and diffuse myocardial dyskinesia along with a decreased left ventricular ejection fraction (LVEF). He was diagnosed with CMV myocarditis with cardiac insufficiency and totally recovered without antiviral therapy. During the COVID-19 pandemic patients may develop myocarditis, still every myocarditis is not a COVID infection. Myocarditis linked to CMV infection may be rare, but life-threatening.
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PMID:A misleading CMV myocarditis during the COVID-19 pandemic: case report. 3295 11


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