title: [Myocardial dysfunction during sepsis: epidemiology, prognosis and treatment].
abstract: About 50% of patients with sepsis show myocardial involvement characterized by biventricular enlargement, reduced contractility and diastolic dysfunction. This increases the risk of death and leads to an extremely poor prognosis in the case of severe sepsis or septic shock, with full recovery of cardiac function seen in survivors at 7-10 days. The pathogenesis of myocardial dysfunction has long been investigated and, although it is still not fully understood, seems not to be due to reduced coronary flow, but to circulating substances released by pathogens (e.g. endotoxins) and host immuno-inflammatory responses (e.g. cytokines and mechanisms related to nitric oxide). First-line therapy is causal and consists of antibiotics plus the surgical excision of the infectious focus; in the presence of severe sepsis or septic shock, it is also necessary to promptly start circulatory and multiorgan support treatment. This review describes current knowledge concerning the instrumental and clinical characteristics, pathophysiology, prognosis and therapy of myocardial dysfunction during sepsis, and briefly considers possible future therapeutic perspectives.
authors.affiliation: Azienda Ospedaliero-Universitaria, Parma. gpaoli@ao.pr.it
authors.forename: Giorgia
authors.initials: G
authors.lastname: Paoli
authors.forename: Serafina
authors.initials: S
authors.lastname: Valente
authors.forename: Diego
authors.initials: D
authors.lastname: Ardissino
authors.forename: Gian Franco
authors.initials: GF
authors.lastname: Gensini
mesh_terms: D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D015415:Biomarkers; D009202:Cardiomyopathies / Q000097:blood / Q000188:drug therapy / Q000453:epidemiology / Q000209:etiology* / Q000503:physiopathology; D002317:Cardiovascular Agents / Q000627:therapeutic use; D003131:Combined Modality Therapy; D015936:Complement C5a / Q000502:physiology; D015908:Counterpulsation; D016207:Cytokines / Q000502:physiology; D016232:Endothelins / Q000502:physiology; D004731:Endotoxins / Q000009:adverse effects; D006801:Humans; D007167:Immunotherapy; D008929:Mitochondria, Heart / Q000187:drug effects / Q000502:physiology; D009200:Myocardial Contraction / Q000187:drug effects; D009569:Nitric Oxide / Q000502:physiology; D011379:Prognosis; D018805:Sepsis / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology / Q000601:surgery; D051197:Toll-Like Receptor 4 / Q000502:physiology
chemical_list: D000900:Anti-Bacterial Agents; D015415:Biomarkers; D002317:Cardiovascular Agents; D016207:Cytokines; D016232:Endothelins; D004731:Endotoxins; C495345:TLR4 protein, human; D051197:Toll-Like Receptor 4; D009569:Nitric Oxide; D015936:Complement C5a