Akutní srdecní selhání a casný rozvoj dysfunkce levé komory a patientů s akutním infarktem myokardu s elevacemi ST lécených primární perkutánní koronární intervencí
[Acute heart failure and early development of left ventricular dysfunction in patients with ST segment elevation acute myocardial infarction managed with primary percutaneous coronary intervention]
Jazyk čeština Země Česko Médium print
Typ dokumentu anglický abstrakt, časopisecké články
PubMed
21351662
- MeSH
- balónková koronární angioplastika * MeSH
- dospělí MeSH
- dysfunkce levé srdeční komory etiologie MeSH
- echokardiografie MeSH
- elektrokardiografie * MeSH
- hemodynamika MeSH
- infarkt myokardu komplikace diagnóza patofyziologie terapie MeSH
- lidé středního věku MeSH
- lidé MeSH
- mortalita v nemocnicích MeSH
- natriuretický peptid typu B krev MeSH
- peptidové fragmenty krev MeSH
- prognóza MeSH
- rizikové faktory MeSH
- senioři MeSH
- srdeční selhání etiologie MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- anglický abstrakt MeSH
- časopisecké články MeSH
- Názvy látek
- natriuretický peptid typu B MeSH
- peptidové fragmenty MeSH
- pro-brain natriuretic peptide (1-76) MeSH Prohlížeč
BACKGROUND: Acute heart failure during ST elevation myocardial infarction (STEMI) makes worse prognosis. The aim of the work was to find independent factors with relationship to acute heart failure (AHF) and the early development of left ventricular dysfunction within the prospective followed patients with STEMI. METHODS: A total of 593 patients with STEMI treated by primary PCI (164 patients with AHF) were the study population. The activity of BNP and NT-ProBNP were measured at hospital admission and 24 h after MI onset. Left ventricular angiography was done before PCI; echocardiography was undertaken between the third and fifth day after MI. RESULTS: The patients with AHF had higher level of glycaemia, creatinine, uric acid, HDL-cholesterol, leukocytosis and natriuretic peptid. The total hospital mortality was 3.7%. 0.2% within the patients without AHF, 3.2%, 14.3%, resp. 63.6% within the patients with mild AHF, with pulmonary oedema, resp. with cardiogenic shock. The patients with AHF had lower ejection fraction (45.4 +/- 11.9% vs 53.0 +/- 10.3%). According to the multiple logistic regression we found higher glycaemia, age, heart rate, anterior wall MI, lower aortic pulse pressure and collaterals of infarct related artery as factors with independent relationship to AHF. Higher glycaemia, age, heart rate, anterior wall MI and lower aortic pulse pressure were found as independent factors with relationship to left ventricular dysfunction. According to ROC analysis possible cut off corresponding with AHF we suggested 29.5 mm Hg for LVEDP, 28.5 for dP/dt/P, 9.5 mmol/l for glycaemia, 50 mm Hg for aortic pulse pressure. CONCLUSIONS: Our results found the development of AHF in one third of patients with STEMI. AHF increases the risk of in-hospital mortality and the risk depends upon severity of failure. As the independent factors with relationship to development of AHF or left ventricular dysfunction we detected higher glycaemia, heart rate, anterior wall MI, age. Lower risk had patients with higher aortic pulse pressure.