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Biomedical subjects

I Chlewicka

Publications and source records attributed to I Chlewicka.

At least 19 recordsLinked to original sources

N-terminal pro-brain natriuretic peptide in patients with acute pulmonary embolism.

Plasma brain natriuretic peptide (BNP), released from myocytes of ventricles upon stretch, has been reported to differentiate pulmonary from cardiac dyspnoea. Limited data have shown elevated plasma BNP levels in acute pulmonary embolism (APE), frequently accompanied by dyspnoea and right ventricular (RV) dysfunction. The aim of this study was to assess plasma N-terminal proBNP (NT-proBNP) in APE, and to establish whether it reflects the severity of RV overload and if it can be used to predict adverse clinical outcome. On admission, NT-proBNP and echocardiography for RV overload were performed in 79 APE patients (29 males), aged 63 +/- 16 yrs. Plasma NT-proBNP was elevated in 66 patients (83.5%) and was higher in patients with (median 4,650 pg x mL(-1) (range 61-60,958)) than without RV strain (363 pg x mL(-1) (16-16,329)). RV-to-left ventricular ratio and inferior vena cava dimension correlated with NT-proBNP. All 15 in-hospital deaths and 24 serious adverse events occurred in the group with elevated NT-proBNP, while all 13 (16.5%) patients with normal values had an uncomplicated clinical course. Plasma NT-proBNP predicted in-hospital mortality. Plasma N-terminal pro-brain natriuretic peptide is elevated in the majority of cases of pulmonary embolism resulting in right ventricular overload. Plasma levels reflect the degree of right ventricular overload and may help to predict short-term outcome. Acute pulmonary embolism should be considered in the differential diagnosis of patients with dyspnoea and abnormal levels of brain natriuretic peptide.

Acute Disease↗

[Primary prostaglandins PGE2, PGF2, prostacyclin and thromboxane in patients with myocardial infarction].

In 47 patients with acute myocardial infarction and in 17 healthy volunteers blood concentration and urinary excretion of PGE2, PGF2 alpha, 6-keto-PGF1 alpha--hydrolysis product of prostacyclin--and TXB2 were determined using RIA. Myocardial infarction patients were found to have significantly higher blood level and urinary excretion of 6-keto-PGF1 alpha, higher blood level of PGF2 and higher urinary excretion of TXB2 than controls, PGE2 urinary excretion was significantly lower. Increased excretion of 6-keto-PGF1 alpha was observed in patients with ventricular arrhythmias. Excretion of all determined prostaglandins was increased in patients with myocardial infarction complicated by atrioventricular block as compared to the other patients. The results suggest, that increase of prostacyclin synthesis in the acute phase of myocardial infarction may provide protection mechanism against heart muscle damage and improve coronary blood flow.

Adult↗