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.

Factors related to the early and late success of direct current cardioversion of chronic nonrheumatic atrial fibrillation: An echocardiographic study.

OBJECTIVES: To assess factors related to the success of restoration and one-year maintenance of sinus rhythm in chronic (more than 48 h) nonrheumatic atrial fibrillation (AF). METHODS AND RESULTS: One hundred and fifty consecutive patients aged 62+/-9 years with AF lasting 123+/-254 days were evaluated clinically with transthoracic and transesophageal echocardiography before elective direct current cardioversion. Heart chamber dimensions and left ventricular ejection fraction were measured. The presence of left atrial thrombi and spontaneous echocardiographic contrast as well as flow velocities in the left atrial appendage were assessed. The first cardioversion was followed by standardized two-step antiarrhythmic treatment including a second cardioversion, if necessary. Twenty patients (13%) spontaneously reverted to sinus rhythm (S) during anticoagulation preceding cardioversion, 81 (54%) were successfully cardioverted (Y), and in 49 (33%) cardioversion failed initially (N). No differences were noted between the two latter groups. However, S patients had smaller left atria measured in the short and long axes (42+/-4 mm, P=0.05, and 53+/-7 mm, P=0.005, respectively) than both the Y (45+/-4 and 61+/-8 mm) and the N patients (46+/-4 and 61+/-8 mm). One-year follow-up was obtained in 95 patients: 64 (67%) were in sinus rhythm while 31 (33%) had AF. Again, no initial differences predicting the maintenance of sinus rhythm were found. CONCLUSIONS: Spontaneous reversion of AF seems more likely with smaller left atria. Echocardiography, including trans-esophageal echocardiography, is unlikely to identify patients in whom attempts to restore and maintain sinus rhythm will fail or succeed.

[Primary prostaglandins PGE2, PGF2, prostacyclin and thromboxane in patients with myocardial infarction]. / Prostaglandyny pierwotne PGE2, PGF2 alpha, oraz prostacyklina i tromboksan u chorych z zawalem serca.

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.