Simultaneous measurement of serum cTnT and NT-proBNP allows for precise APE prognosis. Normotensive patients on admission with cTnT> or =0.07 microg/L and NT-proBNP> or =600 ng/L are at high risk of APE mortality, whereas NTproBNP<600 ng/L indicates excellent prognosis.

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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 (NTproBNP) 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?mL -1 (range 61-60,958)) than without RV strain (363 pg?mL -1 329)). 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. Eur Respir J 2003; 22: 649-653. Elevated plasma levels of brain natriuretic peptide (BNP) released from myocytes of ventricles upon stretch have been found in patients with congestive heart failure and even in those with asymptomatic left ventricular (LV) systolic dysfunction [1,2]. Moreover, elevated plasma BNP was found in patients with primary pulmonary hypertension and chronic thromboembolic pulmonary hypertension [3,4]. Interestingly, elevated plasma BNP was reported to help differentiate pulmonary from cardiac aetiologies of acute dyspnoea [5]. Plasma N-terminal proBNP (NT-proBNP) is also increased in congestive heart failure patients [6] and it may help to stratify their prognosis [7,8]. However, limited data suggest that plasma BNP may be elevated in patients with acute pulmonary embolism (APE), frequently accompanied by acute dyspnoea and right ventricular (RV) dysfunction [9][10][11]. Therefore, the aim of this study was to assess plasma levels of NT-proBNP in patients with APE, and to establish whether the levels reflect the severity of RV overload and whether they can be used to predict adverse clinical outcome. Materials and methods Clinical dataThe study analysed consecutive patients with symptomatic APE. APE was confirmed by contrast-enhanced spiral computed tomography or by high-probability lung scintigraphy according to PIOPED (Prospective Investigation of Pulmonary Embolism Diagnosis) criteria [12]. On admission, systemic blood pressure (BP) and cardiac frequency...

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SummaryBackground and hypothesis: Hemodynamic and functional consequences of acute pulmonary embolism (APE) are believed to be reversible with antithrombotic treatment. To verify this hypothesis, we reassessed our patients at least 1 year after an episode of APE.Methods: We compared echo Doppler indices and 6-min walking test parameters (6-MWT) of 36 patients (13 men, 23 women, age 66 ± 11 years), studied on average 3.1 ± 2.2 years after an acute episode of pharmacologically treated massive or submassive APE, with data of 30 age-matched subjects (12 men, 18 women, age 67 ± 12 years).Results: At least 1 year after APE, right ventricular (RV) diameter remained increased in patients compared with controls (27 ± 2 vs. 23 ± 2 mm, p < 0.001). Also, acceleration time of pulmonary ejection (AcT) was markedly shorter (97 ± 19 vs. 123 ± 19 ms, p < 0.001) and the diameter of the pulmonary trunk was significantly larger in patients than in controls (21 ± 2.6 vs. 18 ± 2.2, p < 0.001). Although the mean value of the tricuspid valve peak systolic gradient (TVPG) in the APE group at follow-up was similar to that in controls, TVPG > 30 mmHg was recorded in three patients with APE (8.3%). There was no difference in the distance of 6-MWT between both groups; however, the mean desaturation after 6-MWT was higher in the APE group than in controls (3.04 ± 2.08 vs. 1.45 ± 0.69%, p = 0.0005).

The aim of the present study was to analyze the profiles of cardiac microRNAs (miRNAs/miRs) in healthy pregnant women and non-pregnant controls. A total of 61 healthy women >18 years of age with singleton pregnancies in the third trimester were compared with 19 non-pregnant controls. Specifically, expression of miRNAs associated with cardiac hypertrophy (miR-1, miR-17-5, miR-22, miR-34a, miR-124, miR-133a, miR-195, miR-199a-3p, miR-199b, miR-210, miR-222 and miR-1249) and miRNAs associated with cardiac hypertrophy and fibrosis (miR-15b, miR-21, miR-26a, miR-29-a, miR-29c, miR-30c, miR-101, miR-146a, miR-191, miR-208a-5p and miR-328) were analyzed and compared with echocardiographic examination results. Both groups had similar cardiac miRNA expression profiles, but differed in quantitative evaluation. Women in the third trimester of physiological pregnancy exhibited downregulation of certain profibrotic miRNAs (miR-21, miR-30c and miR-328), decreased expression of a hypertrophic and antimetabolic miRNAs (miR-146a), downregulation of an antifibrotic miRNA (miR-222), and downregulation of a hypertrophic miRNA (miR-195). In pregnant women, the indices of systolic function were associated with miR-195 expression, and an interplay between miR-17-5p and diastolic function was observed. While the profiles of cardiac miRNAs expressed in healthy pregnant women and healthy non-pregnant controls were similar, these two groups differed in terms of expression of specific miRNAs. In the third trimester of physiological pregnancy, a downregulation of miR-17-5p, miR-21, miR-30c, miR-146a, miR-195, miR-222 and miR-328 was observed. The differences in the association between echocardiographic indices with miRNAs in pregnant and non-pregnant women suggest that miRNAs regulate both the structure and function of the pregnant heart, influencing cardiac muscle thickness as well as systolic and diastolic function.

In the 3rd trimester of physiological pregnancy, there is a 244% increase in expression of miR-101a and a decrease by 73% in expression of miR-328. Both of these changes can protect against fibrosis during volume overload occurring in physiological pregnancy.