Home About us Contact
|
Home About us Contact | ||
|
|
||
Systolic Pulmonary Artery Pressure (systolic + pulmonary_artery_pressure)
Selected AbstractsTonsil size as a predictor of cardiac complications in children with sleep-disordered breathing,THE LARYNGOSCOPE, Issue 6 2010Eduardo Homrich Granzotto MD Abstract Objectives/Hypothesis: The primary objective was to evaluate the association of palatine (T/P) tonsil size determined by radiography with pulmonary artery pressure (PAP) measured by Doppler echocardiography in children with surgical indication for adenotonsillar hypertrophy. The secondary objective was to evaluate if tonsil size could help to identify children at higher risk of pulmonary artery hypertension (PAH). Study Design: Cross-sectional study. Methods: The study was conducted with a consecutive sample of children with indication of adenotonsillectomy for sleep-disordered breathing. T/P was measured by lateral neck radiography, PAP by echodopplercardiography, and symptoms and quality of life by the Obstructive Sleep Apnea (OSA)-18 questionnaire. T/P was plotted in a receiver operating characteristic (ROC) curve to determine the best cut-off point to identify children with PAH. Results: A total of 45 children participated in the study. The mean age was 72.0 ± 32.3 months, and six (13%) patients had PAH. Correlation between systolic PAP and T/P was strong (r = 0.624; P < .0001). T/P was significantly higher in patients with PAH (P < .001). OSA-18 score did not significantly correlate with the variables. The cut-off point identified in the ROC was 0.66, which was the minimum T/P where sensitivity was still 100%. Mean systolic pulmonary artery pressure in children with T/P >0.66 was significantly higher than in those with T/P <0.66 (P < .001). Conclusions: T/P showed a good correlation with PAP in children with adenotonsillar hypertrophy and surgical indication for sleep-disordered breathing. Children with T/P >0.66 can be at greater risk for cardiac complications and should be submitted to complementary studies with echodopplercardiography or given preference for surgery. [source] High N-terminal pro,brain natriuretic peptide levels and low diffusing capacity for carbon monoxide as independent predictors of the occurrence of precapillary pulmonary arterial hypertension in patients with systemic sclerosisARTHRITIS & RHEUMATISM, Issue 1 2008Y. Allanore Objective To evaluate predictors of pulmonary arterial hypertension (PAH) in a prospective cohort of patients with systemic sclerosis (SSc). Methods Routine clinical assessments as well as measurements of the diffusing capacity for carbon monoxide/alveolar volume (DLCO/VA) ratio and N-terminal pro,brain natriuretic peptide (NT-proBNP) level were performed in a prospective cohort of 101 SSc patients who did not have PAH or severe comorbidities. After a planned 36-month followup, we evaluated the predictive value of these parameters for the development of precapillary PAH, as demonstrated by cardiac catheterization, disease progression, and death. Criteria for cardiac catheterization were a systolic pulmonary artery pressure (PAP) of >40 mm Hg on echocardiography, a DLCO value of <50% without pulmonary fibrosis, and unexplained dyspnea. Results Eight patients developed PAH, 29 had disease progression, and 10 died during a median followup of 29 months. Kaplan-Meier analysis identified the following baseline parameters as being predictors of PAH: DLCO/VA ratio <70% or <60% (P < 0.01 for each comparison), elevated plasma NT-proBNP level (>97th percentile of normal; P = 0.005), echocardiographically estimated systolic PAP >40 mm Hg (P = 0.08), and erythrocyte sedimentation rate >28 mm/hour (P = 0.015). In multivariate analyses, an elevated baseline NT-proBNP level (hazard ratio [HR] 9.97 [95% confidence interval (95% CI) 1.69,62.42]) and a DLCO/VA ratio <60% (HR 36.66 [95% CI 3.45,387.6]) were predictors of the occurrence of PAH during followup. An increased NT-proBNP level together with a decreased DLCO/VA ratio of <70% was highly predictive of the occurrence of PAH during followup (HR 47.20 [95% CI 4.90,450.33]). Conclusion This prospective study identified a decreased DLCO/VA ratio and an increased NT-proBNP as predictors of PAH in SSc. Use of these markers should result in improved PAH risk stratification and allow earlier initiation of therapy. [source] N-terminal pro,brain natriuretic peptide as a diagnostic marker of early pulmonary artery hypertension in patients with systemic sclerosis and effects of calcium-channel blockersARTHRITIS & RHEUMATISM, Issue 12 2003Y. Allanore Objective To evaluate N-terminal pro,brain natriuretic peptide (NT-proBNP) as a marker of early pulmonary artery hypertension (PAH) and to study changes in the levels of this marker following treatment with dihydropyridine-type calcium-channel blocker (DTCCB) in patients with systemic sclerosis (SSc). Methods We evaluated 40 consecutive SSc patients who had been hospitalized for followup care (mean ± SD age 56 ± 11 years and mean ± SD duration of cutaneous disease 9 ± 9 years; 27 with limited cutaneous and 13 with diffuse cutaneous disease) but who had no clinical symptoms of heart failure and had a normal left ventricular ejection fraction. At baseline, 10 patients had PAH, defined as a systolic pulmonary artery pressure (sPAP) >40 mm Hg, as measured by echocardiography. Levels of NT-proBNP were determined at baseline (after discontinuation of DTCCB treatment for 72 hours), after taking 3 doses of DTCCB following treatment reinitiation (assessment 1), and after 6,9 months of continuous DTCCB treatment (assessment 2) in the 20 patients who attended regular appointments (including the 10 patients with PAH at baseline). Results At baseline, 13 patients had high NT-proBNP values for their ages. High NT-proBNP levels identified patients with PAH with a sensitivity of 90%, a specificity of 90.3%, a positive predictive value of 69.2%, and a negative predictive value of 96%. The NT-proBNP level correlated with the sPAP (r = 0.44; P = 0.006). By assessment 1, the number of patients with PAH and high levels of NT-proBNP had decreased from 9 of 10 to 2 of 10 (P = 0.02). This decrease was partially sustained at assessment 2 (4 of 10 patients; P = 0.06). Conclusion NT-proBNP is a useful biologic marker that can be used to diagnose early PAH in SSc patients without clinical heart failure. Measurement of NT-proBNP may be valuable for the evaluation of treatment with DTCCB and vasodilators in patients with PAH. [source] Levosimendan versus Dobutamine in Heart Failure Patients Treated Chronically with CarvedilolCARDIOVASCULAR THERAPEUTICS, Issue 3 2008Hamza Duygu Introduction: Although beta-blockers are highly effective in the treatment of heart failure (HF), many patients with HF receiving a beta-blocker continue to become decompensated and require hospitalization for worsening HF. Levosimendan and dobutamine are used to manage decompensated HF, but their comparative effects on left ventricular (LV) function in patients prescribed beta-blockers are unknown. Aims: The aim of this study was to compare the effects of dobutamine and levosimendan on LV systolic and diastolic functions in chronic HF patients treated chronically with carvedilol. Forty patients with chronic HF who had NYHA class III to IV symptoms, a LV ejection fraction (LVEF) <40%, and ongoing treatment with carvedilol were enrolled in this randomized (1:1), dobutamine controlled, open-label study. Before and 24 h after treatment, LVEF, mitral inflow peak E and A wave velocity, E/A ratio, the deceleration time of the E wave (DT), isovolumic relaxation time (IVRT), peak systolic (Sm) and early diastolic (Em) mitral annular velocity, and systolic pulmonary artery pressure (SPAP) were measured by echocardiography. Results: Levosimendan produced a statistically significant increase in LVEF (28 ± 5% vs. 33 ± 3%), Sm (6.5 ± 1.2 cm/s vs. 7.4 ± 0.9 cm/s), DT (120 ± 10 ms vs. 140 ± 15 ms), and Em (7.5 ± 0.4 cm/s vs. 8.1 ± 0.5 cm/s) and significant decrease in E/A ratio (2.1 ± 0.3 vs. 1.7 ± 0.4) and SPAP (55 ± 5 mmHg vs. 40 ± 7 mmHg). No significant change occurred in LV systolic and diastolic function parameters, or SPAP with dobutamine treatment. Levosimendan did not significantly alter the heart rate (72 ± 4 bpm vs. 70 ± 3 bpm), systolic (105 ± 5 mmHg vs. 102 ± 4 mmHg), or diastolic blood pressure (85 ± 5 mmHg vs. 83 ± 5 mmHg) whereas with dobutamine treatment, all these parameters significantly increased. Conclusions: Dobutamine and levosimendan have different effects on LV functions in patients treated chronically with carvedilol. These differences should be considered when selecting inotropic therapy for decompensated HF receiving long-term carvedilol. [source] Novel percutaneous catheter thrombectomy in acute massive pulmonary embolism: Rotational bidirectional thrombectomy (ROBOT)CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 1 2006Masashi Yoshida MD Abstract Background: Although thrombolysis is a standard therapy in cases of pulmonary embolism (PE), fatal outcome is often observed. We designed and investigated the efficacy of a novel percutaneous catheter therapy, rotational bidirectional thrombectomy (ROBOT), for PE. Methods and Results: Eighteen patients with acute massive PE (Miller score , 20) were included in this study. We separated them into two groups [group A (n = 10), thrombolysis; group B (n = 8): thrombolysis and ROBOT or ROBOT alone]. There was no difference in the hemodynamic indices between the groups at diagnosis. ROBOT was designed to fragment emboli by rotating a regular pigtail catheter. Three deaths occurred in group A because of hemodynamic impairment, but there was no death in group B. One day after treatment, systolic pulmonary artery pressure had decreased from 53 ± 8 to 30 ± 8 mm Hg (P < 0.05) in group B and from 54 ± 5 to 42 ± 19 mm Hg (NS) in group A. The hospitalization period in group B was shorter than that in group A (17 ± 6 vs. 27 ± 10 days, P < 0.05). Conclusion: ROBOT therapy results in a significant, rapid improvement in the hemodynamic situation and in a better outcome than conventional therapy in patients with acute massive pulmonary embolism. © 2006 Wiley-Liss, Inc. [source] | ||||||||||