Accuracy of Doppler echocardiography in the hemodynamic assessment of pulmonary hypertension

Division of Pulmonary and Critical Care Medicine, Department of Medicine, Johns Hopkins University, Baltimore, Maryland, USA.
American Journal of Respiratory and Critical Care Medicine (Impact Factor: 11.99). 02/2009; 179(7):615-21. DOI: 10.1164/rccm.200811-1691OC
Source: PubMed

ABSTRACT Transthoracic Doppler echocardiography is recommended for screening for the presence of pulmonary hypertension (PH). However, some recent studies have suggested that Doppler echocardiographic pulmonary artery pressure estimates may frequently be inaccurate.
Evaluate the accuracy of Doppler echocardiography for estimating pulmonary artery pressure and cardiac output.
We conducted a prospective study on patients with various forms of PH who underwent comprehensive Doppler echocardiography within 1 hour of a clinically indicated right-heart catheterization to compare noninvasive hemodynamic estimates with invasively measured values.
A total of 65 patients completed the study protocol. Using Bland-Altman analytic methods, the bias for the echocardiographic estimates of the pulmonary artery systolic pressure was -0.6 mm Hg with 95% limits of agreement ranging from +38.8 to -40.0 mm Hg. Doppler echocardiography was inaccurate (defined as being greater than +/-10 mm Hg of the invasive measurement) in 48% of cases. Overestimation and underestimation of pulmonary artery systolic pressure by Doppler echocardiography occurred with a similar frequency (16 vs. 15 instances, respectively). The magnitude of pressure underestimation was greater than overestimation (-30 +/- 16 vs. +19 +/- 11 mm Hg; P = 0.03); underestimates by Doppler also led more often to misclassification of the severity of the PH. For cardiac output measurement, the bias was -0.1 L/min with 95% limits of agreement ranging from +2.2 to -2.4 L/min.
Doppler echocardiography may frequently be inaccurate in estimating pulmonary artery pressure and cardiac output in patients being evaluated for PH.

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    • "Furthermore, we measured the peak velocity of the tricuspid regurgitant signal by continuous wave doppler and calculated the RVSP with the modified Bernoulli equation, which is believed to reflect systolic PA-pressure in the absence of RV outflow tract obstruction. Theoretically, calculation of mPAP from systolic PA-pressure (PASP) is possible, {mPAP = (0.61×PASP) + 2 mmHg} (23). "
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    ABSTRACT: Pulmonary hypertension (PH) is an important cause of heart failure in chronic obstructive pulmonary disease (COPD). The pro brain natriuretic peptide N-terminal (NT-proBNP) has been suggested as a noninvasive marker to evaluate ventricular function. However, there is no evidence to support the use of NT-proBNP in monitoring the benefits of vasodilators in COPD induced PH. Thus, we used NT-proBNP as a biomarker to evaluate the effect of oral vasodilators on cardiac function in COPD-induced PH. Forty clinically-stable PH patients were enrolled with history of COPD, normal left ventricular ejection-fraction (LVEF), right ventricular systolic pressure (RVSP) > 45 mmHg and baseline blood NT-proBNP levels >100 pg/mL. Patients were randomized into two groups, one group received sildenafil and second group were given amlodipine for two weeks. NT-proBNP and systolic pulmonary arterial pressure (systolic PA-pressure) were measured at the beginning and the end of study. Mean NT-proBNP level in the first group was 1297 ± 912 pg/mL before therapy and 554 ± 5 pg/mL after two weeks drug therapy, respectively. Similarly, in second group NT-proBNP level was 1657 ± 989 pg/mL and 646 ± 5 pg/mL before and after treatment. Amlodipine or sildenafil significantly reduced NT-proBNP levels in COPD-induced PH patients (p < 0.05). Our study shows that amlodipine and sildenafil have a similar effect on NT-proBNP levels. In both groups NT- proBNP levels were significantly reduced after treatment. Therefore, our findings support the potential benefits of treatment with vasodilators in COPD induced PH. Pulmonary hypertension, Chronic obstructive pulmonary disease, NT-proBNP, Amlodipine, Sildenafil
    Iranian journal of pharmaceutical research (IJPR) 03/2014; 13(Suppl):161-8. · 0.51 Impact Factor
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    • "It also provides important information on left heart function. Despite having much greater sensitivity and specificity for PH than the ECG and CXR, the cardiac echo may under- or overestimate the degree of pulmonary artery pressure [31], which is also true for patients with HIV-related PAH [28]. "
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    ABSTRACT: Human immunodeficiency virus- (HIV-) related pulmonary arterial hypertension (PAH) is a rare complication of HIV infection. The pathophysiology of HIV-related PAH is complex, with viral proteins seeming to play the major role. However, other factors, such as coinfection with other microorganisms and HIV-related systemic inflammation, might also contribute. The clinical presentation of HIV-related PAH and diagnosis is similar to other forms of pulmonary hypertension. Both PAH-specific therapies and HAART are important in HIV-related PAH management. Future studies investigating the pathogenesis are needed to discover new therapeutic targets and treatments.
    08/2013; 2013. DOI:10.1155/2013/903454
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    • "The criterion for diagnosis of COPD is post-bronchodilator forced expiratory volume in onesecond/forced vital capacity of less than 70%.8 Systolic BP of the pulmonary artery of 40 mmHg or higher during the silent phase is accepted as pulmonary hypertension.9 CRD is diagnosed with a permanently elevated serum creatinine level of 1.3 mg/dL or higher on the silent phase. "
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    ABSTRACT: Objective: To find out gender differences in severity of sickle cell diseases (SCDs) in non-smokers. Methods: Three groups of SCDs patients on the basis of red blood cell (RBC) transfusions were included. Less than 10 units in their lives were kept in Group-1, Ten units of higher in Group-2 and 50 units or higher as the Third Group. Patients with a history of using one pack of cigarettes -year or above were excluded. Results: The study included 269 patients. Mean ages of the groups were similar (28.4, 28.5, and 28.9 years, respectively). Prevalences of cases without any RBC transfusion in their lives were 7.2% and 3.7% in females and males, respectively (p<0.05). Prevalences of cases without any painful crisis were 13.8% and 6.0% in females and males, respectively (p<0.001). There was progressive increase according to mean painful crises, clubbing, chronic obstructive pulmonary disease (COPD), leg ulcers, stroke, chronic renal disease (CRD), pulmonary hypertension, and male ratio from the first towards the third groups (p<0.05, nearly for all). Mean ages of mortal cases were 29.1 and 26.2 years in females and males, respectively (p>0.05). Conclusion: The higher painful crises per year, digital clubbing, COPD, leg ulcers, stroke, CRD, pulmonary hypertension, and male ratio of the third group, lower male ratio of patients without any RBC transfusion, lower male ratio of patients without any painful crisis, lower mean ages of male SCDs patients with mortality, and longer overall survival of females in the world could not be explained by well known strong atherosclerotic effects of smoking alone, instead it may be explained by the dominant role of male sex in life.
    Pakistan Journal of Medical Sciences Online 07/2013; 29(4):1050-4. DOI:10.12669/pjms.294.3697 · 0.23 Impact Factor
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