Right atrium contractility and right ventricular diastolic function assessed by pulsed Tissue Doppler Imaging can predict brain natriuretic peptide in adults with acquired pulmonary hypertension
Introduction
The elevated right atrial (RA) pressure and right ventricular (RV) dysfunction are associated with increased mortality in patients with chronic pulmonary hypertension (PH) [1], [2]. Although RA and RV show adaptive responses and dynamic changes in order to maintain RV filling and cardiac output [3], few studies have focused on RA contractility and RV diastolic function in adult patients with acquired chronic PH, because assessment of these parameters is difficult due to the complicated morphological remodeling.
To evaluate RA contractility and RV dysfunction, right side heart catheter examinations is the most accurate technique available [4] but cannot be routinely performed in daily practice because of its invasive nature. Therefore, alternative, non-invasive methods are needed to assess RA contractility and RV dysfunction in such patients.
Pulsed Tissue Doppler Imaging (TDI) [5], [6], [7], [8], [9], [10], [11] is a very useful and easy technique to assess RA as well as RV function. Some studies have reported that RV systolic function is initially preserved with RV pressure overload, but that diastolic dysfunction occurs as a consequence of myocardial hypertrophy and remodeling [12]. Both RV contractility and RV stiffness are also very important factors for right heart failure in patients with chronic PH, and TDI is a useful technique in this situation to assess RV diastolic function.
Elevated serum levels of brain natriuretic peptide (BNP) [13], [14], [15], [16], [17], [18], [19], [20], [21] are also associated with poor prognosis in patients with PH [22], [23], which is greatly influenced by volume overload, age, and renal function [24]. Here, we evaluated RA contractility and RV diastolic function in adult subjects with acquired chronic PH and normal electrocardiographic sinus rhythms by pulsed TDI and assessed their relationship with serum BNP using multiple regression analysis.
Section snippets
Study population
From April 2006 to March 2007, 77 consecutive adult patients with acquired PH were enrolled (22 males and 55 females, mean age 54 ± 15 years, 55 of which had chronic pulmonary thromboembolism (CPTE), 13 had primary PH and 9 had PH due to collagen disease). They all received anticoagulant and other treatment, including iloprost infusion therapy, endothelin antagonists or sildenafil for at least 6 months, but thromboendarterectomy was not performed. PH was diagnosed by the presence of an estimated
Results
All data are presented in Table 1.
All subjects had elevated BNP (mean 188.9 ± 244.0 pg/dl) and elevated PASP estimated at 62.9 ± 26.7 mm Hg by transthoracic echocardiography. The BNP level was positively correlated with RV E/Ea and PASP (r = 0.47, p < 0.0001; and r = 0.35, p < 0.01, respectively) but negatively with Aa (r = − 0.29, p < 0.05) (Fig. 2).
Next, all predictor variables, including age, sex, Sa, Ea, Aa, E/Ea, PASP, and cardiac output, were used in a stepwise multiple regression model with serum BNP
Discussion
In contrast to acute PH, chronic PH has a unique cardiovascular circulation such that it is not possible to estimate its severity solely from measuring the pulmonary arterial pressure. CPTE induces pulmonary arterial bed occlusion, resulting in remodeling of small pulmonary arteries and abnormal vascular reactivity with endothelial dysfunction even in the vessels with no occlusions [27], [28]. Furthermore, chronic PH causes RV remodeling, including hypertrophy and dilatation. This phenomenon is
Conclusions
Serum BNP correlates with RA contractility and RV diastolic dysfunction by RV TDI in adults with acquired PH. Increased BNP may be related to decreased RA systolic function and RV diastolic function in these patients.
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