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doi:10.1378/chest.06-2475
(Chest. 2007; 131:339-341)
© 2007 American College of Chest Physicians
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Echocardiography in Pulmonary Arterial Hypertension*

An Essential Tool

Eduardo Bossone, MD, PhD, FCCP; Rodolfo Citro, MD; Francesco Blasi, MD and Luigi Allegra, MD, FCCP

Salerno, Italy
Milan, Italy
Dr. Bossone is Professor at the Institute of Respiratory Disease, University of Milan, IRCCS Ospedale Maggiore, Fondazione Policlinico, Milan, Italy. Dr. Citro is Director of Echocardiography Laboratory, San Luca Hospital, Vallo della Lucania Salerno, Italy. Dr. Blasi is Professor of Respiratory Medicine, Univesity of Milan, IRCCS Ospedale Maggiore Fondazione Policlinico Milan Italy. Dr. Allegra is Professor of Respiratory Medicine, Univesity of Milan, IRCCS Ospedale Maggiore Fondazione Policlinico Milan Italy.

Correspondence to: Eduardo Bossone, MD, PhD, FCCP, Istituto Malattie Respiratorie, Università degli Studi di Milano, Padiglione Sacco, Ospedale Maggiore Milano, IRCCS Fondazione Policlinico-Mangiagalli-Regina Elena, via F. Sforza 35, 20122 Milan, Italy; e-mail: ebossone{at}hotmail.com

Pulmonary arterial hypertension (PAH) [mean pulmonary artery pressure > 25 mm Hg at rest or > 30 mm Hg with exercise, pulmonary wedge pressure ≤ 15 mm Hg, and pulmonary vascular resistance > 3 mm Hg/L/min (Wood units)] is a heterogeneous condition brought on by a wide range of causes characterized by structural changes in small pulmonary arteries that produce a progressive increase in pulmonary artery pressure and pulmonary vascular resistance, ultimately leading to right ventricular (RV) failure and death.12

Because of nonspecific symptoms (exertional dyspnea, fatigue, weakness, or complaints of general exertion intolerance) and subtle signs (accentuated pulmonary component of the second heart sound, early systolic pulmonary valve ejection click, midsystolic pulmonary ejection murmur, a prominent jugular "a" wave), particularly in its early stages, the detection of PAH requires a high clinical index of suspicion.123 Along with the careful clinical assessment and ECG/chest radiograph interpretation, and transthoracic Doppler echocardiography (TTE), the accurate estimation of pulmonary artery systolic pressure (PASP) at rest and with exercise is considered an excellent noninvasive way to screen for the patient with suspected pulmonary hypertension (Fig 1 ).34 In fact, tricuspid regurgitation peak velocity has a high linear positive correlation (0.57 to 0.93) with PASP measured at right-heart catheterization; the reported sensitivity of Doppler-estimated PASP for detecting pulmonary hypertension ranges from 0.79 to 1.00 and specificity from 0.6 to 0.98.25 However, to intercept false-positive results, it is important to be aware that the resting physiologic range of PASP is dependent on age, sex, and body mass index, and may include 40 mm Hg in some older or obese subjects.6 On the other hand, we may assist to mild increases in PASP with exercise among the normal population and to higher pressure among athletes; indeed, well-conditioned athletes are capable of reaching PASP of 60 mm Hg with exercise as consequence of increased flow and left atrial pressure.78


Figure 1
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  		Figure 1. Screening for PAH: role of echocardiography. *Contrast may be used to enhance faint Doppler tricuspid and pulmonary flow signals, detect intracardiac shunts, and/or improve border delineation of cardiac chambers in patients with suboptimal echo windows. PH = pulmonary hypertension.

 
Thus, in symptomatic patients (New York Heart Association class II-III) having a TTE findings "suggestive" of pulmonary hypertension (elevated PASP, abnormal Doppler pattern of right ventricular outflow tract velocity curve, enlarged right-side chambers, RV hypertrophy and reduced global RV systolic function, systolic flattening of the interventricular septum with increased thickness and an abnormal interventricular septum/posterior left ventricular (LV) wall ratio, D-shaped LV), right-heart catheterization must be performed in order to confirm the diagnosis and define prognosis and treatment.124910

In the case of asymptomatic subjects with "definite" predisposing risk factors for PAH (namely, a known genetic mutation associated PAH or a first-degree relative with idiopathic PAH, scleroderma spectrum of disease, patients with congenital heart disease and systemic-to-pulmonary shunts, and patients portal hypertension undergoing evaluation for orthotopic liver transplantation), it is advisable the patient undergo a periodic clinical and echocardiographic screening every 6 months so that the disease can be detected at its early stages.12 In this setting, exercise contrast or saline solution-enhanced Doppler echocardiography may unmask latent or exercise pulmonary hypertension.11

However, because of the complexity of RV geometry and anatomy, a comprehensive and accurate evaluation of RV function and structure by means of ultrasound technologies has been a challenge. In this regard, the study by Ruan and Nagueh12 in this issue of CHEST (see page 395) highlights potential novel clinical applications of tissue Doppler imaging in PAH. Tissue Doppler imaging may be a useful additional means for the following: (1) identifying patients with normal or reduced LA pressure and therefore a noncardiac etiology; (2) monitoring the disease process and the efficacy of specific therapeutic interventions; and (3) providing new insights into physiopathologic mechanisms of RV/LV interdependence.1213

Footnotes

The authors have no conflicts of interest to disclose.

References

  1. Galiè, N, Torbicki, A, Barst, R, et al (2004) Guidelines on diagnosis and treatment of pulmonary arterial hypertension. Eur Heart J ,2243-2278
  2. Barst, RJ, McGoon, M, Torbicki, A, et al Diagnosis and differential assessment of pulmonary arterial hypertension. J Am Coll Cardiol 2004;3,40S-47S
  3. McGoon, M, Gutterman, D, Steen, V, et al Screening, early detection, and diagnosis of pulmonary arterial hypertension: ACCP evidence-based clinical practice guidelines. Chest 2004;126(suppl),14S-34S
  4. Bossone, E, Bodini, BD, Mazza, A, et al Pulmonary arterial hypertension: the key role of echocardiography. Chest 2005;127,1836-1843
  5. Yock, PG, Popp, RL Noninvasive estimation of right ventricular systolic pressure by Doppler ultrasound in patients with tricuspid regurgitation. Circulation 1984;70,657-662[Medline]
  6. McQullian, BM, Picard, MH, Leawitt, M, et al Clinical correlates and reference intervals for pulmonary artery pressure among echocardiographically normal subjects. Circulation 2001;104,2797-2802
  7. Bossone, E, Rubenfire, M, Bach, DS, et al Range of tricuspid regurgitation velocity at rest and during exercise in normal adult men: implications for the diagnosis of pulmonary hypertension. J Am Coll Cardiol 1999;33,1662-1666[Abstract/Free Full Text]
  8. West, JB Left ventricular filling pressures during exercise: a cardiological blind spot? Chest 1998;113,1695-1697
  9. McLaughlin, V, Presberg, KW, Doyle, RL, et al Prognosis of pulmonary arterial hypertension: ACCP evidence-based clinical practice guidelines. Chest 2004;126(suppl),78S-92S
  10. Mahapatra, S, Nishimura, RA, Sorajja, P, et al Relationship of pulmonary arterial capacitance and mortality in idiopathic pulmonary arterial hypertension. J Am Coll Cardiol 2006;47,799-803[Abstract/Free Full Text]
  11. Grunig, E, Janssen, B, Mereles, D, et al Abnormal pulmonary artery pressure response in asymptomatic carriers of primary pulmonary hypertension gene. Circulation 2000;102,1145-1150
  12. Ruan, Q, Nagueh, S Clinical application of tissue Doppler imaging in patients with idiopathic pulmonary hypertension. Chest 2007;131,395-401
  13. Ho, CY, Solomon, SD A clinician’s guide to tissue Doppler imaging. Circulation 2006;113,396-398




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