Heart Failure: Hemodynamic Assessment Using Echocardiography James N. Kirkpatrick, MD, and Roberto M. Lang, MD

Corresponding author James N. Kirkpatrick, MD Hospital of the University of Pennsylvania, Echocardiography Laboratory, 9021 Gates Pavilion, 3400 Spruce Street, Philadelphia, PA 19104, USA. E-mail: [email protected] Current Cardiology Reports 2008, 10:240–246 Current Medicine Group LLC ISSN 1523-3782 Copyright © 2008 by Current Medicine Group LLC

Hemodynamics play a crucial role in diagnosing and managing heart failure (HF) as diagnostic markers and therapeutic targets. In an era of declining physical examination skills and questions about the safety of invasive monitoring, quantitative, objective data provided by echo-Doppler measurements can function as a type of “echo Swan-Ganz catheter” as an important adjustment to traditional methods of hemodynamic assessment. Echocardiographic measures of right- and left-sided filling pressures, pulmonary vascular resistance, and cardiac output are possible in many (although not all) HF patients. Recent studies suggest these measurements can have an important role in clinical pathways treating patients admitted with decompensated HF. The availability of miniaturized echocardiographic devices with full echo-Doppler capability may make repeatable, noninvasive hemodynamic assessment readily available and cost-effective for patients in many clinical settings.

Introduction Hemodynamics play a crucial role in diagnosing and managing heart failure (HF). The pulmonary and systemic venous congestion from diastolic dysfunction and hypoperfusion from reduced systolic function originate in pressure and volume derangements. The measures of these derangements are diagnostic markers and therapeutic targets for HF therapies. Traditionally, HF management has relied on physical examination. However, the medical literature demonstrates the difficulties of assessing volume and pressure status by physical examination; declines in physical examination skills among recent trainees will only exacerbate the problem [1,2]. Concurrently, the traditional gold

standard of invasive monitoring has been the subject of many studies, suggesting it provides no clear clinical benefit and may even be harmful [3,4]. In selected patients, echocardiography can make hemodynamic measurements that are more accurate than physical examination findings without the risks of invasive monitoring. For many years, two-dimensional (2D) echocardiographic assessments, such as chamber sizes and septal bowing, have been used as subjective and qualitative indicators of hemodynamic states. These interpretive assessments are subject to considerable intraobserver and interobserver variability, with consequent reduced reproducibility and accuracy. Quantitative, objective data are often more clinically useful. The modern care of cardiovascular patients relies increasingly on such data to guide diagnostic and therapeutic decision making, from the administration of fluids to inotropic support. Although not possible in certain patients, quantitative echo-Doppler measurements can function as a type of “echo Swan-Ganz catheter.” Patients in a variety of clinical settings besides the cardiac care unit may benefit from this application of echocardiography, including the emergency department, the surgical intensive care unit (ICU), the medical ICU, cardiology clinics, and dialysis units.

Filling Pressures 2D and Doppler echocardiography can estimate right-sided and left-sided filling pressures. Measurement of a number that correlates closely to a precise milliliters of mercury (mm Hg) number from invasive validation is generally not feasible. Echocardiography can estimate right atrial pressures (RAPs) and left ventricular end-diastolic pressures (LVEDPs) (or pulmonary capillary wedge or left atrial mean pressures) in clinically meaningful ranges (Fig. 1 and Fig. 2).

Right atrial pressure The inferior vena cava maximal diameter (IVCmax) 1 to 2 cm from the right atrial-IVC junction and the IVC collapsibility index (IVCCI) yield an estimate of RAP:

IVCmax – IVCmin IVCCI = IVCmax

Heart Failure: Hemodynamic Assessment Using Echocardiography Kirkpatrick and Lang 241

Figure 1. Inferior vena cava (IVC) collapsibility index. Demonstrates maximal (max) IVC diameter (white arrows) (A) and minimal (min) IVC diameter (B) during “sniff” from the subcostal view. The IVC is dilated to greater than 2.0 cm and fails to collapse more than 50% of the maximal diameter during sniff. This finding corresponds to a right atrial pressure (RAP) of 15 to 20 mm Hg in nonventilated patients, according to traditional criteria. IVCmax–IVCmin/IVCmax = < 50%, RAP = 15–20 mm Hg.

Figure 2. Early mitral inflow to flow propagation slope. A, Shows inflow at the mitral valve leaflet tips from pulse wave (PW) spectral Doppler in the apical four-chamber view, from which the peak early inflow velocity is measured (E wave). B, A color M-mode of the flow from mitral annulus to apex of the left ventricle in the apical four-chamber view. The slow of this flow (white line) is the propagation velocity (Vp). The ratio of E to Vp greater than 1.5 indicates a left ventricular end-diastolic pressure greater than 15 mm Hg.

If the IVC is less than 1.2 cm and fully collapses (100%), the RAP is near 0 mm Hg. If the IVC is 1.2 to 1.7 cm and collapses more than 50%, the RAP is 0 to 5 mm Hg. If the IVC is less than 1.7 cm and has more than 50% collapse, the RAP is 6 to 10 mm Hg. If the IVC has less than 50% collapse, the RAP is greater than 10 mm Hg. If the IVC is greater than 1.7 cm and does not collapse at all (0%), the

RAP is 15 to 20 mm Hg [5]. When patients “sniff” to augment negative inspiratory pressure, generally leading to a smaller minimal IVC diameter, accuracy is improved [6,7]. A recent study has questioned the traditional cutoff values for IVCmax and IVCCI and suggests a new cutoff range as follows: IVC less than 2 cm and collapse of more than 55% correlates with an RAP of 0 to 5 mm Hg. An IVC less

242 Echocardiography

than 2 cm with 30% to 50% collapse and an IVC greater than 2 cm with more than 55% collapse correspond to an RAP of 0 to 10 mm Hg. An IVC greater than 2 cm with 30% to 55% collapse suggests an RAP of 10 to 15 mm Hg. An IVC greater than 2 cm with less than 30% collapse predicts an RAP of 10 to 20 mm Hg. If the IVC is less than 2 cm and collapses less than 30%, the RAP is indeterminate [8••]. The discrepancy between various studies suggests that direct correlation between IVC measurement and dynamics and actual mm Hg values may not be as clinically pertinent as categories of filling (ie, “underfilled,” “adequately filled,” “overfilled”). Regardless of the cutoff values used, patients should lay supine for the measurements because left lateral positioning may underestimate IVCmax. Tangential plane positioning errors are common, which may also underestimate IVC size. Using M-mode imaging may improve resolution of the near and fall walls of the IVC for measurement; however, care must be taken to avoid placing the M-mode curser diagonally to the walls (rather than perpendicularly), thereby leading to overestimation of IVC size. Unfortunately, a way to standardize the degree of negative inspiratory pressure from “sniff” has not been worked out. Finally, IVCCI estimate of RAP lacks accuracy in mechanically ventilated patients, although an IVC c 12 mm demonstrated reasonable correlation to an RAP c 10 mm Hg in one study [9]. Other methods for estimating RAP exist. The maximal early filling velocity through the tricuspid during diastole (E wave) increases with increasing RAP. Tissue Doppler imaging can measure velocity of tissue relaxation of the tricuspid free wall annulus in diastole (eb wave). A high E wave velocity in the setting of a slow eb wave velocity generally signals high RAP. The ratio of tricuspid E/eb predicts RAP ranges, irrespective of mechanical ventilation. The correlation was best in patients with right ventricular (RV) systolic dysfunction. RAP was reliably greater than 10 mm Hg when the E/eb was greater than 4. Patients who had undergone cardiac surgery had reduced myocardial annular velocities; tricuspid E/eb was not accurate in this population [10,11•]. RV regional isovolumic relaxation time (RV rIVRT) is measured from tissue Doppler tracings of the tricuspid annulus as the time between the end of systolic annular motion and the onset of the eb wave. Mean RAP by RV rIVRT correlates with invasive measures, independent of the pulmonary artery (PA) pressure. An RV rIVRT less than 59 ms corresponds to a mean RAP greater than 8 mm Hg [12]. Pulse wave Doppler of hepatic vein flow can also measure RAP. Normal flow occurs toward the right atrium (RA) through most of systole and early diastole, followed by a reversal of flow with atrial contraction. In the setting of elevated RAP, systolic forward flow declines and atrial reversal augments. The hepatic venous systolic filling fraction (HVFF) is calculated from velocity time

integral of systolic forward flow (SF VTI) and VTI of diastolic forward flow (DF VTI):

SF VTI HVFF = SF VTI + DF VTI A cutoff value of less than 55% predicts an RAP greater than 8 mm Hg [5]. An atrial reversal maximal velocity greater than systolic forward flow maximal velocity also correlates with an increased RAP [13].

Left-sided filling pressures Echo Doppler estimations of left-sided filling pressures are related to echo Doppler measures of LV diastolic function. Diastolic dysfunction comprises a spectrum of abnormal states. Abnormal LV relaxation produces a decrease in early diastolic mitral inflow velocity (E wave) with greater reliance on atrial contraction (A wave) for ventricular filling (E/A < 1). Increasing left atrial pressure at the start of diastole (increased E wave) produces “pseudonormalization”—an increase in early diastolic flow velocity to a level near that of normal filling, with a normalization of the E/A ratio (E/A 1–1.5). Further elevation in left atrial pressure leads to very rapid early diastolic flow, with rapid equalization of atrial and ventricular pressures (because of residual high LV pressure in the setting of poor compliance) during early diastole (E/A > 2, deceleration time < 115–150 ms). The Valsalva maneuver can change a pseudonormalized pattern to an abnormal relaxation pattern or a restrictive pattern to a pseudonormalized one by reducing left atrial volume [14,15]. The final (end) stage of diastolic dysfunction is characterized by inability to convert a restrictive filling pattern to a pseudonormalized one with Valsalva, or after several months of HF therapy [16,17]. Measures of diastolic function have demonstrated considerable prognostic capacity in many populations [18]; however, several caveats in applying these measures to filling pressures should be mentioned. The main problem with determining filling pressures by these measures of diastolic dysfunction is that they are extremely dependent on heart rate (HR) and loading conditions. Also, they do not correlate well with hemodynamic parameters in patients with preserved LV ejection fraction. Several other measures correlate with filling pressures. As with hepatic vein flow and RAP, measurements of pulmonary vein flow correlate with high left atrial pressures, specifically the ratio of the systolic (S) and diastolic (D) velocities of pulmonary venous inflow (S/D < 1) and systolic filling fraction of pulmonary venous systolic forward flow (< 40%) [17]. A combination of transmitral and pulmonary vein flow involves subtracting the duration of the A wave from the duration of pulmonary venous atrial reversal flow. A value greater than 30 ms correlated with an LVEDP greater than 18 mm Hg [19].

Heart Failure: Hemodynamic Assessment Using Echocardiography Kirkpatrick and Lang 243

Adequate Doppler interrogation of pulmonary vein flow is not possible in many patients. Another measure involves early LV filling flow propagation slope (Vp), obtained from color M-mode interrogation of the slope of the inflow from the mitral valve to the apex in the apical four-chamber view. A ratio of peak E to Vp s 1.5 predicts an LVEDP greater than 15 mm Hg [20]. Vp’s limited reproducibility is a significant drawback. The combination of mitral inflow E with tissue Doppler measurement of mitral annular velocity (eb) provides a more reproducible way to assess left-sided filling pressures. A ratio of E/eb c 8 predicts an LVEDP of less than 15 mm Hg. A ratio of more than 15 predicts an LVEDP greater than 15 mm Hg. Values between 8 and 15 cannot reliably estimate LV filling pressures; this measurement may be more robust in patients with reduced LV ejection fraction and diastolic dysfunction versus more normal ventricles [21]. In hypovolemia, the eb decreases, potentially leading to a false conclusion of high LV filling pressures [22]. In clinical practice, multiple parameters are often required to give an assessment of filling dynamics, particularly when poor acoustic windows may limit the ability to make certain measurements. Sometimes parameters conflict in their filling pressure estimates; careful scrutiny for measurement errors and knowledge of the caveats described above are requisite to accurate assessment of filling dynamics. Finally, different echo Doppler techniques have been validated against different measures of LV filling pressures. In some patients, a discrepancy exists between pulmonary capillary wedge pressure (PCWP) and LVEDP. One study suggested that E/eb correlated with PCWP, whereas pulmonary atrial reversal duration–A wave duration (> 10 ms) correlated with LVEDP. Use of both measures reliably distinguished patients with PCWP/LVEDP discrepancy [23].

Pulmonary Arterial Pressures In most patients who have some degree of tricuspid regurgitation (TR), accurate noninvasive assessment of RV systolic pressure is possible. The RV to RA maximal systolic pressure gradient can be directly measured from the TR jet maximal velocity (v) and the modified Bernoulli equation (pressure gradient = 4 v2). This pressure gradient, added to RAP, will equal the PA systolic pressure (PASP) in the absence of RV outflow tract obstruction and pulmonic valve or PA stenosis. In the presence of such obstruction, the maximal gradient across the site of obstruction can often be measured and subtracted from the measured RV to RA gradient to yield a measure of the PASP. Overestimation of true PASP often involves overestimation of the RAP, but the tricuspid valve closing spike may also be mistaken for the maximal velocity. Probably more often, however, echo Doppler PASP underestimates

the true PASP because of nonparallel alignment of the Doppler signal with the TR jet [24]. In cases of inadequate TR jet interrogation, the use of agitated saline contrast, especially when mixed with plasma or blood, or commercially available contrast bubbles, improves the detection of Doppler signals and the accuracy of continuous wave Doppler measurements [25,26]. Echo Doppler measures of PA diastolic pressure (PAd) and PA mean (PAm) pressure use continuous wave Doppler of the pulmonic valve insufficiency (PI) jet. The end-diastolic PI jet velocity is used to calculate the enddiastolic PA-RV pressure gradient. This gradient is added to the RAP to yield PA diastolic pressure [27,28]. The PA mean pressure can be calculated from the PASP and PAd pressure by the formula

PAm (approx) = (PASP – PAd)/3 + PAd or from the peak of the early diastolic velocity (from which the PA to RV pressure gradient at the time of pulmonic valve closure can be calculated). Initial studies found a direct correlation between the PA-RV pressure gradient and invasively derived PAm [29]. A more recent study, however, demonstrated improved correlation when RAP was added to the gradient [30]. The interrogation of the PI jet can lead to significant PAd and PAm inaccuracies because of poor Doppler signal alignment, inadequacy of regurgitant jet, and imprecise RAP estimate. As above, using contrast agents may improve Doppler signal measurements.

Pulmonary Vascular Resistance Several echo Doppler techniques correlate to varying degrees with pulmonary vascular resistance (PVR) [31,32]. One of the more recent and simple techniques approximates the invasive formula for calculating PVR by using the maximal TR jet velocity (TRvel) and RV outflow tract velocity time integral (RVOT VTI) to calculate PVR in Wood Units (WU):

PVR (WU) = (TRvel/RVOT VTI) × 10 + 0.16 Although not yet validated in a large sample size of patients with a wide range of PVRs, the initial study and technical simplicity of measurements and formula may prove clinically useful. Measurement of the TRvel is subject to the pitfalls described above; RVOT VTI is not well interrogated in patients with poor parasternal acoustic windows [33].

Cardiac Output Echo Doppler estimation of stroke volume (SV) and cardiac output (CO) can be calculated from the LV outflow tract (LVOT) area, the LVOT VTI, and HR.

244 Echocardiography SV = LVOT VTI × {(LVOTdiameter/2)2 × π} CO = SV × HR Excellent correlations have been demonstrated [34,35]. Nonetheless, pitfalls exist. Small errors in LVOT diameter measurement will lead to large errors because this measure is squared in the equation. Significant aortic regurgitation (AR) will lead to overestimation of SV and CO. When AR is present, and in the absence of intracardiac shunting, the pulmonic outflow tract can be used instead of the LVOT [36].

Rate of Pressure Change Another traditionally invasive parameter of ventricular performance involves measuring the rate of pressure change (dP/dt). In the early phases of systole (isovolumic contraction), dP/dt is relatively independent of loading conditions as a measure of contractility. The time difference between 1 to 3 m/s on the mitral or TR jet profile is equal to the time it takes to achieve a 32-mm Hg pressure change in the LV cavity: dP/dt = 32 mm Hg per time. Whereas positive dP/dt is a marker of systolic function, negative dP/dt is reflective of diastolic function. Echocardiographic dP/dt has been correlated with invasive dP/dt measures for LV [37,38] and RV, although the latter demonstrated poorer correlation when RAP was elevated [39]. Another drawback of echocardiographic dP/dt is reduced reproducibility and the fact that dyssynchrony can induce reductions in dP/dt not related to global contractility.

HF. Echocardiography on admission may guide application of various treatments, including inotropes, vasodilators, vasopressors, types of diuretics, or ultrafiltration. Echocardiography before discharge may help determine which patients are suitable for home or skilled nursing care or may require a longer hospital stay. Traditional echocardiography involves a highly trained sonographer using an expensive and somewhat unwieldy machine to acquire images. A highly trained cardiologist then interprets these images. Such a configuration does not lend itself to frequent measurements of hemodynamic variables or to echocardiographic hemodynamic assessment after normal working hours. Recent developments in miniaturized echocardiogram machines (officially termed “hand-carried ultrasound” [HCU] devices) have brought high-quality 2D imaging and Doppler and tissue Doppler capacity to a laptop-sized machine. These devices offer dramatically increased portability and reduced cost and may prove useful in off-hours and repeat measurement of hemodynamic parameters in many clinical settings, including medical, cardiac, and surgical intensive care units, and the emergency department. Ongoing studies are testing the feasibility of the use of these machines by noncardiologist clinicians to make focused hemodynamic measurements. In the future, HCU measurement of hemodynamic variables may become a standard component of physician physical examinations or of nursing vital signs [44].

Conclusions Clinical Applications Not every measurement is feasible in every patient because of image quality, lack of regurgitant jets, and other technical factors. Correlation of echo Doppler findings with invasive monitoring does not necessarily establish the clinical applicability of these techniques to improve patient outcomes. Evidence is increasing, on the other hand, that echocardiographic hemodynamic assessment, specifically measures of LV filling pressures, has substantial prognostic value and can be used clinically to manage volume status. In a study of more than 2000 patients greater than 45 years old with different degrees of diastolic dysfunction, investigators demonstrated that E/eb and pulmonary A reversal – A wave duration predicted death with very high hazard ratios [40]. Another study of 115 patients admitted with HF found pulmonary A reversal – A wave duration predicted death or HF readmission [41]. Other work found that E/eb is superior to brain natriuretic peptide (BNP) levels for diagnosing volume overload, even in patients with preserved systolic function [42]. In a separate study, E/eb plus BNP predicted readmission rates for HF patients more accurately than BNP alone [43••]. These and other studies support the conclusion that echocardiographic hemodynamic measurements can have an important role in clinical pathways treating patients admitted with decompensated

In the setting of declining physical examination skills and concerns about invasive monitoring, echocardiography can play a significant role in hemodynamic assessments in selected HF patients. Echocardiographic measures of right-sided and left-sided filling pressures, PVR, and CO are possible in many (although not all) HF patients. The clinical use of these assessments is suggested by several studies and may be expanded by recent developments in hand-carried devices.

Disclosures Roberto M. Lang is on the advisory board for Philips Medical Systems. He also receives grant support from TomTec Imaging Systems and Point Biomedical Corp. No other potential conflicts of interest relevant to this article were reported.

References and Recommended Reading Papers of particular interest, published recently, have been highlighted as: • Of importance •• Of major importance 1.

Eisenberg PR, Jaffe AS, Schuster DP: Clinical evaluation compared to pulmonary artery catheterization in the hemodynamic assessment of critically ill patients. Crit Care Med 1984, 12:549–553.

Heart Failure: Hemodynamic Assessment Using Echocardiography Kirkpatrick and Lang 245 2.

Demeria DD, MacDougall A, Spurek M, et al.: Comparison of clinical measurement of jugular venous pressure versus measured central venous pressure. Chest 2004, 126:747S. 3. Connors AF, Jr, Speroff T, Dawson NV, et al.: The effectiveness of right heart catheterization in the initial care of critically ill patients. SUPPORT Investigators. JAMA 1996, 276:889–897. 4. Binanay C, Califf RM, Hasselblad V, et al.: Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness: the ESCAPE trial. JAMA 2005, 294:1625–1633. 5. Lang RM, Bierig M, Devereaux RB, et al.: Recommendations for chamber quantification. J Am Soc Echocardiogr 2005, 18:1440–1463. 6. Ommen SR, Nishimura RA, Hurrell DG, et al.: Assessment of right atrial pressure with 2-dimensional and Doppler echocardiography: a simultaneous catheterization and echocardiographic study. Mayo Clin Proc 2000, 75:24–29. 7. Kircher BJ, Himelman RB, Schiller NB: Noninvasive estimation of right atrial pressure from the inspiratory collapse of the inferior vena cava. Am J Cardiol 1990, 66:493–496. 8.•• Brennan JM, Blair JE, Goonewardena S, et al.: Reappraisal of the use of inferior vena cava for estimating right atrial pressure. J Am Soc Echocardiogr 2007, 20:857–861. Studies correlating RAP and IVC measurements are small and somewhat inconsistent. This study was one of a few to prospectively validate the technique. The authors review the current literature and suggest a different set of cutoffs than proposed in the chamber quantification guidelines. 9. Jue J, Chung W, Schiller NB: Does inferior vena cava size predict right atrial pressures in patients receiving mechanical ventilation? J Am Soc Echocardiogr 1992, 5:613–619. 10. Nageh MF, Kopelen HA, Zoghbi WA, et al.: Estimation of mean right atrial pressure using tissue Doppler imaging. Am J Cardiol 1999, 84:1448–1451. 11.• Sade LE, Gulmez O, Eroglu S, et al.: Noninvasive estimation of right ventricular filling pressure by ratio of early tricuspid inflow to annular diastolic velocity in patients with and without recent cardiac surgery. J Am Soc Echocardiogr 2007, 20:982–988. This study builds on prior work to test the usefulness of tricuspid E/eb, with specific investigation of patients with and without RV dysfunction and patients with a history of cardiac surgery. 12. Abbas A, Lester S, Moreno FC, et al.: Noninvasive assessment of right atrial pressure using Doppler tissue imaging. J Am Soc Echocardiogr 2004, 17:1155–1160. 13. Appleton CP, Hatle LK, Popp RL: Superior vena cava and hepatic vein Doppler echocardiography in healthy adults. J Am Coll Cardiol 1987, 10:1032–1039. 14. Nagueh SF: Noninvasive evaluation of hemodynamics by Doppler echocardiography. Curr Opin Cardiol 1999, 14:217–224. 15. Ommen SR, Nishimura RA, Appleton CP, et al.: Clinical utility of Doppler echocardiography and tissue Doppler imaging in the estimation of left ventricular filling pressures: a comparative simultaneous Doppler-catheterization study. Circulation 2000, 102:1788–1794. 16. Pinamonti B, Zecchin M, Di Lenarda A, et al.: Persistence of restrictive left ventricular filling pattern in dilated cardiomyopathy: an ominous prognostic sign. J Am Coll Cardiol 1997, 29:604–612. 17. Traversi E, Pozzoli M, Cioffi G, et al.: Mitral flow velocity changes after 6 months of optimized therapy provide important hemodynamic and prognostic information in patients with chronic heart failure. Am Heart J 1996, 132:809–819. 18. Kirkpatrick JN, Vannan MA, Narula J, Lang RM: Echocardiography in heart failure: applications, utility and new horizons. J Am Coll Cardiol 2007, 50:381–396. 19. Rossi A, Loredana L, Cicoira M, et al.: Additional value of pulmonary vein parameters in defining pseudonormalization of mitral inflow pattern. Echocardiography 2001, 18:673–679.

20.

21.

22. 23.

24.

25. 26. 27.

28.

29.

30. 31.

32.

33. 34.

35.

36. 37. 38.

Garcia MJ, Ares MA, Asher C, et al.: An index of early left ventricular filling that combined with pulsed Doppler peak E velocity may estimate capillary wedge pressure. J Am Coll Cardiol 1997, 29:448–454. Firstenberg MS, Levine BD, Garcia MJ, et al.: Relationship of echocardiographic indices to pulmonary capillary wedge pressures in healthy volunteers. J Am Coll Cardiol 2000, 36:1664–1669. Nagueh SF, Sun H, Kopelen HA, et al.: Hemodynamic determinants of the mitral annulus diastolic velocities by tissue Doppler. J Am Coll Cardiol 2001, 37:278–285. Hadano Y, Murata K, Liu J, et al.: Can transthoracic Doppler echocardiography predict the discrepancy between left ventricular end-diastolic pressure and mean pulmonary capillary wedge pressure in patients with heart failure? Circ J 2005, 69:432–438. Currie PJ, Seward JB, Chan KL, et al.: Continuous wave Doppler determination of right ventricular pressure: a simultaneous Doppler-catheterization study in 127 patients. J Am Coll Cardiol 1985, 6:750–756. Lester SJ, Askew JW, Hurst RT, et al.: Contrast echocardiography: experience in a clinical echocardiography laboratory. J Am Soc Echocardiogr 2006, 19:919–923. Fan S, Nagai T, Luo H, et al.: Superiority of the combination of blood and agitated saline for routine contrast enhancement. J Am Soc Echocardiogr 1999, 12:94–98. Stephen B, Dalal P, Berger M, et al.: Noninvasive estimation of pulmonary artery diastolic pressure in patients with tricuspid regurgitation by Doppler echocardiography. Chest 1999, 116:73–77. Lee RT, Lord CP, Plappert T, et al.: Prospective Doppler echocardiographic evaluation of pulmonary artery diastolic pressure in the medical intensive care unit. Am J Cardiol 1989, 64:1366–1370. Masuyama T, Kodama K, Kitabatake A, et al.: Continuouswave Doppler echocardiographic detection of pulmonary regurgitation and its application to noninvasive estimation of pulmonary artery pressure. Circulation 1986, 74:484–492. Abbas AE, Fortuin FD, Schiller NB, et al.: Echocardiographic determination of mean pulmonary artery pressure. Am J Cardiol 2003, 92:1373–1376. Scapellato F, Temporelli PL, Eleuteri, E, et al.: Pulmonary vascular resistance by doppler echocardiography in patients with chronic heart failure. J Am Coll Cardiol 2001, 37:1813–1819. Lanzarini L, Fontana A, Campana C, Klersy C: Two simple echo-doppler measurements can accurately identify pulmonary hypertension in the large majority of patients with chronic heart failure. J Heart Lung Transplant 2005, 24:745–754. Abbas AE, Fortuin FD, Schiller NB, et al.: A simple method for noninvasive estimation of pulmonary vascular resistance. J Am Coll Cardiol 2003, 41:1021–1027. Lewis JF, Kuo LC, Nelson JG, et al.: Pulsed Doppler echocardiographic determination of stroke volume and cardiac output: clinical validation of two new methods using the apical window. Circulation 1984, 70:425–431. Dubin I, Wallerson DC, Cody RJ, et al.: Comparative accuracy of Doppler echocardiographic methods for clinical stroke volume determination. Am Heart J 1990, 120:116–123. Sahn DJ: Determination of cardiac output by echocardiographic Doppler methods: relative accuracy of various sites for measurement. J Am Coll Cardiol 1985, 6:663–664. Rhodes J, Udelson JE, Marx GR, et al.: A new noninvasive method for the estimation of peak dP/dt. Circulation 1993, 88:2693–2699. Chung N, Nishimura RA, Holmes DR, Jr, Tajik AJ: Measurement of left ventricular dp/dt by simultaneous Doppler echocardiography and cardiac catheterization. J Am Soc Echocardiogr 1992, 5:147–152.

246 Echocardiography 39.

40.

41.

42.

Imanishi T, Nakatani S, Yamada S, et al.: Validation of continuous wave Doppler-determined right ventricular peak positive and negative dP/dt: effect of right atrial pressure on measurement J Am Coll Cardiol 1994, 23:1638–1643. Redfield MM, Rodeheffer RJ, Jacobsen SJ, et al.: Plasma brain natriuretic peptide to detect preclinical ventricular systolic or diastolic dysfunction: a community-based study. Circulation 2004, 109:3176–3181. Whaley GA, Doughty RN, Gamble GD, et al.: Pseudonormal mitral filling pattern predicts hospital readmission in patients with congestive heart failure. J Am Coll Cardiol 2002, 39:1787–1795. Mottram PM, Leano R, Marwick TH: Usefulness of B type natriuretic peptide in hypertensive patients with exertional dyspnea and normal left ventricular ejection fraction and correlation with new echocardiographic indexes of systolic and diastolic function. Am J Cardiol 2003, 92:1434–1438.

43.•• Dokainish H, Zoghbi WA, Lakkis NM, et al.: Incremental predictive power of B-type natriuretic peptide and tissue Doppler echocardiography in the prognosis of patients with congestive heart failure. J Am Coll Cardiol 2005, 45:1223–1226. This important study prospectively analyzed the relative and additive benefit of two different markers of HF: echocardiography and BNP. The findings suggest that these two techniques might prove useful in assessing whether patients are ready for discharge after HF hospitalization, and/or the degree of follow-up necessary. 44. Kirkpatrick JN, Furlong K, Mugica VL, et al.: Effectiveness of echocardiographic imaging by nurses to identify left ventricular systolic dysfunction in high-risk patients. Am J Cardiol 2005, 95:1271–1272.