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European Journal of Echocardiography Advance Access published online on August 22, 2008
European Journal of Echocardiography, doi:10.1093/ejechocard/jen217
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Comparison of myocardial contrast echocardiography derived myocardial perfusion reserve with invasive determination of coronary flow reserve{dagger}

S. Michelle Bierig*, Peter Mikolajczak, Steven C. Herrmann, Nicole Elmore, Morton Kern and Arthur J. Labovitz

Echocardiography Laboratory, St Louis University School of Medicine, FDT-14, St Louis, MO 63110, USA

Received 21 March 2007; accepted after revision 27 July 2008.

* Corresponding author. Tel: +1 314 577 8889. E-mail address: bierigsm{at}slu.edu


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Study limitations
 Conclusion
 Funding
 Notes
 References
 
Aims: Invasive measurements of coronary flow reserve (CFR) by Doppler flow wire are an established method for determining coronary blood flow physiology. Myocardial contrast echocardiography (MCE) is a potential non-invasive method for quantifying myocardial blood flow (MBF). However, few studies have compared MCE-derived myocardial perfusion reserve (MPR) with Doppler flow wire-derived CFR, measured simultaneously in human subjects. This study aimed to correlate MCE-derived MPR with Doppler flow wire-derived CFR.

Methods and results: Ten patients with at least two angiographically normal coronary arteries underwent simultaneous invasive Doppler flow wire measurements and MCE imaging at rest and at peak hyperaemia. Hyperaemia was induced by intravenous adenosine infusion. Doppler-derived CFR was calculated as the ratio of hyperaemic to baseline average peak red blood cell velocity. MPR was calculated as the hyperaemic to baseline ratio of the following parameters: myocardial blood volume (MBV), myocardial microbubble velocity (MMV), and MBF. MCE was performed using real-time and triggered imaging with contrast infused intravenously by bolus and continuous methods. Regardless of whether the contrast was infused by bolus or continuous methods, Doppler flow wire-derived CFR had a stronger correlation with MPR derived by MBV (r = 0.8, P = 0.05) than with MPR derived by microbubble velocity (r = 0.3, P > 0.05) or MBF (r = 0.4, P > 0.05). Real-time imaging with continuous infusion provided better correlation with CFR than triggered imaging methods or bolus administration.

Conclusion: Myocardial perfusion reserve derived by real-time infusion MBV measurements correlates with Doppler flow wire-derived CFR. Therefore, MPR may be a potential surrogate for Doppler flow wire-derived CFR in patients with angiographically normal coronary arteries.

Keywords: Myocardial contrast echocardiography; Myocardial perfusion reserve; Coronary flow reserve; Doppler flow wire


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Study limitations
 Conclusion
 Funding
 Notes
 References
 
Myocardial contrast echocardiography (MCE) has been validated as an accurate method for quantifying myocardial blood flow (MBF) in previous animal studies.1–5 Wei et al.6 used continuous intravenous infusions of contrast microbubbles during MCE to quantify MBF. During this study, microbubbles were infused at a steady rate and concentration. After a microbubble steady state was achieved within the myocardium, all microbubbles were destroyed by a high mechanical index (MI) ultrasound pulse. Microbubbles replenished the myocardium and imaged at a specific pulsing interval. The plot for video intensity (VI) over uptake time was fitted to the exponential function: y = A(1–e–βt) with the values obtained for plateau VI (A) and the rate of rise of VI (β) representing myocardial blood volume (MBV) and myocardial microbubble velocity (MMV), respectively.7 MBF is derived as the product of A x β.8,9

Intermittent-triggered imaging and real-time imaging are the two principal imaging methods to visualize MCE. Triggered imaging is performed by capturing ultrasound frames of images produced using high MI ultrasound pulses gated to end-systole or end-diastole. Images of myocardial microbubble opacification acquired a progressively greater number of cardiac cycles.6 Although effective, triggered imaging is time-consuming and technically challenging in both the acquisition and analysis of data. The high MI pulses also create high background noise and are associated with premature ventricular contractions during end-systolic triggering.10 In comparison, real-time imaging uses one high MI pulse to destroy all microbubbles within the myocardium and then images the myocardial re-opacification with ‘real-time’ low MI imaging that minimally destroy the microbubbles.11 Real-time imaging is more easily acquired and provides the ability to simultaneously assess wall motion.12

Coronary angiography identifies the location and extent of stenotic lesions, but it does not determine the physiologic significance.13 As a result, it is difficult to determine the need for intervention in the setting of intermediate coronary stenosis.14 Doppler flow wire-derived coronary flow reserve (CFR) has been validated as an accurate method for determining the physiologic significance of intermediate coronary stenosis.15,16 CFR is calculated by dividing hyperaemic average peak red blood cell (RBC) velocity by baseline average peak RBC velocity. CFR values ≤2.0 have been associated with increased long-term event rates.17

Comparison of hyperaemia over baseline MCE can be performed for the calculation of myocardial perfusion reserve (MPR).18,19 MPR may be considered a surrogate for Doppler-derived CFR.

Therefore, this study aimed to compare MCE-derived MPR with simultaneously measured Doppler flow wire-derived CFR in angiographically normal patients. A comparison of infusion methods and imaging modalities of MCE contrast administration was also performed to evaluate which imaging provides the best correlation.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Study limitations
 Conclusion
 Funding
 Notes
 References
 
All patients underwent diagnostic cardiac catheterization after informed consent was obtained. Eligible patients had at least two angiographically normal coronary arteries. Patients were excluded if they had a left ventricular ejection fraction <35%, significant valvular heart disease, unstable angina, a myocardial infarction within 4 days, or clinical signs of fluid overload. This study was approved by the Saint Louis University Institutional Review Board.

Myocardial contrast echocardiography
Real-time and triggered imaging was performed with a phased-array S3 transducer (Philips Ultrasound, Andover, MA, USA). Ultrasound pulses were transmitted at a frequency range of 1.6–3.2 MHz. Apical two- and four-chamber views were obtained for each patient. Realtime imaging was acquired over 10 cardiac cycles with a frame rate of >18 Hz.

Myocardial contrast echocardiography was performed using bolus and continuous intravenous infusions of Perflutren Protein Type A Microspheres (OptisonTM, GE Healthcare). About 0.5 mL of contrast was administered intravenously by bolus followed by a slow saline flush. The continuous infusion was performed using a previously described method at a rate of 20–60 mL/h.20 In order to ensure optimal myocardial opacification, contrast was titrated to a rate at which left atrial attenuation was visualized. Imaging was performed after steady state was achieved. MCE was performed at baseline and at peak hyperaemia. Intravenous adenosine was infused intravenously at a rate of 140 mcg/kg/min until hyperaemia was induced. Peak hyperaemia was determined by peak RBC velocity visualized by the Doppler flow wire and maintained until all echocardiographic imaging was completed.

Echocardiographic analysis
All data were analysed off-line with proprietary Agilent (Philips) software. A region of interest was placed within the mid-myocardium. After the first frame of the high MI pulse, the region of interest automatically abstracted the VI for every subsequent frame. Every frame obtained throughout the cardiac cycle during real-time imaging was analysed. The region of interest was repositioned with every frame in order to maintain optimal alignment within the same area of myocardium. This procedure was repeated in the 12 myocardial segments visualized in the apical four- and two-chamber views. VI was plotted against pulsing interval and fitted to the exponential function y = A(1 – e–βt). MPR was calculated as the peak hyperaemic to baseline ratios of the following parameters: MBV (A), MMV (β), and MBF (A x β). Microbubble volume [MBV (A)] was derived from the peak amplitude, microbubble velocity [MMV (β)] was derived from the rate of rise, and blood flow [MBF (A x β)] was derived from the product of the first two variables.

The left anterior descending (LAD) coronary artery territory was considered to be an average of the apical four-chamber mid and apical inferoseptum and the apical two-chamber basal anterior, mid-anterior, apical anterior, and apical inferior wall segments. The circumflex territory was considered to be an average of the apical four-chamber basal and mid-anterolateral wall segments.21

Doppler flow wire
Coronary angiography was performed by standard Judkins technique. Patients were heparinized with a 40–60 U/kg intravenous bolus. A #6 French guiding catheter was positioned in the coronary artery of interest under fluoroscopic guidance. A 0.014 inch Doppler flow wire (Volcano Therapeutics, Rando Cordova, CA, USA) was then positioned in the mid-coronary artery to measure coronary flow velocity.22 Heart rate, blood pressure, and coronary flow velocity were measured at baseline, during, and after intravenous infusion of 140 mcg/kg/min of adenosine to reach hyperaemia. Doppler flow measurements were performed simultaneously with MCE. The Doppler flow velocities from five cardiac cycles were digitized and averaged. Doppler flow wire-derived CFR was calculated as peak hyperaemic average peak velocity divided by basal average peak velocity.

Statistical analysis
The MCE-derived MPR was correlated to the Doppler flow wire-derived CFR using Pearson’s correlation coefficient. Student’s paired t-test was utilized for significance, with P < 0.05 considered significant.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Study limitations
 Conclusion
 Funding
 Notes
 References
 
Technically adequate MCE and Doppler flow wire measurements were achieved in 10 patients. Two studies were excluded due to inadequate image acquisition or suboptimal contrast administration. The average age was 48 years old (35–61). Eight patients were men. CFR was calculated for the LAD coronary artery in eight patients and for the circumflex in two patients. None of the patients had angiographic evidence of epicardial coronary artery disease. An apical two-chamber view of one patient at rest and at peak hyperaemia during continuous contrast infusion is shown in Figure 1. Increased MBF during hyperaemia resulted in increased myocardial microbubble flow and increased opacification. The corresponding Doppler flow wire velocity signals at rest and at peak hyperaemia are shown in Figure 2.


Figure 1
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  		Figure 1 (A) Image at rest with an infusion of contrast to visualize myocardial perfusion with echocardiography. (B) Image at peak hyperaemia displaying increased contrast opacification in the myocardium.

 


Figure 2
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  		Figure 2 Comparison of coronary flow measured by Doppler flow wire at (A) base and (B) peak hyperaemia.

 
The mean Doppler flow wire-derived CFR was 2.6 ± 0.48. The imaging methods used to derive MPR are described in Table 1. Infusion rather than bolus administration provided the most consistent reading and stronger correlations of MPR with CFR, regardless of the use of triggered or real-time imaging modalities. The strongest correlation of MPR and CFR was found when MPR was derived from blood volume (MBV). This correlation was strongest when real-time imaging and infusion administration of contrast was performed (MPR = 2.3 + 0.8, r = 0.7, P = 0.04) (Figure 3). The correlation between Doppler flow wire-derived CFR and blood volume (MBV)-derived MPR is shown in Figure 1. MPR derived by microbubble velocity [MMV (β)] and blood flow [MBF (A x β)] trended towards correlation with CFR but did not reach statistical significance (average MPR 2.2 + 1.5 and 2.5 + 1.8, respectively, P = NS). Triggered imaging at end-diastole provided MPR resulting in values <2.0 in the analysis of blood volume [MBV (A)], velocity [MMV (β)], and flow [MBF (A x β)] with poor non-significant correlation (r = 0.4, P = NS). Triggered imaging and end-systole also provided values of MPR which correlated poorly with CFR (r = 0.6, P = NS) (Table 1).


Figure 3
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  		Figure 3 Correlation between Doppler flow wire-derived coronary flow reserve (CFR) and myocardial contrast echocardiography (MCE)-derived myocardial perfusion reserve (MPR) using real-time imaging with continuous contrast infusion (r = 0.7, P = 0.04).

 


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  		Table 1 Comparison of mean MCE MPR from all patients in myocardial blood volume (MBV), myocardial microbubble velocity (MMV), and myocardial blood flow (MBF) using analysis of full R-R intervals, systolic, or diastolic frames

 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Study limitations
 Conclusion
 Funding
 Notes
 References
 
This study demonstrated that blood volume-derived MPR during real-time imaging and continuous contrast infusion has a strong correlation with Doppler flow wire-derived CFR in patients with no angiographic evidence of coronary artery disease.

All contrast values of MBV, MMV, and MBF increased following adenosine-induced hyperaemia. These findings are similar to previous studies that found significant increases in MBV, MMV, and MBF following pharmaceutical vasodilation in patients with normal coronaries.23 MCE MPR correlated with invasively obtained Doppler flow-derived CFR. Doppler flow-derived CFR correlated more closely with blood volume-derived MPR than with MPR derived from either microbubble velocity or flow. These results suggest that MCE can identify normal MPR as a surrogate for CFR in patients with angiographically normal coronary arteries.

Using dipyridamole in a dog model, Cheirif et al.24 reported a similar increase in microbubble blood volume-derived MPR. The measured transmural flow with stress increased relative to baseline with a ratio on average of 2.1 + 0.60 times that of the baseline flow. Likewise, our average microbubble blood volume-derived MPR was 2.3 + 0.8.

Continuous contrast infusion imaging has a stronger correlation with Doppler flow wire-derived CFR than bolus contrast infusion imaging. This finding is consistent with previous studies that showed increased variability and decreased consistency with bolus injections.25 While bolus contrast infusion may be effective for calculating plateau VI, the calculation of microbubble velocity requires the contrast to be at a steady state within the myocardium which can only be achieved with continuous contrast infusion.26 Continuous infusion allows more time to evaluate different imaging planes and to examine the myocardium in detail.

Wei et al.27 reported no significant change in blood volume between baseline and hyperaemic stages. In contrast to this finding, our study found increased blood volume during hyperaemia. An explanation for this discrepancy is that Wei et al. analysed only end-systolic images acquired during triggered imaging. At end-systole, the large intra-myocardial arterioles and venules are closed shut and the capillaries are the only open myocardial vessels.28 However, during diastole, these arterioles and venules are patent and rapidly replenished with microbubbles. Our study analysed frames acquired throughout the cardiac cycle during real-time imaging. As a result, the VIs of vasodilated, microbubble-filled, arterioles and venules measured during diastole likely contributed to the increased blood volume measured during hyperaemia.


   Study limitations
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Study limitations
Conclusion
 Funding
 Notes
 References
 
During MCE, dropout of the anterior wall can occur due to the anisotropy of myocardial fibre orientation.29 This anisotropy causes backscatter to be maximum at angles of interrogation perpendicular to the myocardial fibres and minimum at more acute (60°) angles. The supine patient in the cardiac catherization laboratory minimizes the optimization of imaging planes due to suboptimal patient placement.

Vogel et al.30 have validated a method for overcoming attenuation caused by inhomogenous contrast administration. This method compares the blood volume in the myocardium with that in the cavity and is able to calculate the absolute MBF. Our study did not evaluate the intensity of the cavity and assessed flow reserve rather than absolute MBF.

The patient population was small and impaired endothelial function or microvascular disease was not evaluated to verify patient normality. Invasively determined CFR was used as the definition of normality that has inherent limitations including the lack of a normal reference artery but rather using the same artery as a reference of normal.


   Conclusion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Study limitations
 Conclusion
Funding
 Notes
 References
 
This study suggests MCE-derived MPR using complete R-R or systolic triggering correlates to normal CFR in angiographically normal patients. Further research is required in patients with significant coronary stenosis. MCE may potentially be a non-invasive method to quantify the physiologic significance of stenosis and assess the need for an interventional approach instantaneously.


   Funding
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Study limitations
 Conclusion
 Funding
Notes
 References
 
Funding provided by Amersham Nycomed (currently GE Healthcare).

Conflict of interest: Funding was provided by GE Healthcare, Bristol Myers Squibb Pharmaceuticals.


   Notes
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Study limitations
 Conclusion
 Funding
 Notes
References
 
{dagger} Presented in part at the American College of Cardiology Scientific Sessions 2003. Back


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Study limitations
 Conclusion
 Funding
 Notes
 References
 

  1. Villanueva FS, Gertz EW, Csikari M, Pulido G, Fisher D, Sklenar J. Detection of coronary artery stenosis with power Doppler imaging. Circulation (2001) 103:2624–30.[Abstract/Free Full Text]
  2. Masugata H, Lafitte S, Peters B, Strachan GM, DeMaria AN. Comparison of real-time and intermittent triggered myocardial contrast echocardiography for quantification of coronary stenosis severity and transmural perfusion gradient. Circulation (2001) 104:1550–6.[Abstract/Free Full Text]
  3. Keller MW, Glasheen W, Smucker ML, Burwell LR, Watson DD, Kaul S. Myocardial contrast echocardiography in humans. II. Assessment of coronary blood flow reserve. J Am Coll Cardiol (1988) 12:925–34.[Abstract]
  4. Villanueva FS, Camarano G, Ismail S, Goodman NC, Sklenar J, Kaul S. Coronary reserve abnormalities in the infarcted myocardium. Assessment of myocardial viability immediately versus late after reflow by contrast echocardiography. Circulation (1996) 94:748–54.[Abstract/Free Full Text]
  5. Van Camp G, Ay T, Pasquet A, London V, Bol A, Gisellu G, et al. Quantification of myocardial blood flow and assessment of its transmural distribution with real-time power modulation myocardial contrast echocardiography. J Am Soc Echocardiogr (2003) 16:263–70.[CrossRef][Web of Science][Medline]
  6. Wei K, Jayaweera AR, Firoozan S, Linka A, Skyba DM, Kaul S. Quantification of myocardial blood flow with ultrasound-induced destruction of microbubbles administered as a constant venous infusion. Circulation (1998) 97:473–83.[Abstract/Free Full Text]
  7. Tiemann K, Schlosser T, Pohl C, Bimmel D, Wietasch G, Hoeft A, et al. Are microbubbles free flowing tracers through the Myocardium? Comparison of indicator-dilution curves obtained from dye dilution and echo contrast using harmonic power Doppler imaging. Echocardiography (2000) 17:17–27.[CrossRef][Web of Science][Medline]
  8. Wei K. Detection and quantification of coronary stenosis severity with myocardial contrast echocardiography. Prog Cardiovasc Dis (2001) 44:81–100.[CrossRef][Web of Science][Medline]
  9. Dijkmans PA, Senior R, Becher H, Porter TR, Wei K, Visser CA, et al. Myocardial contrast echocardiography evolving as a clinically feasible technique for accurate, rapid, and safe assessment of myocardial perfusion: the evidence so far. J Am Coll Cardiol (2006) 48:2168–77.[Abstract/Free Full Text]
  10. van Der Wouw PA, Brauns AC, Bailey SE, Powers JE, Wilde AA. Premature ventricular contractions during triggered imaging with ultrasound contrast. J Am Soc Echocardiogr (2000) 13:288–94.[CrossRef][Web of Science][Medline]
  11. Leong-Poi H, Le E, Rim SJ, Sakuma T, Kaul S, Wei K. Quantification of myocardial perfusion and determination of coronary stenosis severity during hyperemia using real-time myocardial contrast echocardiography. J Am Soc Echocardiogr (2001) 14:1173–82.[CrossRef][Web of Science][Medline]
  12. Dolan M, Bierig M, Vrain St, Sheriff D, Watts W, Labovitz A. Assessment of myocardial perfusion and wall motion by real-time contrast echocardiography. J Am Soc Echocardiogr (2000) 13:461.
  13. White CW, Wright CB, Doty DB, et al. Does visual interpretation of the coronary arteriogram predict the physiologic importance of a coronary stenosis? N Engl J Med (1984) 310:819.[Abstract]
  14. Bach RG, Kern MJ. Clinical application of the Doppler flow velocity guide wire. Intravascular Imaging and Doppler (1997) 15:77–99.
  15. Ofili EO, Kern MJ, Labovitz AJ, St Vrain JA, Segal J, Aguirre FV, et al. Analysis of coronary blood flow velocity dynamics in angiographically normal and stenosed arteries before and after endolumen enlargement by angioplasty. J Am Coll Cardiol (1993) 21:308–16.[Abstract]
  16. Kern MJ, Bach RG, Mechem C, Caracciolo EA, Aguirre FV, Miller LW, et al. Variations in normal coronary vasodilatory reserve stratified by artery, gender, heart transplantation and coronary artery disease. J Am Coll Cardiol (1996) 28:1154–60.[Abstract]
  17. Chamuleau SA, Tio RA, de Cock CC, de Muinck ED, Pijls NH, van Eck-Smit BL, et al. Prognostic value of coronary blood flow velocity and myocardial perfusion in intermediate coronary narrowings and multivessel disease. J Am Coll Cardiol (2002) 39:852–8.[Abstract/Free Full Text]
  18. Osório AF, Tsutsui JM, Kowatsch I, Guerra VC, Ramires JA, Lemos PA, et al. Evaluation of blood flow reserve in left anterior descending coronary artery territory by quantitative myocardial contrast and Doppler echocardiography. J Am Soc Echocardiogr (2007) 20:709–16.[CrossRef][Web of Science][Medline]
  19. Ghanem A, DeMaria AN, Lohmaier S, El-Sayed MA, Strachan M, Sommer T, et al. Triggered replenishment imaging reduces variability of quantitative myocardial contrast echocardiography and allows assessment of myocardial blood flow reserve. Echocardiography (2007) 24:149–58.[CrossRef][Web of Science][Medline]
  20. Miller JJ, Tiemann K, Podell S, Doerr Stevens JK, Kuvelas T, Greener Y, et al. In vitro, animal, and human characterization of OPTISON infusions for myocardial contrast echocardiography. J Am Soc Echocardiogr (1999) 12:1027–34.[CrossRef][Web of Science][Medline]
  21. Lang RM, Bierig M, Devereux RB, Flachskampf FA, Foster E, Pellikka PA, et al. Recommendations for chamber quantification. J Am Soc Echocardiogr (2005) 18:1440–63.[CrossRef][Web of Science][Medline]
  22. Kern MJ. Coronary physiology revisited: practical insights from the cardiac catheterization laboratory. Circulation (2000) 101:1344–51.[Abstract/Free Full Text]
  23. Dawson D, Rinkevich D, Belcik T, Jayaweera AR, Rafter P, Kaul S, et al. Measurement of myocardial blood flow velocity reserve with myocardial contrast echocardiography in patients with suspected coronary artery disease: comparison with quantitative gated Technetium 99m sestamibi single photon emission computed tomography. J Am Soc Echocardiogr (2003) 16:1171–7.[CrossRef][Web of Science][Medline]
  24. Cheirif J, Zoghbi WA, Bolli R, O’Neill PG, Hoyt BD, Quinones MA. Assessment of regional myocardial perfusion by contrast echocardiography. II. Detection of changes in transmural and subendocardial perfusion during dipyridamole-induced hyperemia in a model of critical coronary stenosis. J Am Coll Cardiol (1989) 14:1555–65.[Abstract]
  25. Kisanuki A, Yuasa T, Kuwahara E, Takasaki K, Yoshifuku S, Otsuji Y, et al. Reproducibility of intravenous intermittent triggered myocardial contrast echocardiography in healthy subjects. Jpn Heart J (2004) 45:461–73.[CrossRef][Medline]
  26. Wei K, Jayaweera AR, Firoozan S, Linka A, Skyba DM, Kaul S. Basis for detection of stenosis using venous administration of microbubbles during myocardial contrast echocardiography: bolus or continuous infusion? J Am Coll Cardiol (1998) 32:252–60.[Abstract/Free Full Text]
  27. Wei K, Ragosta M, Thorpe J, Coggins M, Moos S, Kaul S. Noninvasive quantification of coronary blood flow reserve in humans using myocardial contrast echocardiography. Circulation (2001) 103:2560–5.[Abstract/Free Full Text]
  28. Krams R, Pieter S, Westerhof N. Coronary oscillatory flow amplitude is more affected by perfusion pressure than ventricular pressure. Am J Physiol (1990) 258:H1889–98.[Web of Science][Medline]
  29. Madaras EI, Perez J, Sobel BE, Mottley JG, Miller JG. Anisotropy of the ultrasonic backscatter of myocardial tissue: II. Measurements in vivo. J Acoust Soc Am (1988) 83:762–9.[CrossRef][Web of Science][Medline]
  30. Vogel R, Indermühle A, Reinhardt J, Meier P, Siegrist PT, Namdar M, et al. The quantification of absolute myocardial perfusion in humans by contrast echocardiography: algorithm and validation. J Am Coll Cardiol (2005) 45:754–62.[Abstract/Free Full Text]

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