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Physiological basis for identifying viable myocardium with MCE

Contrast Echocardiography in Practice: Contrast for Assessment of Myocardial Perfusion

Non-invasive Imaging: Echocardiography
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As contrast microbubbles remain entirely within the intravascular space[1], their presence within any myocardial territory denotes the status of microvascular perfusion within that region.[2] The volume of blood present in the entire coronary circulation (arteries, arterioles, capillaries, venules and veins) is approximately 12 ml/100 g of cardiac muscle[3]; approximately one third of this is present within the myocardium itself, and is termed ‘myocardial blood volume’ (MBV). 90% of the MBV resides within the capillaries[4] and thus MBV is essentially equivalent to the capillary blood volume (CBV).

 

Myocardial contrast intensity reflects the concentration of microbubbles within the myocardium. When a steady state of microbubble concentration has been achieved in the myocardium, during a continuous infusion of contrast, the observed signal intensity therefore denotes the CBV.[4-5] Any alteration of signal intensity in this situation thus occurs principally as a result of a change in CBV.

Key work previously published has demonstrated that myocyte loss is associated with loss of the microvasculature[6]and that contrast signal intensity correlated strongly with capillary density on biopsy samples obtained from corresponding segments.[7]

Practical Point - Using MCE to assess myocardial viability

Rest contrast images are acquired as described previously in this chapter. However, when real-time imaging is used, it is important to acquire at least 15s post-flash for optimal assessment (it has been shown that both the presence of homogenous contrast uptake and, alternatively, the absence of contrast uptake are very accurate indicators of the presence or absence of myocardial viability, respectively). It is, however, important to exclude apical and basal artefacts before concluding that there is absent contrast uptake. High MI imaging should also include imaging up to 15s post-flash[8]. The transmit focus should be moved towards the apex to confirm an apical perfusion defect when suspected. A thin and scarred (bright) myocardium of <5 mm in size indicates non-viable tissue and it is unnecessary to assess perfusion in these segments.

Therefore, MCE is able to detect presence or absence of viable myocardium by virtue of its ability to assess the integrity of the microcirculation.

In conclusion, Myocardial Contrast Echocardiography:
  • accurately differentiates stunned and necrotic myocardium
  • delineates the transmural extent of infarction
  • predicts recovery of regional and global left ventricular systolic function
  • identifies patients at high risk of left ventricular remodeling
  • provides incremental viability data when performed in conjunction with low-dose dobutamine echocardiography
Technological advances have identified MCE as a safe and practical bedside technique for the evaluation of myocardial viability. It has comparable accuracy with other non-invasive imaging techniques, such as dobutamine stress echocardiography, radionuclide scintigraphy and cardiovascular magnetic resonance imaging.

References

1. Kaul S. Clinical applications of myocardial contrast echocardiography. Am J Cardiol 1992;69(20):46H-55H.
2. Kaul S, Jayaweera AR. Myocardial contrast echocardiography has the potential for the assessment of coronary microvascular reserve. J Am Coll Cardiol 1993;21(2):356-8.
3. Kaul S, Jayaweera AR. Coronary and myocardial blood volumes: noninvasive tools to assess the coronary microcirculation? Circulation 1997;96(3):719-24.
4. 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(1):252-60.
5. 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(5):473-83.
6. Kloner RA, Rude RE, Carlson N, Maroko PR, DeBoer LW, Braunwald E. Ultrastructural evidence of microvascular damage and myocardial cell injury after coronary artery occlusion: which comes first? Circulation 1980;62(5):945-52.
7. Shimoni S, Frangogiannis NG, Aggeli CJ, Shan K, Quinones MA, Espada R, et al. Microvascular structural correlates of myocardial contrast echocardiography in patients with coronary artery disease and left ventricular dysfunction: implications for the assessment of myocardial hibernation. Circulation 2002;106(8):950-6.
8. Swinburn JM, Lahiri A, Senior R. Intravenous myocardial contrast echocardiography predicts recovery of dysynergic myocardium early after acute myocardial infarction. J Am Coll Cardiol 2001;38(1):19-25.

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