Search tips
Search criteria 


Logo of jcarultraJournal of Cardiovascular UltrasoundJournal of Cardiovascular UltrasoundAim and ScopeInstructions to AuthorArchive
J Cardiovasc Ultrasound. 2017 March; 25(1): 3–4.
Published online 2017 March 27. doi:  10.4250/jcu.2017.25.1.3
PMCID: PMC5385315

Role of Echocardiography in Diagnosing Myocardial Ischemia at Emergency Department

Kyoung Im Cho, MD, PhDcorresponding author


Because chest pain is one of the most common complaints that brings a patient to the emergency, the differential diagnosis of chest pain with or without acute coronary syndrome is very important. Traditionally, performing conventional echocardiography for detecting ischemia-related systolic abnormalities involves visually estimating the changes of wall thickening in circular muscle. This has well-documented limitations for both the interobserver variability1) and the ability of the human eye to resolve rapid, short-lived motion.2) Another approach to defining the regional myocardial properties could be to evaluate the deformation of a myocardial segment during the cardiac cycle. During the cardiac cycle, regional deformation of the myocardium occurs in 3 major directions: longitudinally; circumferentially; and radially. Currently, the terms “myocardial strain rate” and “strain” are used as indexes of longitudinal myocardial deformation. The physical definition of strain is the relative change in length of a material related to its original length. Regional strain rate and strain are derivative of myocardial velocities. The actual sequence of the regional changes in the myocardial function that are induced by acute ischemia has been well defined by experimental sonomicrometric techniques.3),4),5),6) Acute ischemia induces a delay in the onset of contraction, a progressive decrease in the rate and degree of thickening, and a progressive delay in the timing of the peak thickening until this event occurs in what is early diastole for the surrounding nonischemic myocardial segments. Finally, systolic thickening is virtually or completely abolished by total occlusion, and only late systolic/early diastolic thinning occurs. Although it has been well documented in the animal laboratory setting, all the components of the above ischemic response have yet to be well documented in the clinical setting by noninvasive imaging techniques. With the introduction of tissue Doppler imaging (TDI), it has also become possible to determine segmental velocities at a sampling rate of more than 140 samples per second by using standard echo views. Prior in vivo animal studies based on TDI have documented a significant reduction in the peak systolic velocities, the velocity gradient7),8) and the peak systolic strain9),10) that occur during acute ischemia. Thus, the quantitation of the segmental systolic parameters derived from high-resolution TDI data might be the optimal solution for functional studies of patients with coronary artery disease. However, the angle dependency of the Doppler technique frequently makes evaluation of regional wall motion abnormalities confusing. 2-dimensional (2D) strain method is another tool for quantitation of regional myocardial deformation within a scan plane. Contrary to strain by TDI, this method is inherently 2D and independent of interrogation angle as it tracks speckle patterns (acoustic markers),11) however, it is widely used for the assessment of global left ventricular (LV) longitudinal strain rather than regional wall motion.

Here, Kim et al.12) showed that regional wall motion assessment using velocity vector imaging (VVI) could be used to detect significant ischemia in the patient with acute chest pain at emergency department. Using a novel feature-tracking algorithm, VVI can display velocity vectors of regional wall motion overlaid onto the B-mode image and allows the quantitative assessment of LV myocardial mechanics without angle dependancy.13) The increase in VMVO is considered to be caused mainly by post-systolic thickening in ischemic myocardium, which is the result of the difference in contractility with the adjacent normal regions. Although the feasibility of this method was limited in some patients with a poor echocardiographic window, and the sensitivity is limited by small number patients, but VVI may have a role in differentiation between ischemic and non-ischemic segments in emergency department.


Editorials published in the Journal of Cardiovascular Ultrasound do not necessarily represent the views of JCU or the Korean Society of Echocardiography.


1. Hoffmann R, Lethen H, Marwick T, Arnese M, Fioretti P, Pingitore A, Picano E, Buck T, Erbel R, Flachskampf FA, Hanrath P. Analysis of interinstitutional observer agreement in interpretation of dobutamine stress echocardiograms. J Am Coll Cardiol. 1996;27:330–336. [PubMed]
2. Kvitting JP, Wigström L, Strotmann JM, Sutherland GR. How accurate is visual assessment of synchronicity in myocardial motion? An in vitro study with computer-simulated regional delay in myocardial motion: clinical implications for rest and stress echocardiography studies. J Am Soc Echocardiogr. 1999;12:698–705. [PubMed]
3. Ehring T, Heusch G. Left ventricular asynchrony: an indicator of regional myocardial dysfunction. Am Heart J. 1990;120:1047–1057. [PubMed]
4. Osakada G, Hess OM, Gallagher KP, Kemper WS, Ross J., Jr Endsystolic dimension-wall thickness relations during myocardial ischemia in conscious dogs. A new approach for defining regional function. Am J Cardiol. 1983;51:1750–1758. [PubMed]
5. Wiegner AW, Allen GJ, Bing OH. Weak and strong myocardium in series: implications for segmental dysfunction. Am J Physiol. 1978;235:H776–H783. [PubMed]
6. Leone BJ, Norris RM, Safwat A, Foëx P, Ryder WA. Effects of progressive myocardial ischaemia on systolic function, diastolic dysfunction, and load dependent relaxation. Cardiovasc Res. 1992;26:422–429. [PubMed]
7. Derumeaux G, Ovize M, Loufoua J, André-Fouet X, Minaire Y, Cribier A, Letac B. Doppler tissue imaging quantitates regional wall motion during myocardial ischemia and reperfusion. Circulation. 1998;97:1970–1977. [PubMed]
8. Derumeaux G, Ovize M, Loufoua J, Pontier G, André-Fouet X, Cribier A. Assessment of nonuniformity of transmural myocardial velocities by color-coded tissue Doppler imaging: characterization of normal, ischemic, and stunned myocardium. Circulation. 2000;101:1390–1395. [PubMed]
9. Armstrong G, Pasquet A, Fukamachi K, Cardon L, Olstad B, Marwick T. Use of peak systolic strain as an index of regional left ventricular function: comparison with tissue Doppler velocity during dobutamine stress and myocardial ischemia. J Am Soc Echocardiogr. 2000;13:731–737. [PubMed]
10. Urheim S, Edvardsen T, Torp H, Angelsen B, Smiseth OA. Myocardial strain by Doppler echocardiography. Validation of a new method to quantify regional myocardial function. Circulation. 2000;102:1158–1164. [PubMed]
11. Korinek J, Wang J, Sengupta PP, Miyazaki C, Kjaergaard J, McMahon E, Abraham TP, Belohlavek M. Two-dimensional strain--a Doppler-independent ultrasound method for quantitation of regional deformation: validation in vitro and in vivo. J Am Soc Echocardiogr. 2005;18:1247–1253. [PubMed]
12. Kim KH, Na SH, Park JS. Role of quantitative wall motion analysis in patients with acute chest pain at emergency department. J Cardiovasc Ultrasound. 2017;25:20–27.
13. Cannesson M, Tanabe M, Suffoletto MS, Schwartzman D, Gorcsan J., 3rd Velocity vector imaging to quantify ventricular dyssynchrony and predict response to cardiac resynchronization therapy. Am J Cardiol. 2006;98:949–953. [PubMed]

Articles from Journal of Cardiovascular Ultrasound are provided here courtesy of Korean Society of Echocardiography