Journal of Medical Ultrasound
Volume 19, Issue 4 , Pages 115-121, December 2011

Clinical Applications of Transthoracic Doppler Echocardiographic Coronary Flow Reserve Measurements in the Left Anterior Descending Coronary Artery

  • Ming-Jui Hung

      Affiliations

    • Corresponding Author InformationCorrespondence to: Dr Ming-Jui Hung, Department of Cardiology, Chang Gung Memorial Hospital, Keelung, 222 Maijin Road, Keelung 20401, Taiwan.
    • ,
  • Wen-Jin Cherng

Department of Cardiology, Chang Gung Memorial Hospital, Keelung, Chang Gung University College of Medicine, Taiwan

Received 29 August 2011; accepted 12 October 2011. published online 31 October 2011.

Article Outline

Transthoracic Doppler echocardiography (TDE) is a noninvasive tool for measuring coronary flow reserve in the epicardial coronary arteries. In the absence of stenosis in the epicardial coronary artery, TDE can detect impaired microvascular vasodilatation associated with diseases, including reperfused myocardial infarct, systemic arterial hypertension, diabetes mellitus, coronary vasospasm, microvascular angina, and hypertrophic cardiomyopathy by demonstrating a decrease in the coronary flow reserve. Because it is noninvasive, TDE allows for serial coronary flow reserve evaluations to explore the effect of various therapies. This noninvasive imaging technique expands the field of diagnostic echocardiography and brings new insight into the pathophysiology of ischemic heart disease. This review outlines rationale of TDE to evaluate coronary flow reserve in the left anterior descending coronary artery and discusses its clinical applications.

Key words: coronary flow reserve, left anterior descending coronary artery, Transthoracic Doppler echocardiography

 

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Introduction 

Coronary flow reserve (CFR) is defined as the ratio of hyperemic (stimulated) to baseline (resting) coronary blood flow for a given perfusion pressure [1]. CFR measurement is used both to assess epicardial coronary stenoses and to examine the integrity of microvascular circulation. In the absence of coronary artery stenoses, the CFR may be decreased when coronary microvascular circulation is compromised by arterial hypertension, diabetes mellitus, coronary vasospasm, cardiac syndrome X, and hypertrophic cardiomyopathy [2].

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Functional anatomy of the coronary arterial system 

The coronary arterial system is composed of three compartments with different functions, although the borders of each compartment cannot be clearly defined anatomically [3]. The first compartment of the coronary arterial system is known as the proximal compartment and is comprised of conductive arteries. It is represented by the large epicardial coronary arteries, which have a capacitance function and offer little resistance to coronary blood flow. The diameter of the epicardial coronary arteries ranges from approximately 500μm to 2–5mm. The second compartment of the coronary arterial system is known as the intermediate compartment. It is comprised of prearterioles that are characterized by a measurable pressure drop along their length. These vessels are not under direct vasomotor control by diffusible myocardial metabolites because of their extramyocardial position and wall thickness. Their diameter ranges from approximately 100–500μm, and their specific function is to maintain pressure at the origin of the arterioles within a narrow range when coronary perfusion pressure or flow changes. The third compartment of the coronary arterial system is known as the distal compartment. It is comprised of intramural arterioles that are characterized by a considerable drop in pressure along their path. The intramural arterioles have diameters of less than 100μm, and their function is the matching of myocardial blood supply and oxygen consumption.

When blood flow changes, epicardial coronary arteries and proximal arterioles have an intrinsic tendency to maintain a given level of shear stress by endothelial-dependent dilatation [4]. When aortic pressure increases, distal prearterioles undergo myogenic constriction to maintain a constant pressure at the origin of the arterioles. Arterioles have a fundamental role in the metabolic regulation of coronary blood flow [5]. They have a high resting tone and dilate in response to the release of metabolites by the myocardium as a result of an increase in oxygen consumption. Arteriolar dilatation decreases both resistance in the overall network and pressure in the distal prearterioles, which in turn induce the dilatation of myogenically sensitive vessels. Furthermore, the dilatation of distal prearterioles and arterioles results in an increase in shear stress, which triggers flow-dependent dilatation in larger prearterioles and conductance arteries. Coronary microvascular dysfunction is defined as disordered function of small coronary resistance vessels (<100–200μm) [6].

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Assessment of the coronary microcirculation 

Presently, there is no technique to visualize coronary microcirculation in vivo in humans. Several measurements that rely on the quantification of blood flow through the coronary circulation are commonly used to assess the function of coronary microvasculature. Coronary blood flow is a measurement of the amount of flow through a given coronary vessel per unit of time and is usually expressed in milliters per minute [7]. Techniques for measuring coronary blood flow include intracoronary thermodilution, which uses a thermal dilution curve to measure blood flow, and an intracoronary Doppler wire, which measures blood flow ultrasonographically according to the Doppler principle. Another invasive technique for assessing coronary blood flow is the Thrombolysis in Myocardial Infarction (TIMI) frame count. It does not quantify the flow, but it is useful for comparative purposes [8]. Recently, transthoracic Doppler echocardiography (TDE) has been used as a noninvasive technique to measure coronary blood flow [6], [9].

CFR is the magnitude of the increase in coronary flow that is achieved from basal coronary perfusion to maximal coronary vasodilation. Since flow resistance is primarily determined by the microvasculature, CFR is a measurement of the ability of the microvasculature to respond to a stimulus and, therefore, presumably of the function of the small vessels. CFR is determined by measuring the coronary or myocardial blood flow both at rest (basal flow) and with maximal hyperemia, and it is achieved with an intracoronary or intravenous infusion of adenosine or an intravenous infusion of dipyridamole. CFR is then expressed as the ratio of blood flow during hyperemia to blood flow at rest. Echocardiographic CFR is defined as the ratio of hyperemic to basal peak diastolic coronary flow. In patients with coronary artery disease (CAD), the extent of the reduction in CFR is directly related to the severity of stenosis, whereas in persons with angiographically normal arteries it is a marker of microvascular dysfunction [7]. A CFR of less than 2.0 is often considered abnormal (Fig. 1) [10].

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  • Fig. 1 

    A synthetic view of different anatomic (first row) and coronary flow reserve (CFR) response (last row). In the normal condition (left), there is a normal CFR response [ratio of hyperemic (light red, A′) to basal (dark red, A) peak diastolic coronary flow velocity >3]. An abnormal CFR response can be noted in the presence of microvascular disease or mild-to-moderate epicardial coronary artery stenosis (second column from left). With more advanced epicardial coronary artery stenosis (third column from left), more reduction of CFR is found.

Coronary microcirculatory dysfunction affects the left ventricle globally [11] and regionally [12]; therefore, CFR assessment of left anterior descending (LAD) artery, which would be inadequate for CAD detection, is an excellent option for evaluating the global coronary microcirculation [10]. The application of the latest ultrasound technology of the second harmonic has gained a great step in ultrasound coronary evaluation. By applying anatomical knowledge and the newest technical applications, it is now possible to make a complete a coronary evaluation of the LAD artery in clinical practice.

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Ultrasound coronary anatomy reference points 

The LAD coronary anatomy is the first artery investigated with ultrasound when using a transesophageal or transthoracic approach. The first anatomical structure is the proximal LAD artery. The left atrial appendage and pulmonary artery represent the key reference points in detecting the proximal LAD coronary tract. The second anatomical structure is the intermediate LAD artery. The septal perforans branches represent the key references obtainable by regulating the probe slightly lower and maintaining the focus on the anterior interventricular sulcus. The third anatomical structure is the distal LAD tract, which can be highlighted by investigating the lower part of the interventricular anterior sulcus near the apex under Color Doppler guidance and by adopting growing delivery frequencies [5–7Mhz in the second harmonic (Fig. 2A)]. The distal LAD tract is more suitable to investigate coronary microvascular function because it is between the large epicardial LAD arteries and microvasculature. By subsequently applying Pulse Doppler inside the coronary vessel, we may obtain the coronary spectrum (Fig. 3A) and therefore quantify it (Fig. 3B). It is now possible to investigate the LAD artery by TDE in 95%–98% of patients [13], [14].

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  • Fig. 2 

    Using a modified parasternal long-axis. (A) Transthoracic color Doppler recording shows coronary blood flow (arrows) in the distal portion of the (B) left anterior descending coronary artery. Ao=aorta; LA=left atrium; LV=left ventricle.

The appropriate TDE settings 

It is important to apply the current parameters to highlight the distal LAD artery: (1) the probe delivery frequencies are 5–7Mhz as the second harmonic, (2) the color Doppler flow velocity range is 12–24 centimeters/second, (3) the wall filter is high, and (4) the pulse Doppler filter is low. The color gain is adjusted to provide optimal images.

Position of the TDE probe 

The acoustic window is around the midclavicular line in the fourth and fifth intercostal spaces in the left lateral decubitus position. The ultrasound beam is transmitted toward the heart to visualize coronary blood flow in the distal portion of the LAD artery by color Doppler flow mapping. First, the left ventricle is imaged in the long-axis cross-section (Fig. 2A), then the ultrasound beam is inclined laterally. Next, the coronary blood flow in the distal LAD is searched for under the color Doppler flow mapping guidance (Fig. 2B). After positioning a sample volume (2.0-, 2.5-, or 3.0-mm wide) on the color signal in the distal LAD artery, Doppler spectral tracings of flow velocity are recorded by fast Fourier transformation analysis. Angle correction is needed in each examination because of the incident Doppler angle. The spectral Doppler tracing of the LAD artery flow shows a characteristic biphasic flow pattern with a larger diastolic component and a smaller systolic one (Figs. 1 and 3A). To obtain a correct CFR, the sample volume should be accurately positioned and maintained throughout the injection of the vasodilator agent. Although dipyridamole (0.84mg/kg/minutes over 6 minutes continuously) and adenosine (140μg/kg/minutes for 2–6 minutes with infusion time, depending on operator skills) can be used as hyperemic stressors, adenosine is preferable because it reaches the hyperemic peak induction within 1 minute, acts mainly at the level of the microcirculation, and it does not significantly alter the diameter of the coronary artery [15]. In addition, the shorter half-life (10 seconds) and rapid onset of action make the CFR measurements more rapid and it produces less adverse reactions [16]. Although adenosine is safe, it is contraindicated in people with bronchial asthma and may be poorly tolerated in others due to its adverse events.

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Clinical applications of TDE CFR 

Angiographically obstructive coronary artery disease 

The cutoff value of <2 of CFR is precise for detecting significant (> 75%) LAD stenosis with a sensitivity of 86% and a specificity of 70% [14]. The same CFR criteria can also be applied to right coronary artery and left circumflex artery [14]. The CFR <1, which suggests coronary steal, may be a predictor of critical stenosis (>90%) [17]. Resting coronary flow pattern can be decreased in the presence of severe coronary artery stenosis. Without pharmacological stress, the cutoff point of 1.6 for peak diastolic to systolic flow velocity ratio has high sensitivities and specificities for predicting coronary artery stenosis (> 85%) [18] and reversible perfusion defects in thallium 201 single photon-emission computed tomography [19].

For angioplasty monitoring, a CFR <2 during follow-up after angioplasty, the restenosis in the LAD is detected with high-sensitivity and specificity [20], [21]. The cutoff value of 2 for CFR at a time point is useful but it probably less sensitive than its evolution over time to detect restenosis after angioplasty. Therefore, a reference value of CFR should be established in a patient to assess the follow-up value in this setting [22]. For postinfarction CFR assessment, the decreased CFR <1.5 predicts an increase in left ventricular volume (i.e., remodeling) after reperfused myocardial infarction [23]. Another study [24] found that preconditioning due to preinfarction angina has a protective role on microvascular function as demonstrated by CFR preservation (>2.5) after myocardial infarction. From a prognostic point of view, a reduced CFR (≤1.92) is the best predictor of future events in patients with known or suspected CAD, and the negative stress echocardiography by wall motion criteria [25] and the prognostic value of CFR are not affected by concomitant antiischemic therapy at the time of testing [26].

Without angiographically obstructive coronary artery disease 

Several diseases such as hypertrophy (due to aortic stenosis, hypertrophic cardiomyopathy, and hypertension), diabetes mellitus, smoking, coronary vasospasm, and menopause can cause structural and/or functional abnormalities of the microcirculation [2]. Because invasive Doppler measurement of CFR is not routinely performed in patients with chest pain and angiographically normal coronary arteries, the extent of such microvascular disease is likely underestimated. Accordingly, recent studies [27], [28] have demonstrated that 22% of patients with chest pain and normal or near normal coronary angiography have CFR <2.0. Noninvasive assessment of CFR using TDE has been performed in patients with hypertrophic cardiomyopathy [29], aortic stenosis [30], diabetes mellitus [10], and in those who smoke [31]. Additionally, the effect of physiological hypertrophy on CFR is measurable by TDE [32], which could prove useful in differentiating an athlete’s hypertrophic heart, in which CFR is in the normal to supranormal range, and from a patient with hypertrophic cardiomyopathy, in which CFR is markedly attenuated. Importantly, noninvasive TDE allows serial CFR evaluation to explore the effects of various therapies [17], [33], [34], [35].

Diffuse coronary vasospasm was associated with significantly reduced vasodilatory reaction compared with focal vasospasm despite the finding that vasodilatory response of the epicardial coronary artery to isosorbide dinitrate was maintained in patients with focal and diffuse vasospasm compared with controls. Studies using different techniques of the thermal dilution method suggested that microvascular impairment could explain the restricted CFR in patients with diffuse vasoconstriction [36], [37]. Furthermore, CFR was maintained in patients with focal vasospasm, and normal microvascular function was suspected in these cases. Nitrates can provide relief in the treatment of focal vasoconstriction but are less effective in patients with diffuse vasospasm, who may require vasorelaxants of microvessels, such as potassium channels openers [38], [39]. Limited atherosclerotic lesions have been demonstrated at the site of focal vasospasm by using intravascular ultrasound, and it has been suggested as a cause of focal vasospasm [40], [41]. CFR might be maintained in patients with focal vasospasm if the pathologic mechanism is related to localized endothelial dysfunction due to the existence of such limited atherosclerotic lesions as there would be no microvascular dysfunction. Thus, the mechanism of focal vasospasm might be related to localized endothelial dysfunction of the epicardial coronary artery, which causes a hypersensitive vasoconstrictive reaction to ergonovine malate in the coronary artery [42].

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Limitations 

The angle between the Doppler beam and the artery can be large (>30°) ad cause an underestimation of the true flow velocity. However, for the purposes of CFR measurement, the absolute velocity value is not needed because CFR is a quotient of two diastolic velocities. For a poor ultrasound window, under some circumstances such as obesity and chronic lung conditions, the use of an intravenous contrast agent can improve the feasibility and quality of CFR measurements [43], [44].

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Pitfalls 

Mapping different coronary arteries from the LAD artery such as diagonal or the ramus branch cannot be excluded completely. Additionally, CFR must be measured distally to stenosis because CFR measurement at the stenosis site is underestimated due to an increased baseline flow velocity.

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Conclusion 

TDE is a convenient tool for measuring CFR in epicardial coronary arteries (predominantly in the LAD artery). An appropriate echo machine setting is important to study CFR. Resting CFR or pharmacologically induced CFR can effectively predict significant coronary artery stenosis. In the absence of stenosis in the epicardial LAD coronary artery, decreased CFR enables the detection of impaired microvascular vasodilatation in women subjects and in patients with arterial hypertension, diabetes mellitus, and coronary vasospasm [45], [46]. In addition, noninvasive TDE allows serial CFR assessments to explore the effect of various therapies.

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References 

  1. Gould KL, Lipscomb K, Hamilton GW. Physiologic basis for assessing critical coronary stenosis. Instantaneous flow response and regional distribution during coronary hyperemia as measures of coronary flow reserve. Am J Cardiol. 1974;33:87–94
  2. Camici PG, Crea F. Coronary microvascular dysfunction. N Engl J Med. 2007;356:830–840
  3. Crea F, Camici PG, De Caterina R, et al. Chronic ischaemic heart disease. In:  Camm AJ,  Luescher TF,  Surruys PW editor. The ESC textbook of cardiovascular medicine. Oxford, England: Blackwell Publishing; 2006;p. 391–424
  4. Lupi A, Buffon A, Finocchiaro ML, et al. Mechanisms of adenosine-induced epicardial coronary artery dilatation. Eur Heart J. 1997;18:614–617
  5. Kuo L, Chilian WM, Davis MJ. Coronary arteriolar myogenic response is independent of endothelium. Circ Res. 1990;66:860–866
  6. Hozumi T, Yoshida K, Akasaka T, et al. Noninvasive assessment of coronary flow velocity and coronary flow velocity reserve in the left anterior descending coronary artery by Doppler echocardiography: comparison with invasive technique. J Am Coll Cardiol. 1998;32:1251–1259
  7. Kaufmann PA, Camici PG. Myocardial blood flow measurement by PET: technical aspects and clinical applications [Erratum appears in J Nucl Med. 2005;46:291]. J Nucl Med. 2005;46:75–88
  8. Gibson CM, Cannon CP, Murphy SA, et al. Relationship of TIMI myocardial perfusion grade to mortality after administration of thrombolytic drugs. Circulation. 2000;101:125–130
  9. Hozumi T, Yoshida K, Ogata Y, et al. Noninvasive assessment of significant left anterior descending coronary artery stenosis by coronary flow velocity reserve with transthoracic color Doppler echocardiography. Circulation. 1998;97:1557–1562
  10. Cortigiani L, Rigo F, Gherardi S, et al. Additional prognostic value of coronary flow reserve in diabetic and nondiabetic patients with negative dipyridamole stress echocardiography by wall motion criteria. J Am Coll Cardiol. 2007;50:1354–1361
  11. L’Abbate A. Large anSd micro coronary vascular involvement in diabetes. Pharmacol Rep. 2005;57 Suppl:3–9
  12. Galderisi M. Diastolic dysfunction and diabetic cardiomyopathy: evaluation by Doppler echocardiography. J Am Coll Cardiol. 2006;48:1548–1551
  13. Rigo F. Coronary flow reserve in stress-echo lab. From pathophysiologic toy to diagnostic tool. Cardiovasc Ultrasound. 2005;3:8
  14. Vegsundvag J, Holte E, Wiseth R, et al. Coronary flow velocity reserve in the three main coronary arteries assessed with transthoracic Doppler: a comparative study with quantitative coronary angiography. J Am Soc Echocardiogr. 2011;24:758–767
  15. Wilson RF, Wyche K, Christensen BV, et al. Effects of adenosine on human coronary arterial circulation. Circulation. 1990;82:1595–1606
  16. Sudhir K, MacGregor JS, Barbant SD, et al. Assessment of coronary conductance and resistance vessel reactivity in response to nitroglycerin, ergonovine and adenosine: in vivo studies with simultaneous intravascular two-dimensional and Doppler ultrasound. J Am Coll Cardiol. 1993;21:1261–1268
  17. Pizzuto F, Voci P, Mariano E, et al. Assessment of flow velocity reserve by transthoracic Doppler echocardiography and venous adenosine infusion before and after left anterior descending coronary artery stenting. J Am Coll Cardiol. 2001;38:155–162
  18. Higashiue S, Watanabe H, Yokoi Y, et al. Simple detection of severe coronary stenosis using transthoracic Doppler echocardiography at rest. Am J Cardiol. 2001;87:1064–1068
  19. Daimon M, Watanabe H, Yamagishi H, et al. Physiologic assessment of coronary artery stenosis without stress tests: noninvasive analysis of phasic flow characteristics by transthoracic Doppler echocardiography. J Am Soc Echocardiogr. 2005;18:949–955
  20. Pizzuto F, Voci P, Mariano E, et al. Noninvasive coronary flow reserve assessed by transthoracic coronary Doppler ultrasound in patients with left anterior descending coronary artery stents. Am J Cardiol. 2003;91:522–526
  21. Ruscazio M, Montisci R, Colonna P, et al. Detection of coronary restenosis after coronary angioplasty by contrast-enhanced transthoracic echocardiographic Doppler assessment of coronary flow velocity reserve. J Am Coll Cardiol. 2002;40:896–903
  22. Djordjevic-Dikic A, Beleslin B, Stepanovic J, et al. Prediction of myocardial functional recovery by noninvasive evaluation of Basal and hyperemic coronary flow in patients with previous myocardial infarction. J Am Soc Echocardiogr. 2011;24:573–581
  23. Ueno Y, Nakamura Y, Kinoshita M, et al. Can coronary flow velocity reserve determined by transthoracic Doppler echocardiography predict the recovery of regional left ventricular function in patients with acute myocardial infarction?. Heart. 2002;88:137–141
  24. Colonna P, Cadeddu C, Montisci R, et al. Reduced microvascular and myocardial damage in patients with acute myocardial infarction and preinfarction angina. Am Heart J. 2002;144:796–803
  25. Rigo F, Cortigiani L, Pasanisi E, et al. The additional prognostic value of coronary flow reserve on left anterior descending artery in patients with negative stress echo by wall motion criteria. A Transthoracic Vasodilator Stress Echocardiography Study. Am Heart J. 2006;151:124–130
  26. Sicari R, Rigo F, Gherardi S, et al. The prognostic value of Doppler echocardiographic-derived coronary flow reserve is not affected by concomitant antiischemic therapy at the time of testing. Am Heart J. 2008;156:573–579
  27. Sicari R, Rigo F, Cortigiani L, et al. Additive prognostic value of coronary flow reserve in patients with chest pain syndrome and normal or near-normal coronary arteries. Am J Cardiol. 2009;103:626–631
  28. Lee DH, Youn HJ, Choi YS, et al. Coronary flow reserve is a comprehensive indicator of cardiovascular risk factors in subjects with chest pain and normal coronary angioram. Circ J. 2010;74:1405–1414
  29. Asami Y, Yoshida K, Hozumi T, et al. Assessment of coronary flow reserve in patients with hypertrophic cardiomyopathy using transthoracic color Doppler echocardiography. J Cardiol. 1998;32:247–252
  30. Hidick-Smith DJ, Shapiro LM. Coronary flow reserve improves after aortic valve replacement for aortic stenosis: an adenosine transthoracic echocardiography study. J Am Coll Cardiol. 2000;36:1889–1896
  31. Otsuka R, Watanabe H, Hirata K, et al. Acute effects of passive smoking on the coronary circulation in healthy young adults. JAMA. 2001;286:436–441
  32. Hildick-Smith DJ, Johnson PJ, Wisbey CR, et al. Coronary flow reserve is supranormal in endurance athletes: an adenosine transthoracic echocardiographic study. Heart. 2000;84:383–389
  33. Dimitrow PP, Krzanowski M, Grodecki J, et al. Verapamil improves the endothelium-dependent vasodilatation in patients with hypertrophic cardiomyopathy. Int J Cardiol. 2002;83:239–247
  34. Kawata T, Daimon M, Hasegawa R, et al. Effect of coronary flow velocity reserve in patients with type 2 diabetes mellitus: comparison between angiotensin-convesrting enzyme inhibitor and angiotensin II type 1 receptor antagonist. Am Heart J. 2006;151:798.e9–798.e15
  35. Løgstrup BB, Høfsten DE, Christophersen TB, et al. Association between coronary flow reserve, left ventricular systolic function, and myocardial viability in acute myocardial infarction. Eur J Echocardiogr. 2010;11:665–670
  36. Cannon RO, Schenke WH, Leon MB, et al. Limited coronary flow reserve after dipyridamole in patients with ergonovine-induced coronary vasoconstriction. Circulation. 1987;75:163–174
  37. Akasaka T, Yoshida K, Hozumi T, et al. Comparison of coronary flow reserve between foal and diffuse vasoconstriction induced by ergonovine in patients with vasospastic angina. Am J Cardiol. 1997;80:705–710
  38. Taria N. Nicorandil as a hybrid between nitrates and potassium channel activators. Am J Cardiol. 1989;63:18J–24J
  39. Yao Z, Gross GJ. Effects of the KATP channel opener bimakalim on coronary blood flow, monophasic action potential duration, and infarct size in dogs. Circulation. 1994;89:1769–1775
  40. Yamagishi M, Miyatake K, Tamai J, et al. Intravascular ultrasound detection of atherosclerosis at the site of focal vasospasm in angiographically normal or minimally narrowed coronary segments. J Am Coll Cardiol. 1994;23:352–357
  41. Bourantas CV, Naka KK, Garg S, et al. Clinical indications for intravascular ultrasound imaging. Echocardiography. 2010;27:1282–1290
  42. Hung MJ. Current advances in the understanding of coronary vasospasm. World J Cardiol. 2010;2:34–42
  43. Takeuchi M, Lodato JA, Furlong KT, et al. Feasibility of measuring coronary flow velocity and reserve in the left anterior descending coronary artery by transthoracic Doppler echocardiography in a relatively obese American population. Echocardiography. 2005;22:225–232
  44. Anantharam B, Janardhanan R, Hayat S, et al. Coronary flow reserve assessed by myocardial contrast echocardiography predicts mortality in patients with heart failure. Eur J Echocardiogr. 2011;12:69–75
  45. Cortigiani L, Rigo F, Gherardi S, et al. Prognostic effect of coronary flow reserve in women versus men with chest pain syndrome and normal dipyridamole stress echocardiography. Am J Cardiol. 2010;106:1703–1708
  46. Mahfouz RA, El Tahlawi MA, Ateya AA, et al. Early detection of silent ischemia and diastolic dysfunction in asymptomatic young hypertensive patients. Echocardiography. 2011;28:564–569

PII: S0929-6441(11)00093-2

doi:10.1016/j.jmu.2011.10.005

Journal of Medical Ultrasound
Volume 19, Issue 4 , Pages 115-121, December 2011

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