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Abnormal Postsystolic Thickening in Acutely Ischemic Myocardium During Coronary Angioplasty: A Velocity, Strain, and Strain Rate Doppler Myocardial Imaging Study
CASE REPORTS
Abnormal Postsystolic Thickening in Acutely Ischemic Myocardium During Coronary Angioplasty: A Velocity, Strain, and Strain Rate Doppler Myocardial Imaging Study Fadi Jamal, MD, Tomasz Kukulski, MD, Jan D’hooge, MSc, Ivan De Scheerder, MD, and George Sutherland, FESC, Leuven, Belgium
We report a case in which the combination of gray scale imaging of wall thickness changes allied to color DMI regional velocity, strain, and strain rate data identified the development and regression of diastolic thickening in the acute ischemic segment
during a right coronary artery percutaneous transluminal coronary angioplasty (PTCA). We also discuss the possible mechanisms and potential clinical implications of this finding. (J Am Soc Echocardiogr 1999;12:994-6.)
Since Tennant and Wiggers first described ischemic
CASE REPORT
myocardial bulging, the patterns of left ventricular dysfunction in acute ischemia have been extensively investigated. Postsystolic thickening (PST) has been recognized as a related phenomenon and has been studied with the use of invasively implanted ultrasonic microcrystals or lead beads.2,3 This phenomenon has been shown to be associated with myocardial viability in open chest animal models, but the underlying mechanisms are unclear. To date, this has not been resolved. However, PST has not been reported in patients in the clinical setting of acute ischemia where both chest and pericardium are closed. If it should be detectable during acute or chronic ischemia, it could serve as a new noninvasive marker for myocardial viability. Doppler myocardial imaging (DMI) has been shown to derive data on myocardial thickening and transmural velocity gradients identical to that obtained by microcrystal implantation.4 DMI quantitation of regional myocardial function has been further extended by computer postprocessing of the color Doppler velocity data to derive regional strain and strain rate.5
A 78-year-old woman with a short history of exercise angina underwent coronary angiography for increasing anginal symptoms.The clinical examination and resting electrocardiogram were normal (with no evidence of ischemia or infarction). Pre-PTCA baseline echocardiography showed the left ventricular diameter, wall thickness, and contractility to be normal. Pulsed Doppler mitral inflow showed a reversed E/A ratio implying abnormal left ventricular relaxation. Angiography showed single-vessel disease within a dominant right coronary artery with a 90% stenosis in the proximal segment. Left ventriculography showed a nondilated ventricle with no wall motion abnormalities (ejection fraction = 65%). During the right coronary artery PTCA, a real-time echocardiographic study was performed (GE Vingmed System V, Horten, Norway) at 2.5 MHz. Color DMI data were recorded at a frame rate of 150 frames/s with a parasternal short-axis mid-ventricular view to obtain an image of the myocardial area at risk. The same view was monitored at baseline, at 5 seconds, at 90 seconds after balloon inflation, and after 60 seconds of reperfusion. Three inflations of 90 seconds each were carried out before stent implantation was performed. During each occlusion the patient described a typical angina comparable to her previous symptoms. DMI data were transferred to a work station for off-line analysis with dedicated software that allowed computation of regional mean velocities, strain, and strain rate values.5 After balloon inflation was performed, posterior wall mean myocardial systolic velocities and radial strain rates decreased rapidly, paralleling the decrease in wall thickening (anatomic M-mode gray scale reconstruction). These changes were totally reversed after balloon deflation
1
From the Department of Cardiology, Gasthuisberg Hospital, Leuven, Belgium. Fadi Jamal, MD, was supported by a grant of the French Federation of Cardiology and the European Society of Cardiology. Reprint requests: George R. Sutherland, MD, Department of Cardiology, University Hospital Gasthuisberg, Herestraat 49, B3000 Leuven, Belgium (e-mail: [email protected]). Copyright © 1999 by the American Society of Echocardiography. 0894-7317/99 $8.00 + 0 27/4/100712
994
Journal of the American Society of Echocardiography Volume 12 Number 11
Jamal et al 995
Figure 1 Myocardial postsystolic thickening of posterior wall during right coronary artery percutaneous transluminal coronary angioplasty was identified with velocity, strain rate, and strain data computed from color DMI short-axis view. Left column shows posterior wall mean velocity curves (cm/s), where S, E’, and A’ are systolic, early, and late diastolic waves, respectively. Note rapid fall in systolic velocity after balloon inflation and abnormal inward wall motion during early diastole (arrows). Middle column shows color-coded radial strain rate (Hz) with curved M-mode of myocardial area at risk. Expansion (ie, thickening) rate is coded blue, and compression (ie, thinning) rate is coded red. During balloon inflation systolic strain rate is dramatically decreased, and high expansion strain rate is detected in early diastole (arrows). Right column represents posterior wall regional strain (%) averaged for mean heart cycle. During ischemia period strain (thickening) is clearly decreased in systole. Arrows show postsystolic thickening phenomenon. Note increase in myocardial systolic thickening after reperfusion caused by reactive hyperkinesia.
occurred (Figure 1). Moreover, during early diastole, gray scale M-mode, strain, and SRI curved M-mode showed an abnormal thickening and expansion strain rate pattern with a simultaneous inward wall motion on the DMI velocity profile (Figure 1). At baseline systolic posterior wall thickening derived from strain data averaged 11%. After a 90-second ischemia period, systolic thinning occurred (–13% in early systole and –6% in end systole), whereas posterior wall thickness increased in early diastole by 18% (Figure 1, right column). This PST phenomenon was reproducible during all 3 inflations occurring within 5 seconds of ischemia onset and was reversed after inflation relief (Figure 2).
DISCUSSION Regional myocardial strain rate and its time integral, myocardial strain, can now be calculated by the spatial interrogation of a high frame rate color DMI data set.5-7 The measurement of regional strain rate and strain can be performed in either the longitu-
dinal or radial direction for a myocardial segment, and they directly reflect different aspects of regional myocardial function. Local strain rate (ie, the temporal derivative of strain) measures the instantaneous spatial gradient of regional velocities normalized by the distance between 2 points within the region of myocardium being interrogated. The radial component of strain rate measures rate of change of wall thickness (and is directly equivalent to the transmural DMI velocity gradient first described by Fleming et al,8 whereas relative changes in wall thickness during the cardiac cycle can be measured with the use of the radial component of regional strain (where increase in strain parallels wall thickening and decrease in strain parallels thinning). Initial studies have suggested that regional myocardial strain and strain rate estimation can be performed in the clinical setting and may prove to be a robust and sensitive tool to define alterations in either contractile function or passive elastic deformation within a myocardial segment.9 One major
996 Jamal et al
Journal of the American Society of Echocardiography November 1999
Figure 2 Color-coded strain rate curved M-mode shows reproducibility of myocardial postsystolic thickening during all 3 balloon inflation periods (arrows).
advantage of these new cardiac ultrasound modalities is their potentially greater signal to clutter ratio compared with gray scale imaging and thus the ability to acquire data from regions of myocardium that cannot be accurately seen by gray scale imaging. A second advantage is that they allow quantitative indexes of regional myocardial function to be derived. Currently, echocardiographic assessment of regional wall motion abnormalities is achieved with a semiquantitative visual method.This approach may fail to identify complex contraction abnormality patterns such as PST, mainly because of the inability of the eye to resolve complexities of myocardial motion combined with the low frame rate of data acquisition. In this case noninvasive high frame rate acquisition of regional velocity, strain, and strain rate data identified noninvasively the occurrence and regression of the PST phenomenon during PTCA.Two differing explanations can be proposed: active fiber shortening related to delayed contraction after segment unloading and regional wall stress decrease, or passive thickening, possibly load-dependent and caused by interaction with the normal surrounding contracting muscle. Further studies are necessary to answer this issue and to determine the clinical relevance of this phenomenon in terms of myocardial viability.
REFERENCES 1. Tennant R, Wiggers CJ. The effect of coronary occlusion on myocardial contraction. Am J Physiol 1935;112:351-61. 2. Akaishi M, Weintraub WS, Schneider RM, et al. Analysis of systolic bulging. Mechanical characteristics of acutely ischemic myocardium in the conscious dog. Circ Res 1986;58:209-17. 3. Villarreal FJ, Lew WY, Waldman LK, Covell JW. Transmural myocardial deformation in the ischemic canine left ventricle. Circ Res 1991;68:368-81. 4. Gorcsan Jr, Strum DP, Mandarino WA, Gulati VK, Pinsky MR. Quantitative assessment of alterations in regional left ventricular contractility with color-coded tissue Doppler echocardiography. Comparison with sonomicrometry and pressure- volume relations. Circulation 1997;95:2423-33. 5. Heimdal A, Stoylen A, Torp H, Skjaerpe T. Real-time strain rate imaging of the left ventricle by ultrasound. J Am Soc Echocardiogr 1998;11:1013-9. 6. Pasquet A, Armstrong G, Garcia M, Thomas J, Marwick T. Quatification of abnormal wall motion by strain rate during exercice echo correlates with dual isotope spect. J Am Soc Echocardiogr 1999;12:346. 7. Pasquet A, Armstrong G, Garcia M, Thomas J, Marwick T. Strain rate: the best myocardial Doppler index for interpretation of stress echocardiography? J Am Soc Echocardiogr 1999;12:349. 8. Fleming AD, Xia X, McDicken WN, Sutherland GR, Fenn L. Myocardial velocity gradients detected by Doppler imaging. Br J Radiol 1994;67:679-88. 9. Voigt JU, Arnold M, Kukulski T, Karlsson M, Sutherland GR. Is strain rate imaging applicable to the clinical setting? Preliminary in vivo data [abstract]. J Am Coll Cardiol 1999;33 (suppl A):429A.
Abnormal Postsystolic Thickening in Acutely Ischemic Myocardium During Coronary Angioplasty: A Velocity, Strain, and Strain Rate Doppler Myocardial Imaging Study Fadi Jamal, MD, Tomasz Kukulski, MD, Jan D’hooge, MSc, Ivan De Scheerder, MD, and George Sutherland, FESC, Leuven, Belgium
We report a case in which the combination of gray scale imaging of wall thickness changes allied to color DMI regional velocity, strain, and strain rate data identified the development and regression of diastolic thickening in the acute ischemic segment
during a right coronary artery percutaneous transluminal coronary angioplasty (PTCA). We also discuss the possible mechanisms and potential clinical implications of this finding. (J Am Soc Echocardiogr 1999;12:994-6.)
Since Tennant and Wiggers first described ischemic
CASE REPORT
myocardial bulging, the patterns of left ventricular dysfunction in acute ischemia have been extensively investigated. Postsystolic thickening (PST) has been recognized as a related phenomenon and has been studied with the use of invasively implanted ultrasonic microcrystals or lead beads.2,3 This phenomenon has been shown to be associated with myocardial viability in open chest animal models, but the underlying mechanisms are unclear. To date, this has not been resolved. However, PST has not been reported in patients in the clinical setting of acute ischemia where both chest and pericardium are closed. If it should be detectable during acute or chronic ischemia, it could serve as a new noninvasive marker for myocardial viability. Doppler myocardial imaging (DMI) has been shown to derive data on myocardial thickening and transmural velocity gradients identical to that obtained by microcrystal implantation.4 DMI quantitation of regional myocardial function has been further extended by computer postprocessing of the color Doppler velocity data to derive regional strain and strain rate.5
A 78-year-old woman with a short history of exercise angina underwent coronary angiography for increasing anginal symptoms.The clinical examination and resting electrocardiogram were normal (with no evidence of ischemia or infarction). Pre-PTCA baseline echocardiography showed the left ventricular diameter, wall thickness, and contractility to be normal. Pulsed Doppler mitral inflow showed a reversed E/A ratio implying abnormal left ventricular relaxation. Angiography showed single-vessel disease within a dominant right coronary artery with a 90% stenosis in the proximal segment. Left ventriculography showed a nondilated ventricle with no wall motion abnormalities (ejection fraction = 65%). During the right coronary artery PTCA, a real-time echocardiographic study was performed (GE Vingmed System V, Horten, Norway) at 2.5 MHz. Color DMI data were recorded at a frame rate of 150 frames/s with a parasternal short-axis mid-ventricular view to obtain an image of the myocardial area at risk. The same view was monitored at baseline, at 5 seconds, at 90 seconds after balloon inflation, and after 60 seconds of reperfusion. Three inflations of 90 seconds each were carried out before stent implantation was performed. During each occlusion the patient described a typical angina comparable to her previous symptoms. DMI data were transferred to a work station for off-line analysis with dedicated software that allowed computation of regional mean velocities, strain, and strain rate values.5 After balloon inflation was performed, posterior wall mean myocardial systolic velocities and radial strain rates decreased rapidly, paralleling the decrease in wall thickening (anatomic M-mode gray scale reconstruction). These changes were totally reversed after balloon deflation
1
From the Department of Cardiology, Gasthuisberg Hospital, Leuven, Belgium. Fadi Jamal, MD, was supported by a grant of the French Federation of Cardiology and the European Society of Cardiology. Reprint requests: George R. Sutherland, MD, Department of Cardiology, University Hospital Gasthuisberg, Herestraat 49, B3000 Leuven, Belgium (e-mail: [email protected]). Copyright © 1999 by the American Society of Echocardiography. 0894-7317/99 $8.00 + 0 27/4/100712
994
Journal of the American Society of Echocardiography Volume 12 Number 11
Jamal et al 995
Figure 1 Myocardial postsystolic thickening of posterior wall during right coronary artery percutaneous transluminal coronary angioplasty was identified with velocity, strain rate, and strain data computed from color DMI short-axis view. Left column shows posterior wall mean velocity curves (cm/s), where S, E’, and A’ are systolic, early, and late diastolic waves, respectively. Note rapid fall in systolic velocity after balloon inflation and abnormal inward wall motion during early diastole (arrows). Middle column shows color-coded radial strain rate (Hz) with curved M-mode of myocardial area at risk. Expansion (ie, thickening) rate is coded blue, and compression (ie, thinning) rate is coded red. During balloon inflation systolic strain rate is dramatically decreased, and high expansion strain rate is detected in early diastole (arrows). Right column represents posterior wall regional strain (%) averaged for mean heart cycle. During ischemia period strain (thickening) is clearly decreased in systole. Arrows show postsystolic thickening phenomenon. Note increase in myocardial systolic thickening after reperfusion caused by reactive hyperkinesia.
occurred (Figure 1). Moreover, during early diastole, gray scale M-mode, strain, and SRI curved M-mode showed an abnormal thickening and expansion strain rate pattern with a simultaneous inward wall motion on the DMI velocity profile (Figure 1). At baseline systolic posterior wall thickening derived from strain data averaged 11%. After a 90-second ischemia period, systolic thinning occurred (–13% in early systole and –6% in end systole), whereas posterior wall thickness increased in early diastole by 18% (Figure 1, right column). This PST phenomenon was reproducible during all 3 inflations occurring within 5 seconds of ischemia onset and was reversed after inflation relief (Figure 2).
DISCUSSION Regional myocardial strain rate and its time integral, myocardial strain, can now be calculated by the spatial interrogation of a high frame rate color DMI data set.5-7 The measurement of regional strain rate and strain can be performed in either the longitu-
dinal or radial direction for a myocardial segment, and they directly reflect different aspects of regional myocardial function. Local strain rate (ie, the temporal derivative of strain) measures the instantaneous spatial gradient of regional velocities normalized by the distance between 2 points within the region of myocardium being interrogated. The radial component of strain rate measures rate of change of wall thickness (and is directly equivalent to the transmural DMI velocity gradient first described by Fleming et al,8 whereas relative changes in wall thickness during the cardiac cycle can be measured with the use of the radial component of regional strain (where increase in strain parallels wall thickening and decrease in strain parallels thinning). Initial studies have suggested that regional myocardial strain and strain rate estimation can be performed in the clinical setting and may prove to be a robust and sensitive tool to define alterations in either contractile function or passive elastic deformation within a myocardial segment.9 One major
996 Jamal et al
Journal of the American Society of Echocardiography November 1999
Figure 2 Color-coded strain rate curved M-mode shows reproducibility of myocardial postsystolic thickening during all 3 balloon inflation periods (arrows).
advantage of these new cardiac ultrasound modalities is their potentially greater signal to clutter ratio compared with gray scale imaging and thus the ability to acquire data from regions of myocardium that cannot be accurately seen by gray scale imaging. A second advantage is that they allow quantitative indexes of regional myocardial function to be derived. Currently, echocardiographic assessment of regional wall motion abnormalities is achieved with a semiquantitative visual method.This approach may fail to identify complex contraction abnormality patterns such as PST, mainly because of the inability of the eye to resolve complexities of myocardial motion combined with the low frame rate of data acquisition. In this case noninvasive high frame rate acquisition of regional velocity, strain, and strain rate data identified noninvasively the occurrence and regression of the PST phenomenon during PTCA.Two differing explanations can be proposed: active fiber shortening related to delayed contraction after segment unloading and regional wall stress decrease, or passive thickening, possibly load-dependent and caused by interaction with the normal surrounding contracting muscle. Further studies are necessary to answer this issue and to determine the clinical relevance of this phenomenon in terms of myocardial viability.
REFERENCES 1. Tennant R, Wiggers CJ. The effect of coronary occlusion on myocardial contraction. Am J Physiol 1935;112:351-61. 2. Akaishi M, Weintraub WS, Schneider RM, et al. Analysis of systolic bulging. Mechanical characteristics of acutely ischemic myocardium in the conscious dog. Circ Res 1986;58:209-17. 3. Villarreal FJ, Lew WY, Waldman LK, Covell JW. Transmural myocardial deformation in the ischemic canine left ventricle. Circ Res 1991;68:368-81. 4. Gorcsan Jr, Strum DP, Mandarino WA, Gulati VK, Pinsky MR. Quantitative assessment of alterations in regional left ventricular contractility with color-coded tissue Doppler echocardiography. Comparison with sonomicrometry and pressure- volume relations. Circulation 1997;95:2423-33. 5. Heimdal A, Stoylen A, Torp H, Skjaerpe T. Real-time strain rate imaging of the left ventricle by ultrasound. J Am Soc Echocardiogr 1998;11:1013-9. 6. Pasquet A, Armstrong G, Garcia M, Thomas J, Marwick T. Quatification of abnormal wall motion by strain rate during exercice echo correlates with dual isotope spect. J Am Soc Echocardiogr 1999;12:346. 7. Pasquet A, Armstrong G, Garcia M, Thomas J, Marwick T. Strain rate: the best myocardial Doppler index for interpretation of stress echocardiography? J Am Soc Echocardiogr 1999;12:349. 8. Fleming AD, Xia X, McDicken WN, Sutherland GR, Fenn L. Myocardial velocity gradients detected by Doppler imaging. Br J Radiol 1994;67:679-88. 9. Voigt JU, Arnold M, Kukulski T, Karlsson M, Sutherland GR. Is strain rate imaging applicable to the clinical setting? Preliminary in vivo data [abstract]. J Am Coll Cardiol 1999;33 (suppl A):429A.