- Email: [email protected]
Commentary on: CMR study of systolic myocardial volume gain in the dilated, hypertrophied, and normal heart
Clinical Radiology 72 (2017) 293e294
Contents lists available at ScienceDirect
Clinical Radiology journal homepage: www.clinicalradiologyonline.net
Commentary
Commentary on: CMR study of systolic myocardial volume gain in the dilated, hypertrophied, and normal heart S. Mirsadraee a, *, F. Alpendurada b a b
Department of Radiology, Royal Brompton Hospital, London, UK Department of Cardiology, Royal Brompton Hospital, London, UK
art icl e i nformat ion Article history: Received 30 December 2016 Accepted 3 January 2017
The theory of non-compressibility assumes that the myocardial volume does not change between systole and diastole. This theory is the basis for performance measurements such as ejection fraction1,2; however, experimental and human studies suggest changes in myocardial volume during the contractile phases. Most studies observed a reduction in myocardial volume during systole that was attributed to a squeezing effect from contracting myocardium.3,4 The reduction was reported to be most in the subendocardial region5 and in the range of 1e8%, depending on the model and measurement technique used.4,6e8 In healthy and hypertensive patients, freehand three-dimensional (3D) echocardiography and steady-state free precession gradientecho cine imaging did not detect a significant difference in the myocardial volume between end-diastole and end-systole.1,9 Conversely, the data presented by Mazurkiewicz et al.10 documented a systolic increase in myocardial volume in healthy controls and in patients with hypertrophic and dilated cardiomyopathies and aortic stenosis. Similarly, a study using computed tomography in dogs demonstrated a 12% increase in left ventricular volume in one of the dogs.11
Although some of the differences in the presented results can be attributed to the heterogeneity of the models and techniques used in each of these studies, potential sources of measurement errors have to be considered. A potential cause of bias in the latter two studies10,11 is the limited spatial resolution of the techniques that might have prevented the separation of compacted trabeculae from true endocardium resulting in overestimation of the volumes. It is known that the systolic myocardial thickening that is observed on magnetic resonance imaging is a combination of wall thickening but also compression and folding of the trabecularepapillary muscle complex resulting in poor resolution of the real inner endocardial borders in end-systole.12e14 This is especially observed in the lateral and anterior wall segments where trabecular zones are more prominent.13 Examination of the presented images from the earlier mentioned dog study highlights the limited spatial resolution of the computed tomography (CT) techniques that resulted in similar measurement error.11 Perhaps further studies could be performed to address this conundrum.
References DOI of original article: http://dx.doi.org/10.1016/j.crad.2016.10.024. * Guarantor and correspondent: S. Mirsadraee, Department of Radiology, Royal Brompton Hospital, London, UK. Tel.: þ44 20 7352 8121. E-mail address: [email protected] (S. Mirsadraee).
1. King DL, Coffin Lel-K, Maurer MS. Noncompressibility of myocardium during systole with freehand three-dimensional echocardiography. J Am Soc Echocardiogr 2002 Dec;15(12):1503e6.
http://dx.doi.org/10.1016/j.crad.2017.01.001 0009-9260/Ó 2017 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved.
294
S. Mirsadraee, F. Alpendurada / Clinical Radiology 72 (2017) 293e294
2. Tsuiki K, Ritman EL. Direct evidence that left ventricular myocardium is incompressible throughout systole and diastole. Tohoku J Exp Med 1980;132:119e20. 3. Gaasch WH, Bernard SA. The effect of acute changes in coronary blood flow on left ventricular end-diastolic wall thickness. An echocardiographic study. Circulation 1977;56:593e8. 4. Rodriguez I, Ennis DB, Wen H. Noninvasive measurement of myocardial tissue volume change during systolic contraction and diastolic relaxation in the canine left ventricle. Magn Reson Med 2006 Mar;55(3):484e90. 5. Ashikaga H, Coppola BA, Yamazaki KG, et al. Changes in regional myocardial volume during the cardiac cycle: implications for transmural blood flow and cardiac structure. Am J Physiol Heart Circ Physiol 2008 Aug;295(2):H610e8. 6. Spaan JA. Coronary diastolic pressureeflow relation and zero flow pressure explained on the basis of intramyocardial compliance. Circ Res 1985;56:293e309. 7. Tsuiki K, Ritman EL. Direct evidence that left ventricular myocardium is incompressible throughout systole and diastole. Tohoku J Exp Med 1980 Sep;132(1):119e20. 8. Liu YH, Bahn RC, Ritman EL. Dynamic intramyocardial blood volume: evaluation with a radiological opaque marker method. Am J Physiol 1992;263:H963e7.
9. Swingen C, Wang X, Jerosch-Herold M. Evaluation of myocardial volume heterogeneity during end-diastole and end-systole using cine MRI. J Cardiovasc Magn Reson 2004;6(4):829e35. 10. Mazurkiewicz q, Or1owska-Baranowska E, Petrykaet J, et al. Systolic myocardial volume gain in dilated, hypertrophied and normal heart. CMR study. Clin Radiol 2017;72:286e92. 11. Iwasaki T, Sinak LJ, Hoffman EA, et al. Mass of left ventricular myocardium estimated with dynamic spatial reconstructor. Am J Physiol Heart Circ Physiol 1984;246:H138e42. 12. Osman NF, Kerwin WS, McVeigh ER, et al. Cardiac motion tracking using CINE harmonic phase (HARP) magnetic resonance imaging. Magn Reson Med 1999 Dec;42(6):1048e60. 13. Peters DC, Ennis DB, McVeigh ER. High-resolution MRI of cardiac function with projection reconstruction and steady-state free precession. Magn Reson Med 2002;48:82e8. 14. Plein S, Smith WH, Ridgway JP, et al. Qualitative and quantitative analysis of regional left ventricular wall dynamics using real-time magnetic resonance imaging: comparison with conventional breath-hold gradient echo acquisition in volunteers and patients. J Magn Reson Imaging 2001;14(1):23e30.
Contents lists available at ScienceDirect
Clinical Radiology journal homepage: www.clinicalradiologyonline.net
Commentary
Commentary on: CMR study of systolic myocardial volume gain in the dilated, hypertrophied, and normal heart S. Mirsadraee a, *, F. Alpendurada b a b
Department of Radiology, Royal Brompton Hospital, London, UK Department of Cardiology, Royal Brompton Hospital, London, UK
art icl e i nformat ion Article history: Received 30 December 2016 Accepted 3 January 2017
The theory of non-compressibility assumes that the myocardial volume does not change between systole and diastole. This theory is the basis for performance measurements such as ejection fraction1,2; however, experimental and human studies suggest changes in myocardial volume during the contractile phases. Most studies observed a reduction in myocardial volume during systole that was attributed to a squeezing effect from contracting myocardium.3,4 The reduction was reported to be most in the subendocardial region5 and in the range of 1e8%, depending on the model and measurement technique used.4,6e8 In healthy and hypertensive patients, freehand three-dimensional (3D) echocardiography and steady-state free precession gradientecho cine imaging did not detect a significant difference in the myocardial volume between end-diastole and end-systole.1,9 Conversely, the data presented by Mazurkiewicz et al.10 documented a systolic increase in myocardial volume in healthy controls and in patients with hypertrophic and dilated cardiomyopathies and aortic stenosis. Similarly, a study using computed tomography in dogs demonstrated a 12% increase in left ventricular volume in one of the dogs.11
Although some of the differences in the presented results can be attributed to the heterogeneity of the models and techniques used in each of these studies, potential sources of measurement errors have to be considered. A potential cause of bias in the latter two studies10,11 is the limited spatial resolution of the techniques that might have prevented the separation of compacted trabeculae from true endocardium resulting in overestimation of the volumes. It is known that the systolic myocardial thickening that is observed on magnetic resonance imaging is a combination of wall thickening but also compression and folding of the trabecularepapillary muscle complex resulting in poor resolution of the real inner endocardial borders in end-systole.12e14 This is especially observed in the lateral and anterior wall segments where trabecular zones are more prominent.13 Examination of the presented images from the earlier mentioned dog study highlights the limited spatial resolution of the computed tomography (CT) techniques that resulted in similar measurement error.11 Perhaps further studies could be performed to address this conundrum.
References DOI of original article: http://dx.doi.org/10.1016/j.crad.2016.10.024. * Guarantor and correspondent: S. Mirsadraee, Department of Radiology, Royal Brompton Hospital, London, UK. Tel.: þ44 20 7352 8121. E-mail address: [email protected] (S. Mirsadraee).
1. King DL, Coffin Lel-K, Maurer MS. Noncompressibility of myocardium during systole with freehand three-dimensional echocardiography. J Am Soc Echocardiogr 2002 Dec;15(12):1503e6.
http://dx.doi.org/10.1016/j.crad.2017.01.001 0009-9260/Ó 2017 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved.
294
S. Mirsadraee, F. Alpendurada / Clinical Radiology 72 (2017) 293e294
2. Tsuiki K, Ritman EL. Direct evidence that left ventricular myocardium is incompressible throughout systole and diastole. Tohoku J Exp Med 1980;132:119e20. 3. Gaasch WH, Bernard SA. The effect of acute changes in coronary blood flow on left ventricular end-diastolic wall thickness. An echocardiographic study. Circulation 1977;56:593e8. 4. Rodriguez I, Ennis DB, Wen H. Noninvasive measurement of myocardial tissue volume change during systolic contraction and diastolic relaxation in the canine left ventricle. Magn Reson Med 2006 Mar;55(3):484e90. 5. Ashikaga H, Coppola BA, Yamazaki KG, et al. Changes in regional myocardial volume during the cardiac cycle: implications for transmural blood flow and cardiac structure. Am J Physiol Heart Circ Physiol 2008 Aug;295(2):H610e8. 6. Spaan JA. Coronary diastolic pressureeflow relation and zero flow pressure explained on the basis of intramyocardial compliance. Circ Res 1985;56:293e309. 7. Tsuiki K, Ritman EL. Direct evidence that left ventricular myocardium is incompressible throughout systole and diastole. Tohoku J Exp Med 1980 Sep;132(1):119e20. 8. Liu YH, Bahn RC, Ritman EL. Dynamic intramyocardial blood volume: evaluation with a radiological opaque marker method. Am J Physiol 1992;263:H963e7.
9. Swingen C, Wang X, Jerosch-Herold M. Evaluation of myocardial volume heterogeneity during end-diastole and end-systole using cine MRI. J Cardiovasc Magn Reson 2004;6(4):829e35. 10. Mazurkiewicz q, Or1owska-Baranowska E, Petrykaet J, et al. Systolic myocardial volume gain in dilated, hypertrophied and normal heart. CMR study. Clin Radiol 2017;72:286e92. 11. Iwasaki T, Sinak LJ, Hoffman EA, et al. Mass of left ventricular myocardium estimated with dynamic spatial reconstructor. Am J Physiol Heart Circ Physiol 1984;246:H138e42. 12. Osman NF, Kerwin WS, McVeigh ER, et al. Cardiac motion tracking using CINE harmonic phase (HARP) magnetic resonance imaging. Magn Reson Med 1999 Dec;42(6):1048e60. 13. Peters DC, Ennis DB, McVeigh ER. High-resolution MRI of cardiac function with projection reconstruction and steady-state free precession. Magn Reson Med 2002;48:82e8. 14. Plein S, Smith WH, Ridgway JP, et al. Qualitative and quantitative analysis of regional left ventricular wall dynamics using real-time magnetic resonance imaging: comparison with conventional breath-hold gradient echo acquisition in volunteers and patients. J Magn Reson Imaging 2001;14(1):23e30.