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1095 Noninvasive Assessment of Myocardial Composition and Function in the Hypertrophied Heart David J. Skorton, MD yocardial hypertrophy is both a useful physiologic adaptive process and an abnormal response to a variety of stimuli.1-4Hypertrophy as an adaptive response to excessive loading conditions is an important compensatory mechanism that tends to minimize abnormalities in myocardial stress related to the inciting load.4 However, recent See p 925 studies have indicated that hypertrophied muscle differs from normal muscle in many respects, including its structure, mechanical properties, vascularity, biochemistry, and electrophysiology.5-11 Current noninvasive imaging methods permit the clinical differentiation of several etiologies of left ventricular hypertrophy, including pressure or volume overload, infiltration, and hypertrophic cardiomyopathy. This differentiation is usually accurately accomplished with echocardiography or other tomographic imaging methods, such as computed tomography or nuclear magnetic resonance imaging. Unfortunately, some diagnostic ambiguities occur that may not be easily resolved with current diagnostic methods. For example, amyloid cardiomyopathy presents the picture of concentric left (and right) ventricular hypertrophy.12 Although many patients with amyloid heart disease display an unusual, "speckled" myocardial appearance on standard echocardiograms,13 this phenomenon is not always noted, and the amyloid-infiltrated left ventricle may thus be confused with pressure-overload hypertrophy. Hypertrophic cardiomyopathy may resemble infiltrative cardiomyopathy on echocardiograms14; conversely, amyloid cardiomyopathy may be misM Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017 The opinions expressed in this editorial comment are not necessarily those of the editors or of the American Heart Association. From the Cardiovascular Center and the Departments of Internal Medicine and Electrical and Computer Engineering, University of Iowa and Veterans Administration Medical Center, Iowa City, Iowa. Supported in part by Research Career Development Award K04-HL-01290 from the National Heart, Lung, and Blood Institute. Address for correspondence: David J. Skorton, MD, Department of Internal Medicine, University of Iowa, Iowa City, IA 52242. taken for hypertrophic cardiomyopathy.15,6 Finally, the elderly patient with left ventricular hypertrophy related to hypertension may present an echocardiographic appearance difficult to distinguish from concentric hypertrophic cardiomyopathy.17 These diagnostic problems emphasize the continuing need for more specific methods of differentiating among the several etiologies of left ventricular hypertrophy. One potential method of defining the structural basis of cardiac hypertrophy is that of ultrasound tissue characterization.18 Echocardiographers have frequently noted anomalies of regional tissue appearance on the ultrasound image in several disorders associated with hypertrophy. Unusual patterns of echo reflection can be seen in regions of myocardium with abnormal myofibrillar architecture such as hypertrophic cardiomyopathy19 or with infiltration of abnormal material such as amyloid.13 Although occasionally useful clinically, visual assessment of standard echocardiographic images is prone to the variability associated with all subjective observations. Further, the several image-processing manipulations performed during the recording of an echocardiogram (altering gain, time-gain compensation, and gray scale mapping functions) may have dramatic and confounding effects on image appearance. Thus, attempts have been made to develop objective methods of evaluating myocardial acoustic properties toward the goal of quantitative ultrasound tissue characterization. Substantial previous investigation has established that the amount of ultrasound energy returning to the echocardiographic transducer from the myocardium (referred to as ultrasound "backscatter") is reproducibly altered by acute and chronic ischemic injury'5 as well as by experimental cardiomyopathies.20 Similarly, as alluded to above, an abnormal two-dimensional spatial pattern or "texture" of echo reflections from the myocardium has been associated with particular histopathologic abnormalities.13,19,20 Computerized methods of analyzing echocardiographic tissue texture have recently been shown capable of discriminating among hypertensive left ventricular hypertrophy, amyloid cardiomyopathy, hypertrophic cardiomyopathy, and normal myocardium.21 The 1096 Circulation Vol 80, No 4, October 1989 Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017 fact that these latter observations were made by analyzing standard, clinical echocardiograms recorded on videotape suggested that sufficient information may be contained in the ultrasound reflections from hypertrophied myocardium to begin to distinguish particular etiologies of hypertrophy in the clinical setting. Unfortunately, methods reported up to this time have had significant drawbacks, particularly the need for complex, off-line assessment of echocardiographic amplitude data with an additional computing system and frequently requiring substantial analysis time. In this issue of Circulation, Masuyama and coworkers22 present intriguing evidence to support the notion that a novel echocardiographic imaging system yielding real-time images and measurements of integrated ultrasound backscatter may help to characterize pressure-overload hypertrophy and hypertrophic cardiomyopathy. In reviewing these interesting and provocative observations, I will briefly consider the mechanisms potentially responsible for the findings, the strengths and limitations of the particular method reported, and the place of these methods in the overall investigative field of cardiac tissue characterization. Masuyama and coworkers evaluated the acoustic properties of normal and hypertrophic myocardium by measuring relative ultrasound backscatter throughout the heart cycle. These investigators noted that the amplitude of cardiac cycle-dependent (cyclic) backscatter variation was significantly smaller in the ventricular septum of both pressureoverload hypertrophy and hypertrophic cardiomyopathy than in the septum of normal subjects. The authors attribute these decrements in cyclic backscatter variation to two mechanisms: abnormalities of myocardial contractile function and myocardial fibrosis. In fact, previous observations have suggested that myocardial contractile function is an important determinant of the amplitude of cyclic backscatter variation.23 However, Masuyama et al observed a nonlinear relation between wall thickening and the amplitude of cyclic backscatter variation, a phenomenon previously noted by others.24 These data suggest that factors other than contractile function may be contributing to alterations in cyclic backscatter variation. A decrement in septal thickening in hypertrophic cardiomyopathy is a well-described phenomenon that may serve as one mechanism of decreased cyclic backscatter variation. However, wall thickening of the septum in pressure-overload hypertrophy should be normal or nearly so; thus, an additional mechanism must be implicated to explain a decrease in cyclic backscatter variation in pressure-overload hypertrophy. Myocardial fibrosis is suggested by Masuyama et a122 to explain acoustic abnormalities in the septum of pressure-overloaded hearts. Previous observations concerning the deposition of collagen in pressure-overload hypertrophy have varied. Some authors have found an increase in regional fibrosis, assessed histologically or biochemically,25,26 while others have found an increase in total myocardial collagen but not an increase in the concentration of collagen in hypertensive left ventricular hypertrophy.27 Further, the degree of fibrosis may differ greatly between hypertensive hypertrophy and hypertrophic cardiomyopathy.27 Because histologic data concerning the presence and degree of fibrosis in the patients studied by Masuyama et al were not available, the contribution of collagen deposition to alterations in ultrasound backscatter data remains conjectural. Further, fibrosis in pressure-overload left ventricular hypertrophy would not be expected to vary greatly in different regions of the myocardium, whereas there was a substantial difference in the degree of cyclic backscatter variation in ventricular septum versus posterior wall in the present study. Further research is indicated to evaluate mechanisms of backscatter variability and its alteration by the hypertrophic process. The key strength of the system reported by Masuyama et al appears to be its online capability. Thus. data on regional backscatter variation are available for qualitative interpretation at the time of examination, and assessment of the quantitative characteristics of backscatter variation may be accomplished rapidly after the examination. Two important limitations of the technique, however, should be recognized. First, in the present study, the estimation of regional myocardial backscatter was performed with an M-mode echocardiographic method, thus providing a spatially limited sample of myocardium. Given the dramatic regional differences in backscatter variation noted by these authors, sampling-related variability of data must be considered an important problem. A second limitation of this method is the wide range of cyclic backscatter variation noted in ventricular septum in normals and, particularly, in the hypertrophic groups. This may be due in part to the complex fiber architecture of the septum and inherent transmural variations in contractile function.28 Similar wide variability of septal cyclic backscatter amplitude has been noted by others in normal myocardium29 and may make the interpretation of data in a given patient extremely difficult. The observations made by Masuyama et al are timely in that they build on substantial previous investigative work suggesting that the measurement of ultrasound backscatter, either averaged through the heart cycle or sampled at many points during contraction and relaxation, is a robust although technically demanding method of identifying abnormalities in myocardial composition or physiologic state. 18 This study is also of importance because of its validation in a clinical setting of the value of this method of backscatter estimation. Unfortunately, the finding of blunted cyclic backscatter variation must be considered somewhat nonspecific, being found in hypertrophic cardiomyopathy and pressureoverload hypertrophy in the present study as well as Skorton Noninvasive Assessment of Hypertrophy in acute and chronic myocardial infarction and dilated cardiomyopathy.30 Thus, the lack of normal cyclic variation may indicate that myocardium is abnormal but not the specific nature of the abnormality. The interesting observations made by Masuyama et al give further impetus to consideration of the use of ultrasound tissue characterization methods both to distinguish normal from abnormal myocardium and to begin to dissect the specific nature of myocardial abnormalities. Further research aimed at determining the mechanisms of backscatter variation and at evaluating acoustic features of myocardium that may differentiate among the several etiologies of decreased cyclic backscatter variation will be important for further development of this promising area of cardiac diagnosis. 14. 15. 16. 17. 18. 19. 20. References Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017 1. Anversa P, Ricci R, Olivetti G: Quantitative structural analysis of the myocardium during physiologic growth and induced cardiac hypertrophy: A review. JAm Coll Cardiol 1986;7:1140-1149 2. Mann DL, Spann JF, Cooper G IV: Basic mechanisms and models in cardiac hypertrophy: Part I. Pathophysiological models. Mod Concepts Cardiovasc Dis 1988;57:7-11 3. Mann DL, Spann JF, Cooper G IV: Basic mechanisms and models in cardiac hypertrophy: Part II. Hypertrophy into failure. Mod Concepts Cardiovas Dis 1988;57:13-17 4. Grossman W, Jones D, McLaurin LP: Wall stress and patterns of hypertrophy in the human left ventricle. J Clin Invest 1975;56:56-64 5. Takahashi M, Sasayama S, Kawai C, Kotoura H: Contractile performance of the hypertrophied ventricle in patients with systemic hypertension. Circulation 1980;62:116-26 6. Marcus ML: The Coronary Circulation in Health and Disease. New York, McGraw-Hill Book Co, 1983, pp 285-306 7. Mirsky I, Laks MM: Time course of changes in the mechanical properties of the canine right and left ventricles during hypertrophy caused by pressure overload. Circ Res 1980; 46:530-42 8. Grover-McKay M, Schwaiger M, Krivokapich J, Perloff JK, Phelps ME, Schelbert HR: Regional myocardial blood flow and metabolism at rest in mildly symptomatic patients with hypertrophic cardiomyopathy. J Am Coll Cardiol 1989; 13:317-324 9. Swynghedauw B, Schwartz K, Apstein CS: Decreased con10. 11. 12. 13. tractility after myocardial hypertrophy: Cardiac failure or successful adaptation? Am J Cardiol 1984;54:437-440 McLenachan JM, Henderson E, Morris KI, Dargie HJ: Ventricular arrhythmias in patients with hypertensive left ventricular hypertrophy. N Engl J Med 1987;317:787-792 Weber KT, Janicki JS, Pick R, Abrahams C, Shroff SG, Bashey RI, Chen RM: Collagen in the hypertrophied, pressure-overloaded myocardium. Circulation 1987;75(suppl I):I-40-1-47 Cueto-Garcia L, Reeder GS, Kyle RA, Wood DL, Seward JB, Naessens J, Offord KP, Greipp PR, Edwards WD, Tajik AJ: Echocardiographic findings in systemic amyloidosis: Spectrum of cardiac involvement and relation to survival. J Am Coll Cardiol 1985;6:737-743 Siqueira-Filho AG, Cunha CLP, Tajik AJ, Seward JB, Schattenberg TT, Giuliani ER: M-mode and two-dimensional (Circulation 1989;80:1095-1097) 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 1097 echocardiographic features in cardiac amyloidosis. Circulation 1981;63:188-196 Frustaci A, Loperfido F, Pennestri F: Hypertrophic cardiomyopathy simulating an infiltrative myocardial disease. Br Heart J 1985;54:329-332 Sedlis SP, Saffitz JE, Schwob VS, Jaffe AS: Cardiac amyloidosis simulating hypertrophic cardiomyopathy. Am J Cardiol 1984;53:969-970 Oh JK, Tajik AJ, Edwards WD, Bresnahan JF, Kyle RA: Dynamic left ventricular outflow tract obstruction in cardiac amyloidosis detected by continuous-wave Doppler echocardiography. Am J Cardiol 1987;59:1008-1010 Topol EJ, Traill TA, Fortuin NJ: Hypertensive hypertrophic cardiomyopathy of the elderly. N Engl J Med 1985; 312:277-283 Miller JG, Perez JE, Sobel BE: Ultrasonic characterization of myocardium. Prog Cardiovasc Dis 1985;29:85-110 Martin RP, Rakowski H, French J, Popp RL: Idiopathic hypertrophic subaortic stenosis viewed by wide angle, phasedarray echocardiography. Circulation 1979;59:1206-1217 Skorton DJ, Collins SM: Clinical potential of ultrasound tissue characterization in cardiomyopathies. JAm Soc Echo 1988;1:69-77 Chandrasekaran K, Aylward PE, Fleagle SR, Burns TL, Seward JB, Tajik AJ, Collins SM, Skorton DJ: Feasibility of identifying amyloid and hypertrophic cardiomyopathy with the use of computerized quantitative texture analysis of clinical echocardiographic data. J Am Coll Cardiol 1989; 13:832-840 Masuyama T, St Goar FG, Tye TL, Oppenheim G, Schnittger I, Popp RL: Ultrasonic tissue characterization of human hypertrophied hearts in vivo with cardiac cycle dependent variation in integrated backscatter. Circulation 1989; 80:925-934 Wickline SA, Thomas LJ III, Miller JG, Sobel BE, Perez JE: The dependence of myocardial ultrasonic integrated backscatter on contractile performance. Circulation 1985; 72:183-192 Wickline SA, Thomas LJ, Miller JG, Sobel BE, Perez JE: Sensitive detection of the effects of reperfusion on myocardium by ultrasonic tissue characterization with integrated backscatter. Circulation 1986;74:389-400 Tanaka M, Fujiwara H, Onodera T, Wu D-J, Hamashima Y, Kawai C: Quantitative analysis of myocardial fibrosis in normals, hypertensive hearts, and hypertrophic cardiomyopathy. Br Heart J 1986;55:575-581 Grover-McKay M, Scholz TD, Skorton DJ: Increased myocardial collagen content is associated with prolonged nuclear magnetic resonance relaxation times in the spontaneously hypertensive rat (abstract). Clin Res (in press) Caspari PG, Newcomb M, Gibson K, Harris P: Collagen in the normal and hypertrophied human ventricle. Cardiovasc Res 1977;11:554-558 Sagar KB, Rhyne TL, Warltier DC, Pelc L, Wann LS: Intramyocardial variability in integrated backscatter: Effects of coronary occlusion and reperfusion. Circulation 1987; 75:436-442 Vandenberg BF, Rath L, Shoup TA, Kerber RE, Collins SM, Skorton DJ: Cyclic variation of ultrasound backscatter in normal myocardium is view dependent: Clinical studies using a real-time backscatter imaging system (abstract). J Am Coll Cardiol 1989;13:226A Skorton DJ, Miller JG, Wickline S, Barzilai B, Collins SM, Perez JE: Ultrasonic characterization of cardiovascular tissue, in Marcus ML, Skorton DJ, Schelbert HR, Wolf GL (eds): Cardiac Imaging-Principles and Practice. Philadelphia, WB Saunders (in press) Noninvasive assessment of myocardial composition and function in the hypertrophied heart. D J Skorton Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017 Circulation. 1989;80:1095-1097 doi: 10.1161/01.CIR.80.4.1095 Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 1989 American Heart Association, Inc. All rights reserved. Print ISSN: 0009-7322. 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