Intraoperative Echocardiography: Interpretation of Changes in Left Ventricular Wall Thickness

Intraoperative Echocardiography: Interpretation of Changes in Left Ventricular Wall Thickness Henry M. Spotnitz) Santos E. Cabreriza) andJoseph P. Hart Quantitative two-dimensional echocardiography (Q2-0E) may be used to detect intraoperative changes in left ventricular (LV) mass (M) and wall thickness (h). Potential causes of change in h include physiological redistribution of myocardium, myocardial edema, reactive hyperemia, and intramyocardial hemorrhage. Changes in h, in the absence of changes in LV shape and volume, generally indicate increased LVM. When changes in h are accompanied by changes in shape or volume, changes in LVM can only be detected by mathematical modeling, unless the direction of the observed changes is opposite that expected with physiological redistribution. Histological observations essential to understanding current mathematical models are presented and related to the inherent solid geometry. Technical considerations in determination of LV mass by Q2-0E are discussed. New procedures that alter LV volume and geometry, such as the Batista operation, defy modeling by conventional methods. Modeling techniques that allow an experimental approach to understanding LVM and h under such conditions are presented. Copyright © 1998 by W.B. Saunders Company Key words: Quantitative two-dimensional echocardiography, left ventricular wall thickness, myocardial edema.

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uantitative two-dimensional echocardiography (Q2-DE) is uniquely suited for detection of changes in left ventricular mass (LVM). Laboratory experiments have shown increased left ventricular (LV) wall thickness (h) in the absence of a change in LV shape or end-diastolic volume (EDV), indicating an increase in the volume of the LV wall. l -7 Given a narrow variation of the specific gravity of myocardium, approximately 1.055, we have considered an increase in LV wall volume equivalent to an increase in LVM.{ LVM is readily confirmable in experimental studies by weighing the excised and trimmed LVI-7 When changes in h are accompanied by changes in LV shape or EDV, alteration in LVM is difficult to detect. The problem can be approached using geometric principles to determine what should happen to LV dimensions in the absence of a change in LVM. From the Department if Surgery, Columbia Unil'ersi~)' College if Pk)'sicians and Surgeons, New York, NY Presented in part bl!fore the Cardiac Surge»' Biology Club. Boston. MA, Mqy3.. 1998. Address reprint requests to Hen»' M. Spotnit::.. MD, Department of Surgf». Columbia Unil'ersity College of Pk)'sicians and Surgeons. 622 W 168th St, New York. NY 10032. COjJyright © 1998 by WE. Saunders Compan), 1043-0679/98/1004-0005$08.00/0

Recently, however, the development by Batista and others of partial ventriculectomy for the treatment of heart failure 8- 10 has created a difficult problem in the analysis of functional geometry. Partial ventriculectomy not only removes a portion of the LV, but also changes LV shape; in addition, the suture line presents an impediment to symmetrical redistribution of mass over the surface of the reconstructed chamber. Increased h and decreased LVEDV after partial ventriculectomy (Fig 1) could simply be due to physiological redistribution of the remaining myocardium over the smaller LV surface that results from the resection. Alternatively, increased h under these circumstances could indicate pathological increases in myocardial water content (myocardial edema).{.ll The controversial nature of this problem stimulated this review of techniques for the analysis of intraoperative changes in hand LVM. In addition, new concepts are proposed for the analysis of functional anatomy after partial ventriculectomy.

Causes of Changing Wall Thickness The causes of acute changes in h are presented in Table 1. These include physiological redistribution, myocardial edema, reactive hyperemia, and intramyocardial hemorrhage. Although myocardial hypertro-

Seminars in Thoracic and Cardiovascular Surge~)'. J/ollO. No.j (October). 1998: pp 273-283

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Figure 1. Effect of partial ventriculectomy in a pig with pacing-induced heart failure. Echo sections before resection in diastole (A) and systole (B) are compared with images after resection in diastole (C) and systole (D). Afterventriculectomy, chamber volume decreases and wall thickness (h) increases. Without mathematical analysis, the etiology of the postresection increase in h cannot be discerned. The geometry observed could reflect redistribution of unchanged LV mass (LVM) over a smaller chamber, an increase in LVM due to myocardial edema, or both. On the other hand, increasing h during systolic contraction (B vs A or 0 vs C) represents physiological redistribution, because LVM is essentially constant throughout the cardiac cycle. Systolic wall thickening is reduced versus normal (Fig 2), because ejection fraction is diminished by heart failure.

Table 1. Causes of Changes in LV Wall Thickness Acute Physiological redistribution Edema Reactive hyperemia Hemorrhage Chronic Hypertrophy Eccentric Concentric Infiltrative Transplant rejection

phy and infiltrative changes related to cardiac allograft rejection also can alter h,l2-I6 they are not relevant to the present discussion because of the relatively long time course usually associated with their evolution. Approximately 5% to 10% of the ventricular wall is occupied by blood vessels and their contents. Variation in LV wall thickness during reactive hyperemia has been attributed to dilation of blood vessels, referred to as the "erectile" or "garden hose" effect. 17

Physiological Redistribution Echocardiographic short axis cross-sections showing changes in LV systolic and diastolic wall thickness

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Figure 2. Systolic and diastolic echocardiograms during vena caval occlusion in a pig with normal LV function. LVM cannot change significantly during this short time course, but the LV wall thickens as volume decreases. These sections unambiguously show physiological increases in h: the wall appears thicker as volume decreases, but LVM is unchanged. These data differ from Fig I in that there has been no edema and no resection between the initial and subsequent sections. Normal ejection fraction in these sections is associated with systolic wall thickening of 40% to 50%.

during vena caval occlusion are presented in Fig 2. The echo images reveal that h increases during systole by 30% to 50%, consistent with measurements by angiography,18 sonomicrometry,1 9 wall thickness gauges,20 M-mode,21 and two-dimensional echo. 22 Moreover, Fig 1 reveals that h at end-diastole increases as LVEDV decreases. An increase in h as LV volume (LW) decreases during systole or diastole is expected from the law of constant volume and basic geometry; h must increase as the fixed wall volume of the LV is redistributed around a shrinking chamber volume. 23 Studies of changes in LVM are best done with two-dimensional or three-dimensional images obtained at end-diastole, when artifacts owing to asymmetric contraction or imaging errors are minimized. Excellent images are imperative for these studies, and sectioning planes should be reproduced as closely as possible for serial measurements. For these studies, we prefer hand-held probes because they offer the greatest precision and accuracy in imaging.u

Geometric Patterns The geometry relating h and LVV results in two patterns of change that unequivocally indicate alter-

a tion in LVM. As indica ted in Table 2, an increase in h and an increase in EDV una mbiguously imply an increase in LVM, because h decreases with increasing EDV when LVM is constant (Fig 3). Similarly, a decrease in h accompanied by a decrease in EDV implies a decrease in LVM, because h should otherwise increase when EDV decreases (Fig 2). However, quantitative modeling is required to interpret changes that resemble the physiological pattern. Thus, a decrease in EDV accompanied by an increase in h could indicate a red uction, no change, or an increase in LVM (Fig 2); modeling is required to distinguish these possibilities. Similarly, an increase in EDV accompanied by a decrease in h is uninterpretable without modeling.

Table 2. Simultaneous Changes in Wall Thickness (h) and Left Ventricular Volume (LVV)-Relation to LV Mass (LVM) Unambiguous pattern hTLWT = TLVM h! LW! = !LVM Ambiguous h TLW! (eg, postop CHD, transplant) h! LWT (eg, volume overload)

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Figure 3. Effect of dilated heart failure on h in the LV of the rat. (B) lllustrates an echocardiogram in the failure state; (A) is an age- and species-matched control heart. There is little difference in LVM between the two animals; the reduction in h represents physiological redistribution of the myocardium over the dilated LV in the failure state.

Ventricular Modeling 80

Models accurately predicting changes in ventricular dimensions can successfully detect changes in wall volume and negate artifacts owing to physiological redistribution. Modeling techniques developed in our laboratory for this purpose are based in part on studies of ventricular architecture and histology in fIxed hearts, reviewed briefly below.

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Histological Studies Electron microscopic measurements have defIned the relation between myocardial sarcomere length, LV fIxation volume, and fIxation pressure. 25 -28 Variation in sarcomere length was largest in the inner layers of the myocardium and smallest in the epicardial layers, consistent with the geometry of a thickwalled sphere. 25 Changes in midwall sarcomere length were internally consistent with gross ventricular architecture, a 13% decrease in midwall sarcomere length closely matching a predicted 15% decrease in midwall radius and circumference, and a 60% decrease in volume during systole. 26-28 Myocardial fIber orientation was found to resemble a fIber-wound chamber in which fIber angle changes gradually across the wall. Midwall fIbers were parallel to the ventricular equator. Systolic contraction had little effect on this pattern (Fig 4).29 Although percentage change in midwall circumference, sarcomere length, and ventricular volume closely matched predictions of simple models based on spherical or ellipsoidal geometry, changes in

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Figure 5. Upper panel illustrates dimensions of dog LVs weighing roughly 100 g fixed in diastole (left) and systole (right). Systole is associated with a 13% decrease in sarcomere length (SL), a 61 % decrease in fixation volume from 52 to 20 cc (V), and a 50% increase in wall thickness (h). Middle panel illustrates hypothesized changes in fiber dimensions including a 13% decrease in SL and fiber length and a compensatory 13% increase in the cross-sectional area of the fiber (to keep fiber volume constant). A 13% increase in cross-section implies a 6% increase in fiber thickness by the geometry of a circle. The lower panel illustrates dimensions calculated for a spherical model with volume and mass similar to the fixed ventricles. The 37% increase in calculated wall thickness of the model and the 15% decrease in midwall circumference (Cm) are similar to measurements in the fixed ventricles. (Reprinted with permission from Spotnitz HM, Sonnenblick EH: Structural conditions in the hypertrophied and failing heart, in Mason DT (ed): Congestive Heart Failure. New York, NY, York Medical Books, 1976. 28 )

ventricular wall thickness in these studies were more difficult to interpret. Thus, in fixed dog hearts a 61 % reduction in volume and 13% decrease in sarcomere length were associated with a 50% increase in wall thickness. 28 A 6% increase in fiber thickness based on a 13% decrease in fiber length left the bulk of the 50% increase in h unexplained (Fig 5). This was studied in greater detail in rat hearts, in which quantitative phase contrast microscopy could define cellular dimensions across the full thickness of the LV wall from epicardium to endocardium. This study confirmed that the rate of change of wall thickness, which matched predictions based on the change in LV volumes, was too great to be accounted for by changes in fiber thickness. Although small changes in fiber thickness and packing were measurable, changes in wall thickness were more closely related to the number of fibers aligned across the wall than to fiber dimensions (Fig 6).30

The realignment of fibers across the wall with increasing wall thickness appeared to be facilitated by sliding planes within the wall. These planes defined cleavage planes within the wall. These planes tended to be perpendicular to the epicardial and endocardial surfaces in thick-walled, low-volume states and more oblique in thin-walled, high-volume states (Fig 7). LV wall thickness, as well as epicardial, endocardial, and midwall radii and circumferences in these studies, were found to be reproducibly related to ventricular chamber volume, and could be predicted at any given filling volume if LVM was known. This information allowed changes in dimensions to be predicted in advance. Further, it seemed that in short axis cross-sections of the LV, the area of the ring of myocardium forming the ventricular wall (AI\I) should be reproducibly related to the area of the enclosed lumen, AL (Fig 8).

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Technical Considerations The accuracy of Q2-DE generally increases as the number of echo sections analyzed increases. 31 -33 The normal LV is symmetrical around its long axis in both systole and diastole throughout the cardiac cycle. 18,28,32 This symmetry allows properly selected single sections to be used successfully to measure LWand LVM and to analyze changes in ventricular architecture and function.1,31,33,34 However, diastolic asymmetry of the LV, as observed with ventricular aneurysms, and localized akinetic or dyskinetic systolic wall motion abnormalities require a large number of sections for accurate measurement of LW, LVM, and ejection fraction. For laboratory studies of the symmetrical or moderately asymmetric LV, we find a three-section model involving two perpendicular long axis sections and a single short axis section satisfactory for Q2_DE.I,4,31 Numerous studies from our laboratory have applied this methodology to analysis of changes in diastolic compliance and/or LVMI-7,35-37 in the beating heart. Anatomic considerations in patients undergoing open heart surgery are particularly challenging for Q2-DE. The preponderance of LV mass lies behind the sternum, and although low profile phased-array probes have provided some promising results, long axis sections provided by hand-held probes are generally not accurate enough for quantitative studies. 24 Transesophageal echo may eventually provide reproducible, anatomically accurate long axis and short axis sections, facilitated by multiplane imaging and miniaturized probes with augmented angulation.

In light of the limitations of current technology, we have studied the AL-AM relation as a means of improving studies of change in LVM. The premise is that the area of the myocardial ring and the area of the ventricular lumen for a given ventricle will be reproducibly related over a wide range of LW. The geometric assumptions used include spherical geometry and symmetrical distribution of mass. Studies based on ellipsoids with a 2: I long axis/short axis relation yield similar results, as long as dimension changes are proportionately equal and symmetrically distributed along the long axis and two principal short axis directions. 23 ,25 The calculations embodied in this concept are illustrated graphically in Fig 8. Experimental testing of this model required technically excellent short axis echo images during large changes in preload in the absence of changes in LVM. This was most reproducibly achieved during vena caval occlusion.38 Representative AL-AM data are presented in Fig 9; the predicted relation is also illustrated. LVM in the calculated model is adjusted to force the relation through the initial data point, and predicted variation of AL and AM is then predicted by the model. Our data support the view that

Figure 7. Schematic representation of the orientation of sliding planes and myocardial fibers in thick-walled and thin-walled ventricles. The mechanism hypothesized to allow for redistribution of fibers across the wall with decreasing LV volume is shown schematically by the blackened fibers. (Reprinted with permission from Spotnitz HM, Sonnenblick EH: Structural conditions in the hypertrophied and failing heart, in Mason DT (ed): Congestive Heart Failure. New York, NY, York Medical Books, 1976. 28 )

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Figure 8. Results of calculations based on a spherical model for effect of changing volume on LV dimensions. The left panel shows increasing midwall circumference (Cm), decreasing wall thickness (h), and decreasing area of ring of myocardium at the equator (A) as LV volume increases. The right panel indicates postulated changes in the number of fibers aligned in each of the principal dimensions in the left panel: As volume increases and the wall thins, the number of fibers perpendicular to the circumference (Nc) must increase and the number aligned across the wall must decrease, whereas the total number of fibers per unit area stays the same. These changes are illustrated schematically in Fig 7. (Reprinted with permission. 30 )

the AeAM relation is reproducible in skilled hands and fits predictions of the model. Changes in LVM can also be detected, as illustrated in Fig 10. LVM derived from forcing the model through the initial data point is only 80% of the true, echocardiographic LVM.

Clinical Observations Our clinical interest in alterations in LVM relates to myocardial edema produced by hemodilution or ischemic injury. 11,24,39-41 Intraoperative reduction in LVEDV (Fig 11) is common in corrective operations for congenital heart disease,39 in correction of aortic insufficiency,34 and in cardiac transplantation. 41 The AL-AM analysis was applied to several data sets in our laboratory, showing increased AM accompanied by a reduction in AL • These studies in most cases showed that a statistically significant increase in h or AM actually represented physiological redistribution of mass rather than edema; ie, there was no true alteration in LVM (Fig 12),34

Partial Ventriculectomy Ventricular reduction surgery creates conditions opposite to those usually observed during cardiac surgery. Ventriculoplasty reduces LW by excising an elliptical portion of myocardium parallel to the ventricular long axis. The chamber is restored with a suture line parallel to the long axis.s A representative echocardiogram from a laboratory replication of ventriculoplastylO is presented in Fig I. LW is reduced, and wall thickness is clearly increased after surgery. Is the observed increase in h due to physiological redistribution, or has wall volume been augmented by myocardial injury and edema?

Analytical Approach The standard AL-AM analysis cannot be applied following ventriculoplasty, because a substantial portion of the LV has been removed. Model calculations are not consistent enough in our view to calculate what the AL-AM relation "should be" following the

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and postoperative segment lengths were identical. A change in h at matched segment length would indicate an increase in L\IM: (myocardial edema). If all segment lengths were reduced postoperatively, this would indicate mass redistribution as an important cause of increased h, but would not rule out myocardial edema as well. This approach could be flawed if the relation of long axis length to local segment length were altered. Thus, if the ventricle lengthens appreciably, h should decrease despite matching of segment lengths.

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Figure 9. Representative example of the relation between the area of the LV myocardial ring AM and the area of the lumen AL . Ring area increases as chamber size decreases. Observed data (circles) match predictions based on a mathematical model (solid line) ; LV mass is adjusted in the model to force the data to pass through the control data. (Reprinted with permission from Cabreriza SE, et al: A method for detecting changes in left ventricular mass during variations in filling volume.] Am Soc Echocardiogr II :356-364, 1998.38 )

resection, even if the resected portion were weighed and the remaining L\1M: were expressed as a fraction of the original. However, this possibility should be tested as additional data become available. Our proposed approach to analysis of changes in wall thickness following ventriculoplasty is illustrated in Fig 13. The underlying concept is that a modified AL-AM analysis can be applied, provided that changes in preload can be reliably measured. For this purpose, landmarks are required to estimate preload. Although the change in the interpapillary circumference opposite the ventriculoplasty might be used for this purpose, there are many difficulties with this approach, including the possibility that the elastic properties of the myocardium in diastole are anisotropic after ventriculoplasty. Thus, it would not be surprising if the myocardium is stiffer near the suture repair of the ventriculoplasty, so that changes in preload are greater opposite the ventriculoplasty than close to it. A solution might be provided by deploying radiopaque markers for fluoroscopy~2 or sonomicrometry crystals around the equator of the LV before the ventriculoplasty. At the completion of the operation, h from selected regions would be compared with pre-resection values for h. Individual segments would be compared at those times when the preoperative

Summary The interpretation of changes in ventricular wall thickness detected by echocardiography during cardiac surgery is reviewed. A 60% ejection fraction is accompanied by an increase in wall thickness of approximately 30% to 50%. The increase in thickness primarily represents realignment of fibers across the wall. This demands rearrangement of myocardium within the LV wall, because the accompanying increase in fiber diameter and center-to-center separation is less than 10%. Despite the requirement for internal rearrangement of cellular architecture, the gross dimensions of the normal LV conform well to predictions based on simple spherical or ellipsoidal models. This allows changes in wall thickness to be 30

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Figure 10. Representative data illustrate the effect of experimentally induced myocardial edema on the relation between AL and AM - Control data (circle) and the predicted AL-AM relation are compared with data obtained after the induction of myocardial edema (cross) with an independently confirmed increase in LV wall volume. (Reprinted with permission from Cabreriza SE, et al: A method for detecting changes in left ventricular mass during variations in filling volume. ] Am Soc Echocardiogr II :356-364, 1998.38 )

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Figure 11. Diastolic echocardiograms before (A) and after (B) surgical correction of congenital heart disease. The chamber is smaller and the wall is thicker after correction. Definition of the cause of the increase in postoperative wall thickness requires mathematical analysis (see Fig 12).

predicted solely from knowledge of the volume contained in the LV and the volume or mass of the wall itself. Models can be constructed that predict the relation in short a.xis echocardiographic images of the circle defining the area of the lumen (Ad and the surrounding ring defining the volume of the wall (A~f). Mathematical derivations of the AL-AM relation 35

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fit well with echo dimensions from carefully obtained echo images. Limitations include the necessity to use an approximation method to cause the derived relation to pass through actual data obtained in the control state. Once this has been done, a predicted value for AM can be derived for any given value of AL; the predicted value for A:-'b rather than the control value for AI-d, is then compared with the observed 35

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Figure 12. Representative measurements of LVM before (A) and after (B) correction for reduction of LV volume using the AL-AM relation. Intraoperative measurements of AM for each patient before (pre) and after (post) surgical correction of congenital heart disease are connected by a solid line; average results are indicated by the symbols with brackets. The uncorrected data indicate a statistically significant increase in LV mass at the conclusion of surgery. However, after correction for a concomitant mean reduction in LV volume, the difference in A~[ becomes statistically insignificant.

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Principles 1. Match Segment Lengths a. Interpapillary Distance b. Marker Lengths 2. Am = Circumference x h

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Figure 13. Proposed approach to the analysis of ventriculoplasty. Sections in which the circumferential distance between internal landmarks like papillary muscles are matched could be used to compare changes in wall thickness. In view of the fact that postoperative changes in segment length may be heterogeneous, wall thickness in individual segments of the wall should ideally be compared when implanted crystals or markers indicate segment length is precisely matched.

value to determine whether LV mass has changed. In the clinical situation in which postoperative LVEDV decreases, as after correction of aortic insufficiency, heart transplantation or congenital heart disease, the use of the AL-AI\J relation tends to minimize the importance of small increases in AM, suggesting that most of these changes represent physiological redistribution of myocardium rather than an expansion of LVM. For the unique circumstances that occur after partial ventriculectomy, a strategy based on myocardial markers or sonomicrometry crystals is proposed to allow the possible causes of postoperative increases in wall thickness-increased wall volume versus physiologic redistribution-to be distinguished.

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Acknowledgment The authors acknowledge with gratitude the editorial assistance of May Deutsch.

References 1. Spotnitz WD, Clark ME, Rosenblum HM, et al: Effect of cardiopulmonary b}pass and global ischemia on human and

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canine left ventricular mass: Evidence for interspecies differences. Surgery 96:230-239, 1984 Rosenblum HM, Haasler GB, Spotnitz WD, et al: Effects of simulated cardiopulmonary bypass and cardioplegia on mass of the canine left ventricle. Ann Thorae Surg 39: 139-148, 1985 Lazar HL, Haasler GB, Collins RH, et al: Compliance, mass, and shape of the canine left ventricle after global ischemia analyzed with two-dimensional echocardiography.J Surg Res 39:199-208,1985 Haasler GB, Rodigas PC, Collins RH. et al: Two-dimensional echocardiography in dogs: Variation of LV mass, geometry, volume, and ejection fraction on cardiopulmonary bypass. J Thorac Cardiovasc Surg 90:430-440, 1985 Dean DA, Jia CoX, Cabreriza SE, et al: Does myocardial edema cause apparent myocardial depression in severe sepsis and trauma? Surg Forum 47:56-58,1996 Amirhamzeh MMR,Jia CoX, Cabreriza SE, et al: Myocardial edema: Increased diastolic compliance and time course of resolution in vivo. Ann Thorac Surg 62:737-743,1996 Dean DA, Amirhamzeh MMR, Jia CoX, et al: Reversal of iatrogenic myocardial edema and related abnormalities of diastolic properties in the pig left ventricle. J Thorac CardiovascSurg 115:1209-1214, 1998 Batista RJV, Santos ]LV, Takeshita N, et al: Partial left ventriculectomy to improve left ventricular function in endstage heart disease.J Card Surg 11:96-97, 1996 Dickstein ML, Spotnitz HM, Rose EA, Burkhoff D: Heart

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reduction surgery: An analysis of the impact on cardiac function.J Thorac Cardiovasc Surg 113:1032-1040, 1997 10. HartJP, Cabreriza SE,Jia C-X, et al: Left ventricular function in a porcine model of dilated cardiomyopathy during left ventricular reduction surgery. Surg Forum (in press) II. Spotnitz HM, Hsu DT: Myocardial edema-Importance in the study ofleft ventricular function. Adv Cardiac Surg 5: 1-25, 1994 12. Soto P, Jia C-X, Carter YM, et al: Effect of improved myocardial protection on edema and diastolic properties of the rat left ventricle during acute allograft rejection. J Heart Transplant 17:608-616, 1998 13. Dubroff jM, Clark ME, Wong CYR, et al: Changes in left ventricular mass associated with the onset of acute rejection after cardiac transplantation. Heart Transplant 3:105-109, 1984 14. Antunes ML, Spotnitz HM, Clark ME, et al: Long-term function of human cardiac allografts assessed by twodimensional echocardiography. J Thorac Cardiovasc Surg 98:275-284, 1989 15. Amirhamzeh MMR,Jia C-X, StarrJP, et al: Diastolic function in the heterotopic rat heart transplant model: Effects of edema, ischemia and rejection. J Thorac Cardiovasc Surg 108:928-937, 1994 16. Soto P,Jia C-X, Carter YM, et al: Diastolic properties during rejection of the chronically transplanted heart. Surg Forum 46:452-455, 1995 17. Gaasch WH, Bing OH, Pine ME, et al: Myocardial contracture during prolonged ischemic arrest and reperfusion. Am J PhysioI235:H619-H627,1978 18. MitchellJH, Wildenthal K, Mullins CB: Geometric studies of the left ventricle utilizing biplane cinefluorography. Fed Proc 28:1334-1343,1969 19. Nicolosi AC, Weng Z-C, Detwiler PW, Spotnitz HM: Simulated left ventricular aneurysm and aneurysm repair in swine. J Thorac Cardiovasc Surg 100: 745-755, 1990 20. Geffin GA, Vasu MA, O'Keefe DD, et al: Ventricular performance and myocardial water content during hemodilution in dogs. AmJ PhysioI235:767-775, 1978 21. Troy BL, PomboJF, Rackley CEo Ultrasonic measurements of left ventricular wall thickness in man. Circulation 42(III):38, 1970 22. Nicolosi AC, Spotnitz HM: Quantitative analysis of regional systolic function with left ventricular aneurysm. Circulation 78:856-862, 1988 23. Ahmad RM, Spotnitz HM: Computer visualization of left ventricular geometry during the cardiac cycle. Comput Biomed Res 25:201-211,1992 24. Spotnitz HM, Clark ME, Wong CYR, et al: Intraoperative echocardiography in valvular heart disease, in Cikes I (ed): Echocardiography in Cardiac Interventions. The Netherlands, Kluwer Academic Publishers, 1989, pp 313-330 25. Spotnitz HM, Sonnenblick EH, Spiro D: Relation of ultrastructure to function in the intact heart: Sarcomere structure relative to pressure volume curves of intact left ventricles of the dog and cat. Circ Res 18:49-66, 1966 26. Sonnenblick EH, RossJJr, CovellJ, et al: Ultrastructure of the heart in systole and diastole: Changes in sarcomere length. Circ Res 21:424-436,1967

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27. Ross J Jr, Sonnenblick EH, Taylor RR, et al: Diastolic geometry and sarcomere lengths in the chronically dilated canine left ventricle. Circ Res 48:49-61,1971 28. Spotnitz HM, Sonnenblick EH: Structural conditions in the hypertrophied and failing heart, in Mason DT (ed): Congestive Heart Failure. New York, NY York Medical Books, 1976, pp 13-24 29. Streeter DDJr, Spotnitz HM, Patel DP, et al: Fiber orientation in the canine left ventricle during systole and diastole. Circ Res 24:339-347,1969 30. Spotnitz HM, Spotnitz WD, Cottrell TS, et al: Cellular basis for volume related wall thickness changes in the rat left ventricle.J Molec Cell CardioI6:317-331, 1974 31. Collins RH, Haasler GB, Krug JH Jr, et al: Canine left ventricular volume and mass during thoracotomy by twodimensional echocardiography. Increased ventricular mass after ischemia and reperfusion.J Surg Res 33:294-304, 1982 32. Eaton LW, Maughan WL, Shoukas AA, Weiss JL: Accurate volume determination in the isolated ejecting canine left ventricle by two-dimensional echocardiography. Circulation 60:320-326, 1979 33. Clark ME, Spotnitz HM, Marboe C, et al: Limitations and clinical relevance of serial left ventricular mass determination by two-dimensional echocardiography: Studies after orthotopic human cardiac transplantation. J Cardiovasc Ultrasonogr 7:55-66, 1988 34. Dubroff jM, Clark M, Wong CYR, et al: Left ventricular ejection fraction during cardiac surgery: A two-dimensional echocardiographic study. Circulation 68:95-103,1983 35. Haasler GB, Rodigas PC, Spotnitz HM: Absence of temperature effects on end-diastolic pressure-volume relations of the canine left ventricle. J Thorac Cardiovasc Surg 83:878-890, 1982 36. Haasler GB, Rodigas PC, Wei J, Spotnitz HM: Heart-rate effects on canine left ventricular end-diastolic compliance measured by two-dimensional ultrasound.J Surg Res 36:205216, 1984 37. Lazar HL, WeiJ, Dirbas FM, et al: Controlled reperfusion of regional ischemia. Ann Thorac Surg 44:350-355, 1987 38. Cabreriza SE, Dean DA, Amirhamzeh MMR, et al: A method for detecting changes in left ventricular mass during variations in filling volume. J Am Soc Echocardiogr 11 :356-364, 1998 39. Spotnitz HM: Effects of myocardial edema on systolic and diastolic function in vivo.J Cardiac Surg 10:454-459, 1995 40. Spotnitz HM, Antunes ML: Effect of aortic and mitral regurgitation on left ventricular structure and function. Adv Cardiac Surg 2:85-1 16, 1991 41. Slater]p, Amirhamzeh MA, Yano OJ, et al: Discriminating between preservation and reperfusion injury in human cardiac allografts using heart weight and left ventricular mass. Circulation 92:II-467-II-471, 1995 (suppI2) 42. Ingels NB, Daughters GT II, Stinson EB, Alderman EL: Measurement of midwall myocardial d}uamics in man by radiography of surgically implanted markers. Circulation 52:859-867,1975