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BACKGROUND: The use of 3D imaging is becoming increasingly common, so too is the use of fiducial markers to identify/track regions of interest and assess material deformation. While many different materials have been used as fiducials, they are often used in isolation, with little comparison to one another. OBJECTIVE: In the current study, we aim to directly compare different Computed Tomography (CT and μCT) fiducial materials, both metallic and nonmetallic. METHODS: μCT imaging was performed on a soft-tissue structure, in this case heart valve tissue, with various markers attached. Additionally, we evaluated the same markers with DiceCT stained tissue in a fluid medium. Eight marker materials were tested in all. RESULTS: All of the metallic markers generated significant artifacts and were found unsuitable for soft-tissue μCT imaging, whereas alumina markers were found to perform the best, with excellent contrast and consistency. CONCLUSIONS: These findings support the further use of alumina as fiducial markers for soft material and tissue studies that utilize CT and μCT imaging.

BACKGROUND The transmural distribution of fiber angles and the extent of shortening among obliquely oriented fibers are likely to be major determinants of the twisting motion that accompanies left ventricular (LV) ejection. As such, measurements of torsion may provide useful information about LV contractile function, but other factors, such as ventricular loading conditions, may also regulate this motion. METHODS AND RESULTS Torsion angles (theta i) of midventricular and apical regions were measured relative to a reference minor axis near the base in seven human cardiac allografts from biplane radiographic images of metallic midwall markers. Pressure loading with methoxamine (5-10 muk/kg/min) increased LV end-systolic pressure by 41 +/- 14 mm Hg (p less than 0.0001). Volume loading with normal saline raised LV end-diastolic pressure from 9.9 +/- 5.2 to 19.6 +/- 4.9 mm Hg (p less than 0.0001). These alterations in LV loading conditions were associated with no change in theta i (difference not significant) for any marker site. Inotropic stimulation with dobutamine (5 micrograms/kg/min) increased values of theta i by as much as twofold (p less than 0.05); this response varied considerably depending on marker location, with the middle and apical inferior wall and the apical lateral wall being the most sensitive. When the marker site associated with the largest torsion angle (theta max) was considered in each patient, dobutamine increased theta max in all cases (25.2 +/- 10.5 degrees versus 15.8 +/- 7.7 degrees, p less than 0.001), whereas pressure and volume loading had negligible effects. This 59% increase in theta max was greater than that of conventional load-dependent indexes of LV systolic performance such as stroke volume (16%), ejection fraction (22%), and maximum rate of LV pressure rise (52%). CONCLUSIONS This component of LV motion is relatively insensitive to alterations in preload and afterload, while changes in contractile state influence LV torsion in a regionally heterogeneous manner. Quantification of LV torsion may, therefore, provide a sensitive and relatively load-independent measure of contractile performance that may prove to be useful in the serial assessment of LV function.

Changes in the dimensions of 'He's triangle' (formed by mitral leaflet segments subtending two associated chordae tendineae) derived from data obtained in in-vitro mitral valve models have been proposed to provide a mechanistic explanation for mitral leaflet malcoaptation. The in-vivo dynamics of He's triangle, however, have not been hitherto determined.Radio-opaque markers were placed in 13 sheep to delineate the mitral annulus and four (of an infinite number of possible) He's triangles formed by: (i) the anterior mitral leaflet (AML), first- (CT1) and second-order (CT2) chordae tendineae emanating from the anterior papillary tip (APT1) as well as from the posterior papillary tip (PPT1), respectively; and (ii) the posterior mitral leaflet (PML), CT1 and CT2 emanating from other loci on the anterior as well as the posterior papillary tips (APT2 and PPT2), respectively. Immediately postoperatively (anesthetized, open-chest), three-dimensional end-systolic marker positions were measured before and during circumflex coronary artery occlusion sufficient to produce mitral regurgitation, as verified by echocardiography.During ischemia, three leaflet segments constituting one side of three He's triangles elongated: The AML attached to APT1 and to PPT1 by 1.5+/-1.2 mm (p0.001) and 1.3+/-0.8 mm (p0.001), respectively, and the posterior leaflet attached to APT2 by 1.4+/-1.9 mm (p = 0.02). Apart from a 0.9+/-1.1 mm (p = 0.02) increase in the length of CT2 attached to APT2, the length of the seven other CT1 and CT2 remained relatively unchanged during acute left ventricular ischemia.With acute posterolateral ischemia, the lengths of CT1 and CT2 remained relatively constant, but the AML and PML lengths were not constant as the AML and PML 'unfurled' during acute left ventricular ischemia. These geometric changes may provide further insight into the mechanisms of acute ischemic mitral regurgitation, though it is not clear how they will be clinically helpful.

Edge-to-edge approximation of the mitral valve leaflets (Alfieri procedure) is a novel surgical treatment for patients with ischemic mitral regurgitation (IMR). Long-term durability may be limited if abnormal mitral leaflet stresses result from this procedure. The aim of the current study was to measure Alfieri stitch tension (F(A)) and to explore its geometric determinants in an ovine model of acute IMR as a reflection of the mitral leaflet stresses imposed by the procedure.Eight sheep were studied immediately after surgical placement of (1) a force transducer interposed between sutures approximating the central leaflet edges and (2) radiopaque markers around the mitral annulus and leaflet edges. Computer-aided analysis of videofluorograms was used to obtained 3D marker coordinates. Simultaneous measurements of F(A), septal-lateral annular dimension (L(S-L)), leaflet edge separation (L(SEP)), anterior (L(AL)) and posterior (L(PL)) leaflet length, and hemodynamic variables were obtained at baseline (CTL) and during acute IMR (circumflex artery occlusion). F(A) was significantly elevated throughout the cardiac cycle during IMR compared with CTL, with maximum F(A) in diastole (0.26+/-0.05 versus 0.46+/-0.08 N, CTL versus IMR; P0.05). Multivariable analysis revealed L(S-L) as the single independent predictor of maximum F(A) (P0.001). Positive linear correlations were shown between values of F(A) and L(AL) and L(PL) (dependent variables).These experimental data demonstrate higher F(A) during IMR and cyclic changes in F(A) closely paralleling changes in L(S-L), eg, being greatest in diastole when the annulus is largest. Increased F(A) during IMR is probably indicative of successful therapeutic intent, but higher diastolic leaflet stresses resulting from persistent or progressive mitral annular dilatation may adversely affect repair durability. This indirectly implies that concomitant mitral ring annuloplasty should be added to the Alfieri repair.

Ovine mitral valve closure is associated with presystolic mitral annular reduction coincident with atrial contraction, which is abolished with ventricular pacing. Whether lack of properly timed atrial contraction influences mitral valve closure or competence, however, is not known.Eight sheep underwent myocardial marker implantation on the left ventricle, mitral annulus (MA), and mitral leaflets. After 7-10 days, the animals were studied with biplane videofluoroscopy at baseline and during ventricular or atrioventricular (AV) sequential pacing. Valve closure was timed from end-diastole (ED) and defined as minimum distance between two leaflet edge markers. ED was defined as peak of ECG R wave, end-systole as peak negative left ventricular (LV) dP/dt, and end-isovolumic contraction (EIVC) as 83.5 ms after ED. Septal-lateral (S-L) annular diameter was defined as distance between two markers at the middle of the anterior and posterior annulus. Regurgitant volume (RV) was calculated as relative volume change between ED and EIVC.V-pacing was associated with delayed leaflet closure (65 +/- 5 versus 29 +/- 10 ms, p = 0.008); moreover, RV (4.1 +/- 0.5 versus 1.4 +/- 0.5 ml, p = 0.02), end-diastolic S-L diameter (2.87 +/- 0.10 versus 2.67 +/- 0.09 cm, p = 0.0005), and MA area (8.12 +/- 0.37 versus 7.26 +/- 0.31 cm2, p = 0.009) all increased. RV and leaflet and annular dynamics during AV-pacing were similar to baseline.V-pacing increased S-L MA diameter by only 8 +/- 1%, but this change was associated with delayed leaflet coaptation and a 16 +/- 1% regurgitant fraction. These findings provide direct evidence that a properly timed atrial contraction is functionally important for effective mitral leaflet closure.

Previous studies have revealed that rigid mitral annuloplasty rings may be associated with left ventricular (LV) systolic dysfunction, but whether ring type affects regional systolic function at the base of the LV, in the region near the mitral annulus, is unclear. We tested the hypothesis that rigid fixation of the mitral annulus results in significant regional systolic dysfunction at the base of the LV.Twenty-six adult male sheep underwent placement of 13 miniature tantalum markers into the LV epicardium and around the mitral annulus to allow calculation of LV volume and regional epicardial area. Group I (n = 7) sheep served as controls; animals randomized to groups II (n = 11) and III (n = 8) underwent mitral annuloplasty with either a semirigid or flexible ring, respectively. After a 7- to 10-day recovery period, animals were studied in a closed-chest, sedated, autonomically blocked state. Global LV systolic function (end-systolic elastance and preload recruitable stroke work) were not significantly different among the 3 groups (P = 1.0, ANOVA). Regional systolic function at the base of the LV (fractional area shrinkage [FAS] of 4 epicardial areas) at comparable LV preload and afterload was similar in the 4 basal areas (P = 0.223, MANOVA). With the use of load-insensitive indexes (slope and area intercept of the end-systolic pressure-regional area relationship and regional stroke work-end-diastolic area relationship), regional systolic function also was not different between groups at baseline or with inotropic stimulation in any basal region (P0.05, MANOVA). Furthermore, neither annuloplasty ring perturbed the regional pattern of basal LV systolic function.Postoperative LV systolic function, both globally and in the region of the base of the LV (near the mitral annulus), was not altered with either semirigid or flexible ring fixation of the mitral annulus.

The precise geometric determinants of ischemic mitral regurgitation (MR) are incompletely understood, although such knowledge is important to improve mitral valve reparative techniques.The three-dimensional geometry of the mitral apparatus was studied using radiopaque markers in eight closed-chest dogs with acute posterior left ventricular wall ischemia either with (MR) or without (no-MR) MR as assessed by using color Doppler. Using a cylindrical coordinate system (origin at the midpoint between the mitral annulus commissures [anterolateral and posteromedial] and z-axis directed toward the left ventricular apex), we measured the distance to the midpoint (z, in millimeters), radial distance from the z-axis (r, in millimeters), and angle from the intercommissural line (theta) of each marker. A multivariate analysis of variance showed the following differences (P.005) between the MR and the no-MR groups: 1) markedly increased r of the posterior papillary muscle tip (10.3 versus 6.4 mm, MR versus no-MR, at end-systole) and increased r of the anterior papillary muscle tip; 2) dilation (in the septal-lateral direction) of the midpart of the mitral annulus and near the anterolateral region; 3) increased posterior mitral leaflet r near both commissures (eg, 8.3 versus 6.2 mm on the posteromedial side) and increased z (ie, shifted toward the left ventricular apex) of the posterior leaflet on the anterolateral side (eg, 7.0 versus 6.2 mm), which is analogous to restricted (or type III) leaflet motion.These findings indicate that the geometric determinants of ischemic MR in dogs are complex and involve many parts of the mitral valve apparatus. This complexity suggests that surgical attention to the entire annulus and excursion of the posterior leaflet may be helpful when annuloplasty alone is inadequate.

Conventional surgical thinking indicates that mitral annular (MA) size reduction plays a key role in mitral valve closure, and most MA size and shape changes are thought to occur during left ventricular (LV) systole. The influences of left atrial (LA) and LV systole on MA size and shape, however, remain debated.Eight radiopaque markers were placed equidistantly around the MA and imaged using high-speed simultaneous biplane videofluoroscopy in seven closed-chest, sedated sheep before and during asynchronous LV pacing. Marker images were used to compute the three-dimensional coordinates of each marker every 16.7 ms throughout the cardiac cycle, allowing calculation of three-dimensional MA area, septal-lateral (SL) dimension, and commissure-commissure (CC) dimension under control and LV pacing conditions. Maximum MA area occurred in early diastole, and minimum MA area near end-diastole; maximum area reduction was 12+/-1% (Por =.001). Interestingly, 89+/-3% of area reduction occurred before LV systole. During this "presystolic" period, SL decreased by 8+/-1% and CC by 2+/-1%; the SL/CC ratio fell from 0.73+/-0.02 to 0.69+/-0.01 (Por =.005), indicating a less circular shape at end-diastole. With LV pacing, total MA area reduction was similar (13+/-2 versus 12+/-1%, P=NS versus control); however, all MA area reduction occurred during LV systole with minimum MA area occurring at end-systole. Presystolic shortening in both SL and CC dimensions was lost, and presystolic ellipticalization disappeared.Changes in MA size and shape coincident with LA systole included area reduction and shape change prior to the onset of LV contraction. These presystolic changes vanished when LA systole was absent (LV pacing). Thus, LA systole plays a pivotal role in MA size reduction and shape alteration. The unexpected timing of these MA dynamics should be taken into account during mitral valve reparative procedures.

Previous studies have shown that left ventricular (LV) unloading alters right ventricular (RV) systolic mechanics, but the effects of LV assist device (LVAD) support on RV diastolic function have not been examined in intact subjects.Seven closed-chest, sedated dogs were studied after placement of a LVAD and 27 myocardial markers; in four animals, a right coronary artery occluder was placed to induce acute RV free wall ischemia. Data were recorded with the LVAD off and LVAD on before (control) and during RV ischemia. Assessment of RV diastolic function included RV myocardial relaxation (time constant of isovolumic pressure decay [tau]), RV chamber stiffness (slope of the end-diastolic pressure-volume relation), and RV filling dynamics (peak filling rate and mean filling rate during early diastole).During control, full LVAD support did not alter RV tau (104 +/- 67 msec LVAD off versus 109 +/- 49 msec LVAD on, p0.50), RV diastolic stiffness (0.56 +/- 0.31 versus 0.51 +/- 0.25 mm Hg/ml, p0.20), peak filling rate (107 +/- 51 versus 119 +/- 82 ml/sec, p0.35) or mean filling rate during early diastole (32 +/- 28 versus 27 +/- 18 ml/sec, p0.40). With right coronary artery occlusion, RV tau rose to 136 +/- 33 msec (p0.001), and RV diastolic stiffness fell to 0.29 +/- 0.13 mm Hg/ml (p0.005), but there was no change in RV filling rates (p0.20). With mechanical LV support during acute RV ischemia, there was no additional change in RV tau, diastolic stiffness, or filling dynamics (p0.20).In intact animals, RV ischemia impaired RV relaxation and decreased chamber stiffness, but there was no change in RV filling rates. Mechanical LV support, during the control state and with RV ischemia, did not affect RV diastolic performance.

This paper develops several working hypotheses regarding the coupling between myocardial fiber architecture and left ventricular function. First, the coupling between spiral myocardial fibers and left ventricular torsional deformation and ejection fraction is examined. A proposal is then made to account for the observed change in orientation of myocardial fibers from a right hand helix in the subendocardium, through circumferential fibers in the midwall, to a left hand helix in the subepicardium in terms of a requirement for generating physiological values of both ejection fraction and pressure as well as equilibration of transmural fiber work. Finally, a pumping hypothesis is developed linking the contraction of each transmural layer of fibers to one another via collagen struts and weaves, with the resulting force transmitted to the epicardium and thence, by means of hydraulic forces associated with the constant volume property of the LV wall, to the endocardium to reduce the volume of the left ventricular chamber.

We have recently described an inhomogeneous pattern of systolic contraction of the mitral annulus (MA) in normovolemic dogs: the posterior annulus shortens, and the anterior annulus lengthens. MA dynamics, however, have not been studied in volume-depleted hearts.Eight radiopaque markers were placed equidistant from each other around the MA in seven dogs. As viewed from the left atrium, the segment between markers 1 and 2 (seg12) began at the posteromedial commissure, and remaining segments were numbered sequentially clockwise around the MA (ie, posterior MA encompassed seg12, seg23, seg34, and seg45; anterior MA encompassed seg56, seg67, seg78, and seg81). Marker images were obtained in sedated dogs by simultaneous biplane videofluoroscopy 7 to 12 days after marker implantation, and three-dimensional marker coordinates at end diastole (ED) and end systole (ES) were computed. Vena caval occlusion (VCO) was used to reduce left ventricular end-diastolic volume to 70 +/- 5% of baseline (BL). With VCO, mean MA area did not change from ED to ES (3.4 +/- 0.8 versus 3.6 +/- 0.7 cm2, P = NS) during the cardiac cycle. MA segmental systolic shortening values (negative values indicate lengthening) were as follows for BL and VCO, respectively (mean +/- SD): seg12, 7 +/- 9% and 0 +/- 13%; seg23, 8 +/- 10%* and 1 +/- 11%; seg34, 16 +/- 6%* and 4 +/- 9% seg45, 10 +/- 7%* and 2 +/- 13%; seg56, -4 +/- 5%* and -16 +/- 11%*; seg67, -7 +/- 7%* and -14 +/- 7%*; seg78, 3 +/- 2%* and -1 +/- 6%; and seg81, 6 +/- 5%* and -5 +/- 11% (*Por = .05 versus zero changes, paired t test).With acute volume depletion, the five annular segments that shortened at BL no longer changed length; two anterior segments (seg56 and seg67) that lengthened at BL continued to lengthen significantly, and to a greater extent. These findings indicate that the anterior MA is a more dynamic structure than previously thought. Such dynamic motion may be important for normal mitral valvular function and possibly needs to be taken into account in the design of mitral valve reparative techniques.

Chordal excision during mitral valve replacement (MVR) impairs left ventricular (LV) systolic function, but the mechanisms responsible for this change remain unclear. This study was performed to determine the influence of annular papillary continuity on regional LV torsional deformation acutely following MVR with and without chordal preservation.Twenty-seven dogs underwent placement of LV subepicardial myocardial markers to measure regional LV systolic torsional deformation throughout the left ventricle. After 1 week, biplane fluoroscopic marker images were obtained pre-MVR in the baseline state and with inotropic stimulation (calcium, 15 mg/kg). Dogs were then randomized to undergo a sham procedure with cardiopulmonary bypass but no valve replacement (n = 6), conventional MVR with chordal excision (n = 7), or chordal-sparing MVR with preservation of the posterior leaflet and reattachment of the anterior leaflet chordae to either the anterior annulus (n = 7) or posterior annulus (n = 7). After chest closure and recovery from anesthesia, post-MVR data were acquired. At the LV apical level, maximal regional LV systolic torsional deformation (theta max) did not fall from pre-MVR values in the baseline state after the sham procedure or anterior or posterior chordal-sparing MVR procedure (Por = .10). After conventional MVR, baseline theta max fell by 66% to 81% in the anteroseptal, anterior, anterolateral, and lateral regions (P.05). With calcium, theta max fell in the anteroseptal through lateral regions and the septal wall (P.05) but did not change in the posterior regions (Por = .10). With calcium, theta max did not fall in any region after either the sham procedure or anterior MVR; however, after posterior chordal-sparing MVR, theta max fell in the lateral, posterior, and posteroseptal regions (P.05).Sham operation and anterior chordal-sparing MVR did not affect regional LV torsion; however, loss of normal valvular-ventricular integrity with conventional MVR reduced regional LV systolic torsion in the anterior and lateral LV regions. Posterior chordal-sparing MVR impaired torsion only after calcium administration. The deleterious effects of chordal excision may be due in part to perturbation of regional systolic torsional deformation.

Despite an incomplete knowledge of the geometry and dynamics of the mitral annulus (MA), papillary muscle (PM), and the chordae tendineac, chordal-sparing MVR is popular.The systolic reduction in three-dimensional distance between each PM tip and eight MA sites (DT-A) was measured in nine normal closed-chest dogs by use of surgically implanted radiopaque markers. Three loci (tip, junction, and base) on each PM were also projected onto the MA plane at end diastole and end systole to assess PM dynamics. The anterior PM tip showed significant shortening of DT-A toward the opposite side of the MA or the midanterior MA region (P.005 or P.05, respectively, versus same MA side [MANOVA]); conversely, the posterior PM tip DT-A shortened toward the opposite side of the MA near the anterior commissure or the area between the anterior commissure and midposterior MA (P.005 versus same MA side). Annular projection revealed three-dimensional motion (relative to the MA) of the anterior PM tip, junction, and base toward the right trigone, while posterior PM motion was oriented toward the opposite side of the MA.Both PMs in normal canine hearts demonstrated systolic relative motion in a direction compatible with the "oblique" chordal configuration, ie, from the anterior PM to the anterior MA near the right trigone and from the posterior PM to the opposite side of the posterior MA. These observations warrant further investigation of three-dimensional PM-MA dynamics with various methods of chorda preservation during MVR to assess their impact on left ventricular systolic and diastolic function.

Although chordal-sparing mitral valve replacement (MVR) is popular, the optimal tension for preserved or reattached chordae tendineae (CT) or for synthetic (ePTFE) CT is unknown.Changes in left ventricular (LV) systolic and diastolic function in nine dogs with anterior CT preservation with different levels of end-diastolic chordal tension (0, 10, 20, 30, and 40 gm, measured by spring scale) were compared using an isovolumic double-balloon technique.LV function data at each level of tension were compared to control data using 0 gm of tension. Systolic function assessed as Emax (mmHg/ml) at 10, 20, 30, and 40 gm versus control was: 5.7 +/- 2.6/4.9 +/- 2.7, 4.7 +/- 2.2/4.7 +/- 2.7, 4.8 +/- 3.1/4.7 +/- 2.8, and 5.0 +/- 3.5/5.1 +/- 2.9; delta improvement from the control at 10 gm was larger than that at 20 gm (p0.05 by paired t-test). Diastolic function assessed as diastolic stiffness (Sd, mmHg/ml) at the same CT tensions versus control was: 0.56 +/- 0.23/0.56 +/- 0.34, 0.53 +/- 0.30/0.57 +/- 0.37, 0.56 +/- 0.39/0.52 +/- 0.38, and 0.60 +/- 0.36/0.58 +/- 0.39; delta Sd was smaller at 20 gm than at 30 gm (p = 0.05 by ANOVA). LV equilibrium volume (Veq, ml) was: 10.7 +/- 3.9/10.1 +/- 3.9, 9.6 +/- 3.4/9.9 +/- 3.8, 10.8 +/- 4.0/10.3 +/- 3.4, and 10.6 +/- 4.0/10.6 +/- 3.5; delta Veq was larger (i.e., more compliant chamber) at 10 gm than at 40 gm (p0.05 by rm-ANOVA). Arrhythmias precluding satisfactory measurements occurred in two dogs at 30 or 40 gm CT tension.With chordal tension exceeding 10 gm, which is barely palpable, there was no additional enhancement in LV systolic function compared to zero CT tension. Veq was largest at the lowest tension; LV diastolic function (assessed as Sd) deteriorated with tensions of 30 gm or higher. The optimal end-diastolic tension of preserved CT should enhance systolic LV performance without adversely affecting diastolic function; in this isovolumic model, minimal CT tension (10 gm) best met these goals. Excessive tension may negate the potential hemodynamic benefits of chordal preservation during mitral valve replacement.

The optimal direction to preserve artificial chordae tendineae (CT) during mitral valve replacement (MVR) is not known, especially in regard to the response to inotropic stimulation which simulates exercise conditions.Using a non-distorting isovolumic balloon technique, we compared left ventricular (LV) systolic and diastolic mechanics in 11 dogs in a control state (no chordal sparing) and with four different methods of chordal preservation: posterior, anterior, oblique (anterior papillary muscle chordae directed anteriorly and others posteriorly, the direction which theoretically augments LV systolic twist), and counter-oblique (counter, chordae preserved in directions opposite to oblique).Before dobutamine, delta Emax from the control was: 0.32 +/- 0.82, 0.10 +/- 0.43, 0.64 +/- 1.07, and 0.51 +/- 0.78 (anterior, posterior, oblique, and counter method, respectively). With dobutamine (3 mg/kg/min), delta Emax (mmHg/ml) was: 0.41 +/- 1.21, -0.13 +/- 0.75, 0.59 +/- 0.82*, and -0.34 +/- 0.71. Before dobutamine, delta LV stiffness (Sd, mmHg/ml) was -0.01 +/- 0.09, -0.02 +/- 0.12, 0.02 +/- 0.10, and 0.01 +/- 0.12; with dobutamine it was 0.01 +/- 0.09, 0.00 +/- 0.15, 0.03 +/- 0.15, and -0.06 +/- 0.11. Similarly, before dobutamine delta LV equilibrium volume (Veq) was -1.2 +/- 3.8, -0.3 +/- 3.0, -0.7 +/- 2.7, and -0.2 +/- 3.5, whereas with dobutamine zeta eq was -0.1 +/- 1.1, -0.4 +/- 0.8, 0.6 +/- 1.7, and -0.4 +/- 1.1. (Mean +/- S.D.; *p = 0.005 posterior and counter by ANOVA; p = NS (0.06) versus counter and posterior by ANOVA).The oblique method enhanced systolic LV function both with and without dobutamine, while a tendency towards better diastolic LV function (Veq) was observed with dobutamine. The anterior method was next best in preserving systolic function, both with and without dobutamine. LV diastolic function tended to deteriorate with dobutamine in the posterior group. Systolic function with the counter method deteriorated with dobutamine. These results warrant further study in an ejecting model to investigate LV systolic and diastolic mechanics with the oblique method of CT preservation, including interactions with LV systolic twist and diastolic recoil.

Left ventricular (LV) assist device (LVAD) support has been associated with right ventricular (RV) failure in humans, but the etiology remains unknown. Mechanical LV support apparently does not induce RV pump failure in normal hearts, but controlled studies of LV assistance in hearts with preexistent RV dysfunction have been limited. Therefore, this study was performed to determine if LVAD support impairs RV systolic mechanics during acute RV ischemia.Five closed-chest, autonomically blocked, sedated dogs were studied after placement of an LVAD (LV-femoral artery bypass), right coronary artery (RCA) occluder, and 27 miniature radiopaque tantalum markers into the LV and RV walls for independent computation of RV and LV volumes. Biplane videofluoroscopic marker images and hemodynamic data were recorded before RCA occlusion with the LVAD off (maximum LV pressure [LVPmax] = 119 +/- 25 mm Hg), after 3 minutes of RCA occlusion with the LVAD off (LVPmax = 84 +/- 18 mm Hg), and then with the LVAD on (LVPmax = 26 +/- 32 mm Hg). Global RV contractility (end-systolic elastance [RV Ees] and preload recruitable stroke work [RV PRSW]), RV power output, and the mechanical (pump) efficiency of converting potential energy to external work (ratio of RV stroke work/total pressure-volume area) were calculated. As expected, with RCA occlusion there were major decreases in RV Ees (from 2.5 +/- 1.2 to 1.4 +/- 0.5 mm Hg/mL, P.005) and RV PRSW (15 +/- 4 versus 9 +/- 4 mm Hg, P.001). RV power output (overall pump performance) declined by 39 +/- 20% (P.025), and mechanical efficiency fell by 38 +/- 13% (P.001). After initiation of mechanical LV support, however, there was no further impairment of RV contractility or power output (P.80). Pulmonary artery input impedance (RV afterload) decreased from 848 +/- 628 to 673 +/- 577 dyne.sec-1.cm-5 (P.01), which led to a 26 +/- 29% improvement in RV pump efficiency (P.001).While right coronary artery occlusion significantly reduced RV systolic performance, LVAD support during acute RV ischemia did not further impair RV contractility or power output. Furthermore, since RV afterload fell with LV unloading, the mechanical pump efficiency of the right ventricle actually improved. These observations demonstrate that LVAD support does not directly induce RV failure in canine hearts with acute isolated RV ischemia.

Cardiac operations and cardiopulmonary bypass are associated with a host of unphysiological consequences that have widespread systemic effects. Since previous investigations in human cardiac transplant recipients had demonstrated that left ventricular (LV) torsional deformation was a sensitive method to detect subclinical LV dysfunction during acute rejection, we studied LV systolic torsion and diastolic recoil preoperatively and postoperatively in a canine model using myocardial marker techniques.Seven dogs underwent placement of LV subepicardial myocardial markers and creation of mitral regurgitation. Three months later, the animals underwent high-speed, biplane videofluoroscopic analysis for determination of LV systolic function and regional LV systolic torsional deformation and diastolic recoil. The animals then underwent chordal-sparing mitral valve replacement and were restudied 1 to 2 hours postoperatively. One to 2 hours after the cardiac operation, regional maximal systolic torsional deformation decreased significantly in all three LV regions on the lateral LV wall, as well as in the apical and apical-equatorial regions on the anterior wall. During early systole, minimal regional systolic torsion increased significantly in all regions on the lateral wall, as well as in the apical level of the posterior wall. Heterogeneous decreases in torsional deformation were also seen during the early diastolic filling period.Regional systolic torsional deformation and diastolic recoil are markedly perturbed early after a cardiac operation and its associated manipulations. Such changes, however, may potentially serve as sensitive tools to assess the impact of different techniques of intraoperative management, including newer methods of myocardial protection.

Eighteen dogs were randomly chosen to undergo mitral annuloplasty with either a Carpentier-Edwards rigid ring (n = 6 in each group) or a Duran-Medtronic flexible ring or to undergo a sham procedure with an operation, but no ring. Tantalum markers were inserted to measure left ventricular volume and geometry. After 1 and 6 weeks, biplane videofluoroscopic images were obtained during steady-state conditions and during vena caval occlusion. Global and regional systolic function was assessed with load-insensitive indexes. Comparison of all three groups and both times (1 and 6 weeks) showed no significant differences among the three groups in global or regional (basal, equatorial, and apical) left ventricular systolic performance. Furthermore, neither type of annuloplasty ring significantly affected left ventricular pump efficiency, ventricular-arterial coupling ratio, or systolic circumferential contraction and rotation of the basal left ventricular sites.

Previous studies suggest that rigid fixation of the mitral annulus with an annuloplasty ring may impair left ventricular (LV) systolic performance. We used load-insensitive indexes of global and regional LV contractile mechanics to test the hypothesis that rigid fixation of the mitral annulus alters LV systolic function.Global and regional LV systolic mechanics were compared in 10 dogs during two mitral annular conditions: rigidly fixed and freely mobile. Carpentier-Edwards annuloplasty rings (20-24 mm) were inserted using a special buttressing suture technique that permitted alternate cinching of the ring down onto the annulus and subsequent removal away from the annulus. Aortic flow was measured with an electromagnetic flow probe, LV pressure by a micromanometer, and LV wall thickness and three near-orthogonal LV endocardial chamber dimensions using piezoelectric crystals during four sequential ring conditions: 1) down, 2) away, 3) down, and 4) away. The following parameters were analyzed during each ring condition to assess global LV systolic function: end-systolic chamber elastance (end-systolic pressure-volume relation), fiber elastance (end-systolic stress-volume relation), preload recruitable stroke work, and myocardial stress-strain relation. Additionally, regional LV systolic performance was assessed using the end-systolic pressure-diameter relation and a regional analog of preload recruitable stroke work. No significant differences in any of these measurements of LV systolic mechanics were observed between the two mitral annular conditions.Rigid fixation of the mitral annulus alters neither global nor regional LV systolic function in anesthetized, open-chest dogs with normal ventricles.

To determine whether closure of the pericardium after cardiac operations affects the filling characteristics and systolic performance of the left ventricle, we measured left ventricular volume, pressure, cardiac index, and stroke work index in 10 patients between 11 and 15 hours after cardiac operations, with the pericardium first closed and then open. At the time of operation, radiopaque tantalum markers were inserted in the left ventricular myocardium to outline the chamber in the 30-degree right anterior oblique projection, and the pericardium was closed by a continuous polypropylene suture exteriorized at both ends of the sternotomy. The patient was then transferred to the surgical intensive care unit, where left atrial pressure was measured via a fluid-filled catheter, left ventricular pressure with a micromanometer-tipped catheter, and myocardial oxygen consumption via a coronary sinus catheter. Left ventricular volume was measured by computer-aided analysis of fluoroscopic images (recorded at 30 frames per second) of the implanted myocardial markers. Left atrial pressure was maintained at target values of 10, 15, and 20 mm Hg by intravenous augmentation of blood volume. Left ventricular and left atrial pressures and volumes were measured with the pericardium closed; the pericardium was then opened by withdrawal of the pericardial suture. Radiopaque clips on the pericardial edges confirmed opening of the pericardium seconds after withdrawal of the suture. Repeated measurements of left ventricular pressures and volumes were then made at the target left atrial pressures with the pericardium open. End-diastolic volume index, peak positive time derivative of pressure, stroke work index, and cardiac index all increased significantly when the pericardium was opened (p0.001). Thus we found the following: (1) At physiologic pressures, the pericardium had a significant constraining effect on diastolic filling of the left ventricle, and (2) opening of the pericardium resulted in increased cardiac index and stroke work index. These increases may be attributed to the Frank-Starling response to increased left ventricular preload. The demonstrated improvement in left ventricular systolic performance should be considered when contemplating closure of the pericardium after cardiac operations, especially in patients with preoperative left ventricular dysfunction.

The effects of volume overload associated with mitral regurgitation on left ventricular systolic mechanics, energetics, mechanical to external stroke work efficiency, and ventriculoarterial coupling were examined in 11 conscious, closed-chest dogs. Miniature radiopaque tantalum markers were implanted into the myocardium to measure left ventricular volume, and biplane cinefluoroscopic images were obtained 1 week and 3 months after creation of mitral regurgitation. Echocardiographically determined left ventricular mass increased from 116 +/- 28 to 152 +/- 29 gm (p less than 0.001). Left ventricular end-diastolic and end-ejection volumes increased by 24% and 27%, respectively. Global left ventricular systolic performance was assessed by the slopes (linear regression) of the end-systolic pressure-volume and end-systolic stress-volume relationships corrected for change in end-diastolic volume; normalized end-systolic pressure-volume relationships fell by 36% (p less than 0.001), and normalized end-systolic stress-volume relationships declined by 21% (p less than 0.005). The normalized end-systolic volume at 100 mm Hg end-systolic left ventricular pressure increased from 0.63 to 0.75 (p less than 0.05). Similar results were observed based on a nonlinear (quadratic) fit of the end-systolic pressure-volume data. In terms of energetics, the slopes of the stroke volume-end-diastolic volume and pressure-volume area-end-diastolic volume relationships fell significantly, indicating reduced external stroke work and mechanical energy at any given level of preload. Additionally, the efficiency of energy transfer from pressure-volume area to external pressure-volume work at matched end-diastolic volume was 25% lower (p = 0.006) at 3 months compared with the 1-week measurements. While overall effective arterial (or total vascular) elastance tended to decrease after a period of time, the effective ventriculovascular coupling ratio increased from 1.6 +/- 0.6 to 2.7 +/- 1.1 (p less than 0.005), indicating a greater degree of mismatch between the left ventricle and the total (forward and regurgitant) vascular load. Therefore the low pressure-volume overload of mitral regurgitation not only resulted in depressed left ventricular systolic mechanics but also was associated with deterioration of global left ventricular energetics and efficiency and exacerbated mismatch in coupling between the left ventricle and the systemic arterial bed and left atrium.

The importance of the mitral subvalvular apparatus in terms of left ventricular (LV) mechanics and energetic efficiency in the chronically dilated canine heart was assessed in nine dogs with surgically induced mitral regurgitation. Miniature radiopaque tantalum markers were implanted into the myocardium to measure LV volume. Biplane cinefluoroscopic images obtained 1 week and 3 months after creation of mitral regurgitation confirmed the presence of LV dilatation. Mitral valve replacement with preservation of all chordae tendineae was then performed. LV systolic function and derived energetics were then assessed during transient caval occlusion both before and after chordal division by using exteriorized snares. Global LV systolic mechanics, as assessed by the slopes of the end-systolic pressure volume (Ees) and end-systolic stress volume (Ms) relations, fell by 46% (11.7 +/- 2.8 versus 6.3 +/- 1.4 mm Hg/ml, p less than 0.001) and 33% (17.8 +/- 4.0 versus 12.0 +/- 5.1 kdyne/cm5, p = 0.0001), respectively, when the chordae were divided. Chordal severing also increased systolic LV wall stress or LV afterload. In terms of calculated myocardial energetics, the slopes of the stroke work-end-diastolic volume and pressure volume area-end-diastolic volume relations declined significantly by 20% (85 +/- 14 versus 68 +/- 16 mm Hg) and 11% (116 +/- 20 versus 104 +/- 20 mm Hg) after cutting the chordae, thereby indicating reduced external stroke work and mechanical energy generated at any given level of preload. Moreover, the efficiency of energy transfer from pressure volume area to external stroke work fell by 19% (p less than 0.001). Since effective systemic arterial elastance (Ea) did not change, the Ea/Ees ratio (index of ventriculoarterial [V-A] coupling) increased from 0.93 +/- 0.27 to 1.67 +/- 0.62 (p = 0.006). Therefore, chordal division in dilated dog hearts due to chronic mitral regurgitation resulted not only in deterioration of systolic LV mechanics but also deleterious changes in calculated LV energetics and efficiency due to exacerbated mismatch in V-A coupling between the left ventricle and the systemic arterial bed, unfavorable loading conditions, and exhaustion of preload reserve. These observations in the low-pressure, volume-overloaded heart due to chronic mitral regurgitation underscore the importance of the mitral subvalvular apparatus for optimal LV systolic performance and energetic efficiency.

We investigated the possibility that myocardial asynergy (dyscoordinate contraction) is a contributing mechanism to the impairment of cardiac function produced by halothane. Coronary cineangiograms were performed in seven dogs, awake and at 1, 2, and 3 MAC halothane. The relative motions between four arterial bifurcations (six segments) were plotted as an indication of changing ventricular dimensions. To quantitate ventricular asynergy, we calculated anisotropy (AI) and asynchrony (AS), the coefficient of variation of mean shortening (S-) and of mean time to half shortening (T-50), respectively, of the six segments. From these a myocardial performance index (MPI) was derived: MPI = S-/AI + T-50 + AS. In general, S- and MPI decreased with increasing halothane concentration. Anisotropy showed a trend, although usually insignificant, toward increasing, while AS did not change. These observations have two implications. First, asynergy of contraction contributes little, if anything, to halothane-induced impairment of myocardial performance. Second, changes in measurements of intact cardiac performance, such as dP/dtmax, may be reasonably valid during halothane, provided loading conditions are taken into account.

The effects of early volume loading in terms of isovolumetric-phase and ejection-phase indexes of left ventricular systolic function were studied in 12 patients 5 hr after myocardial revascularization, with myocardial markers used to measure left ventricular volume directly and with simultaneous transmural left ventricular pressure measurements by micromanometers. Volume loading (increasing transmural left ventricular end-diastolic pressure from 11 +/- 4 to 15 +/- 5 mm Hg) induced a significant 14% increase in left ventricular end-diastolic volume index (LVEDVI), which was associated (as expected) with significant (p less than .005) augmentation of stroke work (+26%), left ventricular pressure-volume loop area (+35%), and stroke volume index (+22%) and with increments in left ventricular dP/dt and mean velocity of circumferential fiber shortening despite a simultaneous increase in left ventricular afterload. In contrast to previous radionuclide studies, however, left ventricular ejection fraction increased significantly (+9%) and the left ventricular end-systolic pressure-volume ratio did not fall. The relative change in ejection fraction was directly proportional to the increment in LVEDVI (r = .54, p = .03) and inversely related to the change in left ventricular end-systolic volume index (r = -.71, p = .0005). Patients who demonstrated a small or no increase in ejection fraction generally had a larger simultaneous increase in afterload, but one patient exhibited exhaustion of preload reserve. Ejection fraction, as an ejection-phase index of left ventricular performance, is highly dependent on afterload; therefore, interpretation of postoperative changes in ejection fraction must be undertaken only with strict caution.(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular hemodynamics, dimensions and coronary sinus blood flows were measured simultaneously after infusions of dobutamine and dopamine. Ten patients were studied 6, 10 to 15, and 24 hr after cardiopulmonary bypass surgery. The dose of each drug was adjusted to increase cardiac output by 25%. Heart rate was held constant with atrial pacing. Dobutamine and dopamine increased peak left ventricular dP/dt from baseline values by 72% vs 58% during the early study, 77% vs 78% in the intermediate study, and 95% vs 79% in the late study (all NS, difference between drugs). Similarly, there were no significant differences in hemodynamic response or in cardiac dimensions after the two drugs in any period. Both drugs increased myocardial oxygen uptake during the intermediate and late studies (32% vs 33% and 34% vs 25%). With dobutamine this increase was matched by a similar increase in coronary blood flow; however, failure of the expected increase in coronary blood flow with dopamine suggested coronary constriction. Although dobutamine and dopamine have similar hemodynamic effects, dobutamine has the advantage of not limiting the increase in coronary blood flow associated with increased oxygen demand.

The response of the donor left ventricle to atrial pacing was measured in 11 patients 12 to 64 days after cardiac transplantation. At operation seven miniature tantalum coils were placed into the midwall of the donor left ventricle so as to outline the ventricle in a 30 degrees right anterior oblique projection. Computer aided fluoroscopic analysis of marker dynamics allowed calculation of end-diastolic and end-systolic volumes, stroke volume, cardiac output, and ventricular filling characteristics. Recipients were studied in a resting, unsedated state during a period of clinical stability that did not immediately follow or precede an episode of graft rejection. Augmentation of heart rate by an average of 40 beats per minute above sinus rate produced significant reductions in end-diastolic volume (-19%), end-systolic volume (-8%), stroke volume (-31%), and the duration of systole (-19%), and diastole (-40%). Cardiac output was invariant with rate. In all patients, end-diastolic volume reduction at augmented rates was brought about by abbreviated diastolic filling as initiation of contraction occurred at an earlier point on a common, incremental filling curve. Previous studies have shown that the normal inverse relationship between heart rate and stroke volume is not available to the transplanted heart in the immediate postoperative period. The present study shows that this intrinsic mechanism becomes available to the denervated heart in the subsequent recovery period after surgery.