The role of atrial contraction in mitral valve closure.

BACKGROUND AND AIM OF THE STUDY: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.

The effects of ring annuloplasty on mitral leaflet geometry during acute left ventricular ischemia.

BACKGROUND: The perturbed mitral leaflet geometry that leads to acute ischemic mitral regurgitation during acute left ventricular ischemia has not been quantified, nor is it known whether annuloplasty rings affect these detrimental changes in leaflet geometry. METHODS: Radiopaque markers were implanted on both mitral leaflets and around the anulus in 3 groups of sheep: one group without rings served as the control group (n = 7); the others underwent Duran (n = 6; Medtronic Heart Valve Division, Minneapolis, Minn) or Carpentier-Edwards Physio (n = 5; Baxter Cardiovascular Division, Santa Ana, Calif) ring annuloplasty. After recovery, 3-dimensional marker coordinates were obtained by means of biplane videofluoroscopy before and during acute posterolateral left ventricular ischemia. Leaflet geometry was defined by measuring distances between annular and leaflet markers and perpendicular distances to the leaflet markers from a best-fit annular plane. RESULTS: In all control animals, left ventricular ischemia was associated with acute ischemic mitral regurgitation and apical displacement (away from the annular plane) of the posterior leaflet edge and base markers by 0.6 +/- 0.4 mm (P =.01) and 0.7 +/- 0.2 mm (P <.001), respectively. The distance between the posterior leaflet markers and the mid-posterior anulus did not change significantly during ischemia. The anterior leaflet edge marker extended 1.0 +/- 0. 5 mm (P =.01) away from the mid-anterior anulus during ischemia, but compared with its nonischemic position, the anterior leaflet was not displaced apically away from the annular plane. In all animals in the Duran and Physio groups, leaflet geometry was unchanged during ischemia, and acute ischemic mitral regurgitation was not detected. CONCLUSION: Acute ischemic mitral regurgitation was associated with restricted motion of the posterior leaflet and extension of the anterior leaflet. Annuloplasty rings prevented these geometric perturbations of the mitral leaflets during acute left ventricular ischemia and preserved valvular competence.

Mitral annular dynamics during rapid atrial pacing.

INTRODUCTION: Ovine mitral annular area (MAA) reduction predominantly occurs before ventricular systole. We used the myocardial marker methods to investigate left atrial and MAA dynamics during rapid atrial pacing. METHODS: Seven sheep underwent implantation of 21 myocardial markers around the mitral annulus, the left ventricle and left atrium. After 7 to 10 days, animals were studied with biplane videofluoroscopy to determine 3-dimensional marker coordinates unpaced and during rapid atrial pacing at 140 minutes(-1). Left ventricle volume, left atrial volume (LAV), and MAA were calculated from marker coordinates. End diastole (ED) was defined at peak of the electrocardiogram R wave; times of minimum MAA and minimum LAV were expressed relative to ED (t = 0). Percent reduction in MAA and LAV were calculated from maximum and minimum values between diastole and early systole. RESULTS: The time of minimum MAA occurred earlier relative to ED during rapid pacing compared with control (-48 +/- 21 vs 19 +/- 14 msec; P <.001), as did the time of minimum LAV (-47 +/- 18 vs 4 +/- 16 msec; P <.001). Minimum MAA and LAV were significantly smaller with rapid pacing (6. 8 +/- 0.6 vs 6.5 +/- 0.5 cm(2); P <.05, respectively; and 15.4 +/- 2. 4 vs 16.5 +/- 2.3 mL; P <.01, respectively), and a relatively greater fractional reduction in MAA and LAV was observed during presystole. CONCLUSIONS: Rapid atrial pacing resulted in greater MAA and LAV reduction, both of which occurred entirely during diastole. This study supports the notion that MAA reduction is closely linked to LA dynamics.

Ring annuloplasty prevents delayed leaflet coaptation and mitral regurgitation during acute left ventricular ischemia.

OBJECTIVE: Incomplete mitral leaflet coaptation during acute left ventricular ischemia is associated with end-diastolic mitral annular dilatation and ischemic mitral regurgitation. Annular rings were implanted in sheep to investigate whether annular reduction alone is sufficient to prevent mitral regurgitation during acute posterolateral left ventricular ischemia. METHODS: Radiopaque markers were inserted around the mitral anulus, on papillary muscle tips, and on the central meridian of both mitral leaflets in three groups of sheep: control (n = 5), Physio ring (n = 5) (Baxter Cardiovascular Div, Santa Ana, Calif), and Duran ring (n = 6) (Medtronic Heart Valve Div, Minneapolis, Minn). After 8 +/- 1 days, animals were studied with biplane videofluoroscopy before and during left ventricular ischemia. Annular area was calculated from 3-dimensional marker coordinates and coaptation defined as minimal distance between leaflet edge markers. RESULTS: Before ischemia, leaflet coaptation occurred just after end-diastole in all groups (control 17 +/- 41, Duran 33 +/- 30, Physio 33 +/- 24 ms, mean +/- SD, P >.2 by analysis of variance). During ischemia, regurgitation was detected in all control animals, and leaflet coaptation was delayed to 88 +/- 8 ms after end-diastole (P =.02 vs preischemia). This was associated with increased end-diastolic annular area (8.0 +/- 0.9 vs 6.7 +/- 0.6 cm(2), P =.004) and septal-lateral annular diameter (2.9 +/- 0.1 vs 2.5 +/- 0.1 cm, P =.02). Mitral regurgitation did not develop in Duran or Physio sheep, time to coaptation was unchanged (Duran 25 +/- 25 ms, Physio 30 +/- 48 ms [both P >.2 vs preischemia]), and annular area remained fixed. CONCLUSION: Mitral annular area reduction and fixation with an annuloplasty ring eliminated delayed leaflet coaptation and prevented mitral regurgitation during acute left ventricular ischemia after ring implantation.

Mitral annular dilatation and papillary muscle dislocation without mitral regurgitation in sheep.

BACKGROUND: Asymmetrical mitral annular (MA) dilatation and papillary muscle dislocation are implicated in the pathogenesis of functional mitral regurgitation (MR). METHODS AND RESULTS: To determine the mechanism by which annular and papillary muscle geometric alterations result in MR, we implanted radiopaque markers in the left ventricle, mitral annulus, anterior and posterior mitral leaflets, and papillary muscle tips and bases in 2 groups of sheep. One group served as controls (CTL, n=7); an experimental group (EXP, n=9) underwent topical phenol application to obliterate anterior annular and leaflet muscle (confirmed histologically ex vivo). After 1 week of recovery, markers were imaged with biplane videofluoroscopy, and hemodynamic data were recorded. MA area (computed from 3-dimensional marker coordinates) was 11% to 13% larger in the EXP group than in the CTL group (P<0.05 by ANOVA). This area increase resulted exclusively from intercommissural axis increase except in 1 heart with large (>1 cm) increases in both the intercommissural and septolateral annular axes. The anterior papillary muscle tip in EXP was displaced from CTL by 2.9+/-0.23 mm toward the anterolateral left ventricle and 2.5+/-0.12 mm toward the mitral annulus at end systole; the posterior papillary muscle geometry was unchanged. Transthoracic echocardiography revealed MR only in the heart exhibiting biaxial annular enlargement. CONCLUSIONS: MA dilatation in the intercommissural dimension with anterior papillary muscle tip displacement toward the annulus is insufficient to produce MR in sheep. Functional MR may require MA dilatation in the septolateral axis, as observed with proximal circumflex coronary occlusion.

Potential mechanism of left ventricular outflow tract obstruction after mitral ring annuloplasty.

OBJECTIVES: The purpose of this study was to explore whether geometric changes that predispose to left ventricular outflow tract obstruction after mitral ring annuloplasty are coupled to subvalvular apparatus disturbances. METHODS: Radiopaque markers were implanted in sheep: 9 in the ventricle, 1 in the high interventricular septum, 1 on each papillary muscle tip, 8 around the mitral anulus, 4 on the anterior mitral leaflet, and 2 on the posterior leaflet. One group served as control (n = 5); the others were randomized to undergo annuloplasty with the Duran ring (n = 6; Medtronic, Inc, Minneapolis, Minn) or Carpentier-Edwards Physio ring (n = 6; Baxter Healthcare Corp, Irvine, Calif). After a 7- to 10-day recovery period, 3-dimensional marker coordinates were measured with biplane videofluoroscopy. RESULTS: At the beginning of ejection, (1) the anterior leaflet was displaced toward the left ventricular outflow tract; (2) the normal atrially flexed anterior anulus was flattened into the left ventricular outflow tract; (3) the posterior anulus was displaced toward the left ventricular outflow tract; (4) the anterior papillary muscle was displaced septally; and (5) the posterior papillary muscle was dislocated inwardly toward the anterior papillary muscle in the Physio ring group compared with the control group. During ejection, all these structures moved septally, encroaching further on the left ventricular outflow tract. In the Duran ring group, only the posterior anulus was displaced toward the left ventricular outflow tract; the anterior leaflet was not displaced toward the left ventricular outflow tract, and it did not move septally during ejection. CONCLUSIONS: The semirigid Physio ring was associated with perturbations in annular dynamics that caused changes in papillary muscle geometry. We propose an integrated valvular-subvalvular mechanism to explain displacement of the anterior leaflet into the left ventricular outflow tract after mitral ring annuloplasty.

Mitral annular size and shape in sheep with annuloplasty rings.

BACKGROUND: Mitral annuloplasty is an important element of most mitral repairs, yet the effects of various types of annuloplasty rings on mitral annular dynamics are still debated. Recent studies suggest that flexible rings preserve physiologic mitral annular area change during the cardiac cycle, while rigid rings do not. METHODS: To clarify the effects of mitral ring annuloplasty on mitral annular dynamic geometry, we sutured 8 radiopaque markers equidistantly around the mitral anulus in 3 groups of sheep (n = 7 each: no ring, Carpentier-Edwards semi-rigid Physio-Ring [Baxter Healthcare Corp, Edwards Division, Santa Ana, Calif], and Duran flexible ring [Medtronic, Inc, Minneapolis, Minn]). Ring sizes were selected according to anterior leaflet area and inter-trigonal distance (Physio-Ring 28 mm, n = 7; Duran ring 31 mm, n = 5, and 29 mm, n = 2). After 8 +/- 1 days of recovery, the sheep were sedated and studied by means of biplane videofluoroscopy. Mitral annular area was calculated from 3-dimensional marker coordinates without assuming circular or planar geometry. RESULTS: In the no ring group, mitral annular area varied during the cardiac cycle by 11% +/- 2% (mean +/- SEM; maximum = 7.6 +/- 0.2, minimum = 6.8 +/- 0.2 cm2; P

Restricted posterior leaflet motion after mitral ring annuloplasty.

BACKGROUND: The effects of ring annuloplasty on mitral leaflet motion are incompletely known. The three-dimensional dynamics of the mitral valve in vivo were examined to determine how two types of annuloplasty rings affect leaflet motion during valve closure. METHODS: Miniature radiopaque markers on the mitral leaflets, annulus, and left ventricle were implanted in three groups of sheep. One group served as control (n = 7); other sheep were randomly assigned to receive either a flexible Duran (n = 6) or a semirigid Carpentier-Edwards Physio ring (n = 6). After recovery, three-dimensional marker coordinates were computed from simultaneous (60 Hz) biplane videofluoroscopic marker images. RESULTS: Both types of rings immobilized the middle scallop of the posterior leaflet without affecting anterior leaflet motion. The excursion of the anterior leaflet edge from maximally open to fully closed was not different between the groups (control, 13+/-2 mm; Duran 13+/-1 mm; Physio ring, 14+/-1 mm; p > 0.05), but posterior leaflet edge excursion was restricted (control, 7.4+/-0.4 mm; 2.3+/-0.3 mm [p < 0.001]; Physio, 2.7+/-0.2 mm [p < 0.001]) by both rings. CONCLUSIONS: Mitral annuloplasty with either ring type markedly reduced the mobility of the central posterior leaflet in normal ovine hearts such that valve closure became essentially a single (anterior) leaflet process with the frozen posterior leaflet serving only as a buttress for closing.

Semirigid or flexible mitral annuloplasty rings do not affect global or basal regional left ventricular systolic function.

BACKGROUND: 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. METHODS AND RESULTS: 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 (P > 0.05, MANOVA). Furthermore, neither annuloplasty ring perturbed the regional pattern of basal LV systolic function. CONCLUSIONS: 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.

Effects of partial left ventriculectomy on left ventricular geometry and wall stress in excised porcine hearts.

BACKGROUND AND AIMS OF THE STUDY: Partial left ventriculectomy (PLV, the "Batista procedure") has received recent attention as a surgical treatment for patients with dilated cardiomyopathy and end-stage congestive heart failure; however, the mechanisms responsible for the purported short-term improvement in left ventricular (LV) function are poorly characterized. This study examined the effects of PLV on three-dimensional (3-D) LV geometry, wall stress and passive LV mechanics in excised porcine hearts. METHODS: Thirty-three radio-opaque tantalum markers were placed into the LV wall of nine freshly excised, porcine hearts (arrested with cold crystalloid cardioplegia) to measure three dimensional LV geometry and volume. Simultaneous biplane video-fluoroscopic marker images and LV pressure (LVP) were obtained over a wide range of LV volumes generated with an intracavitary LV balloon. Measurements were repeated after excision of a diamond-shaped wedge of the lateral LV wall between the papillary muscles (mean: 8 x 3 x 2 cm; 10 +/- 2% of LV mass). RESULTS: Following PLV, the ventricle assumed a more elliptical shape (LV eccentricity rose from 0.71 +/- 0.15 to 0.81 +/- 0.09, p < 0.01). Circumferential radius of curvature fell in the anterior, lateral and posterior regions at the equatorial level (p < 0.01), while the posterior wall longitudinal radius of curvature increased at the basal, equatorial and apical levels (p < 0.01). No change in the longitudinal radius of curvature was observed in the other walls. These changes were associated with a fall in average equatorial LV wall stress from 176 +/- 34 to 159 +/- 30 kdyne/cm2 (p < 0.02). Myocardial stiffness (slope of the LV stress-strain relation) fell from 12.4 +/- 4.0 to 10.0 +/- 3.4 (p < 0.004), indicating lower global LV wall stress at any given LV size. CONCLUSIONS: In flaccid porcine hearts, the left ventricle became more elliptical and chamber size decreased after PLV, which resulted in lower regional LV wall stress and myocardial stiffness. LV ellipticalization may improve systolic LV performance by decreasing regional LV afterload (e.g., systolic wall stress), which would thereby lower myocardial oxygen consumption and improve LV pump efficiency.

Early systolic mitral leaflet "loitering" during acute ischemic mitral regurgitation.

BACKGROUND: The mechanism by which incomplete mitral leaflet coaptation develops during ischemic mitral regurgitation is debated, with recent studies suggesting that incomplete mitral leaflet coaptation may be due to apically displaced papillary muscle tips. Yet quantitative in vivo three-dimensional mitral leaflet motion during ischemic mitral regurgitation has never been described. METHODS: Radiopaque markers (sutured around the mitral anulus, to the central free mitral leaflet edges, and to both papillary muscle tips and bases) were imaged with the use of biplane videofluoroscopy in six closed-chest, sedated sheep before (control) and during induction of acute ischemic mitral regurgitation. Leaflet coaptation was defined as the minimum distance measured between edge markers during control conditions. RESULTS: During control, leaflet coaptation occurred 23 +/- 7 msec (mean +/- standard error of the mean) after end-diastole, when left ventricular pressure was 27 +/- 6 mm Hg. During ischemic mitral regurgitation, coaptation was delayed to 115 +/- 19 msec after end-diastole (p < or = 0.01 vs control [n = 4]) when left ventricular pressure was 88 +/- 4 mm Hg. At end-diastole during ischemic mitral regurgitation, the mitral anulus area was 14% +/- 2% larger than control (7.4 +/- 0.3 cm2 vs 6.5 +/- 0.2 cm2, p < or = 0.005) as the result of the lengthening of muscular annular regions (76.0 +/- 2.5 mm vs 70.5 +/- 1.4 mm, p < or = 0.01). Mitral anulus shape (ratio of two diameters) at end-diastole was more circular during ischemic mitral regurgitation (0.79 +/- 0.01 vs 0.71 +/- 0.02, p < 0.01). At end-diastole during ischemic mitral regurgitation, the posterior papillary muscle tip was displaced 1.5 +/- 0.5 mm laterally and 2.0 +/- 0.6 mm posteriorly (p < or = 0.02 vs control), but there was no apical displacement of either papillary muscle tip. CONCLUSIONS: Incomplete mitral leaflet coaptation during acute ischemic mitral regurgitation occurred early in systole, not at end-systole, and was due to "loitering" of the leaflets associated with posterior mitral anulus enlargement and circularization, as well as some posterolateral, but not apical, posterior papillary muscle tip displacement. These data suggest that early systolic mitral anulus dilatation and shape change and altered posterior papillary muscle motion are the primary mechanisms by which incomplete mitral leaflet coaptation occurs during acute ischemic mitral regurgitation.

Mitral valve opening in the ovine heart.

To study the three-dimensional size, shape, and motion of the mitral leaflets and annulus, we surgically attached radiopaque markers to sites on the mitral annulus and leaflets in seven sheep. After 8 days of recovery, the animals were sedated, and three-dimensional marker positions were measured by computer analysis of biplane videofluorograms (60/s). We found that the oval mitral annulus became most elliptical in middiastole. Both leaflets began to descend into the left ventricle (LV) during the rapid fall of LV pressure (LVP), before leaflet edge separation. The anterior leaflet exhibited a compound curvature in systole and maintained this shape during opening. The central cusp of the posterior leaflet was curved slightly concave to the LV during opening. Markers at the border of the "rough zone" were separated by 10 mm during systole. We conclude that coaptation occurs very near the leaflet edges, that the annulus and leaflets move toward their open positions during the rapid fall of LVP, and that leaflet edge separation, the last event in the opening sequence, occurs near the time of minimum LVP.

Most ovine mitral annular three-dimensional size reduction occurs before ventricular systole and is abolished with ventricular pacing.

BACKGROUND: 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. METHODS AND RESULTS: 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% (P< or =.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 (P< or =.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. CONCLUSIONS: 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.

Geometric determinants of ischemic mitral regurgitation.

BACKGROUND: The precise geometric determinants of ischemic mitral regurgitation (MR) are incompletely understood, although such knowledge is important to improve mitral valve reparative techniques. METHODS AND RESULTS: 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. CONCLUSIONS: 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.

Complete unloading alone may not adequately protect the left ventricle.

BACKGROUND: The benefit of left ventricular (LV) unloading for preserving LV function is commonly accepted, but its efficacy remains incompletely defined. METHODS: We studied the influence of complete LV unloading on LV systolic and diastolic mechanics using an in situ isovolumic preparation with two different coronary perfusion pressures (CPPs) in 12 dogs during prolonged normothermic cardiopulmonary bypass. RESULTS: Multivariate analysis of covariance with time as a covariate revealed that a high CPP (143 +/- 36 mm Hg; n = 6) was associated with better preservation of systolic LV function over time as assessed by LV end-systolic elastance (p < 0.001) and the end-systolic pressure-volume relation physiologic intercept (p < 0.001) compared with a moderate CPP (107 +/- 18 mm Hg; p < 0.005 versus a high CPP by t-test; n = 6). Dobutamine (2 micrograms.kg-1.min-1) improved LV end-systolic elastance (p < 0.005) and LV physiologic intercept (p < 0.01) only in the high-CPP group. Conversely, impaired LV diastolic function (as measured by LV stiffness) was observed (p < 0.001) with a high CPP, but did not change with a moderate CPP. CONCLUSIONS: These observations in canine hearts suggest that complete LV unloading may not preserve LV systolic function adequately over time when CPP is maintained in the accepted clinical range. A higher CPP is required to prevent deterioration over prolonged cardiopulmonary bypass times, but diastolic dysfunction still occurs.

Papillary muscle-left ventricular wall "complex".

OBJECTIVES: Mitral valve homografts, despite theoretical advantages, are not widely used, in part because of lack of basic information about the three-dimensional geometry of the mitral apparatus. METHODS: Radiopaque markers were used in the study of eight closed-chest dogs under four conditions: (1) baseline, (2) caval occlusion, (3) tachycardia (atrial pacing), and (4) nitroprusside infusion. Using a cylindrical coordinate system. defined with the origin at the midpoint between the anterior and posterior commissures, and the left ventricular long axis (z-axis), defined by the origin and the left ventricular apex, DTIP-MA (the z-coordinate [millimeters] of the papillary muscle tip), was measured at 10 time points throughout the entire cardiac cycle. DBASE-MA (the z-coordinate of the papillary muscle base) and LPM (the length of the papillary muscle [millimeters]) were also measured. RESULTS: DTIP-MA varied slightly with time (p < 0.001 by analysis of variance), but the magnitude of change was negligible (< 0.9 mm) (e.g., DTIP-MA of the anterior papillary muscle was 20.7 +/- 2.7/20.8 +/- 2.8 [end-diastolic/end-systolic, mean +/- 1 standard deviation]; DTIP-MA of the posterior papillary muscle was 25.8 +/- 4.8/25.5 +/- 4.5). DTIP-MA was minimally influenced by the above perturbations. DBASE-MA and LPM of each papillary muscle, however, changed throughout the cardiac cycle (p < 0.001 by analysis of variance) by about 4 mm, and both parameters were dependent on loading conditions. CONCLUSIONS: Papillary muscle length changed to keep the DTIP-MA distance constant such that the papillary muscle and left ventricular wall functioned together as a unit ("J-shaped complex"). These results provide a physiologic rationale for measuring DTIP-MA, define its potential surgical usefulness, and imply that using the entire length of the donor's papillary muscle (i.e., maintaining the entire J-shaped complex) is important in operations in which homograft or stentless xenograft mitral valves are used.

Loss of three-dimensional canine mitral annular systolic contraction with reduced left ventricular volumes.

BACKGROUND: 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. METHODS AND RESULTS: 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% (*P < or = .05 versus zero changes, paired t test). CONCLUSIONS: 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.

Three-dimensional dynamic geometry of the normal canine mitral annulus and papillary muscles.

BACKGROUND: 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. METHODS AND RESULTS: 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. CONCLUSIONS: 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.

Three-dimensional dynamics of the canine mitral annulus during ischemic mitral regurgitation.

BACKGROUND: It has been suggested that ischemic mitral regurgitation results, at least in part, from generalized end-systolic mitral annulus (MA) dilatation, but the role of the MA is incompletely understood and the segmental dynamics of the MA during left ventricular ischemia have not been described. METHODS: We used radiopaque markers and simultaneous biplane videofluoroscopy to measure three-dimensional in vivo lengths of eight MA segments in 7 sedated dogs before and after induction of ischemic MR (produced by circumflex coronary artery balloon occlusion and verified by Doppler echocardiography). As viewed from the left atrium, the MA segment between markers 1 and 2 (S12) was defined as starting at the posteromedial commissure, and remaining segments were numbered sequentially clockwise around the MA (ie, the posterior MA encompassed S12, S23, S34, S45,; the anterior MA included S56, S67, S78, S81). Marker images obtained 7 to 12 days after implantation were used to construct x, y, and z coordinates of each marker at end-diastole and end-systole. RESULTS: During regional (posterolateral walls) left ventricular ischemia, the end-systolic MA area increased (4.9 +/- 0.8 cm2 [control] versus 5.9 +/- 0.6 cm2; p = 0.005). End-systolic MA segment lengths were as follows (control, ischemia [mm, mean +/- standard deviation]): S12 = 9 +/- 2, 10 +/- 3; S23 = 10 +/- 2, 12 +/- 3; S34 = 13 +/- 1, 15 +/- 1; S45 = 8 +/- 2, 9 +/- 2; S56 = 11 +/- 2, 11 +/- 2; S67 = 12 +/- 2, 12 +/- 2; S78 = 10 +/- 3, 11 +/- 2; and S81 = 11 +/- 1, 12 +/- 1. Values for S12, S23, S34, and S81 were significant (p < or = 0.05 for control versus ischemia by paired t test). CONCLUSIONS: During ischemic mitral regurgitation, the MA enlarged at end-systole, but in an asymmetric manner; most posterior annular segments lengthened, whereas most anterior annular segment lengths did not change. These data suggest that alterations in regional MA mechanics may be important in the pathogenesis of ischemic mitral regurgitation. Further three-dimensional studies of MA dynamics and shape should be conducted so that new knowledge may result in improved mitral valve surgical techniques.

Improving methods of chordal-sparing mitral valve replacement--Part II: Optimal tension for chordal resuspension.

BACKGROUND AND AIMS OF THE STUDY: 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. METHODS: 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. RESULTS: 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 (p < 0.05 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 (p < 0.05 by rm-ANOVA). Arrhythmias precluding satisfactory measurements occurred in two dogs at 30 or 40 gm CT tension. CONCLUSIONS: 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.