Biomedical subjects

N B Ingels

Publications and source records attributed to N B Ingels.

At least 37 records · Page 2Linked to original sources

PubMed1998

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.

Animals↗

PubMed1998

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.

Acute Disease↗

PubMed1998

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.

Animals↗

PubMed1997

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.

Animals↗

PubMed1997

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.

Animals↗

PubMed1997

Septal function during left ventricular unloading.

BACKGROUND: Left ventricular (LV) unloading with mechanical support devices alters biventricular geometry and impairs right ventricular (RV) contractility, but its effect on septal systolic function remains unknown. METHODS AND RESULTS: To evaluate the effects of LV volume and pressure unloading on septal geometry and function, LV preload was abruptly reduced by clamping left atrial pressure between 0 and -2 mm Hg in seven open-chest, anesthetized dogs by use of a pressure-control servomechanism to withdraw blood from the left atrium. With left atrial pressure clamping, maximal LV pressure decreased 30 +/- 12% (mean +/- SD) (P < .0001) and LV end-diastolic cross-sectional area (determined by two-dimensional echocardiography) decreased by 53 +/- 16% (P < .0001). This caused the septum to shift toward the left (RV septal free-wall dimension increased; P < .004) and flatten (radius of curvature increased; P < .0002), while LV septal free-wall dimension fell (P < .0001). Septal end-diastolic thickness increased 23 +/- 15% (P < .0005), reflecting a decline in septal preload. Systolic septal thickening decreased (P < .002), while systolic septal output (Septal Output = Septal Thickening x Heart Rate) fell from 30 +/- 17 to 15 +/- 22 cm/min (P < .002). This was associated with movement along the septal Frank-Starling equivalent (septal output versus end-diastolic septal thickness [preload] relation) to a less productive portion of the curve. CONCLUSIONS: LV unloading not only altered interventricular septal geometry but also reduced septal systolic thickening and output, all of which may contribute to impaired RV contractility during mechanical LV support.

Animals↗

PubMed1997

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.

Animals↗

PubMed1997

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.

Animals↗

PubMed1997

Myocardial fiber architecture and left ventricular function.

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.

Anisotropy↗

PubMed1997

Effects of mechanical left ventricular support on right ventricular diastolic function.

BACKGROUND: 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. METHODS: 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). RESULTS: During control, full LVAD support did not alter RV tau (104 +/- 67 msec LVAD off versus 109 +/- 49 msec LVAD on, p > 0.50), RV diastolic stiffness (0.56 +/- 0.31 versus 0.51 +/- 0.25 mm Hg/ml, p > 0.20), peak filling rate (107 +/- 51 versus 119 +/- 82 ml/sec, p > 0.35) or mean filling rate during early diastole (32 +/- 28 versus 27 +/- 18 ml/sec, p > 0.40). With right coronary artery occlusion, RV tau rose to 136 +/- 33 msec (p < 0.001), and RV diastolic stiffness fell to 0.29 +/- 0.13 mm Hg/ml (p < 0.005), but there was no change in RV filling rates (p > 0.20). With mechanical LV support during acute RV ischemia, there was no additional change in RV tau, diastolic stiffness, or filling dynamics (p > 0.20). CONCLUSIONS: 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.

Animals↗

PubMed1996

Effects of chordal disruption on regional left ventricular torsional deformation.

BACKGROUND: 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. METHODS AND RESULTS: 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 (P > or = .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 (P > or = .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). CONCLUSIONS: 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.

Animals↗

PubMed1996

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.

Animals↗

PubMed1996

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.

Animals↗

PubMed1996

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.

Animals↗

PubMed1996

Three-dimensional regional dynamics of the normal mitral anulus during left ventricular ejection.

The mitral anulus is a dynamic structure that undergoes alterations in size and shape throughout the cardiac cycle, contracting during systole. Numerous reports have shown this systolic orifice reduction to be due chiefly to posterior annular contraction, whereas the anterior perimeter was unchanged. Segmental motion of the mitral anulus from true in vivo three-dimensional data, however, has not been described. We used radiopaque markers and simultaneous biplane videofluoroscopy to measure the lengths of mitral anular segments in seven closed-chest, sedated dogs. Eight markers were placed equidistant from each other around the mitral anulus, As viewed from the left atrium, segment 1 began at the posteromedial commissure, and the remaining segments were numbered sequentially clockwise around the anulus (that is, the posterior mitral anulus encompassed segments 1 to 4 and the anterior anulus encompassed segments 5 to 8). Marker image coordinates obtained from two orthogonal views 7 to 12 days after implantation were merged to construct three-dimensional marker coordinates at end-diastole and end-systole. From end-diastole to end-systole, mean annular area decreased by 11% +/- 8% (5.5 +/- 0.9 cm2 to 4.9 +/- 0.8 cm2, p = 0.005) and perimeter by 5% +/- 4% (8.8 +/- 0.7 cm to 8.3 +/- 0.7 cm, p < 0.01). Mitral annular segmental percent systolic shortening (negative values indicate lengthening) were as follows (mean +/- standard deviation): segment 1, 7% +/- 9%; segment 2, 8% +/- 10%; segment 3, 16% +/- 6%; segment 4, 10% +/- 7%; segment 5, -4% +/- 5%, segment 6, -7% +/-7%; segment 7, 3% +/- 2%; and segment 8, 6% +/- 5%. With the exception of segment 1, all posterior (2 to 4) and two anterior (7 and 8) mitral annular segments contracted significantly (p < or = vs zero, paired t test). Two anterior annular segments (5 and 6, regions overlapping aortic-mitral continuity), however, unexpectedly lengthened during left ventricular systole. We conclude that the anterior mitral anulus may be a much more dynamic component of the mitral apparatus that previously thought. Such heterogeneous dynamic annular motion should be taken into account when various mitral valve reparative techniques are being designed.

Animals↗

PubMed1996

Left ventricular diastolic suction with zero left atrial pressure in open-chest dogs.

We investigated left ventricular (LV) diastolic volume changes (suction inflows) with left atrial pressure (LAP) clamped to ambient pressure in six open-chest, anesthetized dogs. The left atrium was cannulated and connected to a servo pump, and LAP was clamped to a set point near 0 mmHg for four beats by withdrawing blood. LAP averaged 5.88 +/- 1.44 mmHg before the clamp and fell to 0.74 +/- 0.61 mmHg (P < 0.0001) after the clamp. During the first clamped beat a transmitral pressure gradient of 1.0 +/- 0.6 mmHg was observed, resulting in LV filling of 2.6 +/- 1.8 ml. Subsequent beats developed suction-driven (mean negative LV pressure: -1.5 +/- 1.3 mmHg; P < 0.005 vs. zero) LV filling of 4.5 +/- 2.8 ml/beat with a peak transmitral pressure gradient of 1.7 +/- 0.6 mmHg. These data are consistent with the hypothesis that LV suction can be an important filling mechanism under condition in which LV end-systolic volume is reduced, e.g., reduced filling pressures, high heart rates, exercise, or increased inotropic drive.

Animals↗

PubMed1996

Improving methods of chordal sparing mitral valve replacement. Part I: A new, non-distorting isovolumic balloon preparation for the left ventricle with intact mitral subvalvular apparatus.

BACKGROUND AND AIMS OF THE STUDY: The conventional isovolumic preparation with a single balloon, although employed for many years, distorts the chordae tendineae of the intact mitral apparatus. MATERIAL AND METHODS: Anterior balloon (one balloon inserted via a slit in the anterior leaflet) and double balloon (two balloons through slits in both leaflets) methods were developed and compared to the conventional method and natural conditions (LV filled with saline, or 'gold standard') in six ex-vivo, non-beating porcine hearts. RESULTS: LV volumes measured by the double balloon, anterior balloon, and conventional techniques all correlated highly with natural conditions, but the conventional method had a lower correlation coefficient (r = 0.99, 0.98, p < 0.0001 and < 0.001; and 0.92 p < 0.01, respectively at a left ventricular (LV) pressure of 50 mmHg, while r = 1.00, 1.00, both p < 0.0001; and 0.92, p < 0.01, respectively at 70 mmHg). Epicardial echocardiography revealed that the double balloon technique filled the space behind the chordae while maintaining normal chordal geometry, but the anterior balloon alone did not (p < 0.001). Similarly, the conventional method did not fill the LV outflow tract (p < 0.001) and had a mitral annular shift toward the left atrium (p < 0.001). Photography of both leaflets showed that only the double balloon method maintained normal geometry as assessed by leaflet length ratio; the other methods produced distorted geometry compared to natural filling conditions. CONCLUSIONS: With an intact mitral valve, the double balloon method provides more precise LV pressure-volume measurements while preserving the normal geometry of the chordae tendineae and mitral annulus.

Animals↗

PubMed1996

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.

Animals↗