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Biomedical subjects

D Craig Miller

Publications and source records attributed to D Craig Miller.

At least 37 records · Page 2Linked to original sources

Altered mitral valve kinematics with atrioventricular and ventricular pacing.

BACKGROUND AND AIM OF THE STUDY: Pacing-induced mitral regurgitation contributes to the 'pacemaker syndrome', which usually is observed with ventricular (V) pacing, but has also been reported with atrioventricular (AV) sequential pacing. Effects of different pacing modes on 3-D kinematics of the mitral apparatus are incompletely understood. METHODS: Radio-opaque markers were placed on the left ventricular (LV) and mitral apparatus including the annulus, leaflets and papillary muscles of eight sheep. Hemodynamic and 3-D dynamic marker geometry were obtained one week later with biplane videofluoroscopy (60 Hz) during atrial (pacing site = left atrium), AV-sequential (140 ms interval) and (anterolateral LV epicardial) ventricular pacing. RESULTS: Compared with A-pacing (*p <0.05): 1) The regurgitant fraction increased with both AV- and V-pacing (A: 6 +/- 3%, AV: 13 +/- 3%*, V: 15 +/- 2%*); 2) AV and V-pacing delayed closure at the leaflet center (A: 21 +/- 10 ms, AV: 52 + 5 ms*, V: 92 +/- 6 ms*) and posterior commissure (A: 17 +/- 10 ms, AV: 46 +/- 8 ms*, V: 94 +/- 6 ms*). V-pacing delayed valve closure at the anterior commissure (A: 27 +/- 9 ms, V: 94 +/- 6 ms*); 3) The end-diastolic leaflet opening angle was greater with AV- and V-pacing (anterior mitral leaflet (AML): A: 32 +/- 2 degrees, AV: 41 +/- 4 degrees*, V: 46 +/- 4 degrees*; posterior mitral leaflet (PML): A: 56 +/- 4 degrees, AV: 62 +/- 3 degrees*, V: 68 +/- 3 degrees*); 4) 'Effective' end-diastolic PML midline length was reduced with AV- and V-pacing (A: 11.2 +/- 0.7 mm, AV: 10.0 +/- 0.4 mm*, V: 10.2 +/- 0.3 mm*), as was the distance from each papillary muscle (PM) tip to the AML edge ('effective' chordal length) close to the commissures (anterior PM-AML: A: 31.5 +/-1.8 mm, AV: 30.5 +/- 1.9 mm*, V: 29.7 +/- 1.8 mm*; posterior PM-AML: A: 33.7 +/- 1.8 mm, AV: 33.1 +/- 1.9 mm*, V: 32.8 +/- 1.9 mm*). CONCLUSION: Both ventricular and AV-sequential-pacing resulted in a more widely opened valve at end-diastole and leaflet dyssynchrony with delayed mitral valve closure and early systolic mitral regurgitation. These alterations which result in pacing-induced mitral regurgitation may be clinically important in patients with impaired LV function.

Animals↗

Effect of cutting second-order chordae on in-vivo anterior mitral leaflet compound curvature.

BACKGROUND AND AIM OF THE STUDY: Leaflet curvature determines leaflet stress. In order to assess the influence of second-order chordae (2 degrees CT) on anterior mitral valve leaflet (AMVL) geometry, AMVL curvature was measured before (Baseline) and after (CUT) cutting the 2 degrees CT. METHODS: Miniature radiopaque markers were sutured onto the AMVL in eight sheep: four along the central-meridian from mid-septal annulus to the free-margin; and one each at the 2 degrees CT insertion. Biplane videofluoroscopic data were acquired (open-chest) before and after CUT. Marker-triplet 3-D coordinates were used to calculate radii-of-curvature at LVPmax along the central-meridian (ROCm) and across the AMVL belly (commissure-commissure axis, ROCc-c). RESULTS: CUT did not change LVPmax (111 +/- 12 versus 106 +/- 11 mmHg; p = 0.19). At baseline, the AMVL central-meridian had compound curvature: Convex to the left ventricle near the annulus (-ROCm) and concave near the free-margin (+ROCm). After CUT, the AMVL flattened: ROCm increased near the annulus (from -1.37 +/- 0.52 to -12.58 +/- 29.04 cm; p = 0.02), but did not change near the edge. In the commissure-commissure axis, ROCc-c was concave to the left ventricle at baseline and increased after CUT in all eight animals. In five sheep, ROCc-c was increased (from 1.93 +/- 1.01 to 2.80 +/- 1.36 cm; p = 0.03), but in three sheep ROCc-c was increased and inverted (from 3.65 +/- 2.17 to -1.72 +/- 0.53 cm; p = 0.03), becoming convex to the left ventricle. CONCLUSION: Compound curvature along the AMVL central-meridian appears to be an intrinsic leaflet property that persists even without support from second-order chordae, whereas concave curvature in the commissure-commissure axis is more dependent on intact second-order chordae. Leaflet compound curvature must be incorporated into future finite element models to characterize leaflet stresses accurately. The importance of second-order chordae in maintaining leaflet shape must be considered during mitral repair. A larger ROC increases leaflet stresses, while reversal of ROC changes tensile stress to compressive stress; this might trigger deleterious leaflet remodeling after chordal cutting.

Animals↗

Transmural cardiac strains in the lateral wall of the ovine left ventricle.

The constant-volume property of contracting cardiac muscle has been invoked in models of heart wall mechanics that predict that systolic subendocardial left ventricular (LV) wall thickening must significantly exceed subepicardial thickening. To examine this prediction, we implanted arrays of radiopaque markers to measure lateral equatorial wall transmural strains and global and regional LV geometry in seven sheep and studied the four-dimensional dynamics of these arrays using biplane videofluoroscopy (60 Hz) in anesthetized intact animals 1 and 8 wk after surgery. A transmural gradient of systolic lateral wall thickening was observed at 1 wk (P = 0.009; linear regression) but was no longer present at 8 wk (P = 0.243). Referenced to end diastole, group mean (+/-SD) end-systolic radial subepicardial, midwall, and subendocardial wall thickening strains were, respectively, 0.08 +/- 0.08, 0.14 +/- 0.08, and 0.22 +/- 0.12 at 1 wk and 0.19 +/- 0.07 (P = 0.02; 1 vs. 8 wk), 0.20 +/- 0.04, and 0.23 +/- 0.07 at 8 wk. With the exception of an 8-ml (7%) increase in end-diastolic volume (P = 0.04) from 1 to 8 wk, LV shape and hemodynamics were otherwise unchanged. We conclude that equivalent hemodynamics can be generated by the left ventricle with or without a transmural gradient of systolic wall thickening in this region; thus such a gradient is unlikely to be a fundamental property of the contracting LV myocardium. We discuss some implications of these findings regarding mechanisms involved in systolic wall thickening.

Animals↗

Direct measurement of transmural laminar architecture in the anterolateral wall of the ovine left ventricle: new implications for wall thickening mechanics.

Laminar, or sheet, architecture of the left ventricle (LV) is a structural basis for normal systolic and diastolic LV dynamics, but transmural sheet orientations remain incompletely characterized. We directly measured the transmural distribution of sheet angles in the ovine anterolateral LV wall. Ten Dorsett-hybrid sheep hearts were perfusion fixed in situ with 5% buffered glutaraldehyde at end diastole and stored in 10% formalin. Transmural blocks of myocardial tissue were excised, with the edges cut parallel to local circumferential, longitudinal, and radial axes, and sliced into 1-mm-thick sections parallel to the epicardial tangent plane from epicardium to endocardium. Mean fiber directions were determined in each section from five measurements of fiber angles. Each section was then cut transverse to the fiber direction, and five sheet angles (beta) were measured and averaged. Mean fiber angles progressed nearly linearly from -41 degrees (SD 11) at the epicardium to +42 degrees (SD 16) at the endocardium. Two families of sheets were identified at approximately +45 degrees (beta(+)) and -45 degrees (beta(-)). In the lateral region (n = 5), near the epicardium, sheets belonged to the beta(+) family; in the midwall, to the beta(-) family; and near the endocardium, to the beta(+) family. This pattern was reversed in the basal anterior region (n = 4). Sheets were uniformly beta(-) over the anterior papillary muscle (n = 2). These direct measurements of sheet angles reveal, for the first time, alternating transmural families of predominant sheet angles. This may have important implications in understanding wall mechanics in the normal and the failing heart.

Animals↗

Alterations in left ventricular torsion and diastolic recoil after myocardial infarction with and without chronic ischemic mitral regurgitation.

BACKGROUND: Chronic ischemic mitral regurgitation (CIMR) is associated with heart failure that continues unabated whether the valve is repaired, replaced, or ignored. Altered left ventricular (LV) torsion dynamics, with deleterious effects on transmural gradients of oxygen consumption and diastolic filling, may play a role in the cycle of the failing myocardium. We hypothesized that LV dilatation and perturbations in torsion would be greater in animals in which CIMR developed after inferior myocardial infarction (MI) than in those that it did not. METHODS: 8+/-2 days after marker placement in sheep, 3-dimensional fluoroscopic marker data (baseline) were obtained before creating inferior MI by snare occlusion. After 7+/-1 weeks, the animals were restudied (chronic). Inferior MI resulted in CIMR in 11 animals but not in 9 (non-CIMR). End-diastolic septal-lateral and anterior-posterior LV diameters, maximal torsional deformation (phi(max), rotation of the LV apex with respect to the base), and torsional recoil in early diastole (phi(5%), first 5% of filling) for each LV free wall region (anterior, lateral, posterior) were measured. RESULTS: Both CIMR and non-CIMR animals demonstrated derangement of LV torsion after inferior MI. In contrast to non-CIMR, CIMR animals exhibited greater LV dilation and significant reductions in posterior maximal torsion (6.1+/-4.3 degrees to 3.9+/-1.9 degrees * versus 4.4+/-2.5 degrees to 2.8+/-2.0 degrees; mean+/-SD, baseline to chronic, *P<0.05) and anterior torsional recoil (-1.4+/-1.1 degrees to -0.2+/-1.0 degrees versus -1.2+/-1.0 degrees to -1.3+/-1.6 degrees ). CONCLUSIONS: MI associated with CIMR resulted in greater perturbations in torsion and recoil than inferior MI without CIMR. These perturbations may be linked to more LV dilation in CIMR, which possibly reduced the effectiveness of fiber shortening on torsion generation. Altered torsion and recoil may contribute to the "ventricular disease" component of CIMR, with increased gradients of myocardial oxygen consumption and impaired diastolic filling. These abnormalities in regional torsion and recoil may, in part, underlie the "ventricular disease" of CIMR, which may persist despite restoration of mitral competence.

Animals↗

Undersized mitral annuloplasty alters left ventricular shape during acute ischemic mitral regurgitation.

BACKGROUND: Underlying left ventricular (LV) dysfunction contributes to poor survival after operation to correct ischemic mitral regurgitation (IMR). Many surgeons do not appreciate that a key component of the Bolling undersized mitral ring annuloplasty concept is to decrease LV wall stress by altering LV shape, but precise 3-dimensional (3-D) geometric data do not exist substantiating this effect. We tested the hypothesis that annular reduction decreases regional circumferential LV radius of curvature (ROC) in a model of acute IMR. METHODS: Eight adult sheep underwent insertion of an adjustable Paneth-type annuloplasty suture and radiopaque markers on the LV and mitral annulus. The animals were studied with biplane videofluoroscopy during baseline conditions, then before and after tightening the annuloplasty suture during proximal left circumflex occlusion. End-systolic circumferential regional LV ROC and mitral annular area were computed. RESULTS: Acute IMR was eliminated (MR grade 2.1+/-0.4 to 0.4+/-0.4, mean+/-SD, P<0.05) by tightening the Paneth annuloplasty suture. Paneth suture tightening during circumflex occlusion also decreased end-systolic regional circumferential radii of curvature at the basal (anterior, 3.40+/-0.16 to 3.34+/-0.14 cm; posterior, 3.31+/-0.23 to 3.24+/-0.26 cm; P<0.05) and equatorial levels (anterior, 2.99+/-0.21 to 2.89+/-0.29 cm; posterior, 2.86+/-0.38 to 2.81+/-0.41 cm; P<0.05). CONCLUSIONS: Acute proximal circumflex occlusion caused IMR and increased end-systolic LV radii of curvature in this experimental preparation. Annular reduction sufficient to abolish IMR also decreased end-systolic anterior and posterior LV ROC, which would be expected to reduce LV wall stress and oxygen consumption in these regions, both potentially beneficial effects. The long-term effects of undersized annuloplasty on LV remodeling and function, however, will require further study in chronic animal preparations or patients with chronic IMR.

Acute Disease↗

Cutting second-order chords does not prevent acute ischemic mitral regurgitation.

BACKGROUND: Cutting anterior mitral leaflet second-order chordae has been proposed for repair in ischemic mitral regurgitation (IMR). We examined the efficacy of such chordal cutting in preventing acute IMR. METHODS AND RESULTS: Six sheep underwent radiopaque marker placement (left ventricle, mitral annulus, papillary muscles [PMs], and leaflets). The largest second-order chord from each PM was encircled with exteriorized wire snares. Three-dimensional marker coordinates were obtained with biplane videofluoroscopy before and during acute ischemia (80 seconds of mid-circumflex occlusion). Color Doppler transesophageal echocardiography was used to grade MR on a 0 to 4+ scale. Data were acquired immediately before and after dividing second-order chordae. Slope of the end-diastolic volume-stroke work relationship (PRSW) was calculated to assess systolic function. Chordal cutting increased anterior leaflet inflection angle (155+/-12 versus 162+/-9 degrees; P=0.03), resulting in a flatter leaflet, but did not increase effective leaflet length (1.97+/-0.24 versus 2.08+/-0.23 cm; P=0.15); PRSW decreased (63+/-15 versus 56+/-12 mm Hg; P=0.008). Both before and after chordal cutting, ischemia caused: Septal-lateral annular dilation (P=0.005), posterior PM displacement away from the mid-septal annulus (P=0.06), increased leaflet tenting area (P=0.001), and increased leaflet tenting volume (P=0.002). Before chordal cutting, MR increased significantly during ischemia (0.5+/-0.3 versus 1.7+/-0.4; P<0.001), and IMR increased similarly even after the second-order chords were cut (0.7+/-0.4 versus 1.9+/-0.9; P<0.001). CONCLUSIONS: Cutting second-order chordae resulted in LV systolic dysfunction and neither prevented nor decreased the severity of acute IMR, septal-lateral annular dilation, leaflet tenting area, or leaflet tenting volume.

Acute Disease↗

Importance of mitral valve second-order chordae for left ventricular geometry, wall thickening mechanics, and global systolic function.

BACKGROUND: Mitral valvular-ventricular continuity is important for left ventricular (LV) systolic function, but the specific contributions of the anterior leaflet second-order "strut" chordae are unknown. METHODS AND RESULTS: Eight sheep had radiopaque markers implanted to silhouette the LV, annulus, and papillary muscles (PMs); 3 transmural bead columns were inserted into the mid-lateral wall between the PMs. The strut chordae were encircled with exteriorized wire snares. Three-dimensional marker images and hemodynamic data were acquired before and after chordal cutting. Preload recruitable stroke work (PRSW) and end-systolic elastance (E(es)) were calculated to assess global LV systolic function (n=7). Transmural strains were measured from bead displacements (n=4). Chordal cutting caused global LV dysfunction: E(es) (1.48+/-1.12 versus 0.98+/-1.30 mm Hg/mL, P=0.04) and PRSW (69+/-16 versus 60+/-15 mm Hg, P=0.03) decreased. Although heart rate and time from ED to ES were unchanged, time of mid-ejection was delayed (125+/-18 versus 136+/-19 ms, P=0.01). Globally, the LV apex and posterior PM tip were displaced away from the fibrous annulus and LV base-apex length increased at end-diastole and end-systole (all +1 mm, P<0.05). Locally, subendocardial end-diastolic strains occurred: Longitudinal strain (E22) 0.030+/-0.013 and radial thickening (E33) 0.081+/-0.041 (both P<0.05 versus zero). Subendocardial systolic shear strains were also perturbed: Circumferential-longitudinal "micro-torsion" (E12) (0.099+/-0.035 versus 0.075+/-0.025) and circumferential radial shear (E13) (0.084+/-0.023 versus 0.039+/-0.008, both P<0.05). CONCLUSIONS: Cutting second-order chords altered LV geometry, remodeled the myocardium between the PMs, perturbed local systolic strain patterns affecting micro-torsion and wall-thickening, and caused global systolic dysfunction, demonstrating the importance of these chordae for LV structure and function.

Animals↗

Effects of paracommissural septal-lateral annular cinching on acute ischemic mitral regurgitation.

BACKGROUND: Previous experimental studies demonstrated that central septal-lateral (SL) annular cinching (SLAC) abolishes acute ischemic mitral regurgitation (IMR), but whether localized cinching near the anterior (ACOM) or posterior (PCOM) commissure is equally effective is unknown. METHODS: Six adult sheep underwent implantation of 9 radiopaque markers on the left ventricle, 8 around the mitral annulus (MA) and 1 on each papillary muscle (PM) tip. Transannular SL sutures were placed at the valve center (CENT) and near ACOM and PCOM and externalized. Acute IMR was induced by proximal circumflex coronary snare occlusion. Biplane videofluoroscopy and transesophageal echocardiography were performed before and continuously during 3 episodes of myocardial ischemia including 20 seconds of SLAC at each different location. End-systolic MA SL dimension at each suture location and distances between the anterior and posterior PM tips and mid-septal annulus ("saddle horn") were calculated from the 3-dimensional (3D) marker coordinates. RESULTS: SLAC interventions in all 3 locations reduced the degree of IMR, but cinching at the center, SLAC(CENT), had a significantly greater effect on reducing the magnitude of IMR than SLAC(PCOM) or SLAC(ACOM) (mean grade of IMR reduction=1.0+/-0.5, 1.8+/-0.5, and 0.9+/-0.2 for SLAC(ACOM), SLAC(CENT), and SLAC(PCOM), respectively; P=0.044). Although ACOM and PCOM cinching reduced SL(CENT) somewhat, only SLAC(CENT) simultaneously reduced both SL(ACOM) and SL(PCOM) and also repositioned both PM tips closer to the annular saddle horn. CONCLUSIONS: SLAC in all 3 positions reduced acute IMR, but central SLAC cinching was most effective, reduced all mitral annular SL dimensions, and relocated both PM tips closer to the mid-septal annulus. Central SLAC is most capable of correcting the annular and subvalvular perturbations accompanying acute left ventricular ischemia that lead to IMR.

Acute Disease↗

Simple modification of "T. David-V" valve-sparing aortic root replacement to create graft pseudosinuses.

The absence of sinuses of Valsalva is postulated to perturb coronary flow patterns and to create abnormal leaflet stresses, which theoretically may limit the long-term durability of valve-sparing aortic root replacement with the original Tirone David-I reimplantation technique with a cylindrical tube graft. David developed the "T. David-V" procedure in 2001; it creates large billowing Dacron pseudosinuses while retaining the reimplantation concept. To illustrate a simple modification of the T. David-V technique, we describe a patient with Marfan's syndrome who underwent valve-sparing aortic root replacement with 1 large and 1 small graft to create pseudosinuses in the Dacron graft, to facilitate suturing the valve inside the graft, and to make the distal graft-to-aorta anastomosis a better size match.

Adult↗

Fixed-apex mitral annular descent correlates better with left ventricular systolic function than does free-apex left ventricular long-axis shortening.

Echocardiographic measures of mitral annular descent (MAD) assume a fixed left ventricular (LV) apex throughout the cardiac cycle, ignoring the apical component of LV long-axis shortening (LAS). We tested whether apical motion contributes significantly to LAS, making LAS a better surrogate of LV systolic function than MAD. Three-dimensional LV systolic MAD, LAS, and apical motion were measured in sheep using implanted radiopaque markers and biplane videofluoroscopy. End-diastolic volume-stroke work relationship (preload recruitable stroke work) was computed as a load-independent index of LV systolic function. Apical motion was 1.4 +/- 0.8 mm, representing 22% of LAS (P <.05). Linear regression demonstrated that MAD correlated slightly better with preload recruitable stroke work (r = 0.808) than LAS (r = 0.792, both P <.001). Receiver operating characteristic curves demonstrated MAD was more accurate in predicting depressed LV function than LAS (93% vs 84%, respectively). Although LV apical motion contributed significantly to LAS, MAD measured with a fixed-apex assumption, as currently done echocardiographically, correlated more closely with LV preload recruitable stroke work.

Animals↗

Can the principles of evidence-based medicine be applied to the treatment of aortic dissections?

Surgical treatment of patients with acute type A aortic dissections has improved early survival from 10-20 to approximately 80%. Data supporting several other treatment recommendations in patients with aortic dissection, however, are less convincing. We hypothesized that applying strict principles of evidence-based medicine would invalidate most of the recommendations in these published papers. We conducted a literature search asking three questions: (1) Is the use of routine circulatory arrest and an 'open distal' anastomosis technique better than traditional aortic cross clamping? (2) Does a persistent false lumen in the distal aorta wall have an adverse influence on long-term event-free survival? and (3) Is primary surgical or medical treatment of patients with Stanford acute type B dissections preferable in terms of long-term event-free survival? We searched Entrez Pubmed (National Library of Medicine) for all papers on these topics from 1980 to January 2003. Screening 3164 papers identified using the search terms 'aortic dissection' and 'treatment' yielded 15 papers fulfilling a set of a priori inclusion criteria. No study had a design that allowed unequivocal conclusions; moreover, the heterogeneity in study design and patient populations precluded formal meta-analysis. The difficulties inherent in conducting stringent clinical studies addressing various treatment strategies for patients with aortic dissection hamper their quality and weaken their recommendations for different treatment options. Specifically, no conclusive evidence exists favoring use of an open distal anastomosis in patients with acute type A dissections or complete elimination of flow in the distal aortic false lumen; similarly, medical therapy of patients with acute type B aortic dissections has no proven advantage over surgical treatment.

Acute Disease↗

Does septal-lateral annular cinching work for chronic ischemic mitral regurgitation?

OBJECTIVES: Ring annuloplasty, the current treatment of choice for chronic ischemic mitral regurgitation, abolishes dynamic annular motion and immobilizes the posterior leaflet. In a model of chronic ischemic mitral regurgitation, we tested septal-lateral annular cinching aimed at maintaining normal annular and leaflet dynamics. METHODS: Twenty-five sheep had radiopaque markers placed on the mitral annulus and anterior and posterior mitral leaflets. A transannular suture was anchored to the midseptal mitral annulus and externalized through the midlateral mitral annulus. After 7 days, biplane cinefluoroscopy provided 3-dimensional marker data (baseline) prior to creating inferior myocardial infarction by snare occlusion of obtuse marginal branches. After 7 weeks, the 9 animals that developed chronic ischemic mitral regurgitation were restudied before and after septal-lateral annular cinching. Anterior and posterior mitral leaflet angular excursion and annular septal-lateral and commissure-commissure dimensions and percent shortening were computed. RESULTS: Septal-lateral annular cinching reduced septal-lateral dimension (baseline: 3.0 +/- 0.2; chronic ischemic mitral regurgitation: 3.5 +/- 0.4 [P <.05 vs baseline by repeated measures analysis of variance and Dunnett's test]; septal-lateral annular cinching: 2.4 +/- 0.3 cm; maximum dimension) and eliminated chronic ischemic mitral regurgitation (baseline: 0.6 +/- 0.5; chronic ischemic mitral regurgitation: 2.3 +/- 1.0 [P <.05 vs baseline by repeated measures analysis of variance and Dunnett's test]; septal-lateral annular cinching: 0.6 +/- 0.6; mitral regurgitation grade [0 to 4+]) but did not alter dynamic annular shortening (baseline: 7 +/- 3; chronic ischemic mitral regurgitation: 10 +/- 5; septal-lateral annular cinching: 6 +/- 2, percent septal-lateral shortening) or posterior mitral leaflet excursion (baseline: 46 degrees +/- 8 degrees; chronic ischemic mitral regurgitation: 41 degrees +/- 13 degrees; septal-lateral annular cinching: 46 degrees +/- 8 degrees ). CONCLUSIONS: In this model, septal-lateral annular cinching decreased chronic ischemic mitral regurgitation, reduced annular septal-lateral diameter (but not commissure-commissure diameter), and maintained normal annular and leaflet dynamics. These findings provide additional insight into the treatment of chronic ischemic mitral regurgitation.

Animals↗

Midterm results of endovascular repair of descending thoracic aortic aneurysms with first-generation stent grafts.

OBJECTIVE: Five years after reporting our initial stent-graft repair of descending thoracic aortic aneurysms experience, we determined the 5- to 10-year results of stent-graft treatment and identified risk factors for adverse late outcomes. METHODS: Between 1992 and 1997, 103 patients (mean age 69 +/- 12 years) underwent repair using first-generation (custom-fabricated) stent grafts. Sixty-two patients (60%) were unsuitable candidates for conventional open surgical repair ("inoperable"). Follow-up was 100% complete (mean 4.5 +/- 2.5 years; maximum 10 years). Outcome variables included death and treatment failure (endoleak, aortic rupture, reintervention, and/or aortic-related or sudden death). RESULTS: Overall actuarial survival was 82% +/- 4%, 49% +/- 5%, and 27% +/- 6% at 1, 5, and 8 years. Survival in open surgical candidates was 93% +/- 4% and 78% +/- 6% and at 1 and 5 years compared with 74% +/- 6% and 31% +/- 6% in those deemed inoperable (P <.001). Independent risk factors for death were older age (hazard ratio = 1.1; P =.008), previous stroke (hazard ratio = 2.8; P =.003), and being designated an inoperable candidate (hazard ratio = 1.9; P =.04). Actuarial freedom from aortic reintervention and treatment failure at 8 years was 70% +/- 6% and 39% +/- 8%, respectively. Earlier operative year (hazard ratio = 1.2; P =.07), larger distal landing zone diameter (hazard ratio = 1.1; P =.001), and transposition of the left subclavian artery (hazard ratio = 3.3; P =.008) were determinants of treatment failure. CONCLUSIONS: Survival after aneurysm repair using crude, first-generation stent grafts was satisfactory in good operative candidates but bleak in the inoperable cohort, raising the question of whether asymptomatic patients should have even been treated. Late aortic complications were detected in many patients, reemphasizing the importance of serial imaging surveillance.

Aged↗

Stent-graft repair of penetrating atherosclerotic ulcers in the descending thoracic aorta: mid-term results.

BACKGROUND: Localized aortic pathoanatomic abnormalities are good targets for endovascular stent-grafting but only short-term results have been reported. Our objective was to determine the effectiveness of endovascular stent-graft treatment of patients with descending thoracic atherosclerotic penetrating atherosclerotic ulcers (PAU) and to identify risk factors for treatment failure. METHODS: Between 1993 and 2000 endovascular repair of PAU with first-generation (custom-fabricated) and second-generation (commercial) stent-grafts was performed in 26 patients (mean age, 70 years), 6 (23%) of whom had rupture. Fourteen patients (54%) were not candidates for open surgical repair. Follow-up was 100% complete (average, 51 months; maximum, 114 months). Outcome variables considered in the multivariable analysis included death and treatment failure (composite end-point comprising early death, endoleak, stent-graft mechanical fault, late aortic event, reintervention, and aortic-related or sudden death). RESULTS: Three patients (12% +/- 7% [+/-70% confidence limits]) died within 30 days and 2 had an early type I endoleak. Primary success rate was 92%. Actuarial survival estimates at 1, 3, and 5 years were 85% +/- 8%, 76% +/- 8% and 70% +/- 10% respectively and actuarial freedom from treatment failure was 81% +/- 8%, 71% +/- 9% and 65% +/- 10%. Multivariable analyses identified previous cerebrovascular accident (hazard ratio [HR] 17.1, p = 0.02) and female sex (HR 7.4, p = 0.08) as independent risk factors for death. For treatment failure the predictors were increasing aortic diameter (HR 1.1 [per mm above the mean value], p = 0.01) and female sex (HR 5.5, p = 0.09). CONCLUSIONS: Endovascular stent-graft repair is effective but not curative treatment for selected, high surgical risk, elderly patients with a descending aortic PAU over the medium term. Assiduous serial follow-up imaging after stent-grafting is mandatory to detect late complications especially in those with a large aorta.

Aged↗

Computer-generated three-dimensional animation of the mitral valve.

OBJECTIVE: Three-dimensional motion-capture data offer insight into the mechanical differences of mitral valve function in pathologic states. Although this technique is precise, the resulting time-varying data sets can be both difficult to interpret and visualize. We used a new technique to transform these 3-dimensional ovine numeric analyses into an animated human model of the mitral apparatus that can be deformed into various pathologic states. METHODS: In vivo, high-speed, biplane cinefluoroscopic images of tagged ovine mitral apparatus were previously analyzed under normal and pathologic conditions. These studies produced serial 3-dimensional coordinates. By using commercial animation and custom software, animated 3-dimensional models were constructed of the mitral annulus, leaflets, and subvalvular apparatus. The motion data were overlaid onto a detailed model of the human heart, resulting in a dynamic reconstruction. RESULTS: Numeric motion-capture data were successfully converted into animated 3-dimensional models of the mitral valve. Structures of interest can be isolated by eliminating adjacent anatomy. The normal and pathophysiologic dynamics of the mitral valve complex can be viewed from any perspective. CONCLUSION: This technique provides easy and understandable visualization of the complex and time-varying motion of the mitral apparatus. This technology creates a valuable research and teaching tool for the conceptualization of mitral valve dysfunction and the principles of repair.

Animals↗

Mitral annular size predicts Alfieri stitch tension in mitral edge-to-edge repair.

BACKGROUND AND AIM OF THE STUDY: Whilst increased 'Alfieri stitch' tension may reduce the durability of 'edge-to-edge' mitral repair, the factors affecting suture tension are unknown. In order to study hemodynamics and left ventricular (LV) and annular dynamics that determine suture tension, the central edge of the mitral leaflets was approximated with a miniature force transducer to measure leaflet tension (T) at the leaflet approximation point. METHODS: Eight sheep were studied under open-chest conditions immediately after surgical placement of a force transducer and implantation of radiopaque markers on the left ventricle and mitral annulus (MA). Hemodynamic variables were altered by two caval occlusion steps (deltaV1 and deltaV2) and dobutamine infusion. Three-dimensional marker coordinates were obtained by simultaneous biplane videofluoroscopy to measure LV volume, MA area (MAA) and septal-lateral (SL) annular dimension throughout the cardiac cycle. RESULTS: At baseline, peak Alfieri stitch tension (0.30 +/- 0.18 N) was observed 96 +/- 61 ms prior to end-diastole coincident with peak annular SL diameter (98 +/- 58 ms before end-diastole). Dobutamine infusion decreased suture tension (from 0.30 +/- 0.18 N to 0.20 +/- 0.12 N, p = 0.01), although peak systolic pressure increased significantly (138 +/- 19 versus 115 +/- 14 mmHg; p = 0.03). A regression model was fitted with the goal of interpreting the hemodynamic and geometric predictors of tension as their influence varied with time: Tt (N) = 0.1916 + 0.2115 x SL (cm) - 0.1996 x MAA/SL (cm2/cm) + ft x LVP (mmHg), where Tt is tension at any time during the cardiac cycle and ft is the time-varying coefficient of LVP. CONCLUSION: Tension on the leaflets in the edge-to-edge repair is determined primarily by MA SL size, and paradoxically is lower when the contractile state is enhanced. This indicates that annular and/or LV dilatation increase stitch tension and may adversely affect durability of the repair if concomitant ring annuloplasty is not performed.

Animals↗

Mitral suture annuloplasty corrects both annular and subvalvular geometry in acute ischemic mitral regurgitation.

BACKGROUND AND AIM OF THE STUDY: Papillary muscle displacement is an important element in the pathogenesis of ischemic mitral regurgitation (IMR). The effects of standard ring annuloplasty on subvalvular geometry are incompletely understood. The hypothesis was tested that annular reduction with a Panethtype suture annuloplasty would correct both annular and papillary muscle geometric abnormalities during acute left ventricular (LV) ischemia. METHODS: Eight adult sheep underwent insertion of an adjustable, double-suture Paneth-type mitral annuloplasty and radiopaque markers on the left ventricle, mitral annulus, leaflet edges, and anterior (APM) and posterior (PPM) papillary muscle tips. Immediately after surgey, 3-D marker coordinates were determined during Control conditions and during proximal left circumflex occlusion before and after tightening the annuloplasty suture. RESULTS: Acute IMR (MR grade 0.3 +/- 0.3 to 2.1 +/- 0.4, Control versus Ischemia) was associated with end-systolic LV dilatation (+27 +/- 16 ml, change relative to Control), greater septal-lateral (+4.6 +/- 3.1 cm) and commissure-commissure (+3.3 +/- 1.6 cm) mitral annular diameters, longer anterior (+1.5 +/- 0.9 cm) and posterior (+0.6 +/- 0.9 cm) papillary muscle tethering distances, greater distance from the APM to the anterior commissure (+0.9 +/- 0.8 cm), and shorter distance from the PPM to the poslerior commissure (-1.3 +/- 1.5 cm). Suture annuloplasty corrected the annular and subvalvular changes, and IMR returned to Control levels (0.5 +/- 0.5); only LV end-systolic volume (ESV) was different from Control (+25 +/- 18 ml) (mean +/- SD, p < 0.05 versus Control by RMANOVA and Dunnett's test). CONCLUSION: Suture annuloplasty corrected ischemia-induced end-systolic distortions of the entire valvular-ventricular complex (i.e. inter-leaflet separation, mitral annular dilatation in both axes, and papillary muscle displacements), and abolished acute IMR, independent of any change in ESV. A better understanding of the effects of annular reduction on papillary muscle geometry may lead to improved subvalvular mitral repair techniques.

Animals↗