Dacron Skirt Reconstruction of the Left Ventricular Outflow Tract: Extending the Capabilities of a Valved Conduit.

Aortic root reconstruction in the setting of redo aortic valve procedures or infective endocarditis may be technically challenging, particularly because of variable destruction or distortion of the left ventricular outflow tract. Homograft aortic root replacement is an excellent option for aortic root abscesses but is limited by homograft availability. We describe a simple technique of a bioprosthetic valved conduit constructed on the table using a Dacron (DuPont, Wilmington, DE) skirt below the valve. The use of the Dacron skirt facilitates easy reconstruction of the left ventricular outflow tract.

Complex Tricuspid Valve Repair in Patients With Pacer Defibrillator-Related Tricuspid Regurgitation.

Tricuspid valve regurgitation in patients with heart failure or in those undergoing complex cardiac operations is associated with increased morbidity and mortality. We report our results with a technique of repairing the tricuspid valves while retaining the pacer defibrillator lead. Patients had tricuspid valve repairs that included repositioning of the pacer defibrillator lead, approximation of septal and inferior/posterior leaflets in a modified cleft repair, and implantation of a tricuspid annuloplasty ring. This procedure was performed in more than 42 patients with good success.

Geometric perturbations in multiheaded papillary tip positions associated with acute ovine ischemic mitral regurgitation.

BACKGROUND: Novel surgical approaches are focusing on the "ventricular disease" of ischemic mitral regurgitation (IMR), to correct altered papillary muscle (PM) tip positions (apical displacement) and ameliorate leaflet tethering. Due to the anatomic complexity of the subvalvular apparatus, however, the precise geometric perturbations of the multiheaded PM tips associated with IMR remain uncharacterized. METHODS: In 6 adult sheep, we implanted 3 markers on each PM. To specifically identify distinct PM tips, 1 marker was placed on the PM origin of the dominant chord to the anterior, posterior, and commissural leaflets. Nine markers were placed on the edge of the posterior mitral leaflet, and 5 on the edge of the anterior mitral leaflet. Eight markers were sewn around the mitral annulus. Animals were studied immediately postoperatively, with biplane videofluoroscopy and transesophageal echocardiography, before and during acute snare occlusion of the proximal left circumflex coronary artery, to induce IMR. Papillary muscle tip and leaflet edge geometry was expressed as the orthogonal distance of each respective marker to the least-squares mitral annulus plane at end-systole. In addition, the distance from each PM tip marker to the mitral annulus "saddle horn" was calculated. RESULTS: Acute left circumflex occlusion significantly increased mitral regurgitation from a baseline of 0.7 ± 0.3 to 2.5 ± 0.5 (P < .05). The IMR was associated with posterior leaflet restriction near the central leaflet edge, with simultaneous prolapse of both leaflets near the posterior commissure. No apical displacement of PM tips was observed during IMR, although the posterior PM moved farther away from the midseptal annulus. CONCLUSIONS: During acute ischemia, no apical displacement of any PM tip was observed. Posterior PM movement away from the annular saddle horn, and toward the annulus, was associated with IMR and leaflet prolapse near the posterior commissure, and with restriction near the valve center. These data may help guide development of surgical interventions aimed at PM repositioning.

Determinants of evolution and progression of acute ovine ischemic mitral regurgitation.

BACKGROUND AND AIM OF THE STUDY: The optimal treatment of moderate ischemic mitral regurgitation (IMR) remains contested. Thus, radiopaque markers were implanted on valvular structures to investigate the geometric and hemodynamic variables associated with the evolution and progression of acute ovine IMR. METHODS: Eight adult sheep underwent implantation of five radiopaque markers on the edge of the posterior mitral leaflet (PML), and five on the edge of the anterior mitral leaflet (AML). Eight additional markers were sewn around the mitral annulus (MA). The animals were studied immediately after surgery, using biplane videofluoroscopy and transesophageal echocardiography. Data were acquired at Baseline and at two time points (IMR1 and IMR2) during acute snare occlusion of the proximal left circumflex coronary artery and progressive IMR. The orthogonal distance of each leaflet edge marker to the least-squares annular plane, mitral annular area (MAA), and septal-lateral diameter (SL) were calculated at end-systole. The leaflet tenting area (TA) was calculated at valve center (CENT) and near the anterior (ACOM) and posterior (PCOM) commissures. RESULTS: The degree of MR was 0.6 +/- 0.4, 1.8 +/- 0.7, and 2.8 +/- 0.7 for Baseline, IMR1, and IMR2, respectively (p < 0.005). IMR1 was associated with annular dilatation and leaflet restriction near the valve center, and prolapse near the PCOM versus Baseline. Although both left ventricular pressure (LVP) and left ventricular dP/dt decreased significantly from IMR1 to IMR 2, there were no differences in leaflet or annular geometry. CONCLUSION: The initiation of moderate IMR was associated with significant alterations in annular and leaflet geometry, but only a small decrease in LV systolic function, was needed for IMR progression. These data suggest that the surgical repair and optimization of LV function may be important in combination to treat moderate IMR, as only small hemodynamic deterioration and perturbations in valvular geometry are necessary for significant IMR progression.

Regional mitral leaflet opening during acute ischemic mitral regurgitation.

BACKGROUND AND AIM OF THE STUDY: Diastolic mitral valve (MV) opening characteristics during ischemic mitral regurgitation (IMR) are poorly characterized. The diastolic MV opening dynamics were quantified along the entire valvular coaptation line in an ovine model of acute IMR. METHODS: Ten radiopaque markers were sutured in pairs on the anterior (A1-E1) and corresponding posterior (A2-E2) leaflet edges from the anterior (A1/A2) to the posterior (E1/E2) commissure in 11 adult sheep. Immediately after surgery, 4-D marker coordinates were obtained before and during occlusion of the proximal left circumflex coronary artery. Distances between marker pairs were calculated throughout the cardiac cycle every 16.7 ms. Leaflet opening was defined as the time after end-systole (ES) when the first derivative of the distance between marker pairs was greater than a threshold value of 3 cm/s. Valve opening velocity was defined as the maximum slope of marker pair tracings. RESULTS: Hemodynamics were consistent with acute ischemia, as reflected by increased MR grade (0.5 +/- 0.3 versus 2.3 +/- 0.7, p < 0.05), decreased contractility (dP/dt(max): 1,948 +/- 598 versus 1,119 +/- 293 mmHg/s, p < 0.05), and slower left ventricular relaxation rate (dP/dt(min): -1,079 +/- 188 versus -538 +/- 147 mmHg/s, p < 0.05). During ischemia, valve opening occurred earlier (A1/A2: 112 +/- 28 versus 83 +/- 43 ms, B1/B2: 105 +/- 32 versus 68 +/- 35 ms, C1/C2: 126 +/- 25 versus 74 +/- 37 ms, D1/D2: 114 +/- 28 versus 71 +/- 34 ms, E1/E2: 125 +/- 29 versus 105 +/- 33 ms; all p < 0.05) and was slower (A1/A2: 16.8 +/- 9.6 versus 14.2 +/- 9.4 cm/s, B1/B2: 40.4 +/- 9.9 versus 32.2 +/- 10.0 cm/s, C1/C2: 59.0 +/- 14.9 versus 50.4 +/- 18.1 cm/s, D1/D2: 34.4 +/- 10.4 versus 25.5 +/- 10.9 cm/s; all p < 0.05), except at the posterior edge (E1/E2: 13.3 +/- 8.7 versus 10.6 +/- 7.2 cm/s). The sequence of regional mitral leaflet separation along the line of coaptation did not change with ischemia. CONCLUSION: Acute posterolateral left ventricular ischemia causes earlier leaflet opening, probably due to a MR-related elevation in left-atrial pressure; reduces leaflet opening velocity, potentially reflecting an impaired left ventricular relaxation rate; and does not perturb the homogeneous temporal pattern of regional valve opening along the line of coaptation. Future studies will confirm whether these findings are apparent in patients with chronic IMR, and may help to refine the current strategies used to treat IMR.

Effects of acute ischemic mitral regurgitation on three-dimensional mitral leaflet edge geometry.

BACKGROUND: Improved quantitative understanding of in vivo leaflet geometry in ischemic mitral regurgitation (IMR) is needed to improve reparative techniques, yet few data are available due to current imaging limitations. Using marker technology we tested the hypotheses that IMR (1) occurs chiefly during early systole; (2) affects primarily the valve region contiguous with the myocardial ischemic insult; and (3) results in systolic leaflet edge restriction. METHODS: Eleven sheep had radiopaque markers sutured as five opposing pairs along the anterior (A(1)-E(1)) and posterior (A(2)-E(2)) mitral leaflet free edges from the anterior commissure (A(1)-A(2)) to the posterior commissure (E(1)-E(2)). Immediately postoperatively, biplane videofluoroscopy was used to obtain 4D marker coordinates before and during acute proximal left circumflex artery occlusion. Regional mitral orifice area (MOA) was calculated in the anterior (Ant-MOA), middle (Mid-MOA), and posterior (Post-MOA) mitral orifice segments during early systole (EarlyS), mid systole (MidS), and end systole (EndS). MOA was normalized to zero (minimum orifice opening) at baseline EndS. Tenting height was the distance of the midpoint of paired markers to the mitral annular plane at EndS. RESULTS: Acute ischemia increased echocardiographic MR grade (0.5+/-0.3 vs 2.3+/-0.7, p<0.01) and MOA in all regions at EarlyS, MidS, and EndS: Ant-MOA (7+/-10 vs 22+/-19 mm(2), 1+/-2 vs 18+/-16 mm(2), 0 vs 17+/-15 mm(2)); Mid-MOA (9+/-13 vs 25+/-17 mm(2), 3+/-6 vs 21+/-19 mm(2), 0 vs 25+/-17 mm(2)); and Post-MOA (8+/-10 vs 25+/-16, 2+/-4 vs 22+/-13 mm(2), 0 vs 23+/-13 mm(2)), all p<0.05. There was no change in MOA throughout systole (EarlyS vs MidS vs EndS) during baseline conditions or ischemia. Tenting height increased with ischemia near the central and the anterior commissure leaflet edges (B(1)-B(2): 7.1+/-1.8mm vs 7.9+/-1.7 mm, C(1)-C(2): 6.9+/-1.3mm vs 8.0+/-1.5mm, both p<0.05). CONCLUSIONS: MOA during ischemia was larger throughout systole, indicating that acute IMR in this setting is a holosystolic phenomenon. Despite discrete postero-lateral myocardial ischemia, Post-MOA was not disproportionately larger. Acute ovine IMR was associated with leaflet restriction near the central and the anterior commissure leaflet edges. This entire constellation of annular, valvular, and subvalvular ischemic alterations should be considered in the approach to mitral repair for IMR.

Mitral leaflet remodeling in dilated cardiomyopathy.

BACKGROUND: Normal mammalian mitral leaflets have regional heterogeneity of biochemical composition, collagen fiber orientation, and geometric deformation. How leaflet shape and regional geometry are affected in dilated cardiomyopathy is unknown. METHODS AND RESULTS: Nine sheep had 8 radio-opaque markers affixed to the mitral annulus (MA), 4 markers sewn on the central meridian of the anterior mitral leaflet (AML) forming 4 distinct segments S1 to S4 and 2 on the posterior leaflet (PML) forming 2 distinct segments S5 and S6. Biplane videofluoroscopy and echocardiography were performed before and after rapid pacing (180 to 230 bpm for 15+/-6 days) sufficient to develop tachycardia-induced cardiomyopathy (TIC) and functional mitral regurgitation (FMR). Leaflet tethering was defined as change of displacement of AML and PML edge markers from the MA plane from baseline values while leaflet length was obtained by summing the segments between respective leaflet markers. With TIC, total AML and PML length increased significantly (2.11+/-0.16 versus 2.43+/-0.23 cm and 1.14+/-0.27 versus 1.33+/-0.25 cm before and after pacing for AML and PML, respectively; P<0.05 for both), but only segments near the edge of each leaflet (S4 lengthened by 23+/-17% and S5 by 24+/-18%; P<0.05 for both) had significant regional remodeling. AML shape did not change and no leaflet tethering was observed. CONCLUSIONS: TIC was not associated with leaflet tethering or shape change, but both anterior and posterior leaflets lengthened because of significant remodeling localized near the leaflet edge. Leaflet remodeling accompanies mitral regurgitation in cardiomyopathy and casts doubt on FMR being purely "functional" in etiology.

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 type A aortic dissection complicated by aortic regurgitation: composite valve graft versus separate valve graft versus conservative valve repair.

OBJECTIVE: To clarify the merits of various surgical approaches, we studied the outcome after composite valve graft versus separate valve and graft replacement versus conservative valve treatment with replacement of the ascending aorta in patients with acute type A aortic dissection complicated by aortic regurgitation. METHODS: Between 1967 and 1999, 123 patients (mean age 56 +/- 15 years) underwent composite valve graft replacement (n = 21), separate valve and graft replacement (n = 20), or conservative valve treatment (n = 82 [commissural resuspension in 46]); follow-up averaged 6.5 years (95% complete). RESULTS: The 30-day, 1-year, and 6-year survival estimates of 85% +/- 4%, 79% +/- 5%, and 69% +/- 5% (+/-1 standard error of mean), respectively, after conservative valve treatment were similar to 86% +/- 8%, 81% +/- 9%, and 65% +/- 16%, respectively, with composite valve graft replacement and better (but insignificantly so) than 70% +/- 10%, 70% +/- 10%, and 45% +/- 11%, respectively, with separate valve and graft replacement. The 6-year freedom from proximal reoperation was 95% +/- 3%, 89% +/- 10%, and 100% in conservative valve graft, separate valve and graft, and composite valve graft subgroups, respectively (P = not significant). Cox regression multivariable analysis identified that previous sternotomy (hazard ratio [or e(beta)] 95% confidence interval 1.4-10.9, P =.006), hypertension (0.99-2.9, P =.05), cardiac tamponade (1.1-4.0, P =.03), and stroke (1.7-7.0, P =.001) increased the hazard of death. No factors predicting a higher likelihood of late proximal reoperation were identified. CONCLUSIONS: In patients with acute type A aortic dissection and aortic regurgitation, there was no significant difference in overall survival or reoperation rates among these surgical approaches. We try to save the valve whenever possible unless the aortic root is pathologically dilated (eg, Marfan syndrome or annuloaortic ectasia) or destroyed by the dissection process, when composite valve graft or valve-sparing aortic root replacement is indicated.

Aorto-mitral annular dynamics.

BACKGROUND: The aortic and mitral valves are coupled through fibrous aorto-mitral continuity, but their synchronous dynamic physiology has not been completely characterized. METHODS: Seven sheep underwent implantation of five radiopaque markers on the left ventricle, 10 on the mitral annulus, and 3 on the aortic annulus. One of the mitral annulus markers was placed at the center of aorto-mitral continuity (mitral annulus "saddle horn"). Animals were studied with bi-plane videofluoroscopy 7 to 10 days postoperatively. Total circumference and lengths of mitral fibrous annulus, mitral muscular annulus, aortic fibrous annulus, and aortic muscular annulus were calculated throughout the cardiac cycle from three dimensional marker coordinates as was mitral annular area and aortic annular area. Aorto-mitral angle was determined as the angle between the centroid of the aortic annulus markers, the saddle horn, and the centroid of the mitral annulus markers. Aortic annulus and mitral annulus flexion was expressed as the difference between maximum and minimum values of the aortic and mitral annulus angles during the cardiac cycle. RESULTS: Mitral and aortic annular areas changed in roughly a reciprocal fashion during late diastole and early systole with an overall 32 +/- 8% change in aortic annular area and a 13 +/- 13% change in mitral annular area. Aortic fibrous annulus changed much less than aortic muscular annulus (6 +/- 2% vs 18 +/- 4%; p = 0.0003) as did mitral fibrous annulus relative to mitral muscular annulus (4 +/- 1% vs 8 +/- 2%; p = 0.004). Aortic annulus and mitral annulus flexion was 8 +/- 2 degrees and increased to 11 +/- 2 degrees (p = 0.009) with inotropic stimulation. CONCLUSIONS: Dynamic aortic and mitral annular area changes were not mediated through the anatomic fibrous continuity. Aorto-mitral flexion, which increased with enhanced contractility, may facilitate left ventricle ejection. The effect of valvular surgical interventions on aorto-mitral flexion needs further investigation.

Ablation of mitral annular and leaflet muscle: effects on annular and leaflet dynamics.

Mitral annular (MA) and leaflet three-dimensional (3-D) dynamics were examined after circumferential phenol ablation of the MA and anterior mitral leaflet (AML) muscle. Radiopaque markers were sutured to the left ventricle, MA, and both mitral leaflets in 18 sheep. In 10 sheep, phenol was applied circumferentially to the atrial surface of the mitral annulus and the hinge region of the AML, whereas 8 sheep served as controls. Animals were studied with biplane video fluoroscopy for computation of 3-D mitral annular area (MAA) and leaflet shape. MAA contraction (MAACont) was determined from maximum to minimum value. Presystolic MAA (PS-MAACont) reduction was calculated as the percentage of total reduction occurring before end diastole. Phenol ablation decreased PS-MAACont (72 +/- 6 vs. 47 +/- 31%, P = 0.04) and delayed valve closure (31 +/- 11 vs. 57 +/- 25 ms, P = 0.017). In control, the AML had a compound sigmoid shape; after phenol, this shape was entirely concave to the atrium during valve closure. These data indicate that myocardial fibers on the atrial side of the valve influence the 3-D dynamic geometry and shape of the MA and AML.

Ischemia in three left ventricular regions: Insights into the pathogenesis of acute ischemic mitral regurgitation.

BACKGROUND: Acute posterolateral left ventricular ischemia in sheep results in ischemic mitral regurgitation, but the effects of ischemia in other left ventricular regions on ischemic mitral regurgitation is unknown. METHODS: Six adult sheep had radiopaque markers placed on the left ventricle, mitral annulus, and anterior and posterior mitral leaflets at the valve center and near the anterior and posterior commissures. After 6 to 8 days, animals were studied with biplane videofluoroscopy and transesophageal echocardiography before and during sequential balloon occlusion of the left anterior descending, distal left circumflex, and proximal left circumflex coronary arteries. Time of valve closure was defined as the time when the distance between leaflet edge markers reached its minimum plateau, and systolic leaflet edge separation distance was calculated on the basis of left ventricular ejection. RESULTS: Only proximal left circumflex coronary artery occlusion resulted in ischemic mitral regurgitation, which was central and holosystolic. Delayed valve closure (anterior commissure, 58 +/- 29 vs 92 +/- 24 ms; valve center, 52 +/- 26 vs 92 +/- 23 ms; posterior commissure, 60 +/- 30 vs 94 +/- 14 ms; all P <.05) and increased leaflet edge separation distance during ejection (mean increase, 2.2 +/- 1.5 mm, 2.1 +/- 1.9 mm, and 2.1 +/- 1.5 mm at the anterior commissure, valve center, and posterior commissure, respectively; P <.05 for all) was seen during proximal left circumflex coronary artery occlusion but not during left anterior descending or distal left circumflex coronary artery occlusion. Ischemic mitral regurgitation was associated with a 19% +/- 10% increase in mitral annular area, and displacement of both papillary muscle tips away from the septal annulus at end systole. CONCLUSIONS: Acute ischemic mitral regurgitation in sheep occurred only after proximal left circumflex coronary artery occlusion along with delayed valve closure in early systole and increased leaflet edge separation throughout ejection in all 3 leaflet coaptation sites. The degree of left ventricular systolic dysfunction induced did not correlate with ischemic mitral regurgitation, but both altered valvular and subvalvular 3-dimensional geometry were necessary to produce ischemic mitral regurgitation during acute left ventricular ischemia.

Tachycardia-induced cardiomyopathy in the ovine heart: mitral annular dynamic three-dimensional geometry.

BACKGROUND: Ring annuloplasty has been used to correct annular dilatation and mitral regurgitation in dilated cardiomyopathy, but little is known about the dynamic precise 3-dimensional geometry of the mitral annulus in this condition. METHODS: Nine sheep had radiopaque markers sewn to the mitral annulus, creating 8 distinct segments beginning at the posterior commissure (segments 1-4, septal mitral annulus; segments 5-8, lateral mitral annulus). Biplane videofluoroscopy and transesophageal echocardiography were performed before and after rapid pacing (180-230 min(-1) for 15 +/- 6 days) sufficient to develop tachycardia-induced cardiomyopathy and mitral regurgitation. Mitral annular segment contraction was defined as the percentage difference between maximum and minimum lengths. Mitral annular area and mitral annular septal-lateral and commissure-commissure diameters and 3-dimensional shape were determined from marker coordinates. RESULTS: With tachycardia-induced cardiomyopathy, end-diastolic mitral annular area, septal-lateral diameter, and commissure-commissure diameter increased by 36% +/- 14%, 25% +/- 12%, and 9% +/- 5%, respectively (P <.01), whereas mitral regurgitation increased from 0.3 +/- 0.2 to 2.2 +/- 0.9 (P <.0001). All annular segments dilated at end-diastole with tachycardia-induced cardiomyopathy, except the segment between the midseptal annulus and the left fibrous trigone. Annular segment contraction was significantly decreased with tachycardia-induced cardiomyopathy in the lateral, but not in the septal, regions. Three-dimensional reconstruction of annular shape revealed a saddle shape of the annulus at baseline; this shape was also measured with tachycardia-induced cardiomyopathy, but there was some flattening of the septal annulus. CONCLUSIONS: With tachycardia-induced cardiomyopathy, the mitral annulus dilated substantially, being more in the septal-lateral than in the commissure-commissure dimension. Greater annular segmental dilatation and decreased contraction occurred in the lateral annulus. The saddle shape of the annulus was retained but flattened.

The effects of mitral annuloplasty rings on mitral valve complex 3-D geometry during acute left ventricular ischemia.

OBJECTIVE: Annuloplasty rings are used to treat ischemic mitral regurgitation (IMR), but their exact effects on 3-D geometry of the overall mitral valve complex during acute left ventricular (LV) ischemia remain unknown. METHODS: Radiopaque markers were sutured to the mitral leaflet edges, annulus, papillary muscle tips, and ventricle in three groups of sheep. One group served as control (n = 5), and the others underwent Duran (n = 6) or Physio (n = 5) ring annuloplasty. One week later, 3-D marker coordinates at end-systole were obtained before and during balloon occlusion of the circumflex artery. RESULTS: In all control animals, acute LV ischemia was associated with: (i) septal-lateral separation of the leaflet edges, which was predicted by lateral displacement of the lateral annulus during septal-lateral mitral annular dilatation; (ii) apical restriction of the posterior leaflet edge, which was predicted by displacement of the lateral annulus away from the non-ischemic anterior papillary muscle; (iii) displacement of the posterior papillary muscle, which was not predictive of either septal-lateral leaflet separation or leaflet restriction; and (iv) mitral regurgitation. In the Duran group during ischemia, the posterior leaflet edge shifted posteriorly due to posterior movement of the lateral annulus, but no IMR occurred. In the Physio group during ischemia, neither the posterior leaflet edge nor the lateral annulus changed positions, and there was no IMR. In both the Duran and Physio groups, displacement of the posterior papillary muscle did not lead to IMR. CONCLUSIONS: Either annuloplasty ring prevented the perturbations of mitral leaflet and annular--but not papillary muscle tip--3-D geometry during acute LV ischemia. By fixing the septal-lateral annular dimension and preventing lateral displacement of the lateral annulus, annuloplasty rings prevented systolic septal-lateral leaflet separation and posterior leaflet restriction, and no acute IMR occurred. The flexible ring allowed posterior displacement of the posterior leaflet edge and the lateral annulus, which was not observed with a semi-rigid ring.

Does profound hypothermic circulatory arrest improve survival in patients with acute type a aortic dissection?

OBJECTIVE: No evidence exists that profound hypothermic circulatory arrest (PHCA) improves survival or reduces the likelihood of distal aortic reoperation in patients with acute type A aortic dissection. METHODS: Records of 307 patients with acute type A aortic dissection from 1967 to 1999 were retrospectively reviewed. The influence of repair using PHCA (n=121) versus without PHCA (n=186) on death and freedom from distal aortic reoperation was analyzed using multivariable Cox regression models. Propensity score analysis identified a subset of 152 comparable patients in 3 quintiles (QIII-V) in which the effects of PHCA (n=113) versus no PHCA (n=39) were further compared. RESULTS: For all patients, 30-day, 1-year, and 5-year survival estimates were 81+/-2%, 74+/-3%, and 63+/-3% (+/-1 SE). Survival rates and actual freedom from distal aortic reoperation was not significantly different between treatment methods in the entire patient cohort nor in the matched patients in quintiles III-V. Treatment method was not associated with differences in early major complications, late survival, or distal aortic reoperation rates in the entire patient sample or in quintiles III-V. CONCLUSIONS: Aortic repair with or without circulatory arrest was associated with comparable early complications, survival, and distal aortic reoperation rates in patients with acute type A aortic dissection. Despite the lack of concrete evidence favoring the use of PHCA, it does no harm, and most of our group uses PHCA regularly because of its practical technical advantages and theoretical potential merit.

Is medical therapy still the optimal treatment strategy for patients with acute type B aortic dissections?

OBJECTIVE: The optimal treatment of patients with acute type B dissections continues to be debated. METHODS: A 36-year clinical experience of medical and surgical treatments in 189 patients was retrospectively analyzed (multivariable Cox proportional hazards model) with respect to three outcome end points: all deaths, freedom from reoperation, and freedom from late aortic complications or death. Propensity score analysis identified 2 quintiles (quintiles I and II, consisting of 142 comparable patients) for further comparison of the effects of surgical versus medical treatment. RESULTS: Shock (hazard ratio 14.5, 95% confidence interval 4.7-44.5, P <.001) and visceral ischemia (hazard ratio 10.9, 95% confidence interval 3.9-30.3, P <.001) largely predominated as determinants of death, along with 6 other risk factors (arch involvement, rupture, stroke, previous sternotomy, and coronary or lung disease), which roughly doubled the hazard of death. Female sex was a significant but weaker predictor of death. Renal dysfunction, year of presentation, age, and mode of therapy (medical vs surgical) had no important bearing on overall survival. The actuarial survival estimates for all patients were 71%, 60%, 35%, and 17% at 1, 5, 10, and 15 years, respectively, and were similar for the medical and surgical patients. Reoperation and late aortic complications were predicted by the presence of Marfan syndrome. For the propensity-matched patients in quintiles I and II, survival, freedom from reoperation, and freedom from aortic complications were almost identical in the medically treated and surgical subsets. CONCLUSIONS: The prognosis for patients with acute type B aortic dissection is bleak and determined primarily by dissection-related and patient-specific risk factors, which do not appear to be readily modifiable.

Hemodynamic performance of an unstented xenograft mitral valve substitute.

OBJECTIVE: Stentless mitral xenografts offer potential clinical benefits because they mimic the normal bileaflet mitral valve. How best to implant them and their hemodynamic performance and durability, however, remain unknown. METHODS: A stentless porcine mitral xenograft valve (Medtronic physiologic mitral valve) was implanted in 7 sheep with papillary muscle sewing tubes attached with transmural left ventricular sutures. Radiopaque markers were inserted on the leaflets, annular cuff, papillary tips, and left ventricle. After 10 +/- 5 days, the animals were studied with biplane videofluoroscopy to determine 3-dimensional marker coordinates at baseline and during dobutamine infusion. Transesophageal echocardiography assessed mitral regurgitation and valvular gradients. Mitral annular area was calculated from the annular markers. Physiologic mitral valve leaflet and annular dynamics were compared with 8 native sheep valves. RESULTS: Average mitral regurgitation grade at baseline was 1.2 +/- 1.0 (range, 0-4), and the mean transvalvular pressure gradients were 3.6 +/- 1.3 and 6.2 +/- 2.2 mm Hg during baseline and dobutamine infusion, respectively. Xenograft mitral annular area contraction throughout the cardiac cycle was reduced (6% +/- 6% vs 13% +/- 4% for physiologic mitral valve and control valve, respectively; P =.03). Physiologic mitral valve leaflet geometry during closure differed from the native valve, with the anterior leaflet being convex to the atrium and with little motion of the posterior leaflet. Three animals survived more than 3 months; good healing of the annular cuff and papillary muscle tubes was demonstrated. CONCLUSION: This stentless xenograft mitral valve substitute had low gradients at baseline and during stress conditions early postoperatively, with mild mitral regurgitation. Preliminary analysis of healing characteristics appeared favorable at 3 months. Additional studies are needed to determine long-term xenograft mitral valve performance and resistance to calcification.

Alterations in left ventricular torsion in tachycardia-induced dilated cardiomyopathy.

OBJECTIVE: Left ventricular torsion reduces transmural systolic gradients of fiber strain, and torsional recoil in early diastole is thought to enhance left ventricular filling. Left ventricular remodeling in dilated cardiomyopathy may result in changes in torsion dynamics, but these effects are not yet characterized. Tachycardia-induced cardiomyopathy is accompanied by systolic and diastolic heart failure and left ventricular remodeling. We hypothesized that cardiomyopathy would alter systolic and diastolic left ventricular torsion mechanics, and this hypothesis was tested by studying sheep before and after the development of tachycardia-induced cardiomyopathy. METHODS: Implanted miniature radiopaque markers were used in 8 sheep to measure left ventricular geometry and function, maximal torsional deformation, and early diastolic recoil before and after rapid ventricular pacing was used to create tachycardia-induced cardiomyopathy. RESULTS: All animals had significant heart failure with ventricular dilatation and remodeling. With tachycardia-induced cardiomyopathy, maximum torsion relative to control conditions decreased (1.69 degrees +/- 0.61 degrees vs 4.25 degrees +/- 2.33 degrees ), and early diastolic recoil was completely abolished (0.53 degrees +/- 1.19 degrees vs -1.17 degrees +/- 0.94 degrees ). CONCLUSIONS: Cardiomyopathy is accompanied by decreased and delayed systolic left ventricular torsional deformation and loss of early diastolic recoil, which may contribute to left ventricular dysfunction by increasing systolic transmural strain gradients and impairing diastolic filling. Analysis of left ventricular torsion with radiofrequency-tagging magnetic resonance imaging should be explored to elucidate the role of torsion in patients with cardiomyopathy.

Septal-lateral annular cinching abolishes acute ischemic mitral regurgitation.

OBJECTIVE: Ring annuloplasty prevents acute ischemic mitral regurgitation in sheep, but it also abolishes normal mitral annular and posterior leaflet dynamics. We investigated a novel surgical approach of simple septal-lateral annular cinching with sutures to treat acute ischemic mitral regurgitation. METHODS: Nine adult sheep underwent implantation of multiple radiopaque markers on the left ventricle, mitral anulus, and mitral leaflets. A septal-lateral transannular suture was anchored to the midseptal mitral anulus and externalized to a tourniquet through the midlateral mitral anulus and left ventricular wall. Open-chest animals were studied immediately postoperatively. Acute ischemic mitral regurgitation was induced by means of proximal left circumflex artery snare occlusion, and 3 progressive steps of septal-lateral annular cinching (each 2-3 mm suture tightening for 5 seconds) were performed with the transannular suture. Biplane videofluoroscopy for 3-dimensional marker coordinates and transesophageal echocardiography were performed continuously before and during left circumflex ischemia and septal-lateral annular cinching. RESULTS: Acute left circumflex ischemia caused ischemic mitral regurgitation (+0.5 +/- 0.4 [baseline] vs +2.0 +/- 0.7 [ischemia]; P =.005; scale, +0-4), which decreased progressively with each step of septal-lateral annular cinching and was eliminated during the third step (ischemic mitral regurgitation, +0.6 +/- 0.5; P = not significant vs baseline). The third step of septal-lateral annular cinching decreased the septal-lateral diameter by 6.0 +/- 2.6 mm (P =.005); however, mitral anulus area reduction (8.5% +/- 1.0% and 6.9% +/- 1.9% for ischemic mitral regurgitation and septal-lateral annular cinching step 3, respectively; P =.006) and posterior leaflet excursion (50 degrees +/- 9 degrees and 44 degrees +/- 11 degrees for regurgitation and annular cinching step 3, respectively; P =.002) throughout the cardiac cycle were affected only mildly. Normal mitral annular 3-dimensional shape was maintained with septal-lateral annular cinching. CONCLUSIONS: Isolated 22% +/- 10% reduction in mitral annular septal-lateral dimension abolished acute ischemic mitral regurgitation in normal sheep hearts while allowing near-normal mitral annular and posterior leaflet dynamic motion. Septal-lateral annular cinching may represent a simple method for the surgical treatment of ischemic mitral regurgitation, either as an adjunctive technique or alone, which helps preserve physiologic annular and leaflet function.

Septal-lateral annular cinching ('SLAC) reduces mitral annular size without perturbing normal annular dynamics.

BACKGROUND AND AIM OF THE STUDY: Septal-lateral (S-L) mitral annular diameter reduction is thought to be central to the efficacy of ring annuloplasty in correcting functional mitral regurgitation (MR), but rings perturb mitral annulus (MA) dynamic motion and limit posterior leaflet excursion. The effects of S-L annular cinching ('SLAC'), a novel method for mitral annular reduction, were investigated. METHODS: Eight adult sheep had multiple radioopaque markers placed on the left ventricle, leaflet edges, and around the MA. The S-L trans-annular suture was anchored to the mid-septal MA and externalized through the mid-lateral MA and left ventricular wall. Animals were studied immediately postoperatively with biplane videofluoroscopy before and after suture cinching to reduce annular size. MA area (MAA) and S-L dimension were calculated throughout the cardiac cycle from the annular marker coordinates. MAA contraction (AMAA) was expressed as percentage decrease from maximum to minimum MAA. Anterior (AML) and posterior (PML) leaflet angular excursion were calculated as the change in angle between each leaflet edge marker and the S-L annular dimension during the cardiac cycle. MA folding was calculated as the change in distance during systole of the mid-septal annular marker from a plane fitted to the lateral MA markers. RESULTS: SLAC reduced end-diastolic (ED) S-L diameter (21.6+/-2.8 versus 17.1+/-2.6 mm; p = 0.0005) and ED MAA (618+/-126 versus 525+/-114 mm2; p = 0.0004), but did not perturb normal AMAA (15.8+/-4.1 versus 15.1+/-4.8%; p = 0.4), annular flexion (2.0+/-0.7 versus 1.8+/-0.7 mm; p = 0.3) or AML excursion (55+/-7 versus 53+/-7 degrees; p = 0.1). PML excursion was decreased only slightly (52+/-11 versus 44+/-12 degrees; p = 0.002). CONCLUSION: SLAC substantially reduced S-L annular size, but without perturbing normal MA contraction dynamics, MA flexion, or anterior leaflet excursion. This novel surgical method might represent an alternative to mitral annuloplasty for patients with certain types of mitral pathology.