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PURPOSE: This study presents analytic techniques to quantify cardiac pulsatility-induced deformations of thoracic aortic endografts in patients with thoracic aortic aneurysm (TAA), dissection (TAD), and blunt thoracic aortic injury (BTAI) after thoracic endovascular aortic repair (TEVAR). TECHNIQUE: We analyzed 19 image data sets from 14 patients treated for TAA, TAD, and BTAI with cardiac-gated post-TEVAR CTs. Systolic and diastolic geometric models were constructed and diametric, axial, and bending deformations were quantified. For patients with cardiac-gated pre-op scans, the damping of pulsatile diametric distension was computed. Maximum localized diametric distension was 2.4±1.0%, 4.2±1.7%, and 5.5±1.6%, and axial deformation was 0.0±0.1%, -0.1±0.3%, and 1.1±0.6% in the endografts of TAA, TAD, and BTAI cohorts, respectively. Diametric distension damping from pre- to post-TEVAR was ~50%. Diametric and bending deformations were localized at certain axial positions on the endograft, and the inner curve bends more than the centerline, especially adjacent to overlapping regions. CONCLUSION: The presented techniques support investigation of multi-axial endograft deformations between disease causes and geometric locations on the device. Discretized quantification of deformation is needed to define device fatigue testing conditions and predict device durability in patients. CLINICAL IMPACT: This study demonstrates analytic techniques to quantify discretized deformation of thoracic endografts. Cardiac-resolved computed tomography is sometimes acquired for surgical planning and follow-up, however, the dynamic data are not typically used to quantify pulsatile deformations. Our analytic techniques extract the centerline and surface geometry of the stented thoracic aorta during the cardiac cycle, which are used to quantify diametric, axial, and bending deformations to provide better understanding of device durability and impact on the native anatomy.

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OBJECTIVE: The study objective was to evaluate the safety and effectiveness of the second-generation, low-profile RelayPro (Terumo Aortic) thoracic endograft for the treatment of descending thoracic aortic aneurysm or penetrating atherosclerotic ulcer. METHOD: A prospective, international, nonblinded, nonrandomized, pivotal trial analyzed a primary safety end point of major adverse events at 30 days (death, myocardial infarction, stroke, renal/respiratory failure, paralysis, bowel ischemia, procedural blood loss) and a primary effectiveness end point of treatment success at 1 year (technical success, patency, absence of aneurysm rupture, type I/III endoleaks, stent fractures, reinterventions, aneurysm expansion, and migration) compared with performance goals from the previous generation Relay pivotal study. The study was conducted in 36 centers in the United States and Japan and enrolled participants between 2017 and 2019. RESULTS: The study population of 110 patients had a median (interquartile range) age of 76 (70-81) years, 69 (62.7%) were male, and 43 (39.1%) were Asian. Patients were treated for 76 fusiform aneurysms (69%), 24 saccular aneurysms (22%), and 10 penetrating atherosclerotic ulcers (9%). Most patients (82.7%) were treated with a non-bare stent configuration. Technical success was 100%. The median (interquartile range) procedure time was 91 (64-131) minutes, and the deployment time was 16 (10-25) minutes. A total of 50 patients (73.5%) in the US cohort had percutaneous access, whereas centers in Japan used only surgical cutdown. The 30-day composite major adverse events rate was 6.4% (95% upper confidence interval, 11.6%; P = .0002): 2 strokes, 2 procedural blood losses greater than 1000 mL requiring transfusion, 2 paralysis events, and 1 renal failure. Primary effectiveness was 89.2% (lower 95% confidence interval, 81.8%; P = .0185). Nine subjects experienced 11 events (1 aneurysm expansion, 6 secondary interventions, and 4 type I endoleaks). There was no loss of stent-graft patency, no rupture, no fractures, and no migration. CONCLUSIONS: The low-profile RelayPro thoracic endograft met the study primary end points and demonstrated satisfactory 30-day safety and 1-year effectiveness for the treatment of patients with aneurysms of the descending thoracic aorta or penetrating atherosclerotic ulcers. Follow-up is ongoing to evaluate longer-term outcomes and durability.

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OBJECTIVE: Transcarotid access for transcatheter aortic valve replacement is emerging as an alternative to more traditional nonfemoral access options such as transapical or transaortic; however, comparative data are limited. The purpose of the study was to analyze outcomes after transcatheter aortic valve replacement using transcatheter compared with transthoracic (transapical/transaortic) access. METHODS: The Society of Thoracic Surgeons/American College of Cardiology Transcatheter Valve Therapy Registry was queried for patients who underwent transcarotid, transapical, or transaortic transcatheter aortic valve replacement with the SAPIEN 3 (Edwards Lifesciences, Irvine, Calif) transcatheter heart valve between June 2015 and July 2019. Thirty-day unadjusted outcomes were evaluated, and propensity score matching and logistic regression were used to compare transcatheter access with transthoracic access. RESULTS: In the propensity-matched analysis, 667 transcarotid transcatheter aortic valve replacement procedures were compared with 1334 transthoracic procedures. Transcarotid transcatheter aortic valve replacement was associated with lower mortality (4.2% vs 7.7%, P = .004), less new-onset atrial fibrillation (2.2% vs 12.1%, P < .0001), fewer readmissions at 30 days (9.8% vs 16.1%, P = .0006), shorter median length of stay (3.0 vs 6.0 days, P < .0001), shorter median intensive care unit stay (25 vs 47.2 hours, P < .0001), and greater 30-day Kansas City Cardiomyopathy Questionnaire score improvement from baseline (25.1 vs 20.8, P = .007). Stroke (4.3% vs 3.7%, P = .44) and major vascular complications (1.4% vs 1.9%, P = .40) were similar. CONCLUSIONS: Transcatheter aortic valve replacement using transcarotid access is associated with lower 30-day mortality, less atrial fibrillation, shorter intensive care unit and overall length of stay, fewer readmissions, greater improvement in Kansas City Cardiomyopathy Questionnaire scores, and no significant difference in stroke or major vascular complications compared with transthoracic access.

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BACKGROUND: Subclavian/axillary (TAx) access has become the most frequently used alternative access route for transcatheter aortic valve replacement (TAVR). Transcarotid (TC) TAVR has grown in popularity recently. Comparative data between these 2 contemporary access methods is lacking. METHODS: Data were extracted from The Society of Thoracic Surgeons/American College of Cardiology Transcatheter Valve Therapy (TVT) Registry™ (June 2015 to October 2019) for patients undergoing TAVR by TC or TAx access with the SAPIEN 3 and SAPIEN 3 Ultra (Edwards Lifesciences, Irvine, CA) transcatheter heart valves. Procedural, index hospitalization, and 30-day outcomes were analyzed for TC vs TAx groups after 1:2 propensity matching of patient baseline characteristics. RESULTS: The study included 3903 cases, of which 801 TC and 3102 TAx procedures were compared. After 1:2 propensity matching, TC TAVR was associated with similar 30-day mortality (4.3% vs 5.2%, P = .34) but a significantly lower risk of stroke (4.2% vs 7.4%; hazard ratio, 0.56; 95% confidence interval, 0.38-0.83; P = .003) compared with TAx access. Other outcomes that favored TC over TAx included shorter procedure time (117.0 vs 132.4 minutes; P < .001) and fluoroscopy time (16.6 vs 21.6 min; P < .001), lower contrast volume (78.5 vs 96.7 mL; P < .001), shorter length of stay in the intensive care unit (24.3 vs 25.0 hours; P = .02) and hospital (2.0 vs 3.0 days; P = .002), and more patients discharged to home (82.9% vs 74.6%; P < .001). CONCLUSIONS: TC TAVR is associated with similar mortality and a significant reduction in stroke compared with the TAx approach. If femoral access is precluded, TC may be a safe, or at times, preferred avenue of transcatheter valve delivery.

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BACKGROUND: Open surgical closure and small-bore suture-based preclosure devices have limitations when used for transcatheter aortic valve replacement, percutaneous endovascular abdominal aortic aneurysm repair, or percutaneous thoracic endovascular aortic aneurysm repair. The MANTA vascular closure device is a novel collagen-based technology designed to close large bore arteriotomies created by devices with an outer diameter ranging from 12F to 25F. In this study, we determined the safety and effectiveness of the MANTA vascular closure device. METHODS AND RESULTS: A prospective, single arm, multicenter investigation in patients undergoing transcatheter aortic valve replacement, percutaneous endovascular abdominal aortic aneurysm repair, or thoracic endovascular aortic aneurysm repair at 20 sites in North America. The primary outcome was time to hemostasis. The primary safety outcomes were accessed site-related vascular injury or bleeding complications. A total of 341 patients, 78 roll-in, and 263 in the primary analysis cohort, were entered in the study between November 2016 and September 2017. For the primary analysis cohort, transcatheter aortic valve replacement was performed in 210 (79.8%), and percutaneous endovascular abdominal aortic aneurysm repair or thoracic endovascular aortic aneurysm repair was performed in 53 (20.2%). The 14F MANTA was used in 42 cases (16%), and the 18F was used in 221 cases(84%). The mean effective sheath outer diameter was 22F (7.3 mm). The mean time to hemostasis was 65±157 seconds with a median time to hemostasis of 24 seconds. Technical success was achieved in 257 (97.7%) patients, and a single device was deployed in 262 (99.6%) of cases. Valve Academic Research Consortium-2 major vascular complications occurred in 11 (4.2%) cases: 4 received a covered stent (1.5%), 3 had access site bleeding (1.1%), 2 underwent surgical repair (0.8%), and 2 underwent balloon inflation (0.8%). CONCLUSIONS: In a selected population, this study demonstrated that the MANTA percutaneous vascular closure device can safely and effectively close large bore arteriotomies created by current generation transcatheter aortic valve replacement, percutaneous endovascular abdominal aortic aneurysm repair, and thoracic endovascular aortic aneurysm repair devices. CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov . Unique identifier: NCT02908880.

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The aims of this analysis were to characterize the burden and timing of bleeding events in females versus males on left ventricular assist device (LVAD) support. A single-center retrospective review of 375 patients receiving continuous-flow LVADs was performed. Bleeding events included gastrointestinal, naso-oropharyngeal, gynecologic (GYN), intracranial hemorrhage (ICH), and mediastinal bleeding. Cox hazard ratios (HRs) [95% CI] and incident event rates for females versus males were calculated. Eighty-four females (22%) and 291 males (78%) received an LVAD. There were 189 patients with 406 bleeding events over a median 399 days of support. Two-year freedom from bleeding was 33 ± 6.2% in females and 46 ± 3.7% in males (p = 0.027). Correlates of bleeding included female sex (adjusted HR = 1.6 [1.1-2.2]) and older age (adjusted HR = 1.2 [1.1-1.3] per 10 years). There was no sex-associated difference in 30 day mediastinal bleeding (males 12%; females 16% at 30 days; overall p = 0.35), but incident event rates for overall bleeding and naso-oropharyngeal bleeding were higher in females (p < 0.05) and trends were noted in ICH (eppy: 0.06 male vs. 0.10 female, p = 0.14). Eight females (10%) experienced 12 GYN bleeding events; five required surgical intervention. In summary, females had a 60% higher hazard of bleeding than males with significant morbidity encountered from mucosa (including vaginal) bleeding. Future large device studies should be inclusive of sex-specific outcomes.

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The aim of this study was to evaluate the performance of an adjusted HeartMate II risk score (HMRS) in Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS; n = 9,733) and in HeartWare Ventricular Assist Device (HVAD) bridge to transplant (BTT) trial patients (n = 360). Interagency Registry for Mechanically Assisted Circulatory Support data were used to calculate an adjusted HMRS, omitting center volume, for all patients on continuous-flow left ventricular assist device (LVAD) support. Ninety day mortality was then evaluated in INTERMACS and HVAD-BTT patients. Four risk groups were identified based on INTERMACS patient-adjusted HMRS: very low (<5%, 90 day mortality; score <0.20), low (5-10%, 90 day mortality; score 0.20-1.97), medium (10-20%, 90 day mortality; score 1.98-4.48), and high risk (>20%, 90 day mortality; score >4.48). Within INTERMACS, there were significant differences in survival between all-adjusted HMRS risk groups (p < 0.001 in pairwise comparisons). Controlling for known mortality correlates, the adjusted HMRS mortality hazard ratio was 1.19 (1.25-1.23) per unit HMRS increase. The HVAD cohort was a low-risk cohort with 90 day survivals for very low-, low-, and medium-risk patients of 100%, 97 ± 1.1%, and 90 ± 3.6%, respectively (p = 0.007). Patients in the very low- and low-risk group had significantly improved survival compared with medium-risk patients, respectively (both p < 0.05). The adjusted HMRS appropriately risk stratified a large cohort of INTERMACS patients and was predictive of survival in HeartWare-supported patients.

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OBJECTIVE: As thoracic aortic aneurysms (TAAs) are more frequently being treated with endografts, the anatomic challenges of the thoracic aorta have led to design modifications of endografts. The Conformable GORE TAG (CTAG) device (W. L. Gore & Associates, Flagstaff, Ariz) was specifically designed to be more conformable in tortuous anatomy, more resistant to compression, and more accommodating to various aortic diameters compared with the original GORE TAG device. This prospective, multicenter study evaluated the safety and effectiveness of the CTAG endograft in the repair of descending TAA. METHODS: This was a prospective, multicenter regulatory study with a primary end point of freedom from major device event through 1 month after treatment. Two-year outcomes included aneurysm-related morbidity (endoleaks and morphology changes), aneurysm-related mortality, and all-cause mortality. RESULTS: Fifty-one patients were enrolled between October 2009 and October 2010, with at least one endograft implanted in 50 patients. After the regulatory study successfully completed its primary end point and expanded to a continued-access phase, 15 additional patients were enrolled in the continued-access arm of the study from February 2011 until September 2011, for a total treatment group of 66 patients for the early results and 65 patients for the long-term clinical results with imaging evaluation. There was one 30-day death (1.5%), two patients (3%) with spinal cord ischemia, and two central strokes (3%) ≤30 days. Five patients (7.6%) died ≤1 year; 1 of ascending aortic aneurysm rupture, 2 of cardiac disease, and 2 of respiratory failure. The core laboratory adjudicated 1-month imaging in 60 patients (92.3%), where nine endoleaks (15.0%) were identified (1 type Ia, 4 type II, and 4 indeterminate). Forty-five patients (69.2%) had 2-year imaging with five endoleaks (11.1%; two type II and three indeterminate), and one patient had a distal aortic dilatation that required a secondary intervention. At 2 years, 20 of 38 imaged patients (52.6%) had aneurysm shrinkage ≥5 mm, 15 (39.5%) had no change in diameter, and three patients (7.9%) had an increase in aneurysm diameter of ≥5 mm. There were no conversions, fractures, compressions, or aneurysm ruptures of the treated segment through 2 years. CONCLUSIONS: This next-generation thoracic endograft has a low rate of major device events through 2 years, with no graft compressions or device failures. The data for this new endograft demonstrate favorable outcomes and confirm low risks for treatment for patients with TAA. Follow-up will be continued for 5 years.

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OBJECTIVE: We evaluated a large single center experience of endograft repair of blunt traumatic injury of the thoracic aorta. SUMMARY BACKGROUND DATA: Traumatic aortic transection is a devastating injury with high morbidity and mortality. Endograft repair of these injuries has reduced the rates of death and paraplegia seen with open surgical treatment in the past. However, endograft repair has been associated with a higher incidence of device related failure. METHODS: The records of 43 consecutive cases of endograft treatment of traumatic aortic injury from December 2004 to November 2008 were reviewed. Patient demographics, procedure details, and outcomes were recorded. Aortic morphology was analyzed for predictors of device failure. RESULTS: Forty-three patients (32 men) with a mean age of 44 years (range: 17-88) were treated. Primary technical success was 86%. Six proximal endoleaks (14.3%) occurred. Two were repaired with a more proximal cuff, but 3 required explantation and open repair (7%). Mortality in this series was 11.6%, but no death was aorta related. No patient having endograft treatment suffered postoperative paraplegia. Early device failure is associated with sharp angulation of the aorta and shortened distance between the left subclavian artery and the site of injury. Follow-up ranged from 1 to 38 months (mean: 7.4 months). There were no late device failures or complications. CONCLUSIONS: Endovascular repair of blunt traumatic aortic injury can be performed with a low morbidity and mortality. Anatomic patterns in the aortic arch appear to be predictive of early device failure. Midterm durability is excellent, but reliable follow-up remains challenging in this group of patients.

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Cardiac transplantation remains the first choice for the surgical treatment of end stage heart failure. An inadequate supply of donor grafts that meet existing criteria has limited the application of this therapy to suitable candidates and increased interest in extended criteria donors. Although cold storage (CS) is a time-tested method for the preservation of hearts during the ex vivo transport interval, its disadvantages are highlighted in hearts from the extended criteria donor. In contrast, transport of high-risk hearts using hypothermic machine perfusion (MP) provides continuous support of aerobic metabolism and ongoing washout of metabolic byproducts. Perhaps more importantly, monitoring the organ's response to this intervention provides insight into the viability of a heart initially deemed as extended criteria. Obviously, ex vivo MP introduces challenges, such as ensuring homogeneous tissue perfusion and avoiding myocardial edema. Though numerous groups have experimented with this technology, the best perfusate and perfusion parameters needed to achieve optimal results remain unclear. In the present review, we outline the benefits of ex vivo MP with particular attention to how the challenges can be addressed in order to achieve the most consistent results in a large animal model of the ideal heart donor. We provide evidence that MP can be used to resuscitate and evaluate hearts from animal and human extended criteria donors, including the non-heart beating donor, which we feel is the most compelling argument for why this technology is likely to impact the donor pool.

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OBJECTIVE: Progressive left ventricular remodeling after myocardial infarction has been viewed as an important contributor to progressive heart failure. The objective of this study was to investigate the relationship between myocardial apoptosis and strain during progressive cardiac remodeling. METHODS: Before creation of an anterolateral left ventricular infarction by ligation of diagonal arteries, 16 sonomicrometry transducers were placed in the left ventricular free wall of 8 sheep to assess regional deformation in the infarct, adjacent, and normally perfused remote myocardial regions over 8 weeks' duration. Hemodynamic, echocardiographic and sonomicrometric data were collected before infarction and then 30 minutes and 2, 6, and 8 weeks after infarction. At the end of the study, regional myocardial tissues were collected for apoptotic signaling proteins. RESULTS: At terminal study, an increase in left ventricular end-diastolic pressure of 8.1 +/- 0.1 mm Hg, a decrease in ejection fraction from 54.19% +/- 5.68% to 30.55% +/- 2.72%, and an end-diastolic volume increase of 46.08 +/- 5.02 mL as compared with the preinfarct values were observed. The fractional contraction at terminal study correlated with the relative abundance of apoptotic protein expressions: cytochrome c (r(2) = 0.02, P < .05), mitochondrial Bax (r(2) = 0.27, P < .05), caspase-3 (r(2) = 0.31, P < .05), and poly (adenosine diphosphate-ribose) polymerase (r(2) = 0.30, P < .05). These myocardial apoptotic activities also correlated with remodeling strain: cytochrome c (r(2) = 0.02, P < .05), mitochondrial Bax (r(2) = 0.28, P < .05), caspase-3 (r(2) = 0.43, P < .05), and poly (adenosine diphosphate-ribose) polymerase (r(2) = 0.37, P < .05). CONCLUSION: Increase in regional remodeling strain led to an increase in myocardial apoptosis and regional contractile dysfunction in heart failure.

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BACKGROUND: Thoracic aortic injury remains a leading cause of death after blunt trauma. Thoracic aortic stents have the potential to treat aortic tears using a less invasive approach. We have accumulated the largest series of patients treated with blunt thoracic aortic injury over a 2-year period. METHODS: From July 2005 to present, 26 patients presenting with blunt aortic injury were treated with thoracic aortic endografting; these patients were retrospectively compared with the prior 26 patients presenting with similar aortic injury who were treated by open surgical repair. A Severity Characterization of Trauma score calculated for each patient predicts mortality based on severity of injury and degree of physiologic derangement on presentation. RESULTS: Patients treated with endografting had a significantly shorter length of stay, less intraoperative blood loss, decreased 24-hour blood transfusion, and lower incidence of postoperative tracheostomy compared with patients undergoing open repair. Survival in both groups was similar despite a trend toward higher injury severity among patients treated with endografting. CONCLUSIONS: This early experience suggests that aortic endografting may provide a safe and efficient treatment of aortic tears that cardiac surgeons can be successful in employing.

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BACKGROUND: Cardiac remodeling has been shown to have deleterious effects at both the global and local levels. The objective of this study is to investigate the role of strain in the initiation of structural and functional changes of myocardial tissue and its relation to alteration of calcium-handling proteins during cardiac remodeling after myocardial infarction. METHODS: Sixteen sonomicrometry transducers were placed in the left ventricular free wall of 9 sheep to measure the regional strain in the infarct, adjacent, and remote myocardial regions. Hemodynamic, echocardiographic, and sonomicrometry data were collected before myocardial infarction, after infarction, and 2, 6, and 8 weeks after infarction. Regional myocardial tissues were collected for calcium-handling proteins at the end study. RESULTS: At time of termination, end-systolic strains in 3 regionally distinct zones (remote, adjacent, and infarct) of myocardium were measured to be -14.65 +/- 1.13, -5.11 +/- 0.60 (P < or = .05), and 0.92 +/- 0.56 (P < or = .05), respectively. The regional end-systolic strain correlated strongly with the abundance of 2 major calcium-handling proteins: sarcoplasmic reticulum Ca2+ adenosine triphosphatase subtype 2a (r2 = 0.68, P < or = .05) and phospholamban (r2 = 0.50, P < or = .05). A lesser degree of correlation was observed between the systolic strain and the abundance of sodium/calcium exchanger type 1 protein (r2 = 0.17, P < or = .05). CONCLUSIONS: Regional strain differences can be defined in the different myocardial regions during postinfarction cardiac remodeling. These differences in regional strain drive regionally distinct alterations in calcium-handling protein expression.

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BACKGROUND: Early infarct expansion initiates adverse remodeling, leads to left ventricular dilatation and portends a poor long-term outcome. Early mechanical prevention of infarct expansion has been proposed as a method to improve remodeling, but the extent of ventricular restraint necessary to optimize the salutary effect is not known. We tested the hypothesis that left ventricular restraint (wrap) is superior to infarct stiffening (patch). METHODS: Infarction of 20% to 25% of the left ventricle was induced by coronary ligation in 69 sheep. Infarcts were either anteroapical (n = 33) or posterobasal (n = 36). Animals with each infarct received either no treatment (anteroapical, n = 26; posterobasal, n = 17), infarct stiffening with a localized Marlex mesh patch (posterobasal, n = 9) or left ventricular wrapping with Merseline mesh (anteroapical, n = 7; posterobasal, n = 10). End-systolic volume, end-diastolic volume, end-systolic muscle to cavity area ratio, left ventricular sphericity, ejection fraction, and degree of mitral regurgitation as determined by quantitative echocardiography were assessed before infarction and at 2, 5, and 8 weeks after infarction to evaluate the extent of left ventricular remodeling. RESULTS: Control animals in both groups experienced adverse remodeling. Anteroapical infarct animals developed large left ventricular aneurysms and the posterobasal infarct animals developed severe mitral regurgitation. Early infarct stiffening did not significantly improve any aspect of remodeling due to the posterobasal infarct. Early left ventricular wrapping significantly improved remodeling after both types of infarctions. CONCLUSIONS: Early left ventricular wrapping attenuates infarct expansion and has a salutary effect on remodeling. Simple infarct stiffening alone is not effective.

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OBJECTIVES: Surgical treatment for ischemic mitral regurgitation has become more aggressive. However, no clinical study has demonstrated that surgical correction of chronic ischemic mitral regurgitation improves survival. We used 4 well-developed ovine models of postinfarction left ventricular remodeling to test the hypothesis that ischemic mitral regurgitation does not significantly contribute to postinfarction left ventricular remodeling. METHODS: Infarction of 21% to 24% of the left ventricular mass was induced by means of coronary ligation in 77 sheep. Infarctions varied only by anatomic location in the left ventricle: anteroapical, n = 26; anterobasal, n = 16; laterobasal, n = 9; and posterobasal, n = 20. Six additional sheep had ring annuloplasty before posterobasal infarction. End-systolic and end-diastolic left ventricular volume, end-systolic muscle-to-cavity area ratio, left ventricular sphericity, ejection fraction, and degree of ischemic mitral regurgitation, as determined by means of quantitative echocardiography, were assessed before infarction and at 2, 5, and 8 weeks after infarction. RESULTS: All infarcts resulted in significant postinfarction remodeling and decreased ejection fraction. Anteroapical infarcts lead to left ventricular aneurysms. Only posterobasal infarcts caused severe and progressive ischemic mitral regurgitation. Remodeling because of posterobasal infarcts was not more severe than that caused by infarcts at other locations. Furthermore, prophylactic annuloplasty prevented the development of mitral regurgitation after posterobasal infarction but had no effect on remodeling. CONCLUSION: The extent of postinfarction remodeling is determined on the basis of infarct size and location. The development of ischemic mitral regurgitation might not contribute significantly to adverse remodeling. Ischemic mitral regurgitation is likely a manifestation rather than an important impetus for postinfarction remodeling.

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OBJECTIVES: This study was designed to test the hypothesis that ischemic mitral regurgitation (IMR) results from, but does not influence, the progression of left ventricular (LV) remodeling after posterolateral infarction. BACKGROUND: Surgical correction of chronic IMR is being increasingly recommended. METHODS: Three groups of sheep had coronary snares placed around the second and third obtuse marginal coronary arteries. Occlusion of these vessels in the control group resulted in progressive IMR over eight weeks. In a second group, Merseline mesh was fitted to cover the exposed LV before infarction. In a third group, a ring annuloplasty was placed before infarction to prevent IMR. Remodeling and degree of IMR were assessed with echocardiography at baseline and at 30 min and two, five, and eight weeks after infarction. RESULTS: Eight weeks after infarction, mean IMR grade was significantly higher in control animals than mesh and annuloplasty animals. At eight weeks, LV end-systolic volume and end-systolic muscle-to-cavity-area ratio (ESMCAR) were significantly better in mesh-treated sheep than in control sheep; also, at eight weeks, ESMCAR and akinetic segment length were significantly better in mesh-treated sheep than in annuloplasty sheep. Ejection fraction was significantly higher in the mesh than the annuloplasty group. There was no significant difference in any measure of remodeling between the annuloplasty and control groups. CONCLUSIONS: Prophylactic ventricular restraint reduces infarct expansion, attenuates adverse remodeling, and reduces IMR severity. Prevention of IMR by prophylactic ring annuloplasty does not influence remodeling. Ischemic mitral regurgitation is a consequence, not a cause, of postinfarction remodeling; infarct expansion is the more important therapeutic target.

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BACKGROUND: This study was designed to isolate and quantify the effects of ventricular inotropic and chronotropic state on the normal mitral valve annular sphincter mechanism. METHODS: Sonomicrometry tansducers were placed around the mitral annulus in six sheep; atrial pacing wires were also placed. One week later, esmolol was titrated to produce a baseline hemodynamic state with a heart rate of 90 bpm; hemodynamic and sonomicrometry data were recorded. Then animals were paced at 120 bpm and 150 bpm; data were recorded at each heart rate. Isoproterenol infusion was titrated to achieve a heart rate, without pacing, of 120 and 150 bpm; again, data were recorded. Annular area was calculated at end diastole (ED) and end systole (ES) for all experiments using sonomicrometry array localization. Analysis of variance was used to assess the independent effects of heart rate and inotropic state on annular area. RESULTS: Atrial pacing at 120 bpm produced ES and ED annular areas of 777 +/- 150 mm(2) and 748.8 +/- 140.1 mm(2), respectively. At the same heart rate, isoproterenol-treatment resulted in significantly smaller ES and ED areas: 699 +/- 160 mm(2) and 641.9 +/- 156.5 mm(2), respectively. Atrial pacing at 150 bpm produced ES and ED annular areas of 745.2 +/- 131.3 mm(2) and 723.7 +/- 141.3 mm(2), respectively. At the same heart rate, isoproterenol-treatment resulted in significantly smaller ES and ED areas: 652.8 +/- 146.4 mm(2) and 569.7 +/- 155.9 mm(2), respectively. CONCLUSIONS: The inotropic state of the left ventricle directly affects the mitral valve annular orifice area, independent of heart rate. This inotropic effect on valve size is more pronounced at ED than at ES in the sheep.

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