A geometry-based finite element tool for evaluating mitral valve biomechanics.

Sizing for Mitral Annuloplasty: Where Does Science Stop and Voodoo Begin?

Objective To evaluate the clinic effect of leaflet enlargement with autologous pericardium in repairing mitral valve disease and to describe the technique and discuss its indications. Methods Between July 2004 and June 2008, 45 pa-tients with isolated mitral valve disease, included stenosis in 10 and regurgitation in 35. The causes were congenital heart dis-ease in 8, rheumatic in 21, degenerative in 7 and endecarditis in 9. The procedures were: posterior leaflet enlargement with autologuus pericardium in 14, anterior leaflet enlargement in 8, both anterior and posterior leaflet enlargement in 23. In addi-tion, eye to eye technique was in 12, artificial chordal in 12, chordal transfer in 6, papillary muscle vepesitioning in 4. Mitral anuuloplasty was performed in all cases. Before and after surgery, cardiac function parameters were compared. Results No operative deaths occurred. One case wastransfered to mitral valve replacement due to regurgation, lntraoperative transesophageal echocardiography showed no mitral regurgitation in 38 and small regurgitation in 6 cases. The mean mitral valve effective orifice area(MVEOA) was (2.8±0.6) cm~2, with a mean gradient pressure of (6.21±1.34) mm Hg after operation. The mean followed up was ( 18.0±2.1 ) months. Echocardiography study showed that no mitral regurgitation in 35 cases, slight regurgi-tation in 9, mean mitral effective orifice area was (2.5±0. 8 ) cm~2, mean gradient pressure of (7.21±0. 45 ) mm Hg, no one need reoperation. Postoperative cardiac functions were significantly improved: the average left ventricular end-diastolic diameter (LVEDD) was (48±7) mm [ preoperative (56±6) nun, P <0.05], ejection fraction (EF) was 0.51～0.24( preoperative 0.45± 0.23, P < 0.05 ), the average left atrium diameter ( LA ) was ( 50±11 ) mm [ preoperative ( 62±23 ) mm, P <0. 05 ]. The function of mitral valves was well performed. Conclusion Leaflet enlargement with autologous pericardium com-bined with mitral annuloplasty was effective in repairing of diseased mitral valve. The advantages of the procedure including simplicity, good compatibility, avoiding foreign body and no need for anticoagulation. Key words: Heart valve disease; Cardiac surgical procedure; Autologous pericardium

Artificial chordae

Midterm Outcomes: A Comprehensive Approach to Surgery for Hypertrophic Obstructive Cardiomyopathy

Mitral Valve Dynamics in Severe Aortic Stenosis before and after Aortic Valve Replacement

Although mitral valve (MV) repair initially restores normal leaflets coaptation and stops MV regurgitation, in long term it can also dramatically change the leaflet geometry and stress distribution that may be in-part responsible for limited repair durability. As shown for other collagenous tissues, such changes in geometry and loading reorganize the fiber architecture. In addition, MV interstitial cells may also respond to the altered stress by reducing biosynthetic function, which would affect the load-bearing capabilities of MV and its long-term durability. Thus, investigating the repair-induced MV stress and the concomitant microstructural alterations is a key step in assessing the repaired valve durability. Finite element models have been widely used for stress analysis of the mitral valve. Most of these models, however, have employed only basic constitutive models and above all ignore the complex microstructure of the MV. In addition, the geometry of the valve is usually simplified. Thus, in this work we developed a method to obtain accurate geometrical model of the ovine MV and quantify its fiber structure for the purposes of developing high fidelity computational meshes of the MV. To obtain an accurate geometry of the MV, microcomputed tomography (micro-CT) was used. The entire heart was scanned via a SIEMENS Inveon CT scanner. Three-dimensional scans were segmented semi-automatically using ScanIP segmentation software. The 3D positional data of the fiducial markers were also obtained via ScanIP masks generated by using gray-scale threshold of the CT scans. The segmented geometry was then converted to finite element meshes using ScanIP mesh free mesh generator scheme. Next, the anterior leaflet was then dissected and prepared for measurements of its fiber alignment. The positional data of each point on the accurate mesh was then projected onto the 3D marker mesh. By using a computational domain, the projected point was mapped back to the 2D flattened surface. In addition to mapping, the current method can be used to estimate the changes in connective tissue structure with deformation. This is done by for each point on the valve surface using the local right Cauchy strain tensor C using an in-plane convective curvilinear coordinate system to convect the local fiber orientation to predict the current fiber alignment. To conclude, a robust technique to quantify and map the fibrous microstructure of the MV anterior leaflet to anatomically accurate 3D MV shape derived from micro-CT imaging was developed. The method provides a framework for development of anatomically and micro-structurally accurate finite element models of MV using our tissue structure-based models. It can also be used as a means to validate predicted changes in fibrous structure due to altered stress following surgical interventions.

Closure of the left atrioventricular orifice is achieved when the anterior and posterior leaflets of the mitral valve press together to form a coaptation zone along the free edge of the leaflets. This coaptation zone is critical to valve competency and is maintained by the support of the mitral annulus, chordae tendinae, and papillary muscles. Myocardial ischemia can lead to an altered performance of this mitral complex generating suboptimal mitral leaflet coaptation and a resultant regurgitant orifice. This paper reports on a two-part experiment undertaken to measure the dependence of coaptation force distribution on papillary muscle position in normal and functional regurgitant porcine mitral heart valves. Using a novel load sensor, the local coaptation force was measured in vitro at three locations (A1-P1, A2-P2, and A3-P3) along the coaptation zone. In part 1, the coaptation force was measured under static conditions in ten whole hearts. In part 2, the coaptation force was measured in four explanted mitral valves operating in a flow loop under physiological flow conditions. Here, two series of tests were undertaken corresponding to the normal and functional regurgitant state as determined by the position of the papillary muscles relative to the mitral valve annulus. The functional regurgitant state corresponded to grade 1. The static tests in part 1 revealed that the local force was directly proportional to the transmitral pressure and was nonuniformly distributed across the coaptation zone, been strongest at A1-P1. In part 2, tests of the valve in a normal state showed that the local force was again directly proportional to the transmitral pressure and was again nonuniform across the coaptation zone, been strongest at A1-P1 and weakest at A2-P2. Further tests performed on the same valves in a functional regurgitant state showed that the local force measured in the coaptation zone was directly proportional to the transmitral pressure. However, the force was now observed to be weakest at A1-P1 and strongest at A2-P2. Movement of the anterolateral papillary muscle (APM) away from both the annular and anterior-posterior (AP) planes was seen to contribute significantly to the altered force distribution in the coaptation zone. It was concluded that papillary muscle displacement typical of myocardial ischemia changes the coaptation force locally within the coaptation zone.

We present a technique for mitral valve (MV) replacement that preserves the anterior mitral leaflet (AML) using complete chordal-sparing mitral valve replacement (CCS-MVR), which maintains the architecture of the left ventricle. This technique is beneficial for patients with functional, degenerative, and infective MV disease who were unable to undergo MV repair. The objective of this study is to ascertain the most efficacious treatment for MV disease. Furthermore, the study will contribute to international guidelines for this procedure and provide data on its efficacy in treating MV disease. We performed MV replacement surgery on 161 patients, maintaining the integrity of the entire subvalvular chordae tendineae apparatus. Of these cases, 92 (57.1%) were degenerative, 58 (36.0%) were functional, 9 (5.6%) were infective, and 2 (1.2%) were rheumatic. Of the 93 patients with complicated MV disease, massive calcification was observed in 59 cases (36.6%) and mitral annular disjunction (MAD) was observed in 25 cases (15.5%) while endocarditis with posterior annular abscess was observed in 9 cases (5.6%). The anterior leaflet is detached from its connection to the annulus along the entire extent from the posterior commissure to the anterior commissure. In cases of excess tissue, a section of the free edge of the translocated leaflet must be removed. This must preserve a small section of the edge and the entire chordae tendineae unit. A CCS-MVR requires 24 to 28 individual sutures in routine cases. The AML was reinserted using 12 to 14 single sutures in this specific order: posterior annulus, posterior mitral leaflet, AML, and prosthetic valve. The 30-day mortality rate was 8.7%, based on 14 cases. Ten patients, representing 5% of the total, required reoperation after the initial procedure. Out of 140 patients,74 (52.8%) experienced LV reverse remodeling at the six-month follow-up. Female patients exhibited a significantly higher rate of LV reverse remodeling (71% vs. 29%, P<0.001) compared to male patients. Patients with mitral annular calcification and MAD demonstrated significantly higher rates of left ventricular reverse remodeling compared to patients with coronary artery disease (CAD). We can conclude with certainty that male gender, CAD, atrial fibrillation, and preoperative left ventricular end-diastolic volume indexed (LVEDVI) are significant predictors of LV remodeling. We found that the median survival time after CCS-MVR was 39.5 months. The results of the multivariable analysis revealed that patients with MAD had significantly worse survival rates than those without. For patients presenting with severely calcified posterior mitral annulus, complicated Barlow disease with MAD, or endocarditis involving the posterior annulus, the AML is consolidated with the posterior mitral leaflet to form a neo-annulus. This procedure is safe and effective for a wide range of simple and complex MV pathologies. Its efficacy is unquestionable. It preserves the complete architecture of the left ventricle, avoiding dilatation and promoting reverse remodeling.

The parachute-like asymmetric mitral valve and its two papillary muscles

Breaking the Mold: Lithotripsy for Mitral Annular Calcification.

Mass-spring models for the simulation of mitral valve function: Looking for a trade-off between reliability and time-efficiency

Hypertrophic cardiomyopathy (HCM) is a common monogenetic cardiac disease with a prevalence of 0.2%1 that usually is inherited as an autosomal dominant trait with variable penetrance and expression. Clinically, HCM is defined by the presence of left ventricular (LV) hypertrophy (LVH) unexplained by abnormal loading conditions.1 The natural history varies from an asymptomatic course to drug-refractory angina/dyspnea, sudden cardiac death (SCD), and end-stage heart failure. The incidence of HCM-related SCD is approximately 1% to 2% in children and adolescents and 0.5% to 1% in adults.2,3 In this review, we examine the impact of advanced diagnostic imaging technologies on HCM, with particular emphasis on the detection of particular genetic subtypes. In ≈60% of cases, HCM is inherited as an autosomal dominant trait caused by mutations in genes coding for cardiac sarcomere proteins (Figure 1).4–7 Mutations in genes encoding Z-disc proteins and proteins involved in calcium regulation account for <5% of cases. The absence of sarcomeric gene mutations can be explained by limitations of current mutation detection techniques or mutations in as yet unidentified genes, but in some cases, hypertrophy is caused by other diseases that mimic the phenotype of sarcomeric protein disease. Table 1 lists genetic disorders associated with HCM. Figure 1. A schematic illustration of a cardiac sarcomere. View this table: Table 1. Currently Known Genes Implicated in HCM More than 600 different sarcomeric gene mutations are reported in patients with HCM.8–16 The majority are missense mutations, but nonsense, frameshift, and in-frame insertion/deletion mutations also occur. Most mutations are characterized by incomplete penetrance and variable clinical expression likely due to locus heterogeneity and the effect of mutations at different locations within the same gene. Most mutations probably have a dominant negative effect on sarcomere function, but in some cases, haploinsufficiency (ie, only a single functional …

Pregnancy produces rapid, dramatic volume-overload changes to the maternal circulation. This paper examines pregnancy-induced structural-mechanical changes in bovine aortic and mitral heart valve leaflets. Valve leaflets were harvested from non-pregnant heifers and pregnant cows. Dimensions, biaxial extensibility and creep resistance were assessed and related to changes in the collagen network: histological leaflet and anatomic layer thicknesses plus collagen crimp, and biochemical collagen content. Collagen stability and crosslinking were assessed thermomechanically. Pregnancy altered both aortic and mitral valve leaflets. Both valves demonstrated biphasic changes in leaflet stretch, decreasing in early pregnancy and recovering by late pregnancy. Creep in leaflets from both valves was minimal and decreased even further with pregnancy in the mitral valve. There were valve-specific changes in preconditioning areal extension with pregnancy: increasing in the aortic valve and decreasing in the mitral valve. Leaflet area increased dramatically (84% aortic, 56% mitral), with thickening mainly in the fibrosa, accompanied by increases in collagen content (8% aortic, 16% mitral): together suggesting synthesis of new collagen. Collagen crimp was almost completely lost in pregnancy, with the denaturation temperature decreased by approximately 2 °C. Mature and total crosslinking increased, curiously without a significant increase in immature crosslinking. Mature aortic and mitral heart valve leaflets in the maternal cardiovascular system remodel substantially and similarly-despite their different embryological origins.

Surgical technique of implanting the stentless porcine mitral valve

Mitral valve–sparing operation in subaortic stenosis caused by anomalous papillary muscle and discrete subaortic stenosis