Acute Type A Dissection, Coarctation of Aorta and Levoatriocardinal Vein -- A Rare Combination

Concomitant presence of acute type A dissection and coactation of aorta is rare (1). Levoatriocardinal vein has shown to be associated with left sided hypoplastic lesions as well as with normal hearts (2, 3 ). However, concurrent presence of levoatriocardinal vein with acute type A dissection, severe aortic regurgitation and Coarctation of aortic isthmus was not described. We here described a case of 20 year male presented to emergency department with acute chest pain radiating to back. On evaluation, he was found to have acute type A dissection with dilated aortic root, severe aortic regurgitation, normal mitral valve, severe coarctation of aorta and levoatriocardinal vein. Patient was managed successfully with composite valve conduit replacement of ascending aorta with ascending aortic to descending aortic graft (16mm graft) with levoatriocardinal vein ligation.

Energy loss associated with in-vitro modeling of mitral annular calcification

Introduction Study aims were to compare hemodynamics and viscous energy dissipation (VED) in 3D printed mitral valves–one replicating a normal valve and the other a valve with severe mitral annular calcification (MAC). Patients with severe MAC develop transmitral gradients, without the commissural fusion typifying rheumatic mitral stenosis (MS), and may have symptoms similar to classical MS. A proposed mechanism relates to VED due to disturbed blood flow through the diseased valve into the ventricle. Methods A silicone model of a normal mitral valve (MV) was created using a transesophageal echocardiography dataset. 3D printed calcium phantoms were incorporated into a second valve model to replicate severe MAC. The synthetic MVs were tested in a left heart duplicator under rest and exercise conditions. Fine particles were suspended in a water/glycerol blood analogue for particle image velocimetry calculation of VED. Results Catheter mean transmitral gradients were slightly higher in the MAC valve compared to the normal MV, both at rest (3.2 vs. 1.3 mm Hg) and with exercise (5.9 vs. 5.0 mm Hg); Doppler gradients were 2.7 vs. 2.1 mm Hg at rest and 9.9 vs 8.2 mm Hg with exercise. VED was similar between the two valves at rest. During exercise, VED increased to a greater extent for the MAC valve (240%) versus the normal valve (127%). Conclusion MAC MS is associated with slightly increased transmitral gradients but markedly increased VED during exercise. These energy losses may contribute to the exercise intolerance and exertional dyspnea present in MAC patients.

Pulmonary hypertension and mitral regurgitation in an infant with an anatomically normal mitral valve

A full-term, female presented on her date of birth with severe pulmonary hypertension (PH) and mitral regurgitation (MR), requiring veno-arterial extracorporeal membrane oxygenation. After the treatment, her PH and MR were resolved with no anatomic abnormality present. We propose a positive feedback loop of PH causing right ventricular dilation and interventricular septal shifts, worsening MR, and elevated left atrial, and potentially pulmonary, pressures.

Effect of Edge-to-Edge Mitral Valve Repair on Chordal Strain: Fluid-Structure Interaction Simulations

Edge-to-edge repair for mitral valve regurgitation is being increasingly performed in high-surgical risk patients using minimally invasive mitral clipping devices. Known procedural complications include chordal rupture and mitral leaflet perforation. Hence, it is important to quantitatively evaluate the effect of edge-to-edge repair on chordal integrity. in this study, we employ a computational mitral valve model to simulate functional mitral regurgitation (FMR) by creating papillary muscle displacement. Edge-to-edge repair is then modeled by simulated coaptation of the mid portion of the mitral leaflets. in the setting of simulated FMR, edge-to-edge repair was shown to sustain low regurgitant orifice area, until a two fold increase in the inter-papillary muscle distance as compared to the normal mitral valve. Strain in the chordae was evaluated near the papillary muscles and the leaflets. Following edge-to-edge repair, strain near the papillary muscles did not significantly change relative to the unrepaired valve, while strain near the leaflets increased significantly relative to the unrepaired valve. These data demonstrate the potential for computational simulations to aid in the pre-procedural evaluation of possible complications such as chordal rupture and leaflet perforation following percutaneous edge-to-edge repair.

Histological features of the mitral valve in normal and opioid exposure in experiment

To date, pathology of the cardiovascular system is the most common, tends to increase, most often leads to disability and mortality of the population at a young working age and is an important medical and social problem. The purpose of the study was to establish the features of micro organization of the mitral valve in white rat in norm and after opioid action. The study material is presented by histological samples of a mitral valve of the white rat. The study was performed on 30 adult white reproductive age rats weighing 160-220 g. The experimental animals were injected intramuscularly 1 time per day for the same period of 42 days (6 weeks) with the opioid drug analgesic “Nalbuphine”. Using histological methods, 30 mitral valves of white rat were examined. Microscopy of histological preparations of the valves of the heart was performed sequentially, assessing the morphological changes in the norm and under the action of the opioid after 6 weeks of the experiment. Emphasis was placed on the presence or absence of endothelial layer, as well as the condition of endothelial cells in normal and at the action of the damaging factor, determining the signs of their dystrophy, desquamation and proliferation. It is established that the normal mitral valve is represented by endocardial folds. The rat endocardium consists of three layers: endothelial (endothelial cells rich layer, attached to the basement membrane), subendothelial (connective tissue rich in fibroblasts) and a muscular-elastic layer (represented by smooth myocytes, plaited collagen fibers). After 6 weeks of administration of Nalbuphine, the mitral valve is in a stage of decompensation, when the outer and inner endothelial layers are destroyed, the endothelial cells are deformed, the subendothelial layer is represented by single bundles of different directions. In the musculo-elastic layer, contact between smooth myocytes and fragmented and thinned, collagen and elastic fibers is lost. This study allows us to conclude on the destructive effect of opioid agents on the valvular apparatus of the heart.

Development of a fluid-structure interaction model to simulate mitral valve malcoaptation

Object: Mitral regurgitation (MR) is a condition in which the mitral valve does not prevent the reversal of blood flow from the left ventricle into the left atrium. This study aimed at numerically developing a model to mimic MR and poor leaflet coaptation and also comparing the performance of a normal mitral valve to that of the MR conditions at different gap junctions of 1, 3 and 5 mm between the anterior and posterior leaflets. Results: The results revealed no blood flow to the left ventricle when a gap between the leaflets was 0 mm. However, MR increased this blood flow, with increases in the velocity and pressure within the atrium. However, the pressure within the aorta did not vary meaningfully (ranging from 22 kPa for a ‘healthy’ model to 25 kPa for severe MR). Conclusions: The findings from this study have implications not only for understanding the changes in pressure and velocity as a result of MR in the ventricle, atrium or aorta, but also for the development of a computational model suitable for clinical translation when diagnosing and determining treatment for MR.

EFFECT OF PAPILLARY MUSCLE DISPLACEMENT AND ANNULAR DILATION ON DEVELOPMENT OF FUNCTIONAL MITRAL REGURGITATION

Functional mitral regurgitation (FMR) occurs following left ventricle (LV) dysfunction with normal mitral valve (MV) leaflet. The progress and severity of FMR are closely related to LV dilatation, which often results in displacement of the papillary muscles (PMs) and enlargement of the mitral annulus. We investigated the effect of PM displacement and annular dilation on FMR development to better understand the complex intercorrelation between these pathologic alterations leading to FMR. Virtual MV modeling was performed to create a normal human MV, and several different types of PM displacement, annular dilation, and the combination of PM displacement and annular dilation mimicking the pathology of FMR were modeled. Dynamic finite element evaluation of MV function was performed across the complete cardiac cycle for the normal and FMR MV models. PM displacement to both lateral and apical directions revealed markedly reduced leaflet coaptation and large stress distribution in the P2 scallop. Annular dilation greater than 2% demonstrated the occurrence of leaflet malcoaptation and increased stresses near the anterior saddle-horn region. The pathologic MV model with annular dilation combined with PM displacement provides physiologically realistic biomechanical characteristics as the MVs having FMR. Simulation-based biomechanical evaluation of MV pathology related to LV chamber dilatation provides an excellent tool to better understand the pathophysiologic mechanism of FMR.