Prediction of the Individual Aortic Stenosis Progression Rate and its Association With Clinical Outcomes.

Background: The progression rate of aortic stenosis differs between patients, complicating clinical follow-up and management. Objectives: This study aimed to identify predictors associated with the progression rate of aortic stenosis. Methods: In this retrospective longitudinal single-center cohort study, all patients with moderate aortic stenosis who presented between December 2011 and December 2022 and had echocardiograms available were included. The individual aortic stenosis progression rate was calculated based on aortic valve area (AVA) from at least 2 echocardiograms performed at least 6 months apart. Baseline factors associated with the progression rate of AVA were determined using linear mixed-effects models, and the association of progression rate with clinical outcomes was evaluated using Cox regression. Results: The study included 540 patients (median age 69 years and 38% female) with 2,937 echocardiograms (median 5 per patient). Patients had a linear progression with a median AVA decrease of 0.09 cm2/y and a median peak jet velocity increase of 0.17 m/s/y. Rapid progression was independently associated with all-cause mortality (HR: 1.77, 95% CI: 1.26-2.48) and aortic valve replacement (HR: 3.44, 95% CI: 2.55-4.64). Older age, greater left ventricular mass index, atrial fibrillation, and chronic kidney disease were associated with a faster decline of AVA. Conclusions: AVA decreases linearly in individual patients, and faster progression is independently associated with higher mortality. Routine clinical and echocardiographic variables accurately predict the individual progression rate and may aid clinicians in determining the optimal follow-up interval for patients with aortic stenosis.

Sonication of heart valves detects more bacteria in infective endocarditis.

Optimal antimicrobial treatment of infective endocarditis requires identification and susceptibility patterns of pathogens. Sonication of explanted heart valves could increase the identification and culture of pathogens, as shown in prosthetic joint and pacemaker/ICD infections. We tested 26 explanted heart valves from 20 patients with active definite endocarditis for added diagnostic value of sonication to the standard microbiological workup in a prospective diagnostic proof of concept study. Two sonication protocols (broth enrichment vs. centrifugation) were compared in an additional 35 negative control valves for contamination rates. We selected sonication/centrifugation based on acceptable false positive rates (11.4%; 4/35). Sonication/enrichment yielded many false positive results in negative controls (28.6%; 10/35), mainly Propionibacterium acnes (next-generation sequencing excluded technical problems). Compared to direct culture only, adding sonication/centrifugation (including molecular testing) significantly increased the diagnostic yield from 6/26 to 17/26 valves (p = 0.003). Most importantly, culture positives almost doubled (from 6 to 10), providing unique quantitative information about antimicrobial susceptibility. Even if direct molecular testing was added to the standard workup, sonication/centrifugation provided additional diagnostic information in a significant number of valves (8/26; 31%; p = 0.013). We concluded that sonication/centrifugation added relevant diagnostic information in the workup of heart valves with infective endocarditis, with acceptable contamination rates.

Repositioning of an intraventricular dislocated aortic valve during transcatheter aortic valve implantation.

The case is presented of a 75-year-old man referred for transcatheter aortic valve implantation. During the procedure the prosthetic aortic valve became dislocated into the left ventricle shortly after expansion. The subsequent steps taken to reposition the valve using only materials at hand are described.

Percutaneous aortic valve replacement using a subclavian artery graft.

Over the past few years transcatheter heart valve implantation (THI) has become an alternative treatment for aortic valve replacement. The THI does not require a midline sternotomy or cardiopulmonary bypass and can be performed through a transfemoral or a transapical approach. In case of severe peripheral vascular disease the transapical route is usually chosen. However, when the use of a small anterolateral thoracotomy is not preferred due to comorbidities, the subclavian artery can be considered as a third alternative route. This case report describes an approach for THI through the subclavian artery, by using a Dacron graft.

Percutaneous Edwards SAPIEN valve implantation in the tricuspid position: case report and review of literature.

AIMS: Experience with transcatheter valve-in-valve implantation in a failing bioprosthetic tricuspid valve is very limited. Fewer than 30 cases have been reported, and in most of them the Melody valve (Medtronic, Inc., Minneapolis, MN, USA) was used. With this case report and review of literature we sought to evaluate the safety and feasibility of the Edwards SAPIEN transcatheter valve (Edwards Lifesciences, Irvine, CA, USA) in valve implantation in the tricuspid position and to compare this intervention with the more established Melody valve implantation. METHODS AND RESULTS: We describe one of the rarely reported Edwards SAPIEN valve implantations in a bioprosthetic tricuspid valve which is also the first in a patient with Ebstein's anomaly. A review is presented of all eight case reports on Edwards SAPIEN valve implantations in tricuspid position. The procedure was successful in all cases. Valve performance after implantation was good and no complications were described. In only one procedure pre-stenting was performed. Transatrial, transjugular and transfemoral approaches have been used. The results are comparable to those of the series about Melody valve-in-valve implantation in the tricuspid valve. Mid-term follow-up data are not yet available for both valves. CONCLUSIONS: Edwards SAPIEN valve implantation in tricuspid bioprosthetic valves is feasible and safe. Considering the available sizes of the Edwards SAPIEN valve, it may become the preferred prosthesis for valve-in-valve implantation in the tricuspid position in the future.

Normal and abnormal development of pulmonary veins: state of the art and correlation with clinical entities.

Interest for the pulmonary veins has increased in the past decade after the potential arrhythmogenicity of the myocardial sleeve surrounding these structures has been recognized. Furthermore, there are several clinical entities, such as anomalous connection pattern and pulmonary vein stenosis, that are related to abnormal pulmonary vein development. In this review, we will describe current literature and aim to elucidate and reorganize current opinions on normal and abnormal pulmonary vein development in relation to clinical (management of) diseases. Several unresolved questions will be addressed, as well as current conceptual controversies. First, a general overview of development of structures at the venous pole of the heart, including normal development of the pulmonary vein from a primitive Anlage, will be provided. Recent insights indicate an important contributory role of the mesoderm behind the heart, the so-called second heart field, to this area. Subsequently, the formation of a myocardial and smooth muscle vascular wall of the pulmonary veins and the left atrium is described, as well as current insights in the mechanisms involved in the differentiation of these different cell types in this area. Next, developmental concepts of normal pulmonary venous drainage patterns are reviewed, and an overview is provided of clinical entities related to abnormal development at several anatomical levels. Lastly, attention is paid to arrhythmogenesis in relation to pulmonary vein development, as well the consequences for clinical management.

Pulmonary vein and atrial wall pathology in human total anomalous pulmonary venous connection.

BACKGROUND: Normally, the inside of the left atrial (LA) body and pulmonary veins (PVs) is lined by vessel wall tissue covered by myocardium. In total anomalous pulmonary venous connection (TAPVC), no connection of the PVs with the LA body exists. These veins have an increased incidence of PV stenosis. We describe the consequences of the absent connection for the histopathology of the wall of the LA body and the PVs, and hypothesize on a mechanism predisposing to PV stenosis. METHODS AND RESULTS: In 10 human neonates with TAPVC, the wall of the LA body and PVs were studied using histological and immunohistochemical techniques. As controls, 2 normal neonatal and adult hearts and 5 neonatal hearts with partial anomalous venous connection (PAPVC) or situs inversus were studied. In hearts with TAPVC no vessel wall tissue was found in the LA body and its myocardial layer was hypoplastic. No myocardial sleeve was found around the abnormally draining PVs. In hearts with PAPVC, only the non-LA draining PV lacked myocardial covering, whereas in situs inversus PVs connecting to the right-sided LA, were normally myocardialized. CONCLUSION: An open connection of the PVs with the morphological LA is necessary for the presence of vessel wall tissue in the LA and myocardialization of the PVs. Absence of myocardium covering the PVs is hypothesized to enhance susceptibility to PV stenosis and prevent onset of PV originating arrhythmias. The embryonic posterior heart field may be responsible for the abnormal myocardialization and smooth muscle cell formation in TAPVC.

Pulmonary vein, dorsal atrial wall and atrial septum abnormalities in podoplanin knockout mice with disturbed posterior heart field contribution.

The developing sinus venosus myocardium, derived from the posterior heart field, contributes to the atrial septum, the posterior atrial wall, the sino-atrial node, and myocardium lining the pulmonary and cardinal veins, all expressing podoplanin, a coelomic and myocardial marker. We compared development and differentiation of the myocardium and vascular wall of the pulmonary veins (PV), left atrial dorsal wall, and atrial septum in wild type with podoplanin knockout mouse embryos (E10.5-E18.5) by 3D reconstruction and immunohistochemistry. Expression of Nkx2.5 in the pulmonary venous myocardium changes from mosaic to positive during development pointing out a high proliferative rate compared with Nkx2.5 negative myocardium of the sino-atrial node and cardinal veins. In mutants, myocardium of the PVs, dorsal atrial wall and atrial septum was hypoplastic. The atrial septum and right-sided wall of the PV almost lacked interposed mesenchyme. Extension of smooth muscle cells into the left atrial body was diminished. We conclude that myocardium of the PVs, dorsal atrial wall, and atrial septum, as well as the smooth muscle cells, are derived from the posterior heart field regulated by podoplanin.

Histology of vascular myocardial wall of left atrial body after pulmonary venous incorporation.

During embryonic development, the common pulmonary vein (PV) becomes incorporated into the left atrium, giving rise to separate PV ostia. We describe the consequences of this incorporation process for the histology of the left atrium and the possible clinical implications. The histology of the left atrial (LA) wall in relation to PV incorporation was studied immunohistochemically in 16 human embryos and fetuses, 1 neonate, and 5 adults. The PV wall, surrounded by extrapericardially differentiated myocardial cells, was incorporated into the LA body. After incorporation, the composition of PVs and the smooth-walled LA body wall was histologically identical. The LA appendage, however, consisted of endocardial and myocardial layers without a vessel wall component. In 2 adults, the myocardium in the LA posterior wall was absent. At the transition of the LA body and LA appendage, a smooth-walled myocardial zone lacking the venous wall was observed. This zone was histologically identical to the sinus venarum of the right atrium. In conclusion, the LA body arises by incorporation and growth of PVs, presenting with a histologically identical structure of vessel wall covered by extrapericardially differentiated myocardium of PVs. Discontinuity of myocardium may be the substrate for arrhythmias, and absence of myocardium in some patients makes this area potentially vulnerable to damage inflicted by ablation strategies. A border zone between the LA body and LA appendage is hypothesized to be the left part of the embryonic sinus venosus.

Clinical evaluation of a new fat removal filter during cardiac surgery.

OBJECTIVES: Fat microemboli are generated during cardiac surgery that are associated with post-operative organ injury. Recently, a fat removal filter has been developed, based on a polyester leukocyte depletion filter. However, the efficacy of such a filter in a clinical setting is unknown. In this study we tested the efficacy of this filter. METHODS: Coronary artery bypass patients were randomly divided into two groups. Group I: filtration of cardiotomy suction blood during cardiopulmonary bypass with a fat removal filter (n=14). Group II: control patients without filtration (n=14). Filter efficacy was evaluated in group I using biochemical assays and thin layer chromatography of blood samples taken simultaneously before and after the filter. In addition, clinical and biochemical markers for organ injury were determined in both groups. RESULTS: The fat filter removed triglycerides (0.9+/-0.08 vs. 0.63+/-0.08 mmol l(-1), P=0.004, paired t-test), leukocytes (4.3+/-0.8 x 10(9) vs. 2.3+/-0.6 x 10(9)l(-1), P=0.03), and platelets (116+/-26 x 10(9) vs. 75+/-21 x 10(9)l(-1), P=0.003) from the blood samples taken before and after the filter. Chromatography showed a significant reduction in free fatty acids, phospholipids and triglycerides. Clinically, leukocyte counts were similar, but platelet counts were higher (181+/-14 x 10(9) vs. 117+/-8.6 x 10(9)l(-1) control, P<0.001) in group I on the first postoperative day. CONCLUSIONS: The fat filter removed 40% fat, leukocytes and platelets from cardiotomy suction blood during cardiac surgery. A larger scale study is necessary to determine clinical effects on organ damage.