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  1. Yakub MA, Pau KK, Awang Y
    Ann Thorac Cardiovasc Surg, 1999 Feb;5(1):36-9.
    PMID: 10074567
    A minimally invasive approach to aortic valve surgery through a transverse incision ("pocket incision") at the right second intercostal space was examined. Sixteen patients with a mean age of 30 years underwent this approach. The third costal cartilage was either excised (n = 5) or dislocated (n = 11). The right internal mammary artery was preserved. Cardiopulmonary bypass (CPB) was established with aortic-right atrial cannulation in all except the first case. Aortic valve replacements (AVR) were performed in 15 patients and one had aortic valve repair with concomitant ventricular septal defect closure. There was no mortality and no major complications. The aortic cross-clamp, CPB and operative times were 72 +/- 19 mins, 105 +/- 26 mins and 3 hrs 00 min +/- 29 mins respectively. The mean time to extubation was 5.7 +/- 4.0 hrs, ICU stay of 27 +/- 9 hrs and postoperative hospital stay of 5.1 +/- 1.2 days. Minimally invasive "pocket incision" aortic valve surgery is technically feasible and safe. It has the advantages of central cannulation for CPB, preservation of the internal mammary artery and avoiding sternotomy. This approach is cosmetically acceptable and allows rapid patient recovery.
    Matched MeSH terms: Aortic Valve Insufficiency/etiology
  2. Le Ho Y, Ahmad Zaidi NA, Salleh A, Abdul Kareem BA
    J Cardiothorac Surg, 2021 Apr 17;16(1):92.
    PMID: 33865405 DOI: 10.1186/s13019-021-01458-2
    BACKGROUND: Antiphospholipid syndrome is an antibody mediated pro-thrombotic state leading to various arterial and venous thromboses. The syndrome can be either primary or secondary to other autoimmune diseases, commonly systemic lupus erythematosus. Cardiac involvement, in particular valvular disease is common in patients with antiphospholipid syndrome, occurring in about a third of these patients. Valvular diseases associated with antiphospholipid syndrome often occur as valve thickening and non-bacterial vegetation or Libman-Sacks endocarditis. Deposits of antiphospholipid immunoglobulin and complement components are commonly observed in the affected valves, suggesting an inflammatory process resulting in valvular vegetation and thickening. Libman-Sacks endocarditis has a high propensity towards mitral valve, although haemodynamically significant valvular dysfunction is rare.

    CASE PRESENTATION: We present a successful aortic valve replacement with cardiopulmonary bypass in a 48 years old lady with antiphospholipid syndrome, who has severe aortic regurgitation as a result of Libman-sacks endocarditis. Antiphospholipid antibodies were positive and the clinical data showed both negative cultures and infective parameters. Surgically resected vegetations revealed sterile fibrinous and verrucous vegetations on aortic valve. Valve replacement and the course of cardiopulmonary bypass was uneventful, and the patient was discharged well.

    CONCLUSIONS: Classically Libman-Sacks endocarditis is often and more commonly associated with autoimmune diseases such as systemic lupus erythematosus, although it can occur in both primary and secondary antiphospholipid syndrome. It is not a common entity, and it is a frequent underestimated disease as most clinicians do not routinely screen for valvular lesion in patients with antiphospholipid syndrome unless they are symptomatic. However, due to its high prevalence of cardiac involvement, clinicians should have a high index of suspicion in the attempt to minimize cardiovascular and haemodynamic complications. Valve surgery in patients with antiphospholipid syndrome carries considerable early and late morbidity and mortality, usually caused by thromboembolic and bleeding events. The perioperative anticoagulation management and haemostatic aspect of antiphospholipid syndrome present an exceptional challenges to clinicians, surgeons, anaesthetists and laboratory personnel.

    Matched MeSH terms: Aortic Valve Insufficiency/etiology
  3. Abbas SS, Nasif MS, Al-Waked R, Meor Said MA
    Artif Organs, 2020 Feb;44(2):E20-E39.
    PMID: 31378963 DOI: 10.1111/aor.13536
    Platelet activation induced by shear stresses and non-physiological flow field generated by bileaflet mechanical heart valves (BMHVs) leads to thromboembolism, which can cause fatal consequences. One of the causes of platelet activation could be intermittent regurgitation, which arises due to asynchronous movement and rebound of BMHV leaflets during the valve closing phase. In this numerical study, the effect of intermittent regurgitation on the platelet activation potential of BMHVs was quantified by modeling a BMHV in the straight and anatomic aorta at implantation tilt angles 0°, 5°, 10°, and 20°. A fully implicit Arbitrary Lagrangian-Eulerian-based Fluid-Structure Interaction formulation was adopted with blood modeled as a multiphase, non-Newtonian fluid. Results showed that the intermittent regurgitation and consequently the platelet activation level increases with the increasing implantation tilt of BMHV. For the straight aorta, the leaflet of the 20° tilted BMHV underwent a rebound of approximately 20° after initially closing, whereas the leaflet of the 10°, 5°, and 0° tilted BMHVs underwent a rebound of 8.5°, 3°, and 0°, respectively. For the anatomic aorta, the leaflet of the 20° tilted BMHV underwent a rebound of approximately 24° after initially closing, whereas the leaflet of the 10°, 5°, and 0° tilted BMHVs underwent a rebound of 14°, 10°, and 7°, respectively. For all the implantation orientations of BMHVs, intermittent regurgitation and platelet activation were always higher in the anatomic aorta than in the straight aorta. The study concludes that the pivot axis of BMHV must be implanted parallel to the aortic root's curvature to minimize intermittent regurgitation and platelet activation.
    Matched MeSH terms: Aortic Valve Insufficiency/etiology*
  4. Tamin SS, Dillon J, Aizan K, Kadiman S, Latiff HA
    Echocardiography, 2012 Feb;29(2):E34-8.
    PMID: 22044509 DOI: 10.1111/j.1540-8175.2011.01543.x
    This case report describes a 20-year-old woman with Turner's syndrome who presented with reduced effort tolerance limited by dyspnea. She had previously been on pediatric cardiology follow-up for congenital subvalvular aortic stenosis first diagnosed at age 7. Unfortunately she defaulted after two visits before any intervention could be done. Transthoracic echocardiography demonstrated severe aortic incompetence (AI) with a membrane-like structure in the left ventricular outflow tract (LVOT). The mean pressure gradient across the LVOT on continuous wave Doppler was 41 mmHg. The membranous interventricular septum appeared aneurysmal and it was observed that the "subaortic membrane" had a connection to the anterolateral papillary muscle via a strand of chordal tissue. Further images were captured using two-dimensional and three-dimensional transthoracic and transesophageal echocardiography (iE33, Philips Medical Systems, Andover, MA, USA). After a review of the literature it was concluded that this appeared to be an accessory mitral valve (AMV) leaflet causing LVOT obstruction associated with AI. AMV tissue is a rare congenital malformation causing LVOT obstruction. Because it is so unusual, it may not be immediately recognizable even in a high volume echocardiography laboratory. The clue which helped with the diagnosis was the strand of chordal tissue which connected the mass to the papillary muscle. This anomaly is often associated with LVOT obstruction.
    Matched MeSH terms: Aortic Valve Insufficiency/etiology*
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