Vito Margari

and 8 more

Abstract Objectives: The use of minimally invasive or transcatheter interventions rather than standard full sternotomy operations to treat Tricuspid valve disease is increasing. Debate however is still open regarding venous drainage management during cardiopulmonary bypass and wheatear or not superior and inferior vena cava should be occluded during opening of the right atrium to avoid air entrance in the venous line. The aim of the present study is to report operative outcomes and mid-term follow-up results of minimally invasive tricuspid valve surgery performed without caval occlusion. Methods: This is a retrospective outcome evaluation from institutional records with prospective data entry. We searched for all the patients who underwent right mini-thoracotomy tricuspid valve surgery isolated or combined with mitral valve surgery during the period June 2013 – February 2020. Results: During the study period 68 consecutive patients underwent minimally invasive tricuspid valve surgery without occlusion of cava veins. Survival at a 5-year and 8-year follow up was 100% and 79%, respectively. At follow-up no patient had an NHYA class greater than two, only one patient was re-hospitalized for heart failure for an atrial fibrillation episode. One patient was hospitalized for a pericardiocentesis twenty days after discharge No severe tricuspid regurgitation was evident at echocardiographic follow up. Five patients had 2+ TR. Conclusion Our results show that performing tricuspid surgery without caval occlusion is safe. There is no clinical evidence of gas embolism. Mid-term follow up data confirm that minimally invasive approach does not alter the quality of surgery.

Antonio Calafiore

and 11 more

In secondary mitral regurgitation, the concept that the mitral valve (MV) is an innocent bystander, has been challenged by many studies in the last decades. The MV is a living structure with an intrinsic plasticity that reacts to changes in stretch or in mechanical stress activating bio-humoral mechanisms that have, as purpose, the adaptation of the valve to the new environment. If the adaptation is balanced, the leaflets increase both surface and length and the chordae tendinae lengthen: the result is a valve with different characteristics, but able to avoid or to limit the regurgitation. However, if the adaptation is unbalanced, the leaflets and the chords do not change their size, but become stiffer and rigid, with moderate or severe regurgitation. These changes are mediated mainly by a cytokine, the transforming growth factor β (TGF-β), which is able to promote the changes that the MV needs to adapt to a new hemodynamic environment. In general, mild TGF-β activation facilitates leaflet growth, excessive TGF-β activation, as after a myocardial infarction, results in profibrotic changes in the leaflets, with increased thickness and stiffness. The MV is then a plastic organism, that reacts to the external stimuli, trying to maintain its physiologic integrity. This review has the goal to unveil the secret life of the MV, to understand which stimuli can trigger its plasticity and to explain why the equation “large heart=moderate/severe mitral regurgitation” and “small heart=no/mild mitral regurgitation” does not work into the clinical practice.