Nosocomial infection after off-pump coronary artery bypass grafting is an uncommon but potentially life-threatening complication. The identification of independent risk factors, including arterial hypertension, associated with development of postoperative infection may help in the development of clinical strategies for the prevention, early diagnosis, and treatment of these infections.
Preoperative low-dose amiodarone therapy does not seem to be related to significant postoperative lung toxicity, but it is associated with various cardiac complications and an increased need for more intense inotropic support after cardiac operations. These findings may be related to the drug's depressant effect on the myocardium.
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 intrinsic plasticity that reacts to changes in stretch or in mechanical stress activating biohumoral 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 tendineae 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 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.
In this study, PMV following aorta no-touch OPCAB was related to preoperative variables: age, octogenarians, preoperative IABP, TIA, and stroke. There was no relation between PMV and any of the operative data.
CPB is characterised by pronounced changes in plasma sP-s, sE-s, TN, vWF levels, and ACE activity, which are associated with significant alteration in the intra- and early postoperative endothelial function observed in open heart surgery.
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