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Chronic ischaemic mitral regurgitation (CIMR) remains one of the most complex and unresolved aspects in the management of ischaemic heart disease. This review provides an overview of the present knowledge about the different aspects of CIMR with an emphasis on mechanisms, current surgical treatment results and new mechanism-based surgical approaches. CIMR occurs in approximately 20-25% of patients followed up after myocardial infarction (MI) and in 50% of those with post-infarct congestive heart failure (CHF). The presence of CIMR adversely affects prognosis, increasing mortality and the risk of CHF in a graded fashion according to CIMR severity. The primary mechanism of CIMR is ischaemia-induced left ventricular (LV) remodelling with papillary muscle displacement and apical tenting of the mitral valve leaflets. CIMR is often clinically silent, and colour-Doppler echocardiography remains the most reliable diagnostic tool. The most commonly performed surgical procedure for CIMR (restrictive annuloplasty combined with coronary artery bypass grafting (CABG)) can provide good results in selected patients with minimal LV dilatation and minimal tenting. However, in general the persistence and recurrence rate (at least MR grade 3+) for restrictive annuloplasty remains high (up to 30% at 6 months postoperatively), and after a 10-year follow-up there does not appear to be a survival benefit of a combined procedure compared to CABG alone (10-year survival rate for both is approximately 50%). Patients at risk of annuloplasty failure based on preoperative echocardiographic and clinical parameters may benefit from mitral valve replacement with preservation of the subvalvular apparatus or from new alternative procedures targeting the subvalvular apparatus including the LV. These new procedures include second-order chordal cutting, papillary muscle repositioning by a variety of techniques and ventricular approaches using external ventricular restraint devices or the Coapsys device. In addition, percutaneous transvenous repair techniques are being developed. Although promising, at this point these new procedures still lack investigation in large patient cohorts with long-term follow-up. They will, however, be the subject of much anticipated and necessary ongoing and future research.

Libman-Sacks endocarditis of the mitral valve was first described by Libman and Sacks in 1924. Currently, the sterile verrucous vegetative lesions seen in Libman-Sacks endocarditis are regarded as a cardiac manifestation of both systemic lupus erythematosus (SLE) and the antiphospholipid syndrome (APS). Although typically mild and asymptomatic, complications of Libman-Sacks endocarditis may include superimposed bacterial endocarditis, thromboembolic events, and severe valvular regurgitation and/or stenosis requiring surgery. In this study we report two cases of mitral valve repair and two cases of mitral valve replacement for mitral regurgitation (MR) caused by Libman-Sacks endocarditis. In addition, we provide a systematic review of the English literature on mitral valve surgery for MR caused by Libman-Sacks endocarditis. This report shows that mitral valve repair is feasible and effective in young patients with relatively stable SLE and/or APS and only localized mitral valve abnormalities caused by Libman-Sacks endocarditis. Both clinical and echocardiographic follow-up after repair show excellent mid- and long-term results.

Preemptive reduction of immunosuppression after lung transplantation guided by EBV-DNA load appears to be a safe approach for the prevention of PTLD in lung transplant recipients late after transplantation.