OBJECTIVES
Cardiac biomarkers are indicators of irreversible cell damage. Current myocardial infarction (MI) definitions require concomitant clinical characteristics. For perioperative MI, a correlation of biomarker elevations and mortality has been suggested. Definitions emerged relying on cardiac biomarker release only. This approach is questionable as several clinical and experimental scenarios exist where relevant biomarker release can occur apart from MI.
METHODS
We reviewed the clinical and basic science literature and revealed important aspects regarding the use and interpretation of cardiac biomarker release with special focus on their interpretation in the perioperative setting.
RESULTS
Ischaemic biomarkers may be released without cell death in multiple conditions, such as after endurance runs in athletes, temporary inotropic stimulation in animal models and flow variations in in vitro cell models. In addition, access through atrial tissue during cannulation or concomitant valve procedures adds sources of enzyme release that may not be related to ventricular ischaemia (i.e. MI). Such non-cell death-related mechanisms may explain the lack of poor correlations of enzyme release and long-term outcomes in recent trials. In addition, the 3 main biomarkers, troponin T, I and creatine kinase myocardial band, differ in their release kinetics, which may differentially trigger MI events in trial patients.
CONCLUSIONS
The identification of irreversible myocardial injury in cardiac surgery based only on biomarker release is unreliable. Cell death- and non-cell death-related mechanisms create a mix in the perioperative setting that requires additional markers for proper identification of MI. In addition, the 3 most common ischaemic biomarkers display different release kinetics adding to the confusion. We review the topic.
Subj collection
120, 123
Mitral valve regurgitation is the second most common valve disease in the western world. Surgery is currently the best tool for generating a long-lasting elimination of mitral valve regurgitation. However, the mitral valve apparatus is a complex anatomical and functional structure, and repair results and durability show substantial heterogeneity. This is not only due to differences in the underlying mitral valve regurgitation pathophysiology but also due to differences in repair techniques. Repair philosophies differ substantially from one surgeon to the other, and consensus for the technically best repair strategy has not been reached yet. We had previously addressed this topic by suggesting that ring sizing is "voodoo". We now review the available evidence regarding the various repair techniques described for structural and functional mitral valve regurgitation. Herein, we illustrate that for structural mitral valve regurgitation, resuspension of prolapsing valve segments or torn chordae with polytetrafluoroethylene sutures and annuloplasty can generate the most durable results paired with the best achievable hemodynamics. For functional mitral valve regurgitation, the evidence suggests that annuloplasty alone is insufficient in most cases to generate durable results, and additional subvalvular strategies are associated with improved durability and possibly improved clinical outcomes. This review addresses current strategies but also implausibilities in mitral valve repair and informs the mitral valve surgeon about the current evidence. We believe that this information may help improve outcomes in mitral valve repair as the heterogeneity of mitral valve regurgitation pathophysiology does not allow a one-size-fits-all concept.
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