Secondary mitral regurgitation (SMR) is defined as an insufficiency of the mitral valve, due to an abnormal function of normal valve leafl ets, related to impaired left ventricular (LV) function (Lancellotti et al., Eur J Echocardiogr 11(4):307–32, 2010). Some authors consider it to be a ventricular disease with a “valvular phenotype” (Komeda et al., Circ J 73(Suppl A):A23–8, 2009). SMR can be caused either by ischemic heart disease (with or without LV dilatation), or non-ischemic dilated cardiomiopathy (Marwick et al., Heart 95(20):1711–8, 2009). It has also been described in patients with right ventricular pacing, due to secondary LV dyssynchrony (Barold and Ovsyshcher, Pacing Clin Electrophysiol 28(5):357–60, 2005), or on maintenance dialysis due to end-stage chronic kidney disease (Cirit et al., Nephrol Dial Transplant 13(2):389–92, 1998). Therefore, SMR can result from a heterogeneous group of etiologies, with particular aspects regarding pathophysiology, clinical presentation, and prognosis. After a myocardial infarction, SMR has been reported to occur with an incidence ranging from 20–25 % (Lamas et al., Circulation 96(3):827–33, 1997) up to 40–50 % of patients, (Bursi et al., Circulation 111(3):295–301, 2005; Perezde Isla et al., Eur Heart J 27(22): 2655–60, 2006). Despite the fact that SMR has an independent adverse prognostic value, even when the severity is only mild and there are no signs of congestive heart failure (Lamas et al., Circulation 96(3):827–33, 1997; Lancellotti et al., Circulation 108(14): 1713–7, 2003; St John Sutton et al., Circulation 96(10):3294–9, 1997; Agricola et al., J Am Soc Echocardiogr 24(12):1376–82, 2011), morbidity and mortality are related to SMR severity (Grigioni et al., Circulation 103(13):1759–64, 2001; Amigoni et al., Eur Heart J 28(3):326–33, 2007). Progressive LV remodeling encountered in dilated cardiomiopathy, independent on its etiology, leads to SMR despite anatomically normal mitral valve leafl ets (Yiu et al., Circulation 102(12):1400–6, 2000; Trichon et al., Circulation 108(Suppl 1):II103–10, 2003). In these patients, SMR is a multifactorial condition (Donal et al., Eur J Echocardiogr 10(1):133–8, 2009) associated with poor hemodynamics and adverse clinical prognosis (Grigioni et al., Circulation 103(13):1759–64, 2001; Robbins et al., Am J Cardiol 91(3): 360–2, 2003). The pathophysiology of SMR is at present quite well established, and particular clinical interest is directed towards finding a tailored therapeutic strategy for each particular case (Anyanwu et al., Curr Treat Options Cardiovasc Med 10(6):529–37, 2008). Therefore, it is generally recommended a comprehensive assessment of the mechanism of SMR and its classification before planning the surgical intervention, in order to tailor it on the specific characteristics of each patient. However, despite the multitude of therapeutic strategies developed to correct SMR (Fattouch et al., J Thorac Cardiovasc Surg 138(2):278–85, 2009; Fattouch et al., J Thorac Cardiovasc Surg 143(4 Suppl):S38–42, 2012; Fattouch et al., J Thorac Cardiovasc Surg 143(6):1352–5, 2012; Vassileva et al., Eur J Cardiothorac Surgery 39(3):295–303, 2011; Magne et al., J Am Coll Cardiol 51(17):1692–701, 2008; Braun et al., Ann Thorac Surg 85(2):430–6, 2008), post-intervention recurrence of MR still has a high incidence (Magne et al., Circulation 120(11 Suppl):S104–11, 2009).

Badano, L., Mihaila, S., Muraru, D., Vinereanu, D., Iliceto, S. (2015). Functional classification of secondary mitral valve regurgitation. In Secondary Mitral Valve Regurgitation (pp. 19-28). Springer-Verlag London Ltd [10.1007/9781447164883_4].

Functional classification of secondary mitral valve regurgitation

Badano L.;Muraru D.;
2015

Abstract

Secondary mitral regurgitation (SMR) is defined as an insufficiency of the mitral valve, due to an abnormal function of normal valve leafl ets, related to impaired left ventricular (LV) function (Lancellotti et al., Eur J Echocardiogr 11(4):307–32, 2010). Some authors consider it to be a ventricular disease with a “valvular phenotype” (Komeda et al., Circ J 73(Suppl A):A23–8, 2009). SMR can be caused either by ischemic heart disease (with or without LV dilatation), or non-ischemic dilated cardiomiopathy (Marwick et al., Heart 95(20):1711–8, 2009). It has also been described in patients with right ventricular pacing, due to secondary LV dyssynchrony (Barold and Ovsyshcher, Pacing Clin Electrophysiol 28(5):357–60, 2005), or on maintenance dialysis due to end-stage chronic kidney disease (Cirit et al., Nephrol Dial Transplant 13(2):389–92, 1998). Therefore, SMR can result from a heterogeneous group of etiologies, with particular aspects regarding pathophysiology, clinical presentation, and prognosis. After a myocardial infarction, SMR has been reported to occur with an incidence ranging from 20–25 % (Lamas et al., Circulation 96(3):827–33, 1997) up to 40–50 % of patients, (Bursi et al., Circulation 111(3):295–301, 2005; Perezde Isla et al., Eur Heart J 27(22): 2655–60, 2006). Despite the fact that SMR has an independent adverse prognostic value, even when the severity is only mild and there are no signs of congestive heart failure (Lamas et al., Circulation 96(3):827–33, 1997; Lancellotti et al., Circulation 108(14): 1713–7, 2003; St John Sutton et al., Circulation 96(10):3294–9, 1997; Agricola et al., J Am Soc Echocardiogr 24(12):1376–82, 2011), morbidity and mortality are related to SMR severity (Grigioni et al., Circulation 103(13):1759–64, 2001; Amigoni et al., Eur Heart J 28(3):326–33, 2007). Progressive LV remodeling encountered in dilated cardiomiopathy, independent on its etiology, leads to SMR despite anatomically normal mitral valve leafl ets (Yiu et al., Circulation 102(12):1400–6, 2000; Trichon et al., Circulation 108(Suppl 1):II103–10, 2003). In these patients, SMR is a multifactorial condition (Donal et al., Eur J Echocardiogr 10(1):133–8, 2009) associated with poor hemodynamics and adverse clinical prognosis (Grigioni et al., Circulation 103(13):1759–64, 2001; Robbins et al., Am J Cardiol 91(3): 360–2, 2003). The pathophysiology of SMR is at present quite well established, and particular clinical interest is directed towards finding a tailored therapeutic strategy for each particular case (Anyanwu et al., Curr Treat Options Cardiovasc Med 10(6):529–37, 2008). Therefore, it is generally recommended a comprehensive assessment of the mechanism of SMR and its classification before planning the surgical intervention, in order to tailor it on the specific characteristics of each patient. However, despite the multitude of therapeutic strategies developed to correct SMR (Fattouch et al., J Thorac Cardiovasc Surg 138(2):278–85, 2009; Fattouch et al., J Thorac Cardiovasc Surg 143(4 Suppl):S38–42, 2012; Fattouch et al., J Thorac Cardiovasc Surg 143(6):1352–5, 2012; Vassileva et al., Eur J Cardiothorac Surgery 39(3):295–303, 2011; Magne et al., J Am Coll Cardiol 51(17):1692–701, 2008; Braun et al., Ann Thorac Surg 85(2):430–6, 2008), post-intervention recurrence of MR still has a high incidence (Magne et al., Circulation 120(11 Suppl):S104–11, 2009).
Capitolo o saggio
Functional classification; secondary mitral valve regurgitation;
English
Secondary Mitral Valve Regurgitation
2015
9781447164876
Springer-Verlag London Ltd
19
28
Badano, L., Mihaila, S., Muraru, D., Vinereanu, D., Iliceto, S. (2015). Functional classification of secondary mitral valve regurgitation. In Secondary Mitral Valve Regurgitation (pp. 19-28). Springer-Verlag London Ltd [10.1007/9781447164883_4].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10281/279493
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