Severe coronary artery disease resulting in myocardial ischemia or infarction can be complicated by mitral regurgitation. This so-called ischemic mitral regurgitation is a specific clinical entity and should be differentiated from clinical scenarios in which concomitant ischemic cardiomyopathy and mitral regurgitation due to other etiologies (e.g. degenerative disease, rheumatic fever, or endocarditis) are present.
During the last three decades, experimental studies and clinical investigations using novel imaging modalities have elucidated different mechanisms of ischemic mitral regurgitation. Carpentier's functional classification is applied for the pathophysiological study of ischemic mitral regurgitation. This functional approach enables physicians to describe with clarity various mechanisms of valvular regurgitation and also serves as a guideline to valvular reconstruction.
Type I mitral regurgitation- Normal leaflet motion
Type I mitral regurgitation results from isolated annular dilatation which can occur after basal myocardial infarction. It is a relatively rare condition and is observed in less than 10% of cases of ischemic mitral regurgitation.
Type II mitral regurgitation- Excess leaflet motion
In type II dysfunction, the motion of one or two leaflet(s) is increased and therefore the free edge of one or more leaflet segments overrides the plane of the mitral annulus during systole. In these patients, leaflet prolapse results from papillary muscle rupture (partial or complete) or from papillary muscle elongation or, rarely from isolated chordae rupture.
Papillary muscle rupture is a rare mechanical complication of myocardial infarction. The incidence of this complication has significantly decreased with current thrombolytic and early percutaneous revascularization therapy for acute infarction.
The rupture affects most often the posteromedial papillary muscle (75% versus 25% for anterolateral papillary muscle). This vulnerability of posteromedial papillary muscle is explained by the fact that its vascular supply is dependent on one coronary artery (either the right coronary artery or the left circumflex artery in right or left dominant system respectively), which also supplies the blood to the crux of the heart. In contrast, the anterolateral papillary muscle is revascularized by 2 major coronary vessels: the left anterior descending and the circumflex arteries. Complete papillary muscle rupture occurs in 30 % of patients and results in bileaflet prolapse with severe mitral regurgitation. Partial rupture of a papillary muscle involving one or more heads remains the most common lesion in patients with type II ischemic mitral regurgitation.
Papillary muscle elongation results from fibrotic transformation of papillary muscle following myocardial infarction. The elongation of papillary muscle causes leaflet prolapse leading to mitral regurgitation.
Type IIIb mitral regurgitation- Systolic restricted leaflet motion
The most common mechanism of ischemic mitral regurgitation is restricted leaflet motion, particularly the posterior leaflet, during systole. Following myocardial ischemia or infarction, left ventricular remodeling leads to an apical and lateral displacement of the papillary muscles (mostly the posteromedial papillary muscle) producing a tethering of the mitral leaflets (mostly p2,p3, and posterior commissure leaflet segments) . This apical tenting of the leaflets prevents their free margin to reach the plane of the annulus reducing significantly the surface of coaptation, producing mitral regurgitation. In addition, a tethering of the belly of the anterior leaflet due to excess traction on one or more main secondary chordae can further reduce leaflet mobility and the surface of coaptation.
From Carpentier A, Adams DH, Filsoufi F. Carpentier's Reconstructive Valve Surgery. Saunders (Elsevier), 2010
The localization of myocardial infarction has a direct impact on the degree of left ventricular remodeling and therefore on the severity and localization of leaflet tethering.
In patients with posterolateral infarction, left ventricular remodeling remains segmental. Most patients present with a restricted posterior leaflet motion predominant at the P2, P3 and posteromedial commissural area. Similarly, annular dilatation/deformation is asymmetrical affecting with greater severity the posteromedial aspect of the valve. In contrast, in patients with antero-septal infarction, left ventricular remodeling is global and the ventricle is typically transformed from an elliptical into a spherical shape. Leaflet tethering involves both anterior and posterior leaflets. Annular dilatation/deformation is also global and symmetrical. In general, there is a direct correlation between the degree of left ventricular dilatation and the severity of leaflet tethering. These patho-morphological changes should be analyzed with a great degree of precision on echocardiography considering their prognostic value.
Acute mitral regurgitation complicating myocardial infarction
Patients with papillary muscle rupture often presents with acute severe mitral regurgitation. Although this complication can occur during the acute phase of myocardial infarction most patients are diagnosed within 2 to 7 days after this event. Clinical presentation is characterized by rapid development of congestive heart failure, pulmonary edema and cardiogenic shock. Following myocardial infarction, in previously stable patients, this rapid deterioration of the clinical condition, should strongly suggest the occurrence of a mechanical complication of myocardial infarction. It is important to note that the sudden appearance of a systolic murmur and hemodynamic compromise may result from acute severe mitral regurgitation secondary to papillary muscle rupture as well as from ventricular septal rupture. Clinically, it may be very difficult to distinguish between these two diagnoses despite differences in the characteristics of murmurs (the systolic murmur due to ventricular septal rupture is loud, prominent at the left sternal border and associated with a thrill whereas the systolic murmur of mitral regurgitation due to papillary muscle rupture is softer, intense at the apex and without thrill). Another differential diagnosis is extensive myocardial infarction with cardiogenic shock associated with severe type IIIb ischemic mitral regurgitation. In most instances, however, the clinical symptomatology associated with type IIIb mitral regurgitation is less dramatic and most patients develop mild to moderate mitral regurgitation.
Preoperative examinations including two dimensional transthoracic echocardiography, transesophageal echocardiography with Doppler and cardiac catheterization are crucial to make the accurate diagnosis of ischemic mitral regurgitation due to papillary muscle rupture and to evaluate left ventricular function and the severity of coronary artery disease.
Chronic mitral regurgitation from ischemic cardiomyopathy
Chronic ischemic mitral regurgitation is mainly due to left ventricular remodeling with enlargement after myocardial infarction (Carpentier's type IIIb dysfunction). Risk factors for the occurrence of this condition include: advanced age, female gender, large infarct size, recurrent ischemia, and multi-vessel coronary artery disease. Patients may develop significant mitral regurgitation over time and become symptomatic with the appearance of fatigue, dyspnea on exertion, or atrial fibrillation. Some patients will develop significant mitral regurgitation but remain asymptomatic for a long-period of time as they adapt their physical activity to the functional capacity of the heart. In a subgroup of these patients with multivessel coronary artery disease, the coronary symptomatology predominates and the mitral regurgitation is discovered at the occasion of a routine workup or a new coronary event.
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