title: Mitral regurgitation after anteroapical myocardial infarction: new mechanistic insights.
abstract: BACKGROUND
  Mitral regurgitation (MR) generally accompanies inferobasal myocardial infarction (MI), with leaflet tethering by displaced papillary muscles. Mitral regurgitation is also reported with anteroapical MI without global dilatation or inferior wall motion abnormalities. We hypothesized that anteroapical MI extending to the inferior apex displaces the papillary muscles, tethering the mitral leaflets to cause MR.
  
  
  RESULTS
  In the retrospective part of the study, consecutive anteroapical MI patients were studied. Moderate-severe MR occurred in 9% of 234 patients with only anteroapical MI versus 17% of 242 with inferoapical extension (P<0.001). Ejection fraction was only mildly different (41 ± 4% versus 46 ± 5%; P<0.01). In the human mechanistic portion of the study, 60 anteroapical MI patients (20 with only 2 apical segments involved and 40 with involvement of all 4 apical segments; 20 with MR and 20 without MR) were compared with 20 normal controls. Those with MR (≥ moderate) had higher systolic papillary muscle-to-annulus tethering length (P < 0.01). Mitral regurgitation grade correlated most strongly with tethering length (r = 0.70) and its diminished systolic shortening (r = -0.65). In the animal study, 9 sheep with left anterior descending coronary artery ligation were analyzed. Four sheep that developed MR had inferoapical MI extension with tethering length increasing over 1.5 months (2.1 ± 0.4 to 2.9 ± 0.4 cm, P < 0.001) versus no significant increase in 5 sheep without MR (2.0 ± 0.4 to 2.1 ± 0.3 cm, P not statistically significant). In MR sheep, the normal decrease in tethering length from diastole to systole was eliminated (P < 0.01).
  
  
  CONCLUSIONS
  Anteroapical MI with inferoapical extension can mechanically displace papillary muscles, causing MR despite the absence of basal and midinferior wall motion abnormalities. This suggests the possibility of repositioning treatments for this condition.
authors: Cardiac Ultrasound Laboratory, Harvard Medical School, Massachusetts General Hospital, Boston, MA 02114-2696, USA. rlevine@partners.org
authors: Chaim
authors: C
authors: Yosefy
authors: Ronen
authors: R
authors: Beeri
authors: J Luis
authors: JL
authors: Guerrero
authors: Mordehay
authors: M
authors: Vaturi
authors: Marielle
authors: M
authors: Scherrer-Crosbie
authors: Mark D
authors: MD
authors: Handschumacher
authors: Robert A
authors: RA
authors: Levine
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000818:Animals; D016022:Case-Control Studies; D003331:Coronary Vessels / Q000601:surgery; D015150:Echocardiography, Doppler; D005260:Female; D006801:Humans; D008026:Ligation / Q000009:adverse effects; D008297:Male; D008875:Middle Aged; D008943:Mitral Valve / Q000000981:diagnostic imaging / Q000503:physiopathology; D008944:Mitral Valve Insufficiency / Q000000981:diagnostic imaging / Q000209:etiology* / Q000503:physiopathology*; D023421:Models, Animal; D009203:Myocardial Infarction / Q000150:complications* / Q000000981:diagnostic imaging / Q000209:etiology; D010210:Papillary Muscles / Q000000981:diagnostic imaging / Q000503:physiopathology*; D012189:Retrospective Studies; D012756:Sheep; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000503:physiopathology