Ischemia in three left ventricular regions: Insights into the pathogenesis of acute ischemic mitral regurgitation

BACKGROUND: Acute posterolateral left ventricular ischemia in sheep results in ischemic mitral regurgitation, but the effects of ischemia in other left ventricular regions on ischemic mitral regurgitation is unknown. METHODS: Six adult sheep had radiopaque markers placed on the left ventricle, mitral annulus, and anterior and posterior mitral leaflets at the valve center and near the anterior and posterior commissures. After 6 to 8 days, animals were studied with biplane videofluoroscopy and transesophageal echocardiography before and during sequential balloon occlusion of the left anterior descending, distal left circumflex, and proximal left circumflex coronary arteries. Time of valve closure was defined as the time when the distance between leaflet edge markers reached its minimum plateau, and systolic leaflet edge separation distance was calculated on the basis of left ventricular ejection. RESULTS: Only proximal left circumflex coronary artery occlusion resulted in ischemic mitral regurgitation, which was central and holosystolic. Delayed valve closure (anterior commissure, 58 +/- 29 vs 92 +/- 24 ms; valve center, 52 +/- 26 vs 92 +/- 23 ms; posterior commissure, 60 +/- 30 vs 94 +/- 14 ms; all P <.05) and increased leaflet edge separation distance during ejection (mean increase, 2.2 +/- 1.5 mm, 2.1 +/- 1.9 mm, and 2.1 +/- 1.5 mm at the anterior commissure, valve center, and posterior commissure, respectively; P <.05 for all) was seen during proximal left circumflex coronary artery occlusion but not during left anterior descending or distal left circumflex coronary artery occlusion. Ischemic mitral regurgitation was associated with a 19% +/- 10% increase in mitral annular area, and displacement of both papillary muscle tips away from the septal annulus at end systole. CONCLUSIONS: Acute ischemic mitral regurgitation in sheep occurred only after proximal left circumflex coronary artery occlusion along with delayed valve closure in early systole and increased leaflet edge separation throughout ejection in all 3 leaflet coaptation sites. The degree of left ventricular systolic dysfunction induced did not correlate with ischemic mitral regurgitation, but both altered valvular and subvalvular 3-dimensional geometry were necessary to produce ischemic mitral regurgitation during acute left ventricular ischemia.     

Imbalanced chordal force distribution causes acute ischemic mitral regurgitation: mechanistic insights from chordae tendineae force measurements in pigs

BACKGROUND: Ischemic mitral regurgitation is caused by an imbalance of the entire mitral-ventricular complex. This interaction is mediated through the chordae tendineae force distribution, which may perturb several elements of the mitral valve apparatus. Our objective was to investigate the association between the mitral valvular 3-dimensional geometric perturbations and chordae tendineae force redistribution in a porcine model of acute ischemic mitral regurgitation. METHODS: In 9 pigs, acute ischemic mitral regurgitation was induced by repeated microembolization of the left circumflex coronary artery. Mitral leaflet coaptation geometry was determined by 2-dimensional echocardiography and reconstructed 3-dimensionally. Leading edge chordal forces were measured by dedicated miniature force transducers at control and during ischemic mitral regurgitation. RESULTS: During acute ischemic mitral regurgitation, there was a decreased tension of the primary chorda from the ischemic posterior left ventricular wall to the anterior leaflet (0.295 +/- 0.063 N vs 0.336 +/- 0.071 N [control]; P < .05). The tension of the chorda from the nonischemic anterior left ventricular wall to the anterior leaflet increased (0.375 +/- 0.066 N vs 0.333 +/- 0.071 N [control]; P < .05). In accordance, relative leaflet prolapse was observed at the ischemic commissural side, whereas there was an increase in the leaflet surface area at the nonischemic commissural side, indicating localized leaflet tethering. CONCLUSIONS: Acute ischemic mitral regurgitation due to posterior left ventricular wall ischemia was associated with focal chordal and leaflet tethering at the nonischemic commissural portion of the mitral valve and a paradoxical decrease of the chordal forces and relative prolapse at the ischemic site of the anterior mitral valve leaflet.     

Annular or subvalvular approach to chronic ischemic mitral regurgitation?

OBJECTIVE: We sought to investigate whether annular or subvalvular interventions corrected chronic ischemic mitral regurgitation differently. METHODS: Sheep underwent placement of markers on the left ventricle, mitral annulus, papillary muscles (anterior and posterior), and both leaflet edges. A transannular suture (septal-lateral annular cinching) was anchored to the midseptal mitral annulus and externalized through the midlateral mitral annulus. Another suture (papillary muscle repositioning) from the posterior papillary muscle was passed through the mitral annulus near the posterior commissure and externalized. After 7 days, 3-dimensional marker data were obtained before inducing posterolateral myocardial infarction. After 7 weeks, animals in whom chronic ischemic mitral regurgitation developed (n = 10) were restudied before and after pulling septal-lateral annular cinching or papillary muscle repositioning sutures. End-systolic septal-lateral annular diameter and 3-dimensional displacement of the papillary muscles and leaflet edges were computed. RESULTS: Infarction increased mitral regurgitation (0.6 +/- 0.5 to 2.3 +/- 1.1); mitral annular septal-lateral dilation (4 +/- 1 mm); posterior papillary muscle displacement laterally (4 +/- 2 mm), posteriorly (9 +/- 3 mm), and toward the annulus (2 +/- 1 mm); posterior mitral leaflet apical tethering (3 +/- 1 mm); and interleaflet separation (+3 +/- 1 mm, P < .05 baseline vs chronic ischemic mitral regurgitation). Septal-lateral annular cinching reduced septal-lateral dimension (-9 +/- 3 mm), corrected lateral posterior papillary muscle displacement (4 +/- 1 mm) and septal-lateral interleaflet separation (-4 +/- 2 mm), and decreased mitral regurgitation (0.6 +/- 0.6, P < .05 septal-lateral annular cinching vs chronic ischemic mitral regurgitation) without affecting posterior leaflet restriction. Papillary muscle repositioning reduced septal-lateral diameter (-4 +/- 1 mm), moved the anterior papillary muscle closer to the annulus (2 +/- 1 mm), and relieved posterior leaflet apical restriction (2 +/- 1 mm, P < .05 papillary muscle repositioning vs chronic ischemic mitral regurgitation) but did not change lateral posterior papillary muscle displacement or decrease mitral regurgitation (1.9 +/- 1.2). CONCLUSIONS: Septal-lateral annular cinching moved the lateral annulus and the posterior papillary muscle closer to the septum and reduced mitral regurgitation unlike posterior papillary muscle repositioning, and thus the key mitral subvalvular repair component must correct posterior papillary muscle lateral displacement.     

Annuloplasty ring selection for chronic ischemic mitral regurgitation: lessons from the ovine model

BACKGROUND: Chronic ischemic mitral regurgitation (CIMR) is poorly understood and repair operations are often unsatisfactory. This study elucidates the mechanism of CIMR in an ovine model. METHODS: Sonomicrometry array localization measured the three-dimensional geometry of the mitral annulus and subvalvular apparatus in five sheep before and 8 weeks after a posterior infarction of the left ventricle that produced progressive severe CIMR. RESULTS: End systolic annular area increased from 647 +/- 44 mm(2) to 1,094 +/- 173 mm(2) (p = 0.01). Annular dilatation occurred equally along the anterior (47.0 +/- 5.6 mm to 60.2 +/- 4.9 mm, p = 0.001) and posterior (53.8 +/- 3.1 mm to 68.5 +/- 8.4 mm, p = 0.005) portions of the annulus. The tip of the anterior papillary muscle moved away from both the anterior and posterior commissures by 5.2 +/- 3.2 mm (p = 0.021) and 7.3 +/- 2.2 mm (p = 0.002), respectively. The distance from the tip of the posterior papillary muscle to the anterior commissure increased by 11.0 +/- 5.7 mm (p = 0.032) while the distance from the tip of the posterior papillary muscle to the posterior commissure remained constant. CONCLUSIONS: Progressive dilatation of both the anterior and posterior mitral annuli, increased annular area, and asymmetric ventricular dilatation combine to cause CIMR by distortion of mitral valve geometry and tethering of leaflet coaptation. Therefore complete ring annuloplasty may be superior to partial annuloplasty in the treatment of CIMR.     

Left thoracotomy approach for left ventricular pseudoaneurysm due to myocardial infarction after mitral valve replacement for papillary muscle rupture

A 59-year-old man with acute mitral regurgitation due to papillary muscle rupture after myocardial infarction was admitted to our hospital. He underwent emergent mitral valve replacement with a mechanical valve by median sternotomy. Although postoperative echocardiography showed no sign of a ventricular aneurysm, echocardiography performed 5 weeks after the surgery showed enlarging left ventricular pseudoaneurysm of the inferior to the posterior cardiac wall. He underwent dacron patch closure of the orifice by fifth intercostal left thoracotomy. The postoperative course was uneventful and he was discharged on postoperative day 10. The patient was successfully treated for two life-threatening complications occurring subsequently after myocardial infarction.     

A case of emergency surgery for acute mitral regurgitation due to complete papillary muscle rupture as complication of acute inferior myocardial infarction

We experienced a case with acute mitral regurgitation caused by complete posterior papillary muscle rupture as complication of acute inferior myocardial infarction, who underwent successfully emergency operation of mital valve replacement and coronary revascularization in acute stage. A 64-year-old woman developed sudden cardiogenic shock shortly after the onset of acute inferior myocardial infarction. The diagnosis of acute inferior myocardial infarction was based on the electrocardiographic findings. Under IABP support, preoperative coronary angiography visualized total occlusion of segment 3 of the right coronary artery, and preoperative left ventriculography showed akinesis of inferior wall and severe mitral regurgitation. At 6 hours after onset of papillary muscle rupture, emergency operation was performed. At operation, posterior papillary muscle was found to be totally ruptured. Coronary artery revascularization and mitral valve replacement were performed. Postoperative course was uneventful, with 4 days of IABP and 5 days of ventilatory support. She was discharged on the twentieth postoperative day in NYHA class I. Reports of successful emergency operation for total papillary muscle rupture following acute myocardial infarction are rare. Early diagnosis and surgical treatment are mandatory to save this group of patients.     

Septal-lateral annular cinching abolishes acute ischemic mitral regurgitation

OBJECTIVE: Ring annuloplasty prevents acute ischemic mitral regurgitation in sheep, but it also abolishes normal mitral annular and posterior leaflet dynamics. We investigated a novel surgical approach of simple septal-lateral annular cinching with sutures to treat acute ischemic mitral regurgitation. METHODS: Nine adult sheep underwent implantation of multiple radiopaque markers on the left ventricle, mitral anulus, and mitral leaflets. A septal-lateral transannular suture was anchored to the midseptal mitral anulus and externalized to a tourniquet through the midlateral mitral anulus and left ventricular wall. Open-chest animals were studied immediately postoperatively. Acute ischemic mitral regurgitation was induced by means of proximal left circumflex artery snare occlusion, and 3 progressive steps of septal-lateral annular cinching (each 2-3 mm suture tightening for 5 seconds) were performed with the transannular suture. Biplane videofluoroscopy for 3-dimensional marker coordinates and transesophageal echocardiography were performed continuously before and during left circumflex ischemia and septal-lateral annular cinching. RESULTS: Acute left circumflex ischemia caused ischemic mitral regurgitation (+0.5 +/- 0.4 [baseline] vs +2.0 +/- 0.7 [ischemia]; P =.005; scale, +0-4), which decreased progressively with each step of septal-lateral annular cinching and was eliminated during the third step (ischemic mitral regurgitation, +0.6 +/- 0.5; P = not significant vs baseline). The third step of septal-lateral annular cinching decreased the septal-lateral diameter by 6.0 +/- 2.6 mm (P =.005); however, mitral anulus area reduction (8.5% +/- 1.0% and 6.9% +/- 1.9% for ischemic mitral regurgitation and septal-lateral annular cinching step 3, respectively; P =.006) and posterior leaflet excursion (50 degrees +/- 9 degrees and 44 degrees +/- 11 degrees for regurgitation and annular cinching step 3, respectively; P =.002) throughout the cardiac cycle were affected only mildly. Normal mitral annular 3-dimensional shape was maintained with septal-lateral annular cinching. CONCLUSIONS: Isolated 22% +/- 10% reduction in mitral annular septal-lateral dimension abolished acute ischemic mitral regurgitation in normal sheep hearts while allowing near-normal mitral annular and posterior leaflet dynamic motion. Septal-lateral annular cinching may represent a simple method for the surgical treatment of ischemic mitral regurgitation, either as an adjunctive technique or alone, which helps preserve physiologic annular and leaflet function.     

Surgical management of ventricular septal defects and mitral regurgitation complicating acute myocardial infarction

Sixteen patients were studied subsequent to the development of acute ventricular septal rupture in 7 and severe mitral regurgitation in 9. These lesions occurred within two weeks of acute myocardial infarctions. Intraaortic balloon assistance was initiated when cardiovascular deterioration occurred, and hemodynamic improvement was obtained in all patients. Shunting through a ventricular septal perforation was reduced during balloon assistance, and mitral regurgitation, when present, was decreased. These effects were short-lived, and the patients were subsequently studied with coronary angiography and ventriculography.Two of 3 patients with anterior ventricular septal defect underwent successful surgical correction. Three patients had attempted closure of inferior ventricular septal defect without success. The fourth patient with an inferior ventricular septal defect died of his lesion without any attempt at surgical repair.Four patients with rupture of the papillary muscle were long-term surgical survivors. Coronary artery bypass grafting was carried out when indicated in these patients. Two of 5 patients with papillary muscle dysfunction who underwent operation during the acute period of their infarction were long-term survivors.The findings suggest that the mechanical lesions of mitral regurgitation and ventricular septal perforation are amenable to surgical intervention if a sufficient amount of residual functional muscle can be preserved in the left ventricle. Intraaortic balloon assistance allows a period of time to stabilize the condition of patients with these lesions, to reduce myocardial ischemia, and to carry out studies to determine the degree of associated coronary artery disease and the extent of irreversible myocardial damage. Based on the findings from these studies, surgical procedures may be selected.     

Functional mitral regurgitation in chronic ischemic coronary artery disease: analysis of geometric alterations of mitral apparatus with magnetic resonance imaging

BACKGROUND: Patients with chronic coronary artery disease have double the mortality rate if the condition is combined with functional mitral regurgitation. An understanding based on geometric alterations of the mitral apparatus in functional mitral regurgitation is desirable. METHODS: Twenty-nine subjects were enrolled in the study, including 9 healthy volunteers (control group), 12 patients with chronic coronary artery disease without functional mitral regurgitation (CAD group), and 8 patients with chronic coronary artery disease with functional mitral regurgitation (CAD+FMR group). Cine magnetic resonance imaging was performed to acquire multiple short-axis cine images from base to apex. Left ventricular end-systolic volume, left ventricular ejection fraction, mitral area, and vertices of the mitral tetrahedron, defined by medial and lateral papillary muscle roots and anterior and posterior mitral annulus, were determined from reconstructed images at end-systole. Anterior-posterior annular distance, interpapillary distance, and annular-papillary distance (the distance from the anterior or posterior mitral annulus to the medial or lateral papillary muscle roots) were calculated. RESULTS: Left ventricular end-systolic volume was inversely associated with left ventricular ejection fraction (R(2) = 0.778). Left ventricular end-systolic volume was highly associated with distances related to ventricular geometry (R(2) = 0.742 for interpapillary distance, 0.792 for the distance from the anterior mitral annulus to the medial papillary muscle root, and 0.769 for distance from the anterior mitral annulus to the lateral papillary muscle root) but was moderately associated with distances related to annular geometry (R(2) = 0.458 for anterior-posterior annular distance and 0.594 for mitral area, respectively). Moreover, interpapillary distance of greater than 32 mm and distance from the anterior mitral annulus to the medial papillary muscle root of greater than 64 mm readily distinguished the CAD+FMR group from the other groups. CONCLUSION: In patients with coronary artery disease, an increase in left ventricular end-systolic volume is associated with inadequate approximation of the mitral tetrahedron during systole, which consequently leads to functional mitral regurgitation. Our study suggests that interpapillary distance and distance from the anterior mitral annulus to the medial papillary muscle root are sensitive to the increase in left ventricular end-systolic volume and reliably indicate the presence of functional mitral regurgitation.     

Long term results of mitral valve repair: posterior papillary muscle repositioning versus chordal shortening.

OBJECTIVE: Mitral valve repair is considered as the gold standard to treat mitral regurgitation. However anterior leaflet prolapse in the posterior paramedial and paracommissural area remains a challenging problem. Indeed several elongated chordae may arise from a single posterior papillary muscle head which does not allow safe separate chordal shortening (CS). We therefore suggest use of papillary muscle repositioning in such cases. METHODS: In a cohort of 180 mitral valve repair performed between 1989 and May 1998, we have retrospectively studied 100 consecutive patients who underwent anterior leaflet repair in the posterior paramedial and paracommissural area. Group I (n = 60) had posterior papillary muscle repositioning (PPMR) and group II (n = 40) had CS. There was no statistical difference between the two groups concerning age, functional class and left ventricular function. Etiology was similar in both groups, degenerative process being predominant. At echocardiogram, regurgitation was graded 3.4/4 in both groups. There was no statistical difference concerning preoperative ejection fraction, end systolic and end diastolic left ventricular diameter. RESULTS: There were no in-hospital deaths in group I and two deaths in group II not related to mitral valve repair. Mean follow up is 26.4 +/- 24.2 months in group I and 46.1 +/- 28.8 months in group II. No patient was lost to follow up. Severe mitral regurgitation was not observed. Mean regurgitation at follow up was 0.8 +/- 0.7 in group I and 0.8 +/- 0.8 in group II (P = n.s.); there was no statistical difference between the two groups concerning postoperative ejection fraction, end systolic and end diastolic left ventricular diameter. There was no late cardiac death in either group and there were no thromboembolic events. Actuarial survival rate is 100% and 94.4% in group I and 92% and 84.4% in group II at 2 and 6 years, respectively. CONCLUSION: This experience shows that PPMR provides as good longterm results as CS to repair anterior leaflet prolapse in posterior paramedial and paracommissural area with lesser morbidity and mortality.     

Assessment of perioperative predictive factors influencing survival in patients with postinfarction ventricular septal perforation. Classified by the site of myocardial infarction

BACKGROUND: The present study was designed to identify the perioperative factors and to consider a counterplan for the improvement of surgical results, based on the site of myocardial infarction. METHODS: Sixteen patients with postinfarction ventricular septal perforation underwent surgical repair. The operation was performed 5+/-3 days after the onset of ventricular septal perforation using the same method, an infarctectomy and reconstruction of the septum and right and left ventricular walls with a single Dacron patch. The ventricular septal perforation was anterior in 11 patients and posterior in 5. Preoperative hemodynamics between survivors and non-survivors were compared. Left ventricular wall motion was estimated using echocardiography by wall motion score (divided into 17 segments and each segment was graded on a fourpoint scale: normal, 0; hypokinetic, 1; severe hypokinetic, 2; a- or dyskinetic, 3) and summed up. RESULTS: The operative mortality was 36% in 11 patients with anterior ventricular septal perforation. In non-survivors compared to survivors, wall motion score was greater (25+/-4 vs 18+/-4, p<0.01) and all values were over 20. The value of the cardiac index divided by Qp/Qs was lower (0.98+/-0.09 vs 1.44+/-0.31, p<0.02) and all were under 1.1. In 5 patients with inferior ventricular septal perforation, the operative mortality was 40%. In non-survivors compared to survivors, wall motion score was greater (18, 18 vs 7, 2, 12) and the right atrial pressure was greater (18, 19 vs 10, 9, 9 mmHg) due to a right ventricular infarction. CONCLUSIONS: The patients with poor left ventricular wall motion were lost for reasons unrelated to the site of myocardial infarction. Moreover, a cardiac index over Qp/Qs in anterior ventricular septal perforation and the existence of a right ventricular infarction in inferior ventricular septal perforation was predictive of operative mortality.     

Mitral regurgitation after myocardial infarction. Coronary artery bypass grafting and mitral valve replacement with chordae preservation.

A patient with acute ischemic mitral regurgitation after acute myocardial infarction required emergency coronary artery bypass grafting and mitral valve replacement with chordae preservation. For severe mitral regurgitation and heart failure due to myocardial infarction and ischemic papillary muscle dysfunction, mitral valve replacement with chordae preservation was effective. Here, we discuss the etiology of ischemic mitral regurgitation and the operative method for valve repair or replacement.     

Hemodynamic performance of an unstented xenograft mitral valve substitute

OBJECTIVE: Stentless mitral xenografts offer potential clinical benefits because they mimic the normal bileaflet mitral valve. How best to implant them and their hemodynamic performance and durability, however, remain unknown. METHODS: A stentless porcine mitral xenograft valve (Medtronic physiologic mitral valve) was implanted in 7 sheep with papillary muscle sewing tubes attached with transmural left ventricular sutures. Radiopaque markers were inserted on the leaflets, annular cuff, papillary tips, and left ventricle. After 10 +/- 5 days, the animals were studied with biplane videofluoroscopy to determine 3-dimensional marker coordinates at baseline and during dobutamine infusion. Transesophageal echocardiography assessed mitral regurgitation and valvular gradients. Mitral annular area was calculated from the annular markers. Physiologic mitral valve leaflet and annular dynamics were compared with 8 native sheep valves. RESULTS: Average mitral regurgitation grade at baseline was 1.2 +/- 1.0 (range, 0-4), and the mean transvalvular pressure gradients were 3.6 +/- 1.3 and 6.2 +/- 2.2 mm Hg during baseline and dobutamine infusion, respectively. Xenograft mitral annular area contraction throughout the cardiac cycle was reduced (6% +/- 6% vs 13% +/- 4% for physiologic mitral valve and control valve, respectively; P =.03). Physiologic mitral valve leaflet geometry during closure differed from the native valve, with the anterior leaflet being convex to the atrium and with little motion of the posterior leaflet. Three animals survived more than 3 months; good healing of the annular cuff and papillary muscle tubes was demonstrated. CONCLUSION: This stentless xenograft mitral valve substitute had low gradients at baseline and during stress conditions early postoperatively, with mild mitral regurgitation. Preliminary analysis of healing characteristics appeared favorable at 3 months. Additional studies are needed to determine long-term xenograft mitral valve performance and resistance to calcification.     

Surgical treatment of left ventricular aneurysm associated with mitral regurgitation

The purpose of this study is to analyze the early and late results of left ventricular aneurysmectomy in patients with mitral regurgitation secondary to myocardial infarction. Twenty patients who had left ventricular aneurysm combined with mitral regurgitation underwent the isolated or combined aneurysmectomy during the last 10 years. There were 18 male cases and 2 female cases, and their age ranged from 31 to 64 (mean age 52.6 years). In 19 cases, the left ventricular aneurysm were caused secondary to antero-septal infarction due to the occlusion of the left anterior descending coronary artery. In one case, the coronary spasm of circumflex artery provoked the posterolateral myocardial infarction and the tendon rupture of posterior papillary muscle. The isolated left ventricular aneurysmectomy were performed in 6 cases and the combined operations were coronary artery bypass grafting in 11 cases, mitral annuloplasty in 1 case, mitral annuloplasty and bypass grafting in 1 case, and mitral replacement in 1 case. There were no operative death cases. The preoperative mean functional class (NYHA classification) was 2.9 and the postoperative class was 1.4. The preoperative mitral regurgitation of grade 1 in Sellers' classification was observed in 11 cases. Grade 2 regurgitation was observed in 6 cases, grade 3 in 2 and grade 4 in 1. After surgery, mitral regurgitation more than grade 2 was recognized in 3 cases (group A) and regurgitation less than grade 1 was seen in 17 cases (group B).(ABSTRACT TRUNCATED AT 250 WORDS)     

Does septal-lateral annular cinching work for chronic ischemic mitral regurgitation?

OBJECTIVES: Ring annuloplasty, the current treatment of choice for chronic ischemic mitral regurgitation, abolishes dynamic annular motion and immobilizes the posterior leaflet. In a model of chronic ischemic mitral regurgitation, we tested septal-lateral annular cinching aimed at maintaining normal annular and leaflet dynamics. METHODS: Twenty-five sheep had radiopaque markers placed on the mitral annulus and anterior and posterior mitral leaflets. A transannular suture was anchored to the midseptal mitral annulus and externalized through the midlateral mitral annulus. After 7 days, biplane cinefluoroscopy provided 3-dimensional marker data (baseline) prior to creating inferior myocardial infarction by snare occlusion of obtuse marginal branches. After 7 weeks, the 9 animals that developed chronic ischemic mitral regurgitation were restudied before and after septal-lateral annular cinching. Anterior and posterior mitral leaflet angular excursion and annular septal-lateral and commissure-commissure dimensions and percent shortening were computed. RESULTS: Septal-lateral annular cinching reduced septal-lateral dimension (baseline: 3.0 +/- 0.2; chronic ischemic mitral regurgitation: 3.5 +/- 0.4 [P <.05 vs baseline by repeated measures analysis of variance and Dunnett's test]; septal-lateral annular cinching: 2.4 +/- 0.3 cm; maximum dimension) and eliminated chronic ischemic mitral regurgitation (baseline: 0.6 +/- 0.5; chronic ischemic mitral regurgitation: 2.3 +/- 1.0 [P <.05 vs baseline by repeated measures analysis of variance and Dunnett's test]; septal-lateral annular cinching: 0.6 +/- 0.6; mitral regurgitation grade [0 to 4+]) but did not alter dynamic annular shortening (baseline: 7 +/- 3; chronic ischemic mitral regurgitation: 10 +/- 5; septal-lateral annular cinching: 6 +/- 2, percent septal-lateral shortening) or posterior mitral leaflet excursion (baseline: 46 degrees +/- 8 degrees; chronic ischemic mitral regurgitation: 41 degrees +/- 13 degrees; septal-lateral annular cinching: 46 degrees +/- 8 degrees ). CONCLUSIONS: In this model, septal-lateral annular cinching decreased chronic ischemic mitral regurgitation, reduced annular septal-lateral diameter (but not commissure-commissure diameter), and maintained normal annular and leaflet dynamics. These findings provide additional insight into the treatment of chronic ischemic mitral regurgitation.     

Results of surgery for irreversible moderate to severe mitral valve regurgitation secondary to myocardial infarction.

OBJECTIVE: Moderate to severe irreversible mitral regurgitation secondary to myocardial infarction is an independent risk factor for reduced long-term survival. Late effects of correction of mitral incompetence concomitant with coronary artery bypass grafting (CABG) are less well known and the choice of mitral valve procedure is still debated. METHODS: From 1988 to 1998, 93 consecutive patients (mean age 63+/-9 years) were treated for moderate to severe irreversible mitral regurgitation secondary to myocardial infarction; 84 were in NYHA functional class III-IV and 19 were in cardiogenic shock. Thirty-seven patients underwent emergency surgery. Perioperative intraaortic balloon pump (IABP) was necessary in 33 patients. Follow-up ranged from 6 months to 12 years (mean 51 months+/-41). RESULTS: Mitral valve was repaired in 30 patients and replaced in 63. Replacement was preferably performed in patients with major displacement of papillary muscle and in patients with acute papillary muscle rupture. CABG (3.4 distal anastomoses) was performed in all patients and was complete in 92%. Early mortality was 15% (14/93). Multivariable analysis identified need for IABP (P=0.005) and COPD (P=0.02) as risk factors for early death. Emergency surgery had only a trend (P=0.15) for increased mortality; age, low ejection fraction, repair vs. replacement had no influence. Actuarial survival rates at 1, 5 and 10 years were 81, 65 and 56%, respectively. Late survival was similar in patients with replacement or repair (P=0.46). At last follow-up, all but one patient were in NYHA functional class I or II. CONCLUSIONS: Combined mitral valve procedure and myocardial revascularization, as complete as possible, for moderate to severe mitral regurgitation secondary to myocardial infarction achieve satisfactory early and late outcome despite the increased operative mortality. Acute papillary muscle rupture, severe restriction of the mitral valve by major displacement of the papillary muscle are better managed by valve replacement.     

Ischemic mitral regurgitation: intraventricular papillary muscle imbrication without mitral ring during left ventricular restoration

OBJECTIVES: Functional mitral regurgitation in ischemic cardiomyopathy carries a poor prognosis, and its surgical management remains problematic and controversial. The aim of this study was to report the results of our surgical approach to patients who have had myocardial infarctions and have ventricular dilatation, mitral regurgitation, reduced pump function, pulmonary hypertension and coronary artery disease. This surgical approach consists of endoventricular mitral repair without prosthetic ring, ventricular reconstruction with or without patch, and coronary artery bypass grafting. PATIENTS: Forty-six patients (aged 64 +/- 10 years) with previous anterior transmural myocardial infarction and mitral regurgitation comprised the study group. Indication for surgery was heart failure in 93% of cases; 25 patients were in New York Heart Association functional class IV and 17 were in class III. Mitral regurgitation was moderate to severe in 32 cases (69%). RESULTS: All patients underwent coronary artery bypass grafting, with a mean of 3.2 +/- 1.3 grafts. Associated aortic valve replacement was performed in 4 cases. Global operative mortality rate was 15.2%. End-diastolic and end-systolic volumes significantly decreased after surgery (from 140 +/- 40 to 98 +/- 36 mL/m(2) and from 98 +/- 32 to 63 +/- 22 mL/m(2), respectively, P =.001). Systolic pulmonary pressure decreased significantly (from 55 +/- 13 to 43 +/- 16 mm Hg, P =.001). Ejection fraction did not change significantly. Postoperative mitral regurgitation was absent or minimal in 84% of cases; 1 patient had severe mitral regurgitation necessitating valve replacement. New York Heart Association functional class significantly improved. The mean preoperative functional class was 3.4 +/- 0.6 (median 3, range 2-4); after the operation, this decreased to 1.9 +/- 0.7 (median 2, range 1-3, P <.001). Cumulative survival at a 30-month follow-up was 63%. CONCLUSIONS: Our aggressive, combined surgical approach is aimed at correcting the three components of ischemic cardiomyopathy: relieving ischemia, reducing left ventricular wall tension by decreasing left ventricular volumes, and reducing volume overload and pulmonary hypertension by repairing the mitral valve. Despite a relatively high perioperative mortality rate, surviving patients benefitted from the operation, with improved clinical functional class and thus quality of life.     

Determinants of postinfarction remodeling affect outcome and left ventricular geometry after surgical treatment of ischemic cardiomyopathy

OBJECTIVE: To identify the effects of the time between myocardial infarction and surgery, the site of infarction, mitral involvement on ventricular geometry, and clinical outcome in the treatment of ischemic cardiomyopathy in patients with heart failure. METHODS: Sixty-nine consecutive patients with ischemic cardiomyopathy, indexed end-systolic volume > or =50 mL/m(2), ejection fraction < or =35%, and heart failure underwent surgery 81.9 +/- 100.8 months after myocardial infarction, using different techniques of ventricular restoration. Thirteen geometric parameters were studied pre- and postoperatively. Paired and unpaired t tests and general linear model for multivariate analysis were used to analyze subgroups. Logistic regression and Kaplan-Meier survival curves with pairwise log-rank were used to correlate covariates to clinical outcome. RESULTS: Longer time to surgery and posterior necrosis linearly correlated with higher left ventricular volumes (r(2) =.66) and diameters (r(2) =.40). High grade of mitral regurgitation was always present in posterior infarctions. Hospital mortality was 4.3%. Complicated postoperative course was predicted by mitral surgery (P =.004) and longer time to surgery (P =.04). Survival was significantly lower in the posterior infarction (P =.0002) and mitral surgery (P =.001) subgroups. At a mean follow-up of 1.9 +/- 1.3 years, functional status and geometrical restoration are influenced by the studied covariates. CONCLUSIONS: Longer time to surgery after myocardial infarction, its posterior location, and significant mitral regurgitation can affect left ventricular remodeling, surgical restoration, and clinical outcome in patients with ischemic cardiomyopathy.     

Mitral regurgitation after myocardial infarction

A patient with acute ischemic mitral regurgitation after acute myocardial infarction required emergency coronary artery bypass grafting and mitral valve replacement with chordae preservation. For severe mitral regurgitation and heart failure due to myocardial infarction and ischemic papillary muscle dysfunction, mitral valve replacement with chordae preservation was effective. Here, we discuss the etiology of ischemic mitral regurgitation and the operative method for valve repair or replacement.     

Perioperative outcome and long-term survival of surgery for acute post-infarction mitral regurgitation.

OBJECTIVE: To determine factors predictive of mortality in patients undergoing emergency mitral valve surgery in the setting of severe post-infarction regurgitation. METHODS: Patients admitted for an acute myocardial infarction who required urgent mitral valve surgery for severe regurgitation were studied. Factors predictive of outcome were analysed. RESULTS: Fifty-five consecutive patients (mean 65+/-10 years, 37 males) were included. The infarct was inferior in 31 patients, posterior in 10, anterior in 9 and lateral in 5. Thirty-four patients (62%) were in Killip class IV. Peroperative findings confirmed total papillary muscle rupture in 25 patients (posteromedial in 21, anterolateral in 4), and partial rupture in 12 patients (posteromedial in 10, anterolateral in 2). Papillary muscle dysfunction without rupture was responsible for regurgitation in 18 patients (posteromedial in 15, anterolateral in 3). The mitral valve was replaced by a prosthesis in all but 4 patients, who had valvuloplasty. Coronary angiography was done in 32 patients, of whom 18 underwent concomitant coronary artery bypass grafting and 2 balloon angioplasty. Surgery was performed on average 7 days after infarction. Thirteen patients (24%) died during the perioperative period. Absence of coronary revascularisation was significantly associated with increased perioperative mortality (34% vs. 9%, P = 0.02). Of the 42 surviving patients, there were 5 deaths during a mean follow-up of 4.0+/-3.7 years. CONCLUSION: In patients with acute post-infarction mitral regurgitation, perioperative mortality is high, but can be improved with concomitant CABG in addition to valve surgery. Long-term outcome of survivors is favourable.