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• W2149388003 abstract "HomeCirculationVol. 112, No. 5Ischemic Mitral Regurgitation on the Threshold of a Solution Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBIschemic Mitral Regurgitation on the Threshold of a SolutionFrom Paradoxes to Unifying Concepts Robert A. Levine, MD and Ehud Schwammenthal, MD, PhD Robert A. LevineRobert A. Levine From the Cardiac Ultrasound Laboratory (R.A.L.), Cardiology Division, Massachusetts General Hospital, Department of Medicine, Harvard Medical School, Boston, Mass, and the Cardiac Rehabilitation Institute (E.S.), Sheba Medical Center, Tel Hashomer, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. Search for more papers by this author and Ehud SchwammenthalEhud Schwammenthal From the Cardiac Ultrasound Laboratory (R.A.L.), Cardiology Division, Massachusetts General Hospital, Department of Medicine, Harvard Medical School, Boston, Mass, and the Cardiac Rehabilitation Institute (E.S.), Sheba Medical Center, Tel Hashomer, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. Search for more papers by this author Originally published2 Aug 2005https://doi.org/10.1161/CIRCULATIONAHA.104.486720Circulation. 2005;112:745–758“More than once in history the discovery of paradox has been the occasion for major reconstruction at the foundations of thought.”— W.V. Quine, The WaysOne thing is certain: Ischemic mitral regurgitation (MR) conveys adverse prognosis, doubling mortality after myocardial infarction (MI), in chronic heart failure, and after surgical or catheter revascularization.1–9 It is common and increases mortality even when mild,3–5 with a graded relationship between severity and reduced survival (Figure 1A).5Download figureDownload PowerPointFigure 1. A, Decreased survival after MI with increasing MR. Effective regurgitant orifice (ERO) area of 20 mm2 demarcates mild from moderate. Reprinted with permission from Grigioni et al.5 Copyright 2001, American Heart Association, Inc. B, Decreased survival after cardiogenic shock with increasing MR for comparable LV ejection fraction (LVEF). Reprinted with permission from Picard et al.8 Copyright 2003, American Heart Association, Inc.In many other respects, however, ischemic MR has been a study in controversy and paradox. Its diagnosis is notoriously elusive, both by auscultation and intraoperatively. It may paradoxically decrease as driving pressure increases. Still commonly referred to as “papillary muscle dysfunction,” it cannot generally be produced by direct papillary muscle damage and may actually decrease with papillary muscle ischemia. Although leaflet motion is typically restricted, it may also be excessive, or both. Treatment benefit is hotly debated and will be difficult to resolve so long as existing therapies are incompletely effective in permanently abolishing MR. New therapeutic opportunities are perplexing in their diversity. By exploring such areas of confusion, we aim to clarify fundamental principles and achieve more effective solutions.Ischemic MR is convenient shorthand for MR caused by changes in ventricular structure and function related ultimately to ischemia; it is predominantly postinfarction MR. Active ischemia can contribute, for example, creating intermittent “flash” pulmonary edema, although MR from brief single-vessel occlusion is usually mild, without preexisting ventricular abnormality. “Functional MR” broadly denotes abnormal function of normal leaflets in the context of impaired ventricular function; it typically occurs in globally dilated and hypokinetic ventricles or with segmental damage that affects valve closure (Figure 2). It occurs in roughly 20% to 25% of patients followed up after MI3,4,10,11 and 50% of those with congestive heart failure.12 It differs from the dramatic presentation of ruptured papillary muscle (PM),13 a surgical emergency. Download figureDownload PowerPointFigure 2. A, Ischemic MR in spherical LV with global dysfunction. Left, Mitral leaflet closure is restricted apically relative to annulus (dotted line), with anterior leaflet bent at basal chordal attachment (arrow). LA indicates left atrium. Right, Moderate MR by Doppler color flow mapping. (Courtesy of Dr. J. Hung.) B, Ischemic MR with inferior MI (left on apical long-axis images). Left, Apically tethered leaflets, with anterior leaflet bend (oblique arrow) and chord from posterior wall restricting posterior leaflet motion (horizontal arrow). Right, Moderate MR with prominent vena contracta (narrowest neck, thin arrows) and flow convergence (thick arrow).MechanismsBurch, De Pasquale, and Phillips14,15 initially ascribed ischemic MR to PM dysfunction. Normally, as the left ventricle (LV) shortens, PM contraction maintains the distance between the PM tips and mitral annulus to prevent prolapse. PM damage could then produce prolapse, consistent with its frequently late-systolic murmur. Experimental damage to the PMs themselves, however, fails to produce MR acutely without damage to the underlying myocardial wall as well.16Burch et al14,15 alternatively postulated restricted leaflet motion. The PMs, normally parallel to the LV long axis and perpendicular to the leaflets, efficiently balance forces generated by ventricular pressure on the leaflet surface. Ischemia or heart failure causes the myocardial segments underlying the PMs to bulge posteriorly and outward, displacing the PMs, so that they pull the leaflets nonperpendicularly, away from their normal coaptation (Figure 3). The distance between the PM tips and the annulus also increases, drawing the leaflets into the ventricle and restricting their motion toward closure, as proposed by Paul Dudley White, Levy and Edwards, Silverman and Hurst,17 and Perloff and Roberts.18Download figureDownload PowerPointFigure 3. Left, Balance of forces acting on mitral leaflets in systole. LA indicates left atrium; AO, aorta. Right, Effect of PM displacement. Dark shading indicates inferobasal MI; light hatching, normal baseline. Modified and used with permission from Liel-Cohen et al.31 Copyright 2000, American Heart Association, Inc.Two-dimensional echocardiography first directly demonstrated apically restricted leaflet motion, termed “incomplete mitral leaflet closure” (IMLC; Figure 2).19,20 Godley, Weyman, et al20 associated IMLC with inferior dyskinesis, postulating increased leaflet tethering. On the basis of myocardial injection studies, Alain Carpentier has succinctly renamed PM dysfunction “PM wall dysfunction,” namely, tethering caused by displacement of the leaflet attachments.Kaul et al21 elegantly confirmed that reducing PM perfusion produced neither prolapse nor MR. In contrast, global hypoperfusion with LV dilatation, despite continued PM perfusion and thickening, caused MR with IMLC in direct correlation with LV dysfunction.21 In those studies, however, akinesia of the PMs and their underlying wall also failed to produce MR acutely. This led to the postulate that MR results from global LV dysfunction, decreasing the leaflet closing force,22 as opposed to PM wall tethering. Conceivably, however, the acute PM wall displacement in that study was insufficient to produce MR, and as the authors acknowledged, LV dilatation paralleled global dysfunction, precluding separation of dysfunction from dilatation as primary cause of MR.This distinction has practical implications: LV contractile dysfunction would demand inotropic therapy, revascularization, or transplantation, whereas tethering might respond to modifying LV wall or PM geometry. New models were therefore required to dissect the effects of dysfunction and dilatation.He, Yoganthan, et al23 reproduced MR in excised mitral valves by displacing the PMs apically, posteriorly, and outward, as in patients. In vivo, Schwammenthal, Otsuji, et al24 created global LV dysfunction pharmacologically but limited LV expansion through pericardial restraint and decreased preload. Contractile dysfunction (ejection fraction <20%) without dilatation produced only trace MR; LV dilatation was a prerequisite for IMLC and MR.24 To quantify tethering geometry, Mark Handschumacher24 used 3D echocardiographic data to standardize the tethering length from the PM tips to the anterior mitral annulus (Figure 4A). In global dysfunction, Otsuji et al24 found that tethering length was the only independent predictor of MR, not LV ejection fraction or dP/dt. MR also correlated with LV sphericity, consistent with the key observation of Kono, Sabbah, et al25–27 that MR relates not to LV dilatation per se but to increased sphericity that could potentially displace the PMs posterolaterally, as verified by 3D echocardiography.24Download figureDownload PowerPointFigure 4. A, Tethering length in 3 dimensions. Left, 3D echocardiographic LV reconstruction. Dotted line indicates tethering length from anterior mitral annulus to most posterior PM head. Right, Schematic. Modified and used with permission from Messas et al.40 Copyright 2001, American Heart Association, Inc. LA indicates left atrium. B, Suture approach to reduce tethering length and improve coaptation (insets) by approximating displaced posterior PM (PPM) toward annulus. A indicates anterior leaflet; P, posterior leaflet. Reprinted from Kron et al77 with permission from the authors and the Society of Thoracic Surgeons. Copyright 2002, Society of Thoracic Surgeons.The centrality of geometric change was confirmed in acute segmental inferior ischemia, studied with and without external constraint,28 and in the chronic sheep model of Gorman and Edmunds, in which MR, initially absent, evolves in parallel with LV remodeling and PM displacement.28–31 In patients, Yiu, Enriquez-Sarano, et al32 strongly related PM tethering, leaflet tenting, and MR, which is frequently due to localized remodeling of the posterior PM-bearing walls, without the global remodeling required for MR with anterior infarctions.11 By 3D echocardiography, the medial mitral valve is most tented in ischemic cardiomyopathy, because the inferomedial PM is most displaced33; this asymmetry might augment MR through asymmetrical coaptation between posterior leaflet scallops.34 Although the annulus is dilated in global dysfunction,35 isolated annular dilatation without increased tethering length in atrial fibrillation is not associated with important MR.36 Finally, Otsuji and colleagues37 recognized restricted diastolic as well as systolic leaflet excursion, an echocardiographic clue that tethering is increased.The simple story, however, is often incomplete. First, although PM damage does not produce MR acutely, MR does occur in the chronic phase of ethanol injection, with PM scarring and retraction.16 Second, occasional patients with MI actually do have prolapse with PM elongation.38 These observations, rather than disproving tethering, actually confirm that tethering distance is the final common pathway determining the level of leaflet coaptation. The change in tethering distance is the resultant of 2 vectors: Displacement of the PM-bearing wall is modulated by changes in PM length. As Frater et al39 have shown, MR increases biphasically with too long or too short a tethering length.We can therefore understand how PM contractile dysfunction can paradoxically diminish MR. Messas et al40 created a limited inferobasal MI with wall bulging and MR; making the adjacent PM acutely ischemic caused it to elongate in response to ventricular forces and reduced tethering distance and MR. Preserved PM shortening increases tethering and MR,41 which confirms the central role of tethering length and the concept of PM-ventricular wall complex expressed by Komeda, Miller, et al.42Tethering is one facet of a unifying principle of mitral valve function: that leaflet motion is determined by the 3D geometry of the leaflets and their attachments, relative to the surrounding flow field. Another example is the relation between systolic anterior mitral valve motion and anterior PM displacement combined with leaflet elongation, the converse of posterior PM displacement and leaflet restriction in ischemic MR.The dichotomy between tethering versus closing forces is also a simplification: Both are involved. The equilibrium position of the mitral leaflets is determined by the balance of forces acting on them, including annular and PM tethering forces and LV-generated closing forces (Figure 3). Normally, little force is required to close the thin leaflets, so MR is not produced by global dysfunction without tethering.24 However, once tethering is increased, leaflet closure is further impaired when less force is available to oppose tethering. This balance of competing forces creates a unique dynamic pattern, recognized by Schwammenthal et al,43 with flow and orifice area greatest in early and late systole and often paradoxically decreased in mid systole, when peak LV pressure maximizes leaflet closure (Figure 5A). Tethering sets the stage for MR; transmitral pressure modulates its variation throughout the cardiac cycle.23,44 We therefore understand the early systolic leaflet “loitering” described by Glasson, Miller, et al45 and late-systolic MR and murmurs in patients with inferior MIs, in whom tethering increases as the inferior wall is “left behind” the contracting ventricle.46Download figureDownload PowerPointFigure 5. A, Color Doppler M-mode showing dynamic changes in ischemic MR flow within systole, indicated by proximal flow convergence region on LV side of valve (white line), with early and late systolic peaks (arrows). LA indicates left atrium. B, Schematic relating dynamic changes in transmitral pressure gradient (TMP) and effective regurgitant orifice area (ERO) with cardiac resynchronization. With pacing off (top), LV contractility is low; LV pressure and TMP rise slowly, with delayed maximum. Therefore, ERO area remains large relatively long until its minimum. During cardiac resynchronization therapy (CRT; bottom), LV contractility improves, and TMP rises faster and to higher, earlier maximum. Consequently, ERO falls earlier to lower values for longer. Shaded area represents time during which ERO is <50% of its initial value. Reduced V-wave from initial MR reduction also preserves TMP. Reprinted from Breithardt et al127 with permission of the American College of Cardiology. Copyright 2003, The American College of Cardiology Foundation.The Dynamic LesionA dramatic example of this dynamic behavior is the case of the vanishing intraoperative MR. A patient undergoing coronary revascularization is reported to have moderate ischemic MR by transthoracic echocardiography. After anesthetic induction, transesophageal echocardiography shows only minor MR, so the mitral valve is not approached, and after successful revascularization, transthoracic echocardiography 1 month later again shows moderate MR. This frequent scenario has led to recognition that anesthetic induction and inotropic agents can substantially reduce MR, confounding decisions regarding repair.47–49 Phenylephrine can restore representative driving pressures but may fail to reproduce volume-dependent tethering, so intravenous volume loading has also been advocated, titrated to ventricular diameter, mean blood pressure ≥90 mm Hg, and wedge pressure of 12 mm Hg.47 Practically, some surgeons advocate decisions based on the appearance of restricted leaflet closure and prior MR assessment under routine loading conditions.Ischemic MR also responds dynamically to exercise. Lancellotti, Pierard, et al50,51 recently quantified MR during semisupine bicycle exercise in patients with LV dysfunction, at least mild MR, and no evidence of inducible ischemia. In most, exercise increased MR, with orifice area rising by >20 mm2 (enough to change clinical grade) in nearly 30%, but without extended wall-motion abnormalities. Increased MR correlated best with increased tethering and PM displacement. MR decreased only in patients with recruitable contraction of the inferior wall.50 Exercise-increased MR also correlated with increased pulmonary artery pressure and adverse prognosis.51 Lapu-Bula, Vanoverschelde, et al52 likewise have shown that exercise-induced MR limits stroke volume and exercise capacity in chronic congestive heart failure.Pierard and Lancellotti53 have studied patients with established LV dysfunction admitted with acute pulmonary edema but without evident acute ischemia. When they exercised, these patients, unlike control subjects, doubled their regurgitant volume from mild to moderate-to-severe, with increased pulmonary pressures and limiting dyspnea; they appear sensitive to the volume load imposed by exercise and increased MR.53There are several practical messages54: (1) We can now expand the differential of acute pulmonary edema to include acute exacerbation of ischemic MR without obvious acute coronary insufficiency.55 (2) Exercise can unmask the severity of what might otherwise be considered mild MR. This may help explain the clinical puzzle of patients with exertional dyspnea out of proportion to their resting systolic dysfunction or MR (assuming no intermittent ischemia or diastolic dysfunction). This may also be a reason that apparently mild ischemic MR worsens prognosis.3–5Given the dynamic interplay of tethering and closing forces, why not reduce MR by raising LV pressure? That approach is limited, because increasing afterload dilates compromised ventricles and increases tethering. Therapy must therefore focus on reducing the geometric culprits.TherapyPrompt in-hospital revascularization of acute coronary occlusion can reverse ischemic MR. Leor et al56 and Tenenbaum and colleagues57 showed that early thrombolysis of first inferior MIs reduces localized LV remodeling and MR. This would support revascularization of MIs that, although localized, can cause important MR. Delayed reperfusion may yield less benefit.2In acute MI with shock, MR conveys considerable excess mortality for any level of global LV function (Figure 1B), and as Picard, Hochman, and colleagues have shown,8 early revascularization increases survival across the board. Acute PM rupture may present with acute pulmonary edema despite relatively limited areas of damage, and experience supports aggressive repair.13In contrast to the clear therapeutic opportunity provided by rapid reperfusion, MR relief by revascularization alone in chronic coronary artery disease is problematic. Aklog et al,49 for example, recently found persistent moderate or severe MR in 77% of revascularized patients, without established means to predict improvement.Standard surgical therapy includes annular ring reduction, which aims to improve leaflet apposition by correcting posterior annular dilatation. Although often effective initially, long-term failures are increasingly recognized. Experienced centers consistently report important persistent and recurrent MR, often months after surgery, in 30% or more of patients, casting doubt on whether satisfactory early results represent success.58–61 Disappointing benefits, combined with the added risks of prolonged bypass and ischemic time, with reported mortalities of ≥6% to 12%,62–64 often deter surgeons from performing this procedure.Intraoperative MR underestimation contributes to the impression of recurrence but is only part of the problem. The mitral valve is caught in a tug-of-war between the dilated annulus and the displaced PMs. Reducing annular size alone leaves persistent tethering to the displaced LV wall. Steven Bolling and Bach65 and others indicate that ischemic MR is a ventricular, not a valvular, problem. Calafiore et al58 have shown that annuloplasty failure is predicted by greater preoperative leaflet tethering. Most importantly, the ventricle is a moving target and often continues to remodel and dilate, which renders initial repair ineffective, as quantitatively confirmed by Hung, Duran, and colleagues60 (Figure 6) and Qin, Shiota, Thomas, et al.66Download figureDownload PowerPointFigure 6. Progressive MR despite coronary revascularization and annular ring reduction. A, B, Early postoperative (post-op) mild leaflet tethering and MR. LVID indicates LV internal diameter. C, D, Late postoperative increased MR and tethering paralleling increased LV dilatation. Reprinted with permission from Hung et al.60 Copyright 2004, American Heart Association, Inc.Bolling introduced the increasingly common practice of implanting rings 1 or 2 sizes smaller than predicted by measuring the fibrous intertrigonal annulus.65 However, as Carlos Duran59 has put it, this attempts to compensate for the fundamental problem, not correct it. Recently, McGee, Gillinov, et al61 reported high-grade recurrent MR in 35% of patients 6 months after surgery, highest for pericardial annuloplasty but still 25% for Cosgrove and complete Carpentier rings, with no significant difference between large and small rings. Rings also shift the posterior annulus anteriorly, but the posterior leaflet remains tethered posteriorly, so its anterior excursion is markedly restricted; nearly rigid, it coapts poorly.60,67Modified approaches include asymmetrical annuloplasty, first introduced by Tirone David,68 to reduce the largest leaflet gap, located medially because the inferomedial PM is most affected; apical displacement of the medial annulus to restore its more normal 3D saddle shape,69,70 bringing the vulnerable commissural point closer to the PM to relieve tethering, as shown by He, Yoganathan, and colleagues in a preliminary study; and predominant anteroposterior (septal-lateral) annular reduction to bring the leaflets together most effectively.71 Percutaneous annular reduction by coronary sinus compression may increase applicability but may be limited in reducing the anteroposterior dimension, because the coronary sinus is posterior. Nevertheless, all these approaches share the limitation that if the remodeling ventricle is not addressed, MR may persist or recur.Subvalvular tethering can be relieved by modifying ventricular, leaflet, or chordal structures (Figure 7). Early approaches involved scar resection with PM reimplantation.39 The partial ventriculectomy stress-reduction experience reminded surgeons that decreasing inter-PM separation could cause variable tethering, prolapse, and severe MR unless prevented by an edge-to-edge (Alfieri) stitch. More recent ventricular reconstruction approaches championed by investigators such as Gerald Buckberg and Lynda Mickleborough, as in the STICH trial (Surgical Treatments for Ischemic Heart Failure), restore a less spherical ventricle to optimize contraction and reduce MR.72–75 Dor’s excision and patching of large dysfunctional areas reduces MR, but tethering and MR may recur.76 Tethering can be reduced by infarct plication to reduce bulging, reported by Liel-Cohen et al31 (Figure 8). Plication was inspired by the observation of J. Luis Guerrero,31 an experienced physiological surgeon, that manually repositioning the PM-bearing wall inward and anteriorly reduces tethering and MR; plication prolongs this benefit. Kron et al77 brought displaced PMs closer to the annulus using sutures, in conjunction with annular reduction (Figure 4B). Others use internal slings or surgically buckle displaced PMs anteriorly.78Download figureDownload PowerPointFigure 7. Therapeutic targets. Ao indicates aorta.Download figureDownload PowerPointFigure 8. Infarct plication to bring displaced PM tip back toward anterior mitral annulus, reducing MR. AO indicates aorta. Modified and used with permission from Liel-Cohen et al.31 Copyright 2000, American Heart Association, Inc.To realign the PM simply, Hung, Levine, et al79 have applied a localized patch that contains an epicardial balloon over inferior infarcts (Figure 9). In the beating heart, the injection of saline into the buttressed balloon under echocardiographic guidance repositions the underlying wall and PM anteriorly, which reverses leaflet tenting and MR.79 Effective in both acute and chronic remodeled MIs, this maneuver does not increase LV end-diastolic pressure, decrease LV contractility, or significantly increase stiffness. Initial experience shows efficacy over 2 months; despite instances of continued global remodeling, the patch maintains the critical PM-valve alignment that prevents MR.42 Thus, a relatively simple external device can reverse tethering and MR adjustably under echocardiographic guidance in the beating heart. Moainie, Gorman, et al80 have used a Marlex mesh patch that reduces but does not always eliminate MR in the absence of a PM-realigning balloon; external bands can also reposition the PMs. McCarthy’s Coapsysdevice spans the LV with a reinforced suture that hoists a small pad at the posterior base anteriorly toward the right ventricular free wall.81 The localized LV compression and need for anterior attachment without coronary or right ventricular compromise merit exploration. Download figureDownload PowerPointFigure 9. Patch placement and balloon inflation over infarct region (highlighted) to reposition displaced PM toward anterior annulus and relieve tethering and MR under ultrasound guidance in beating heart. LA indicates left atrium; AO, aorta. Modified and used with permission from Hung et al.79 Copyright 2002, American Heart Association, Inc.External constraint can also limit ventricular remodeling82,83 and parallels development of global constraint devices for congestive heart failure that do not appear to cause constriction. Potential for minimally invasive port-access implantation has particular value in advanced heart failure. Alternatively, repopulating damaged myocardium with cells derived from autologous skeletal myoblasts or from embryonic stem cells could reduce MR mechanically if increased wall thickness decreases bulging and reduces wall stress; in a preliminary report,83a autologous skeletal myoblast engraftment into a large, scarred sheep infarct blunted the progression of remodeling and MR over 8 weeks.The leaflets and chordae also present logical targets. PM elongation and prolapse, although uncommon, respond to PM and leaflet reduction.38 Kunzelman et al84 have shown by elegant finite element modeling that tethering stresses alter collagen deposition and increase leaflet stiffness, but the body appears unable to compensate sufficiently by increasing leaflet area. Leaflet elongation can reduce MR but is seldom attempted, perhaps because of concerns regarding durability, calcification, and complexity. Suturing leaflet edges together (Alfieri), possibly percutaneously, can improve coaptation in flail or prolapse85 but may increase tension on tethered leaflets, unless unstressed, perhaps by annuloplasty.86 A steadily increasing frequency of moderate and severe ischemic MR has been reported after this maneuver87; it may ideally address asymmetrical coaptation or prolapse that persists after relief of tethering (see below).An alternative approach involves modifying the chordal tethering mechanism directly, in ways suggested by valve anatomy18 and clinical observations of valve shape.19,20,88 Fine marginal chordae position the leaflet tips and prevent prolapse; thicker intermediate (basal or strut) chordae insert closer to the leaflet bases. With increased tethering, the basal anterior leaflet near the annulus becomes nearly rigid and tented apically by these basal chordae (Figures 2 and 10). The more distal leaflet pivots around the “knee” where these chordae attach, but only its tip can then approach the posterior leaflet, which decreases the coaptational surface that normally seals the orifice. Download figureDownload PowerPointFigure 10. Anterior leaflet distortion by tethering basal chordae, reducing coapting surface and causing MR; with improved coaptation after basal chordal cutting. Modified and used with permission from Messas et al.89 Copyright 2001, American Heart Association, Inc.Messas, Levine, and colleagues89 therefore proposed that cutting a limited number of these critically positioned basal chordae can reduce ischemic MR; eliminating the anterior leaflet bend can make the leaflets less taut and improve coaptation (Figure 10). The intact marginal chordae should continue to prevent prolapse. As an initial approach, the 2 most central basal chordae to the anterior leaflet were cut at their valvular insertions, because they are most stretched by PM displacement away from the LV center.Relief of MR without prolapse has been confirmed in several settings. (1) In porcine valves studied in vitro at Georgia Tech, chordal cutting decreases leaflet tension for the same tethering length.89 (2) In sheep with acute inferobasal infarction, LV ejection fraction, pressure, and dP/dt are unchanged as MR decreases.89 (3) With greater inferobasal remodeling 2 months after MI, LV ejection fraction is not decreased by chordal cutting.90 (4) With chordal cutting at the onset of inferobasal infarcts known to produce progressive MR,28,29 after a mean follow-up of 33 weeks (up to 43 weeks), no MR or post-MI LV ejection fraction decline occurs.90 Goetz, Duran, et al91 have confirmed that chordal cutting increases leaflet mobility, which could benefit the tethered valve. Alternatively, expanded polytetrafluoroethylene chordal elongation is feasible.Does chordal cutting affect ventricular function? Complete chordal transsection can reduce function, particularly in chronically volume-overloaded ventricles, leading to the current practice of chordal-sparing valve replacement.92 In isolated hearts, even severing all basal chordae only slightly decreased shortening of a single myocardial segment. To reduce tethering, however, only 2 chords are cut, and although they individually bear more stress, Kunzelman and Cochran have suggested “it may be possible surgically t" @default.
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• W2149388003 date "2005-08-02" @default.
• W2149388003 modified "2023-09-27" @default.
• W2149388003 title "Ischemic Mitral Regurgitation on the Threshold of a Solution" @default.
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