Ann Thorac Surg 2000;70:771-777
© 2000 The Society of Thoracic Surgeons
Original articles: cardiovascular
Papillary muscle repair surgery in ischemic mitral valve patients
Roland Fasol, MDa,
Fitzum Lakew, MDa,
Bettina Pfannmüller, MDa,
Marvin J. Slepian, MDa,
Elrina Joubert-Hubner, CTPa
a Herz-und Gefaess-Klinik, Bad Neustadt, Germany
Address reprint requests to Dr Fasol, Division of Cardiothoracic Surgery, IMC, Innovative Medical Care Ltd, Kreutzgasse 70/32, A-1180 Vienna, Austria
e-mail: rfasol{at}heart-surgeon.com
Presented at the Thirty-sixth Annual Meeting of The Society of Thoracic Surgeons, Fort Lauderdale, FL, Jan 31Feb 2, 2000.
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Abstract
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Background. Ischemic mitral regurgitation (MR), when ischemia/infarction has resulted in fibrotic degeneration and elongation of papillary muscles, carries a high risk for the patient and a technical challenge for the surgeon. We have developed a papillary-shortening plasty for this specific pathology.
Methods. Papillary muscle repair was performed in 88 patients (7.2%) where degenerated and fibrotic elongated papillary muscles were found, which resulted in a prolapse of one or more parts of the mitral valve leaflets (MR IIIIV). All patients had a papillary muscle-shortening plasty using a pericardium pledged-reinforced polytetrafluoroethylene suture and a ring annuloplasty. Because the cause of regurgitation in this specific group of patients was ischemic, concomitant coronary bypass grafting was required in all patients, with 2.2 grafts/patient.
Results. There were five hospital deaths (5.7%). Postoperative mitral valve function was satisfactory in all patients: no residual mitral regurgitation (MR 0) was found in 80 patients (90.9%), mild regurgitation (MR I) in 5 patients (5.7%), and moderate regurgitation (MR III) was observed in 3 patients (3.4%). Within a short mean follow-up period of 18.6 months (3 to 40 months), there was one late death (1.2%). The actuarial freedom from reoperation and thromboembolic complications was 100%, but there were two anticoagulation-induced gastric bleeding complications (2.3%). All patients were in New York Heart Association functional class I or II at the time of follow-up.
Conclusions. Our data show that careful assessment of papillary muscle pathology is mandatory, and that a papillary muscle-shortening plasty is a simple but valuable surgical tool to repair the mitral valve in this specific group of high-risk patients with ischemic mitral regurgitation.
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Introduction
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Coronary artery disease is the leading cause of death in women aged over 65 years and men aged over 45 years [1]. The association of coronary artery disease with organic nonischemic valve lesions has been linked to decreased postoperative long-term survival [24]. However, mitral valve regurgitation secondary to ischemic heart disease unfavorably alters prognosis for medical therapy, carries a significant mortality, and is also associated with a dramatically increased surgical mortality [57]. Nevertheless, although most surgeons advocate and prefer repair, ischemic valves are often replaced by them, because the mechanism that causes the otherwise intact valve to leak is normally not understood.
Mitral valve surgery has subsequently evolved through the years, since 1956, when the first mitral annuloplasty was performed by Lillehei [8], and 1968, when the first mitral valve reconstruction using a prosthetic ring was performed by Carpentier [9]. However, patients with ischemic mitral regurgitation still represent a surgical challenge. The results after combined mitral procedures and coronary revascularization with a reported perioperative mortality of 19% to 53% have been poor, and the optional methods of repair are still under discussion [1013].
We have employed a papillary-shortening plasty for this specific pathology of ischemic mitral regurgitation, when ischemia or infarction has resulted in fibrotic degeneration and elongation of papillary muscles with subsequent leaflet prolapse.
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Material and methods
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Patient population
Between January 1996 and March 1999, 11,406 patients underwent open heart surgery in our unit (Herz-und Gefaess-Klinik, Bad Neustadt, Germany). One thousand two hundred twenty patients had mitral surgery during this period of time (10.7%), and the percentage of mitral repair increased from 52.1% in 1996 to 72.7% in 1999. A specific subgroup of 88 patients (7.2%) were identified to have degenerated and fibrotic elongated papillary muscles due to myocardial ischemia and/or infarction, which resulted in a prolapse of one or more parts of the mitral valve leaflets with a subsequent significant mitral regurgitation (MR IIIIV). Of these 88 patients, 54 were male (61.4%), the mean age was 66.5 ± 9.6 years (range 38 to 82 years), and 85.3% were in New York Heart Association (NYHA) class III or IV. Eight patients (9.1%) had a preoperative left ventricular ejection fracture (LVEF) of less than or equal to 19%, 33 patients (37.5%) between 20% and 39%, 23 patients (26.2%) between 40% and 54%, and only 24 patients (27.2%) had a preoperative LVEF of 55% or more. All patients had associated coronary artery disease, but 4 patients had an additional aortic valve lesion, and 3 patients had either an additional atrial septal defect (ASD), a left ventricular aneurysm, or a symptomatic internal carotid artery stenosis.
Surgery
The operation was performed according to the hospital routine in ischemic cardiac arrest under cardiopulmonary bypass with moderate systemic hypothermia, but without cardioplegia. Concomitant coronary artery bypass grafting was performed in all patients, with 2.2 grafts/patient. Other associated procedures included aortic valve replacement (4 patients), and left ventricular aneurysmectomy, atrial septal closure, and thromboendarteriectomy (TEA) of the internal carotid artery (1 patient each). Intraoperative Doppler echocardiography was used, but all patients were studied before discharge from hospital.
Repair techniques
For repairing the mitral valve, the interatrial groove was incised and the right atrium dissected. In addition, both caval veins were mobilized. With the left atrial roof nicely exposed, the left atrial incision was carried out close to the mitral valve. Special care was taken to perform this exposure, because it was experienced that in this specific group of "ischemic mitral valve patients," quite small left atrials were found, which complicated a sufficient exposure of the mitral valve. A self-retaining retractor was used. Accurate valve analysis using the two conceptual approaches, the functional and segmental approach, as advocated by Carpentier [9], was mandatory, in addition to a careful and detailed assessment of papillary muscle pathology. Mitral valve repair details are listed in Table 1. The simplified scheme of the essential concept of a papillary muscle shortening plasty using a pericardium pledged-reinforced polytetrafluoroethylene (PTFE) suture [14] is explained in Figure 1 and close-up intraoperative views of this repair technique are shown in Figure 2. When ischemia or infarction has resulted in fibrotic degeneration with subsequent elongation of papillary muscles leading to leaflet prolapse (Figs 1B, 2A,B) a pericardium pledged-reinforced PTFE suture is placed through the base of the papillary muscle on the one side (Figs 1C, 2C), and through the elongated tip on the other side (Fig 2D), in order to shorten the elongated body of the diseased papillary muscle (Figs 1D, 2E) and thus achieve a correction of the length with a subsequent correction of the leaflet prolapse (Fig 2F).

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Fig 1. (A) The physiological anatomy of a papillary muscle, the chordae, and parts of the mitral valve leaflets. (B) The pathology of a degenerated and fibrotic elongated papillary muscle (arrow), as found in all patients of this study, resulting in a prolapse of one or more parts of mitral valve leaflets, but leafing the chordae intact. (C) The technique of papillary muscle shortening plasty using a pericardium pledged-reinforced PTFE suture. The PTFE suture is placed through the base of the papillary muscle on the one side, and through the elongated tip on the other side, in order to shorten the elongated part of the papillary muscle. (D) The outcome of the papillary muscle-shortening plasty, resulting in a correction of the leaflet prolapse.
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Fig 2. (A) Intraoperative view of an ischemic mitral valve, when ischemia/infarction has resulted in elongation of papillary muscles leading to subsequent leaflet prolapse, causing mitral regurgitation. Clearly shown here is the prolapse (arrow) of the anterior leaflet (A2), compared to the middle scallop of the posterior leaflet (P2). (B) Close-up view of the papillary muscle showing a fibrotic elongated body (arrow). (C and D) A pericardium pledged-reinforced PTFE suture is placed through the base of the papillary muscle on the one side (arrow), and through the elongated tip on the other side (arrow), in order to shorten the elongated body of the papillary muscle. (E) Close-up view of the result of the papillary muscle-shortening plasty, showing the reconstructed papillary muscle. Arrows point at the pericardium pledged-reinforced PTFE suture. (F) Final result of the repair procedure: after the papillary muscle-shortening plasty and implantation of a Carpentier-Edwards "Physio" annuloplasty ring, the mitral valve is competent.
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Follow-up
Follow-up information was obtained by telephone interviews with cardiologists, family physicians, and patients or their relatives. Postoperative events were categorized using the guidelines for reporting morbidity and mortality after cardiac valve operations [15]. All patients received oral anticoagulation starting on the third postoperative day, the efficacy assessed by the International Normalized Ratio (INR). Providing the patient was in sinus rhythm, anticoagulation was discontinued after 3 months and replaced by an antiplatelet therapy.
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Results
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Table 2 summarizes the perioperative and postoperative complications. All but 5 patients of this series of 88 patients undergoing papillary muscle surgery and subsequent mitral repair, when ischemia/infarction has resulted in fibrotic degeneration and elongation of papillary muscles, survived surgery, resulting in a 30-day mortality of 5.7%. The cause of these early deaths were cardiac related in 4 patients (pulmonary embolism, myocardial infarct, arrhythmia, multiorgan failure) and non-cardiac related in 1 patient (cerebral hemorrhage). There was one late death (1.2%); the cause of this late death was diagnosed to be cardiac related due to heart failure. Postoperative Doppler echocardiography, performed shortly before discharge from the hospital on postoperative day 10, showed satisfactory mitral valve function in all patients. No residual regurgitation (MR 0) was found in 80 of all patients (90.9%), mild regurgitation (MR I) in 5 patients (5.7%), and mild to moderate regurgitation (MR III) in 3 patients (3.4%). Preoperative and postoperative echocardiography parameters are listed in Table 3. There was no incidence of early or late failure of a repaired papillary muscle involved.
Follow-up information, collected in 1999 after a mean follow-up time of 18.6 months (3 to 40 months), was 100% complete. The actuarial freedom from reoperation and thromboembolic complications was 100%, but there were two anticoagulation-induced gastric bleeding complications (2.3%). All patients were in NYHA functional class I or II at the time of follow-up.
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Comment
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Mitral regurgitation secondary to ischemic heart disease is well known to be a poor prognostic factor and may affect up to 15% of all patients undergoing coronary artery bypass surgery. In case mitral regurgitation is not corrected, hospital mortality as well as late survival is profoundly worsened, even in patients with good myocardial revascularization, with a reported follow-up survival of only 20% [16]. However, the repair of ischemic mitral regurgitation is advocated by many, but actually performed by few [1719]. This may be explained by the observation that in the absence of papillary muscle rupture, the precise mechanisms that causes mitral regurgitation secondary to myocardial ischemia are difficult to understand and impair subsequent reparative efforts [19]. In case of papillary muscle rupture, recent reports describe simplified papillary muscle reimplantation procedures allowing acceptable survival results in this group of patients [20]. However, in the absence of papillary muscle rupture, a reliable and simple operation to restore valve competence is needed for ischemic mitral valve patients. As one important prerequisite, careful assessment and understanding of the mechanisms causing this type of mitral valve pathology is mandatory. Recent reports indicate that ischemic mitral regurgitation may be the product of small changes in the spartial relations of the anatomic components of the mitral valve and highlight the impact of even small changes in annular shape and, more important, the role of the papillary muscles to contribute to the distortion of leaflet coaptation [19]. It is therefore of great interest that recently the focus of interest has shifted to pay a little more attention also to papillary muscle pathology, resulting in new applied techniques of papillary muscle repair procedures [14].
Our data describe a technique of papillary muscle surgery in a small, very specific group of patients with ischemic mitral regurgitation, when ischemia and/or infarction has resulted in fibrotic degeneration and elongation of papillary muscles with subsequent distortion of leaflet coaptation. We were intrigued to study the feasibility as well as outcome of this simple and physiologic repair method, to correct by the shortening of elongated papillary muscles. The follow-up of our series of 88 patients showed a early mortality of 5.7% and a late mortality of 1.2%. Postoperative Doppler echocardiography, performed shortly before discharge on postoperative day 10, showed satisfactory mitral valve function in 96.6% of all patients; moderate regurgitation (MR III) was observed in only 3 patients. There was no case of papillary muscle rupture or distortion due to the papillary plasty procedure, and there was no reoperation. It may be assumed that this technique may turn out be a save and effective procedure also in the long-term.
If advocating this type of papillary muscle surgery as a viable part to repair specific cases of ischemic mitral regurgitation, the argument of prolonged cross-clamping times will be brought up against this technique. Flameng and associates investigated the determinants of early and late deaths of combined valve and coronary bypass operations. They described that the duration of aortic cross-clamping was a predictor of early death [21]. However, although some even suggest to restrict the number of distal anastomoses to shorten the cross-clamp time [22] and others postulate to "replace the valve without delay" [23], we strongly believe that mitral valve repair is the treatment of choice for this group of patients. Our mean aortic cross-clamp time for performing these combined procedures, mitral reconstruction and papillary repair combined with coronary bypass grafting, was 55 ± 13 minutes (range 26 to 89 minutes). This is not significantly prolonged as compared with the mean cross-clamp times of 52 to 61 minutes described for isolated mitral valve procedures [24, 25], but significantly shorter than the reported 139 ± 6 minutes for combined procedures [26]. However, our perioperative mortality of 5.7% matches favorably with reported 19% to 53% [1013].
Furthermore, we are convinced that even a difficult repair procedure should be strongly preferred to the possible alternative of a valve replacement, because it is well known that early and late results of replacement procedures of the mitral valve, in comparison with repair, have been shown to be associated with decreased survival and higher rates of complications in patients with mitral regurgitation secondary to coronary artery disease [27]. It seems, however, that specifically in patients with ischemic disease, the preservation and reconstruction of the papillary muscles and chordae during mitral valve reconstruction, as well as the lack of an artificial valve prosthesis, contribute to the enhanced systolic function with improved late survival and lower complication rates after mitral repair, as compared with replacement [24]. Some studies reported the immediate decrease of left ventricular function by up to 30% as a result of loss of the annular-chordal-papillary continuity, which may be ill afforded in the ischemic patient [28]. However, even the preservation of the annuloventricular continuity in mitral valve replacement may have some serious complications [29].
In conclusion, even though the follow-up period is short, our data indicate that this physiologic repair method, to correct by the shortening of elongated papillary muscles, may turn out to become a valuable technique of papillary muscle surgery for a small, specific group of patients with ischemic mitral regurgitation.
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