Temporal Changes in Interpapillary Muscle Dynamics as an Active Indicator of Mitral Valve and Left Ventricular Interaction in Ischemic Mitral Regurgitation

Kalra, Kanika; Wang, Qian; McIver, Bryant V.; Shi, Weiwei; Guyton, Robert A.; Sun, Wei; Sarin, Eric L.; Thourani, Vinod H.; Padala, Muralidhar

doi:10.1016/j.jacc.2014.07.988

Cited by 71 publications

(51 citation statements)

References 20 publications

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“…10,17,221,222 The use of 3D echocardiography in experimental studies has proved that global left ventricular dysfunction alone is insufficient to cause IMR. 223–225 Displacement and abnormal contraction of the left ventricular wall underlying the papillary muscles, along with decreased shortening of the distance between the papillary muscles, causes mitral leaflet tethering and restricted closure that leads to IMR (Figures 12a,b), 223–226 which is referred to as a Carpentier type IIIb lesion. Isolated annular dilation, such as occurs in patients with lone atrial fibrillation, also impairs coaptation (Carpentier type I), but relatively mildly unless the leaflets are tethered at both annular and ventricular ends.…”

Section: Ischaemic Mitral Regurgitationmentioning

confidence: 99%

Mitral valve disease—morphology and mechanisms

Levine¹,

Hagège²,

Judge³

et al. 2015

Nat Rev Cardiol

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308

254

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Mitral valve disease is a frequent cause of heart failure and death. Emerging evidence indicates that the mitral valve is not a passive structure, but—even in adult life—remains dynamic and accessible for treatment. This concept motivates efforts to reduce the clinical progression of mitral valve disease through early detection and modification of underlying mechanisms. Discoveries of genetic mutations causing mitral valve elongation and prolapse have revealed that growth factor signalling and cell migration pathways are regulated by structural molecules in ways that can be modified to limit progression from developmental defects to valve degeneration with clinical complications. Mitral valve enlargement can determine left ventricular outflow tract obstruction in hypertrophic cardiomyopathy, and might be stimulated by potentially modifiable biological valvular–ventricular interactions. Mitral valve plasticity also allows adaptive growth in response to ventricular remodelling. However, adverse cellular and mechanobiological processes create relative leaflet deficiency in the ischaemic setting, leading to mitral regurgitation with increased heart failure and mortality. Our approach, which bridges clinicians and basic scientists, enables the correlation of observed disease with cellular and molecular mechanisms, leading to the discovery of new opportunities for improving the natural history of mitral valve disease.

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Section: Ischaemic Mitral Regurgitationmentioning

confidence: 99%

Mitral valve disease—morphology and mechanisms

Levine¹,

Hagège²,

Judge³

et al. 2015

Nat Rev Cardiol

Self Cite

308

254

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“…Acute mitral regurgitation necessitating immediate surgery due to complete or sequential papillary muscle (PM) rupture is a rare major adverse cardiac event [2,3]. In the majority of patients, ischemic mitral regurgitation develops gradually due to remodeling of the ischemic myocardium and altered hemodynamic conditions in the left ventricle [4]. Additionally, PM infarction may contribute to the development of ischemic mitral regurgitation by tethering of the chordae and subsequent dysfunction of the PM-chorda-mitral valve complex [5].…”

Section: Introductionmentioning

confidence: 99%

Impact of Papillary Muscle Infarction on Ischemic Mitral Regurgitation Assessed by Magnetic Resonance Imaging

Bretschneider

Heinrich

Seeger

et al. 2017

Fortschr Röntgenstr

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This document was downloaded for personal use only. Unauthorized distribution is strictly prohibited.the development of mitral regurgitation in patients with chronic myocardial infarction (MI). The aim of the present study was to assess the correlation of PM infarction depicted by MRI with mitral regurgitation and left ventricular function.Methods and Materials 48 patients with chronic MI and recent MRI and echocardiography were retrospectively included. The location and extent of MI depicted by MRI were correlated with left ventricular function assessed by MRI and mitral regurgitation assessed by echocardiography. The presence, location and extent of PM infarction depicted by late gadolinium enhancement (LGE-) MRI were correlated with functional parameters and compared with patients with chronic MI but no PM involvement.Results PM infarction was found in 11 of 48 patients (23 %) using LGE-MRI. 8/11 patients (73 %) with PM infarction and 22/37 patients (59 %) without PM involvement in MI had ischemic mitral regurgitation. There was no significant difference between location, extent of MI and presence of mitral regurgitation between patients with and without PM involvement in myocardial infarction. In 4/4 patients with complete and in 4/7 patients with partial PM infarction, mitral regurgitation was present. The normalized mean left ventricular enddiastolic volume was increased in patients with ischemic mitral regurgitation. ConclusionThe presence of PM infarction does not correlate with ischemic mitral regurgitation. In patients with complete PM infarction and consequent discontinuity of viable tissue in the PM-chorda-mitral valve complex, the probability of developing ischemic mitral regurgitation seems to be increased. However, the severity of mitral regurgitation is not increased compared to patients with partial or no PM infarction.

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“…Indeed, a recent comprehensive study involving MRI evaluation of patients with IMR supplemented with an experimental IMR animal model and computational analysis revealed that loss of lateral shortening of inter-papillary distance may be central to the pathogenesis of IMR. 24 Experimental surgical interventions that relocate the posterior papillary muscle toward the septum such as a cinching stitch 25 or inflating balloon 26 have shown promise in controlling IMR. Repositioning of the posterior papillary muscle with an externally adjusted chord anchored at the fibrous trigone as an adjunct to ring annuloplasty has now also found clinical application.…”

Section: Discussionmentioning

confidence: 99%

Geometric perturbations in multiheaded papillary tip positions associated with acute ovine ischemic mitral regurgitation

Timek

Lai

Bothe

et al. 2015

The Journal of Thoracic and Cardiovascular Surgery

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Background Novel surgical approaches are focusing on the “ventricular disease” of ischemic mitral regurgitation (IMR) to correct altered papillary muscle (PM) tip positions (apical displacement) and ameliorate leaflet tethering. Due to the anatomic complexity of the subvalvular apparatus, however, the precise geometric perturbations of the multi-headed PM tips associated with IMR remain uncharacterized. Methods In six adult sheep we implanted three markers on each papillary muscle (anterior= APM, posterior=PPM). To specifically identify distinct papillary muscle tips, one marker was placed on the PM origin of the dominant chord to the anterior (PMAML), posterior (PMPML), and commissural (PMCM) leaflets. Nine markers were placed on the edge of the posterior mitral leaflet and five on the edge of the anterior mitral leaflet. Eight markers were sewn around the mitral annulus (MA). Animals were studied immediately post-op with biplane videofluoroscopy and transesophageal echocardiography before and during acute snare occlusion of proximal LCx coronary artery to induce IMR. Papillary muscle tip and leaflet edge geometry was expressed as orthogonal distance of each respective marker to the least squares MA plane (MAPL) at end-systole. Distance of each PM tip marker to the MA “saddle horn” (MASH) was also calculated. Results Acute LCx occlusion significantly increased MR from baseline of 0.7±0.3 to 2.5±0.5 (p<0.05). IMR was associated with posterior leaflet restriction near the central leaflet edge with simultaneous prolapse of both leaflets near the posterior commissure. No apical displacement of papillary muscle tips was observed during IMR although the PPM moved farther away from the mid-septal annulus. Conclusions During acute ischemia no apical displacement of any papillary muscle tip was observed. PPM movement away from the annular saddle horn and toward the annulus was associated with IMR and leaflet prolapse near the posterior commissure and restriction near valve center. These data may help guide development of surgical interventions aimed at papillary muscle repositioning.

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Temporal Changes in Interpapillary Muscle Dynamics as an Active Indicator of Mitral Valve and Left Ventricular Interaction in Ischemic Mitral Regurgitation

Cited by 71 publications

References 20 publications

Mitral valve disease—morphology and mechanisms

Mitral valve disease—morphology and mechanisms

Impact of Papillary Muscle Infarction on Ischemic Mitral Regurgitation Assessed by Magnetic Resonance Imaging

Geometric perturbations in multiheaded papillary tip positions associated with acute ovine ischemic mitral regurgitation

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