Excessive Papillary Muscle Traction and Dilated Mitral Annulus in Mitral Valve Prolapse Without Mitral Regurgitation

1996 ◽  
Vol 78 (4) ◽  
pp. 482-485 ◽  
Author(s):  
Tsung-Ming Lee ◽  
Sheng-Fang Su ◽  
Tsuei-Yuen Huang ◽  
Ming-Fong Chen ◽  
Chiau-Suong Liau ◽  
...  
2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
G Babur Guler ◽  
A Kilicgedik ◽  
H Zencirkiran Agus ◽  
G Kahveci

Abstract Introduction Mitral valve prolapse is the most common form of degenerative mitral valve disease. However, ischemic mitral valve prolapse is a rare cause of mitral regurgitation. The mechanism was initially thought to be papillary muscle dysfunction, but more complex mechanisms were suggested recently. Purpose Try to understand the pathophysiology of ischemic mitral valve prolapse on a case example. Case Report A 42-year-old male with a history of inferoposterior myocardial infarction was admitted from outpatient clinic due to NYHA class 3 heart failure symptoms. On physical examination, a 4/6 holosystolic murmur was heard in the apex. He had a permanent pacemaker implanted for sick sinus syndrome. Transthoracic echocardiography showed 1-global dysfunction of the left ventricle (posterior segment akinetic and thinned), 2- prolapse of the posterior mitral leaflet (suspicion of ruptured chordae) 3-severe mitral regurgitation (with anterior eccentric jet), 4- moderate tricuspid regurgitation and high systolic pulmonary artery pressure (65 mmHg), 5- pacemaker lead in the right heart chambers. 6- normal right ventricular systolic function. Transesophageal echocardiography showed P2 scallop prolapse and chordae were intact, there were no redundant or myxamous components of the leaflets. It was observed that the posteromedial papillary muscle was elongated and did not contract. We commented that these echocardiographic findings represented ischemic mitral valve prolapse. Other echo findings in favour of this hypothesis were the posteromedial papillary muscle prolongation in systole and reduced the free strain of papillary muscle in the the apical long axis view. The patient underwent mitral ring anuloplasty and surgical neocord implantation. Surgery also reported the aetiology as ischemic mitral prolapse secondary to chordal extension in accordance with echocardiography. Conclusion(s): Ischemic mitral prolapse is a complex pathology involving multiple components of the mitral valve apparatus as left ventricle, papillary muscle, chordae, annulus, leaflets. The diagnostic criteria for ischemic mitral valve prolapse and its management are not defined. The presence of myocardial infarction and the exclusion of other possible valve pathologies with transesophageal echocardiography are important steps in the diagnosis. Abstract P1689 Figure.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
T Le Tourneau ◽  
C Cueff ◽  
N Piriou ◽  
R Capoulade ◽  
S Le Scouarnec ◽  
...  

Abstract Background Filamin-A mitral valve prolapse/dystrophy (FLNA-MVP) phenotype associates MVP and a paradoxical restricted motion in diastole. Purpose We aim to assess the association of mitral valve prolapse to restricted motion in diastole in MVP patients (restricted MVP). Methods We prospectively enrolled 475 MVP probands (64±13 years) and controls relatives. Patients underwent a clinical examination and a comprehensive echocardiographic analysis of mitral valve apparatus. Results Among 475 consecutive probands, 48 (10.1%, 95% CI 7.7–13.3) had both a MVP and a doming aspect in diastole. Patients with restricted MVP exhibited shorted chordae tendinaes, and a shorter distance between papillary muscle tip and mitral annulus. Compared with controls, mitral valve leaflets were lenghtened, thickened and mitral valve annulus was enlarged. The prevalence of polyvalvular disease and bicuspid aortic valve was not increased in restricted MVP patients compared with conventional MVP. Familial form of restricted MVP was identified even in the absence of Filamin-A mutation. Conclusion Restricted MVP is a quite frequent finding in MVP patients and is associated with unique features of the MV apparatus. Restricted MVP can be regarded as a third type of MVP beside myxomatous Barlow disease and fibro-elastic deficiency MVP. Acknowledgement/Funding PHRC I Mitral, Fédération Française de Cardiologie, Fondation Coeur et recherche


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Shota Fukuda ◽  
Jae-Kwan Song ◽  
Hiroshi Kuwaki ◽  
Jeong-Yoon Jang ◽  
Masaaki Takeuchi ◽  
...  

Introduction: Mitral annulus (MA) is generally enlarged in patients with mitral valve prolapse (MVP), which may raise MV closing force acting to shift the MV and its adjacent basal left ventricular (LV) wall toward left atrium. Hypothesis: MA dilatation with augmented MV closing force may disturb basal LV wall systolic contraction in patients with MVP. Methods: In 11 healthy controls and 34 patients with MVP, 3 apical views were obtained to assess longitudinal strain of basal- and mid-LV segments by speckle tracking analysis. The ratio of basal- to mid-LV strain value was then calculated. MA area was calculated by annulus diameters in apical 4- and 2- chamber views. MV closing force was calculated as MA area х (systolic blood pressure - 10). Results: Patients with MVP showed significantly larger MA area (5.3±1.0 vs 3.8±0.7 cm2/m2) and MV closing force (638±192 vs 431±66 mmHg•cm2/m2), and reduced basal-LV strain (-18±3 vs -21±2%) than controls (all p<0.005), whereas mid-LV strain was similar between the 2 groups (-22±4 vs -22±3%, p=0.4). Consequently, significantly lower basal/middle ratio was observed in patients with MVP compared to controls (0.86±0.11 vs 0.95±0.08, p=0.004). By multivariate analysis, reduced basal/middle strain ratio was associated with augmented MV closing force (β=0.45, p=0.005) (Figure A), independent from the severity of mitral regurgitation (p=0.7). The basal/middle strain ratio significantly increased to 1.07±0.10 after annular size reduction in 5 patients with surgical MV plasty (p=0.04) (Figures B and C). Conclusions: In patients with MVP, an increase in MV closing force corresponding to MA dilatation, as opposed to the severity of mitral regurgitation, was related to attenuated basal LV wall contraction, which can be restored by MV plasty with annular size reduction.


Author(s):  
Evaldas Girdauskas ◽  
Lenard Conradi ◽  
Eva Karolina Harmel ◽  
Hermann Reichenspurner

Objective Pathophysiological background of type IIIb functional mitral regurgitation (FMR) is a progressively increasing distance between papillary muscle tips and mitral annular plane. Standard surgical treatment of such FMR by means of undersized mitral annuloplasty is associated with a high recurrence rate. Methods We propose a modified subannular maneuver to correct type IIIb FMR while combining undersized annuloplasty with a controlled realignment of both papillary muscles, thereby fixing the distance between mitral annular plane and papillary muscle tips. The differences of this subannular maneuver as compared with the previously published techniques are the following: (1) controlled realignment of both papillary muscles, (2) fixation of the papillary muscles to mitral annulus distance on an annuloplasty ring, and (3) application in a three-dimensional endoscopic minithoracotomy setting. Results We describe a surgical technique of minimally invasive mitral valve repair performed due to severe type IIIb FMR, which includes a modified subannular maneuver to realign both papillary muscles. Preliminary results of the first 10 patients who underwent this procedure at our institution are presented. There was no in-hospital mortality and follow-up echocardiography (mean ± SD echocardiographic follow-up = 10 ± 6 months) demonstrated stable functional results. Conclusions Our initial experience indicates that adding of this subannular maneuver to the standard annuloplasty and thereby fixing the distance between papillary muscles and mitral annular plane have a potential to improve results of surgical FMR treatment.


2020 ◽  
Vol 22 (Supplement_N) ◽  
pp. N131-N131
Author(s):  
Massimo Bolognesi

Abstract The Pickelhaube Sign is today recognized as a novel Echocardiographic Risk Marker for Malignant Mitral Valve Prolapse Syndrome. Mitral Valve Prolapse (MVP) has long been recognized to be a relatively common valve abnormality in the general population. Patients with relatively non-specific symptoms and asymptomatic athletes who have MVP still represent an important clinical conundrum for any physician involved in preventive medicine and sports screening. Although cardiac arrhythmias and/or cardiac death are an undesirable problem in MVP patients, when these subjects were studied with Holter Electrocardiogram (ECG) monitoring a prevalence of ventricular arrhythmias up to 34% was observed, with premature ventricular contractions as the most common pattern (66% of cases). At this regard a paper by Anders et al. described a series of cases that suggest that even clinically considered benign cases of MVP in young adults may cause sudden and unexpected death. However, cardiac arrest and Sudden Arrhythmic Cardiac Death (SCD) resulted in rare events only in patients with MVP based on data from a community study. A middle-aged athletic male who has been practicing competitive cycling for about 20 years came to our Sports Medicine Centre to undergo screening of sports preparation for competitive cycling and the related renewal of certification for participation in sports competitions. This athlete was always considered suitable in previous competitive fitness assessments performed in other sports medicine centers. His family history was unremarkable, as well as his recent and remote pathological anamnesis. The physical examination revealed a 3/6 regurgitation heart murmur with a click in the mid late systole. Previous echocardiographic examinations revealed a MVP which was considered benign with mild not relevant mitral regurgitation. He did not complain of symptoms such as dyspnoea or heart palpitations during physical activity. The resting ECG showed negative T waves in the inferior limb leads, and the stress test showed sporadic premature ventricular beats (a couple) with right bundle branch block morphology. An echocardiogram confirmed the presence of a classic mitral valve prolapse with billowing of both mitral leaflets, associated with a mild to moderate valve regurgitation. The TDI exam at the level of the lateral mitral annulus showed a high-velocity mid-systolic spike like a Pickelhaube sign, i.e. spiked German military helmet morphology. Consequently, an in-depth diagnostic imaging with cardiac magnetic resonance imaging was proposed, but the athlete refused it, both because he was totally asymptomatic and above all because he would be forced to pay a considerable amount of money as the examination is not guaranteed by the Italian National Health Service. In conclusion, the athlete remained sub judice as for competitive suitability, Finally, the question is: does MVP really cause sudden death? Is it enough to detect the Pickelhaube signal by echocardiography to stop this athlete? Let us bear in mind that this athlete was asymptomatic, and he had not had any trouble during exercise and maximal effort for many years. Why must we declare him unsuitable to do competitive sports?


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