Spontaneous healing of a ruptured mycotic aneurysm of the posterior mitral leaflet: Unexpected resolution of a severe mitral regurgitation

2021 ◽  
Author(s):  
Cristina Ruisanchez Villar ◽  
Sofia Gonzalez Lizarbe ◽  
Piedad Lerena Saenz ◽  
Aritz Gil Ongay ◽  
Teresa Borderias Villarroel ◽  
...  
2020 ◽  
Vol 04 (05) ◽  
Author(s):  
Laura Piggott ◽  
Ashling Ní Chinnéide ◽  
Laura Worthington ◽  
Paul Shiels

1997 ◽  
Vol 5 (1) ◽  
pp. 25-30 ◽  
Author(s):  
Shiv Kumar Choudhary ◽  
Anil Bhan ◽  
Rajesh Sharma ◽  
Balram Airan ◽  
Bhabhananda Das ◽  
...  

This study assessed the mechanism of acute mitral regurgitation following balloon mitral valvuloplasty for the treatment of symptomatic mitral stenosis. We studied 25 patients who required mitral valve replacement for severe mitral regurgitation following balloon mitral valvuloplasty. All the mitral valves studied had features of severe mitral stenosis. Radial tear of the mitral leaflet was responsible for mitral regurgitation in 18 (72%) cases. Of these, 16 involved the anterior mitral leaflet and in 2 cases the posterior mitral leaflet was torn. Three patients (12%) had chordal rupture, whereas in 4 (16%) patients pseudo-orifices were formed. All the excised mitral valves showed significant subvalvular deformity which was underestimated in prevalvuloplasty echocardiography. No other factor was found to be associated with disruption of the valve. Hence, we conclude that cusp deformity and subvalvular pathology are responsible for faulty transmission of forces and improper engagement of the balloon, resulting in disruption of the valvular apparatus. The incidence of severe mitral regurgitation following balloon mitral valvuloplasty might be decreased by appropriate prevalvuloplasty assessment and patient selection.


2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
E Tafciu ◽  
F Ancona ◽  
S Stella ◽  
C Capogrosso ◽  
G Ingallina ◽  
...  

Abstract A sixty-two years old female presents with shortness of breath. She has Marfan syndrome (c.6448C > T mutation variant) with a previous history relevant for type A aortic dissection which was treated by Bentall procedure with a mechanical aortic prosthesis and ascending aorta prosthesis, coronary artery bypass graft on the right coronary artery and pacemaker for third degree AV block; subsequent aortic arch reconstruction and endovascular repair of the descending aorta for thoracic aorta aneurism rupture. Upon visit she is in NYHA class III, blood pressure of 145/85 mmHg and heart rate of 75 bpm. A systolic murmur with a prosthetic second tone was heard at heart auscultation and bilateral crackles were heard at pulmonary auscultation. Peripheral pulses were symmetrical. ECG showed sinus rhythm, right bundle branch block with left anterior hemiblock and left ventricular hypertrophy. Blood tests were within normal range. Chest X-ray showed bilateral pulmonary congestion. She underwent transesophageal echocardiography which showed severe mitral regurgitation (MR) with a normal bi-ventricular systolic function. Posterior mitral leaflet (PML) was severely hypoplastic especially at the level of P1 which was confirmed by CT (see picture). Diuretic therapy together with an ACE inhibitor was introduced with a decrease in MR severity. The patients was sent home with an indication for strict follow up visits. Congenital mitral valve defects are very rare and can be isolated or associated with other cardiac malformations. Limited data are available about hypoplastic posterior mitral leaflet (PML) including singular case reports or anecdotal descriptions, therefore its etiology, association with other cardiac or systemic syndromes and prognosis is not well understood. However, it is suggested that absence of PML has a high fetal or infant mortality due to severe mitral regurgitation (MR). The degree of MR varies among patients and in the same patient at different timepoints as it depends on anatomical variations of the anterior mitral leaflet, residual PML tissue, posterior ventricular wall conformation and other associated cardiac abnormalities. We showed a case of a patient with hypoplastic PML and advanced age with a concomitant history of Marfan syndrome. Picture legend (A) Mid-esophageal 4-chamber view shows severe hypoplasia of PML (red arrow) and the posterior ventricular myocardial shelf (green arrow). (B) Mid-esophageal commissural view shows a large central MR jet. (C) 3D ventricular perspective of the mitral valve: an almost complete absence of the PML can be appreciated in the central and lateral scallops (grey arrows). (D) CT 3 chamber view shows the myocardial shelf which takes the role of the posterior mitral annulus (blue arrow) and direct PML chordal insertion into the ventricular wall (yellow arrow). (E) CT reconstruction of the mitral valve shows a virtually absent P1 (< 1mm), a P2 length of 4.1 mm, and a P3 length of 5 mm. Abstract P271 Figure. Hypoplastic posterior mitral leaflet


2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Daisuke Kaneyuki ◽  
Hiroyuki Nakajima ◽  
Toshihisa Asakura ◽  
Akihiro Yoshitake ◽  
Chiho Tokunaga ◽  
...  

Abstract Background Good mid-term durability of mitral valve repair of bileaflet lesions has been reported; however, patients may develop failure during follow-up. This study assessed late outcomes and mechanisms of failure associated with mitral valve repair of bileaflet lesions. Methods Fifty-six patients (mean age 67 ± 12 years) underwent mitral valve repair of bileaflet lesions due to degenerative disease in 2011–2018. Mitral annuloplasty was added to all procedures except for 1 patient with annular calcification. Mitral valve lesions were identified by surgical inspection. Mean clinical and echocardiography follow-up occurred at 2.7 ± 2.1 and 2.5 ± 1.9 years, respectively. Results Additional mitral valve repair techniques involved triangular resection (n = 15 patients), quadrangular resection with sliding plasty (n = 12), neochordoplasty (n = 52), and commissural plication (n = 26). Prolapse of ≥2 anterior and posterior leaflet scallops occurred in 22 (39%) and 30 (54%) patients, respectively. During follow-up, 10 (17.8%) patients developed moderate or severe mitral regurgitation. Whereas prolapse or tethering was observed early after neochordoplasty or quadrangular resection, recurrent regurgitation occurred late after commissural repair. Five-year freedom from recurrent moderate or severe mitral regurgitation rates was 71.1 ± 11.0%. Conclusions Seventeen percent of patients developed recurrent mitral regurgitation during follow-up. Repair failure in the early phase occurred owing to aggressive resection of the posterior mitral leaflet or maladjustment of the artificial neochordae. Recurrent mitral regurgitation might occur in the late phase even after acceptable commissural repair. A sequential approach may be useful to improve the quality of mitral valve repair in bileaflet lesions.


2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
A H Ali ◽  
U Alnuaimi ◽  
S I Lacau ◽  
C Badiu ◽  
A C Popescu

Abstract A 60 y/o diabetic and hypertensive lady with previous anterior infarction treated by primary PCI with stenting of the proximal LAD (2011) and CABG for stent thrombosis, presented for chest pain. Admission ECG showed ST segment elevation in II, III aVF, ST segment depression in V1-V2 (A). Urgent coronary angiography was performed. It showed non-significant lesions on RCA and LCX, occlusion of the proximal LAD stent, patent LIMA to LAD and first diagonal with non-significant stenosis of the distal anastomosis (B). Transthoracic echocardiography (C) showed calcific mass involving the mitral annulus and posterior mitral leaflet, moderate mitral regurgitation, hipokinesia of the basal segment of the inferior wall with preserved LV ejection fraction. Transesophageal echocardiography (D) confirmed the calcified mass involving the mitral annulus and the posterior mitral leaflet. There was no significant mitral stenosis, and mitral regurgitation was moderate. Thoracic CT showed massive mitral calcification and a possible thrombus attached to it. (E) Myocardial infarction was confirmed by troponin rise and fall. The patient was discharged on dual antiplatelet therapy, ACE-I, betablocker and statin. At one month follow-up transthoracic echocardiography the central area of the mitral mass became hypoechogenic, and a bilobated hypermobile structure was seen attached to the ventricular side of the mass (F). Blood cultures were negative and there was no inflammatory syndrome. Cardiac magnetic resonance (H) confirmed myocardial infarction and showed massive calcification of the posterior mitral annulus. TEE performed after another month showed a very long hypermobile structure attached to the mitral annulus calcification, which was entering the left ventricular outflow tract reaching the plane of the aortic valve (G). The patient underwent surgical mitral valve replacement and redo CABG and the mass was excised. The pathologic aspect of the excised material was cazeous and friable (I). The initial presentation was presumably an embolic infarct with cazeous material. Abstract P1481 Figure.


2020 ◽  
Vol 8 ◽  
pp. 2050313X2093695
Author(s):  
Abigayle Sullivan ◽  
Pragya Shrestha ◽  
Sijan Basnet ◽  
Ronald Herb ◽  
Emily Zagorski

We report a case of an elderly Caucasian male with past medical history of dextrocardia with situs inversus totalis, polymyalgia rheumatica, history of cryptogenic stroke, and severe mitral regurgitation with mitral valve prolapse, who presented with acute heart failure symptoms, including severe dyspnea on exertion and worsening lower extremity edema in the setting of immunosuppression with steroids for a year-old diagnosis of polymyalgia rheumatica. One month prior to this presentation, the patient suffered a transient ischemic attack and during the workup, his transthoracic echocardiography showed myxomatous degeneration of posterior mitral leaflet, partially flail, with severe mitral regurgitation, which required mitral valve replacement. Genome sequencing of mitral valve anterior leaflet pathology detected Tropheryma whipplei as a causal agent of culture-negative endocarditis. The patient was treated with 6 weeks of ceftriaxone and ampicillin–sulbactam and further continued trimethoprim–sulfamethoxazole for 1 year. He continued antibiotic treatment with resolution of shortness of breath along with arthralgia.


2015 ◽  
Vol 2015 ◽  
pp. 1-4 ◽  
Author(s):  
Cagdas Baran ◽  
Serkan Durdu ◽  
Sadik Eryilmaz ◽  
Mustafa Sirlak ◽  
A. Ruchan Akar

We report here on a 43-year-old female patient presenting with non-ST elevation myocardial infarction, severe mitral regurgitation, and mild mitral stenosis secondary to encroachment of the related structures by a primary cardiac angiosarcoma. A coronary angiography revealed significant stenosis in the left main and left circumflex arteries and at exploration, the tumour was arising from posterior left atrial free wall, invading the posterior mitral leaflet, and extending into all of the pulmonary veins and pericardium. Therefore, no further intervention was performed, except for left internal mammarian artery to left anterior descending artery anastomosis and biopsy. As far as we know, this case is unique with respect to its presentation.


2015 ◽  
Vol 67 (2) ◽  
pp. 161-162 ◽  
Author(s):  
Hatem Ari ◽  
Abdullah Dogan ◽  
İbrahim Ersoy

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