scholarly journals Conservative approach to mitral valve replacement in hypertrophic cardiomyopathy with systolic anterior motion – a case report

2015 ◽  
Vol 4 ◽  
pp. 345-347
Author(s):  
Bogdan Suder ◽  
Krzysztof Bartus ◽  
Krzysztof Szymoński ◽  
Grzegorz Wasilewski ◽  
Jerzy Sadowski ◽  
...  
2018 ◽  
Vol 26 (5) ◽  
pp. 400-403 ◽  
Author(s):  
Praveen Kerala Varma ◽  
Neethu Krishna ◽  
Hisham Ahamed ◽  
Sujatha Madassery

Anomalies of the mitral valve apparatus in hypertrophic cardiomyopathy are an important cause of systolic anterior motion. Patients with significant residual obstruction due to systolic anterior motion after myectomy and anterior mitral leaflet plication may end up having mitral valve replacement. We describe the case of a 52-year-old man who underwent posterior mitral leaflet plication to correct residual systolic anterior motion after anterior mitral leaflet plication.


1982 ◽  
Vol 49 (4) ◽  
pp. 949 ◽  
Author(s):  
Joan C. Kishel ◽  
Altagracia M. Chavez ◽  
Barry J. Maron ◽  
Stephen E. Epstein ◽  
Andrew G. Morrow ◽  
...  

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Raabia N Ahmad ◽  
Barry J Maron ◽  
Ethan J Rowin ◽  
Tammy S Haas ◽  
Joseph A Dearani ◽  
...  

Background: Marked septal hypertrophy is considered a requirement for effective myectomy in obstructive hypertrophic cardiomyopathy (HCM), with mitral valve replacement recommended as the alternative strategy in patients with minimal hypertrophy. However, it remains uncertain whether relief of obstruction can be effectively abolished without mitral valve replacement in patients with minimal septal wall thickening. Methods: Of 500 patients who underwent surgical myectomy from 2004 to January 2014, 21 (4.2%) were identified with a maximum LV wall thickness ≤ 15mm and constitute the study cohort. Results: All 21 patients (56 ± 10 years old; 62% male) were followed for advanced heart failure symptoms refractory to drug therapy with a maximal septal wall thickness of 13.6 ± 1.7 mm (range: 10-15 mm; ≤ 12 mm in 5 patients). Outflow obstruction ≥ 30 mmHg due to mitral valve-septal contact was present after exercise in 17 of 21 patients (range: 50-150 mmHg), and under resting conditions in 4 patients (range: 30-65 mmHg). In all patients, surgical relief of obstruction consisted of muscular resection of the basal septum with revision of abnormal and apically displaced papillary muscles, which were judged intraoperatively to be contributing to obstruction. In addition, in 10 patients (47%) myectomy alone was not sufficient to relieve obstruction due to the limited opportunity for septal reduction and adjunctive mitral valve repair was performed to shorten an elongated anterior leaflet. No patient required mitral valve replacement or incurred a ventricular septal defect. Post-operatively, 4 patients developed complete heart block requiring permanent pacemaker (1 patient with pre-operative right bundle branch block) and 1 had a cerebrovascular event. At most recent follow up 18 ± 19 months post-myectomy, septal thickness was reduced to 10 ± 2 mm, no patient had an outflow gradient at rest or with provocation, and all patients were alive with the majority asymptomatic (class I: n=13; 62% and class II n=8; 38%). Conclusion: In patients with minimal septal hypertrophy, outflow obstruction can be effectively abolished with surgical myectomy and adjunctive mitral valve repair with a small increased risk of heart block, but without the need for mitral valve replacement.


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