Background: Extended myectomy for left ventricular outflow tract obstruction (LVOTO) due to hypertrophic cardiomyopathy (HCM) has good long-term results. In addition to the midseptal resection (R) for HCM, our group has introduced a novel variation in anterior leaflet plication (P) and release (R) of papillary muscle attachments. We sought to investigate the medium-term success of this three-step repair that addresses all aspects of complex HCM pathology.
Methods: Nineteen patients underwent resection-plication-release repair for complex HCM pathology. Transesophageal echocardiography was performed on all patients preoperatively and postoperatively to assess adequacy of resection, left ventricular outflow tract gradients, and mitral valve function. All patients underwent transthoracic outpatient echocardiography at a mean follow-up of 2.4 +/- 2.1 years (range, 0.5 to 6).
Results: The average age of the patients was 57 +/- 14 years. The preoperative peak LVOTO was 137 +/- 45 mm Hg. The average degree of mitral regurgitation was 3.1. The average length of stay was 7.5 +/- 3.3 days. There were no readmissions or deaths in the group. Initial postoperative transesophageal echocardiography demonstrated marked reduction in LVOTO to 10 +/- 17 mm Hg (p < 0.0001) and significant improvement in mitral regurgitation to 0.2 (p < 0.0001). In follow-up, the LVOT gradient remained low at 6 +/- 14 (p > 0.0001) and mitral regurgitation remained insignificant at 0.4 (p < 0.0001).
Conclusions: Anterior leaflet plication and papillary muscle release are logical adjuncts to septal resection in the treatment of the complicated pathophysiology of obstructive HCM. Durable long-term results can be achieved with an aggressive approach to mitral valve pathology in conjunction with extended myectomy.
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http://dx.doi.org/10.1016/j.athoracsur.2005.01.064 | DOI Listing |
Reports (MDPI)
December 2024
Division of Cardiology, Department of Medicine, University of Washington, Seattle, WA 98195, USA.
Unlabelled: The combination of hypertrophic cardiomyopathy with outflow tract obstruction, severe pre-capillary and post-capillary pulmonary hypertension, and severe primary mitral regurgitation is rare and presents distinct management challenges.
Background And Clinical Significance: Pulmonary hypertension is an independent predictor of all-cause mortality in patients with hypertrophic cardiomyopathy managed medically and often precludes patients from undergoing cardiopulmonary bypass due to increased surgical morbidity and mortality. In studies specifically evaluating surgical myectomy, however, survival is favorable in patients with moderate-to-severe pulmonary hypertension.
Sci Rep
October 2024
Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Multimed Man Cardiothorac Surg
August 2024
Department of Cardiovascular Surgery, Japanese Red Cross Nagoya First Hospital, Nagoya, Japan.
SAGE Open Med Case Rep
June 2024
Division of Cardiovascular Surgery, Oita Prefectural Hospital, Oita City, Oita, Japan.
Midventricular obstruction (MVO) is a rare form of hypertrophic cardiomyopathy (HCM). While surgical treatment for HCM is among the most technically challenging cardiac operations for acquired disease, surgery for MVO is rarely reported. A 38-year-old man was admitted to our hospital with a cough and dyspnea.
View Article and Find Full Text PDFJ Mol Cell Cardiol
June 2024
Department of Bioengineering, University of Washington, Seattle, WA 98109, USA; Institute for Stem Cell and Regenerative Medicine, University of Washington, Seattle, WA 98109, USA; Center for Translational Muscle Research, University of Washington, Seattle, WA 98109, USA. Electronic address:
Approximately 40% of hypertrophic cardiomyopathy (HCM) mutations are linked to the sarcomere protein cardiac myosin binding protein-C (cMyBP-C). These mutations are either classified as missense mutations or truncation mutations. One mutation whose nature has been inconsistently reported in the literature is the MYBPC3-c.
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