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Significant left ventricular outflow tract obstruction secondary to systolic anterior motion in a patient without hypertrophic cardiomyopathy: An echocardiographic study
Dynamic left ventricular outflow tract obstruction (LVOTO) can be hemodynamically significant and can adversely affect the heart and quality of life. It is caused by systolic anterior motion (SAM) of the anterior mitral valve into the LVOT. The mechanism underlying SAM has been an area of special in...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6083379/ https://www.ncbi.nlm.nih.gov/pubmed/30100681 http://dx.doi.org/10.1016/j.jsha.2018.07.001 |
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author | Alrammah, Hanan Ghazal, Sami |
author_facet | Alrammah, Hanan Ghazal, Sami |
author_sort | Alrammah, Hanan |
collection | PubMed |
description | Dynamic left ventricular outflow tract obstruction (LVOTO) can be hemodynamically significant and can adversely affect the heart and quality of life. It is caused by systolic anterior motion (SAM) of the anterior mitral valve into the LVOT. The mechanism underlying SAM has been an area of special interest. However, SAM occurrence in the absence of septal hypertrophy is exceedingly uncommon. Here we present a case of a young male patient who sought medical care with a complaint of exertional dyspnea, New York Heart Association functional Class 2–3, and was found to have SAM and severe LVOTO at rest without hypertrophic cardiomyopathy. Continuous wave Doppler signal showed a peak velocity of 4.96 m/s along the LVOT, with a pressure gradient at rest of 98.44 mmHg, calculated using the modified Bernoulli equation. The patient is not known to have any medical conditions, nor had a family history of cardiac condition or sudden death. Trans-thoracic echocardiography showed concentric remodeling of the LV without hypertrophy. Trans-esophageal echocardiography was performed for further assessment of the anatomy. The anterior mitral leaflet (AML) and posterior mitral leaflet (PML) lengths were 3.7 cm and 1.3 cm, respectively (normal AML < 3 cm; normal PML < 1.5 cm). In our patient, the LVOTO is significant enough to result in a decreased cardiac output, which explains the symptoms experienced, due to which he developed concentric remodeling. The only finding in this patient explaining SAM is an elongated AML. |
format | Online Article Text |
id | pubmed-6083379 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-60833792018-08-10 Significant left ventricular outflow tract obstruction secondary to systolic anterior motion in a patient without hypertrophic cardiomyopathy: An echocardiographic study Alrammah, Hanan Ghazal, Sami J Saudi Heart Assoc Article Dynamic left ventricular outflow tract obstruction (LVOTO) can be hemodynamically significant and can adversely affect the heart and quality of life. It is caused by systolic anterior motion (SAM) of the anterior mitral valve into the LVOT. The mechanism underlying SAM has been an area of special interest. However, SAM occurrence in the absence of septal hypertrophy is exceedingly uncommon. Here we present a case of a young male patient who sought medical care with a complaint of exertional dyspnea, New York Heart Association functional Class 2–3, and was found to have SAM and severe LVOTO at rest without hypertrophic cardiomyopathy. Continuous wave Doppler signal showed a peak velocity of 4.96 m/s along the LVOT, with a pressure gradient at rest of 98.44 mmHg, calculated using the modified Bernoulli equation. The patient is not known to have any medical conditions, nor had a family history of cardiac condition or sudden death. Trans-thoracic echocardiography showed concentric remodeling of the LV without hypertrophy. Trans-esophageal echocardiography was performed for further assessment of the anatomy. The anterior mitral leaflet (AML) and posterior mitral leaflet (PML) lengths were 3.7 cm and 1.3 cm, respectively (normal AML < 3 cm; normal PML < 1.5 cm). In our patient, the LVOTO is significant enough to result in a decreased cardiac output, which explains the symptoms experienced, due to which he developed concentric remodeling. The only finding in this patient explaining SAM is an elongated AML. Elsevier 2018-10 2018-07-30 /pmc/articles/PMC6083379/ /pubmed/30100681 http://dx.doi.org/10.1016/j.jsha.2018.07.001 Text en © 2018 The Authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Article Alrammah, Hanan Ghazal, Sami Significant left ventricular outflow tract obstruction secondary to systolic anterior motion in a patient without hypertrophic cardiomyopathy: An echocardiographic study |
title | Significant left ventricular outflow tract obstruction secondary to systolic anterior motion in a patient without hypertrophic cardiomyopathy: An echocardiographic study |
title_full | Significant left ventricular outflow tract obstruction secondary to systolic anterior motion in a patient without hypertrophic cardiomyopathy: An echocardiographic study |
title_fullStr | Significant left ventricular outflow tract obstruction secondary to systolic anterior motion in a patient without hypertrophic cardiomyopathy: An echocardiographic study |
title_full_unstemmed | Significant left ventricular outflow tract obstruction secondary to systolic anterior motion in a patient without hypertrophic cardiomyopathy: An echocardiographic study |
title_short | Significant left ventricular outflow tract obstruction secondary to systolic anterior motion in a patient without hypertrophic cardiomyopathy: An echocardiographic study |
title_sort | significant left ventricular outflow tract obstruction secondary to systolic anterior motion in a patient without hypertrophic cardiomyopathy: an echocardiographic study |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6083379/ https://www.ncbi.nlm.nih.gov/pubmed/30100681 http://dx.doi.org/10.1016/j.jsha.2018.07.001 |
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