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Transthoracic Speckle Tracking Echocardiography for the Quantitative Assessment of Left Ventricular Myocardial Deformation
Published on: October 20, 2016
Speckle tracking echocardiography to assess regional ventricular function in patients with apical hypertrophic
María Cristina Saccheri1, Tomás Francisco Cianciulli1, Luis Alberto Morita1
1María Cristina Saccheri, Tomás Francisco Cianciulli, Luis Alberto Morita, Ricardo José Méndez, Martín Alejandro Beck, Juan Enrique Guerra, Alberto Cozzarin, Luciana Jimena Puente, Lorena Romina Balletti, Jorge Alberto Lax, Division of Cardiology, Echocardiography Laboratory, Hospital "Dr. Cosme Argerich", C1155AHD Buenos Aires, Argentina.
Aim:
To explore regional systolic strain of midwall and endocardial segments using speckle tracking echocardiography in patients with apical hypertrophic cardiomyopathy (HCM).
Methods:
We prospectively assessed 20 patients (mean age 53 ± 16 years, range: 18-81 years, 10 were male), with apical HCM. We measured global longitudinal peak systolic strain (GLPSS) in the midwall and endocardium of the left ventricle.
Results:
The diastolic thickness of the 4 apical segments was 16.25 ± 2.75 mm. All patients had a normal global systolic function with a fractional shortening of 50% ± 8%. In spite of supernormal left ventricular (LV) systolic function, midwall GLPSS was decreased in all patients, more in the apical (-7.3% ± -8.8%) than in basal segments (-15.5% ± -6.93%), while endocardial GLPPS was significantly greater and reached normal values (apical: -22.8% ± -7.8%, basal: -17.9% ± -7.5%).
Conclusion:
This study shows that two-dimensional strain was decreased mainly confined to the mesocardium, while endocardium myocardial deformation was preserved in HCM and allowed to identify subclinical LV dysfunction. This transmural heterogeneity in systolic strain had not been previously described in HCM and could be explained by the distribution of myofibrillar disarray in deep myocardial areas. The clinical application of this novel finding may help further understanding of the pathophysiology of HCM.
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