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Exercise-QTc is associated with diffuse interstitial fibrosis reflected by lower approximated T1 relaxation time in hypertrophic cardiomyopathy patients

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dc.contributor.author Corona-Villalobos, C. P.
dc.contributor.author Saha, S.
dc.contributor.author Pozios, I.
dc.contributor.author Paz, D. H. D.
dc.contributor.author Sorensen, L.
dc.contributor.author Cordoba, J. G.
dc.contributor.author Dolores-Cerna, K.
dc.contributor.author Kamel, I. R.
dc.contributor.author Laurel, W. M.
dc.contributor.author Bluemke, D. A.
dc.contributor.author Abraham, T. P.
dc.contributor.author Zimmerman, S. L.
dc.contributor.author Abraham, M. R.
dc.date.accessioned 2019-01-25T16:36:28Z
dc.date.available 2019-01-25T16:36:28Z
dc.date.issued 2017
dc.identifier.uri https://hdl.handle.net/20.500.12866/4840
dc.description.abstract Hypertrophic cardiomyopathy (HCM) is frequently associated with exercise-related sudden death. One possible contributor to arrhythmias is pathologic hypertrophy, which can lead to QTc prolongation. Since beta-adrenergic stimulation increases inward ionic currents and can increase spatial repolarization heterogeneity, we hypothesized that exercise would prolong QTc and predispose to arrhythmias in HCM patients. We tested this hypothesis by measuring QTc at rest and peak exercise, and examining ECGs for arrhythmias during exercise/recovery in 163 patients with a clinical diagnosis of HCM. Since hypertrophy and fibrosis are risk factors for arrhythmias in HCM, left ventricular (LV) mass and cardiac fibrosis were quantified using cardiac magnetic resonance imaging. Exercise led to an increase in QTc interval (436 +/- 37 to 482 +/- 45, p < 0.001), QRS duration (100 +/- 9 to 109 +/- 12, p < 0.001) and ST-T abnormalities. The proportion of patients with QTc prolongation (>470 ms) increased from 28% at rest, to 58% at peak exercise. An inverse correlation was detected between the approximated T1 relaxation time (using the Look Locker sequence) and rest-QTc (r = -0.68, p < 0.001); this association was increased during exercise (r = -0.81, p < 0.001). Late gadolinium enhancement (LGE) and LV mass were weakly associated with exercise-QTc. A weak inverse correlation was also observed between approximated T1 relaxation time and rest/exercise-QRS duration. A trend for association with arrhythmia (non-sustained ventricular tachycardia on Holler) was observed for rest-QTc >470 ms (OR = 3.0;p = 0.06). We conclude that exercise leads to QTc prolongation in a subset of HCM patients. The association between the approximated T1 relaxation time and QTc interval may reflect concomitant electrical and structural remodeling in HCM. en_US
dc.language.iso eng
dc.publisher Elsevier
dc.relation.ispartofseries Journal of Electrocardiology
dc.rights info:eu-repo/semantics/restrictedAccess
dc.rights.uri https://creativecommons.org/licenses/by-nc-nd/4.0/deed.es
dc.subject Cardiovascular System & Cardiology en_US
dc.subject risk en_US
dc.subject Cardiac magnetic resonance en_US
dc.subject enhancement en_US
dc.subject Exercise-QTc interval en_US
dc.subject Fibrosis en_US
dc.subject Hypertrophic cardiomyopathy en_US
dc.subject mechanisms en_US
dc.subject mice en_US
dc.subject repolarization reserve en_US
dc.subject Rest-QTc interval en_US
dc.subject sudden-death en_US
dc.title Exercise-QTc is associated with diffuse interstitial fibrosis reflected by lower approximated T1 relaxation time in hypertrophic cardiomyopathy patients en_US
dc.type info:eu-repo/semantics/article
dc.identifier.doi https://doi.org/10.1016/j.jelectrocard.2017.02.002
dc.subject.ocde https://purl.org/pe-repo/ocde/ford#3.02.04
dc.relation.issn 1532-8430


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