Abstract
Background: Hypertrophic cardiomyopathy (HCM) is characterized by myocyte hypertrophy, disarray, fibrosis, and increased risk for ventricular arrhythmias. Increased QT dispersion has been reported in patients with HCM, but the underlying mechanisms have not been completely elucidated. In this study, we examined the relationship between diffuse interstitial fibrosis, replacement fibrosis, QTc dispersion and ventricular arrhythmias in patients with HCM. We hypothesized that fibrosis would slow impulse propagation and increase dispersion of ventricular repolarization, resulting in increased QTc dispersion on surface electrocardiogram (ECG) and ventricular arrhythmias. Methods: ECG and cardiac magnetic resonance (CMR) image analyses were performed retrospectively in 112 patients with a clinical diagnosis of HCM. Replacement fibrosis was assessed by measuring late gadolinium (Gd) enhancement (LGE), using a semi-automated threshold technique. Diffuse interstitial fibrosis was assessed by measuring T1 relaxation times after Gd administration, using the Look-Locker sequence. QTc dispersion was measured digitally in the septal/anterior (V1-V4), inferior (II, III, and aVF), and lateral (I, aVL, V5, and V6) lead groups on surface ECG. Results: All patients had evidence of asymmetric septal hypertrophy. LGE was evident in 70 (63%) patients; the median T1 relaxation time was 411±38. ms. An inverse correlation was observed between T1 relaxation time and QTc dispersion in leads V1-V4 (p<0.001). Patients with HCM who developed sustained ventricular tachycardia had slightly higher probability of increased QTc dispersion in leads V1-V4 (odds ratio, 1.011 [1.004-1.0178, . p=0.003). We found no correlation between presence and percentage of LGE and QTc dispersion. Conclusion: Diffuse interstitial fibrosis is associated with increased dispersion of ventricular repolarization in leads, reflecting electrical activity in the hypertrophied septum. Interstitial fibrosis combined with ion channel/gap junction remodeling in the septum could lead to inhomogeneity of ventricular refractoriness, resulting in increased QTc dispersion in leads V1-V4.
| Original language | English (US) |
|---|---|
| Journal | Journal of Arrhythmia |
| DOIs | |
| State | Accepted/In press - Mar 11 2016 |
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Keywords
- Corrected QT dispersion
- Hypertrophic cardiomyopathy
- Late gadolinium enhancement
- T1 relaxation time
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
Cite this
Diffuse interstitial fibrosis assessed by cardiac magnetic resonance is associated with dispersion of ventricular repolarization in patients with hypertrophic cardiomyopathy. / Hurtado-de-Mendoza, David; Corona Villalobos, Celia; Pozios, Iraklis; Gonzales, Jorge; Soleimanifard, Yalda; Sivalokanathan, Sanjay; Montoya-Cerrillo, Diego; Vakrou, Styliani; Kamel, Ihab R; Mormontoy-Laurel, Wilfredo; Dolores-Cerna, Ketty; Suarez, Jacsel; Perez-Melo, Sergio; Bluemke, David A.; Abraham, Theodore P.; Zimmerman, Stefan; Abraham, M. Roselle.
In: Journal of Arrhythmia, 11.03.2016.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Diffuse interstitial fibrosis assessed by cardiac magnetic resonance is associated with dispersion of ventricular repolarization in patients with hypertrophic cardiomyopathy
AU - Hurtado-de-Mendoza, David
AU - Corona Villalobos, Celia
AU - Pozios, Iraklis
AU - Gonzales, Jorge
AU - Soleimanifard, Yalda
AU - Sivalokanathan, Sanjay
AU - Montoya-Cerrillo, Diego
AU - Vakrou, Styliani
AU - Kamel, Ihab R
AU - Mormontoy-Laurel, Wilfredo
AU - Dolores-Cerna, Ketty
AU - Suarez, Jacsel
AU - Perez-Melo, Sergio
AU - Bluemke, David A.
AU - Abraham, Theodore P.
AU - Zimmerman, Stefan
AU - Abraham, M. Roselle
PY - 2016/3/11
Y1 - 2016/3/11
N2 - Background: Hypertrophic cardiomyopathy (HCM) is characterized by myocyte hypertrophy, disarray, fibrosis, and increased risk for ventricular arrhythmias. Increased QT dispersion has been reported in patients with HCM, but the underlying mechanisms have not been completely elucidated. In this study, we examined the relationship between diffuse interstitial fibrosis, replacement fibrosis, QTc dispersion and ventricular arrhythmias in patients with HCM. We hypothesized that fibrosis would slow impulse propagation and increase dispersion of ventricular repolarization, resulting in increased QTc dispersion on surface electrocardiogram (ECG) and ventricular arrhythmias. Methods: ECG and cardiac magnetic resonance (CMR) image analyses were performed retrospectively in 112 patients with a clinical diagnosis of HCM. Replacement fibrosis was assessed by measuring late gadolinium (Gd) enhancement (LGE), using a semi-automated threshold technique. Diffuse interstitial fibrosis was assessed by measuring T1 relaxation times after Gd administration, using the Look-Locker sequence. QTc dispersion was measured digitally in the septal/anterior (V1-V4), inferior (II, III, and aVF), and lateral (I, aVL, V5, and V6) lead groups on surface ECG. Results: All patients had evidence of asymmetric septal hypertrophy. LGE was evident in 70 (63%) patients; the median T1 relaxation time was 411±38. ms. An inverse correlation was observed between T1 relaxation time and QTc dispersion in leads V1-V4 (p<0.001). Patients with HCM who developed sustained ventricular tachycardia had slightly higher probability of increased QTc dispersion in leads V1-V4 (odds ratio, 1.011 [1.004-1.0178, . p=0.003). We found no correlation between presence and percentage of LGE and QTc dispersion. Conclusion: Diffuse interstitial fibrosis is associated with increased dispersion of ventricular repolarization in leads, reflecting electrical activity in the hypertrophied septum. Interstitial fibrosis combined with ion channel/gap junction remodeling in the septum could lead to inhomogeneity of ventricular refractoriness, resulting in increased QTc dispersion in leads V1-V4.
AB - Background: Hypertrophic cardiomyopathy (HCM) is characterized by myocyte hypertrophy, disarray, fibrosis, and increased risk for ventricular arrhythmias. Increased QT dispersion has been reported in patients with HCM, but the underlying mechanisms have not been completely elucidated. In this study, we examined the relationship between diffuse interstitial fibrosis, replacement fibrosis, QTc dispersion and ventricular arrhythmias in patients with HCM. We hypothesized that fibrosis would slow impulse propagation and increase dispersion of ventricular repolarization, resulting in increased QTc dispersion on surface electrocardiogram (ECG) and ventricular arrhythmias. Methods: ECG and cardiac magnetic resonance (CMR) image analyses were performed retrospectively in 112 patients with a clinical diagnosis of HCM. Replacement fibrosis was assessed by measuring late gadolinium (Gd) enhancement (LGE), using a semi-automated threshold technique. Diffuse interstitial fibrosis was assessed by measuring T1 relaxation times after Gd administration, using the Look-Locker sequence. QTc dispersion was measured digitally in the septal/anterior (V1-V4), inferior (II, III, and aVF), and lateral (I, aVL, V5, and V6) lead groups on surface ECG. Results: All patients had evidence of asymmetric septal hypertrophy. LGE was evident in 70 (63%) patients; the median T1 relaxation time was 411±38. ms. An inverse correlation was observed between T1 relaxation time and QTc dispersion in leads V1-V4 (p<0.001). Patients with HCM who developed sustained ventricular tachycardia had slightly higher probability of increased QTc dispersion in leads V1-V4 (odds ratio, 1.011 [1.004-1.0178, . p=0.003). We found no correlation between presence and percentage of LGE and QTc dispersion. Conclusion: Diffuse interstitial fibrosis is associated with increased dispersion of ventricular repolarization in leads, reflecting electrical activity in the hypertrophied septum. Interstitial fibrosis combined with ion channel/gap junction remodeling in the septum could lead to inhomogeneity of ventricular refractoriness, resulting in increased QTc dispersion in leads V1-V4.
KW - Corrected QT dispersion
KW - Hypertrophic cardiomyopathy
KW - Late gadolinium enhancement
KW - T1 relaxation time
UR - http://www.scopus.com/inward/record.url?scp=85006931245&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85006931245&partnerID=8YFLogxK
U2 - 10.1016/j.joa.2016.10.005
DO - 10.1016/j.joa.2016.10.005
M3 - Article
C2 - 28607615
AN - SCOPUS:85006931245
JO - Journal of Arrhythmia
JF - Journal of Arrhythmia
SN - 1880-4276
ER -