TY - JOUR
T1 - Association of Concentric Left Ventricular Hypertrophy with Subsequent Change in Left Ventricular End-Diastolic Volume
T2 - The Dallas Heart Study
AU - Garg, Sonia
AU - de Lemos, James A
AU - Matulevicius, Susan A
AU - Ayers, Colby
AU - Pandey, Ambarish
AU - Neeland, Ian J
AU - Berry, Jarett D
AU - McColl, Roderick W
AU - Maroules, Christopher
AU - Peshock, Ronald M
AU - Drazner, Mark H
N1 - Funding Information:
Dr Drazner has received support from the James M. Wooten Chair in Cardiology, University of Texas Southwestern Medical Center. Dr de Lemos has received grant support from Roche Diagnostics and from Abbott Diagnostics and consulting income from Abbott Diagnostics, Siemen’s Healthcare Diagnostics, and Radiometer. The other authors report no conflicts.
Funding Information:
The Dallas Heart Study was funded by the Donald W. Reynolds Foundation and was partially supported by the National Center for Advancing Translational Sciences of the National Institutes of Health under award number UL1TR001105. This work was also supported by the American Heart Association Strategically Focused Research Grant (14SFRN20740000).
Publisher Copyright:
© 2017 American Heart Association, Inc.
PY - 2017/8/1
Y1 - 2017/8/1
N2 - Background In the conventional paradigm of the progression of left ventricular hypertrophy, a thick-walled left ventricle (LV) ultimately transitions to a dilated cardiomyopathy. There are scant data in humans demonstrating whether this transition occurs commonly without an interval myocardial infarction. Methods and Results Participants (n=1282) from the Dallas Heart Study underwent serial cardiac magnetic resonance ≈7 years apart. Those with interval cardiovascular events and a dilated LV (increased LV end-diastolic volume [EDV] indexed to body surface area) at baseline were excluded. Multivariable linear regression models tested the association of concentric hypertrophy (increased LV mass and LV mass/volume0.67) with change in LVEDV. The study cohort had a median age of 44 years, 57% women, 43% black, and 11% (n=142) baseline concentric hypertrophy. The change in LVEDV in those with versus without concentric hypertrophy was 1 mL (-9 to 12) versus -2 mL (-11 to 7), respectively, P<0.01. In multivariable linear regression models, concentric hypertrophy was associated with larger follow-up LVEDV (P≤0.01). The progression to a dilated LV was uncommon (2%, n=25). Conclusions In the absence of interval myocardial infarction, concentric hypertrophy was associated with a small, but significantly greater, increase in LVEDV after 7-year follow-up. However, the degree of LV enlargement was minimal, and few participants developed a dilated LV. These data suggest that if concentric hypertrophy does progress to a dilated cardiomyopathy, such a transition would occur over a much longer timeframe (eg, decades) and may be less common than previously thought. Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT00344903.
AB - Background In the conventional paradigm of the progression of left ventricular hypertrophy, a thick-walled left ventricle (LV) ultimately transitions to a dilated cardiomyopathy. There are scant data in humans demonstrating whether this transition occurs commonly without an interval myocardial infarction. Methods and Results Participants (n=1282) from the Dallas Heart Study underwent serial cardiac magnetic resonance ≈7 years apart. Those with interval cardiovascular events and a dilated LV (increased LV end-diastolic volume [EDV] indexed to body surface area) at baseline were excluded. Multivariable linear regression models tested the association of concentric hypertrophy (increased LV mass and LV mass/volume0.67) with change in LVEDV. The study cohort had a median age of 44 years, 57% women, 43% black, and 11% (n=142) baseline concentric hypertrophy. The change in LVEDV in those with versus without concentric hypertrophy was 1 mL (-9 to 12) versus -2 mL (-11 to 7), respectively, P<0.01. In multivariable linear regression models, concentric hypertrophy was associated with larger follow-up LVEDV (P≤0.01). The progression to a dilated LV was uncommon (2%, n=25). Conclusions In the absence of interval myocardial infarction, concentric hypertrophy was associated with a small, but significantly greater, increase in LVEDV after 7-year follow-up. However, the degree of LV enlargement was minimal, and few participants developed a dilated LV. These data suggest that if concentric hypertrophy does progress to a dilated cardiomyopathy, such a transition would occur over a much longer timeframe (eg, decades) and may be less common than previously thought. Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT00344903.
KW - animals
KW - dilation, left ventricular
KW - heart
KW - hypertrophy, left ventricular
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U2 - 10.1161/CIRCHEARTFAILURE.117.003959
DO - 10.1161/CIRCHEARTFAILURE.117.003959
M3 - Article
C2 - 28775115
AN - SCOPUS:85025432886
SN - 1941-3289
VL - 10
JO - Circulation: Heart Failure
JF - Circulation: Heart Failure
IS - 8
M1 - e003959
ER -