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 - 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 -