TY - JOUR
T1 - "Malignant" left ventricular hypertrophy identifies subjects at high risk for progression to asymptomatic left ventricular dysfunction, heart failure, and death
T2 - MESA (Multi-Ethnic Study of Atherosclerosis)
AU - Peters, Matthew N.
AU - Seliger, Stephen L.
AU - Christenson, Robert H.
AU - Hong-Zohlman, Susie N.
AU - Daniels, Lori B.
AU - Lima, Joao A.C.
AU - de Lemos, James A.
AU - Neeland, Ian J.
AU - de Filippi, Christopher R.
N1 - Funding Information:
This research was supported by contracts HHSN 268201500003I, N01-HC-95159, N01-HC-95160, N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168, and N01-HC-95169 from the National Heart, Lung, and Blood Institute and by grants UL1-TR-000040 and UL1-TR-001079 from NCRR. Roche Diagnostics supported the measurement of hs-cTnT and additional NT-proBNP through an investigator-initiated grant (PI: deFilippi).
Funding Information:
deFilippi receives grant support from Roche Diagnostics and Abbott Diagnostics, consulting for Alere, Roche Diagnostics, Siemens Healthcare Diagnostics, Metanomics, Thermo-Fisher and Ortho Clinical Diagnostics, and participates on the endpoint review committee for Radiometer. Seliger has received grant support from Roche Diagnostics. Christenson receives grant support from Roche Diagnostics, Ortho Clinical Diagnostics and Abbott Diagnostics, consulting for Siemens Healthcare and Ortho Clinical Diagnostics. Daniels has received speaking fees from Roche Diagnostics and consulting for Siemens Healthcare Diagnostics. de Lemos has received grant support and consulting income from Roche Diagnostics and Abbott Diagnostics, and has participated on endpoint review committees for Siemen’s Health Care Diagnostics and Radiometer. The remaining authors have no disclosures to report.
Publisher Copyright:
© 2018 The Authors.
PY - 2018/2/1
Y1 - 2018/2/1
N2 - Background--As heart failure (HF)-associated morbidity and mortality continue to escalate, enhanced focus on prevention is increasingly important. "Malignant" left ventricular (LV) hypertrophy (LVH): LVH combined with an elevated cardiac biomarker reflecting either injury (high-sensitivity cardiac troponin T), or strain (amino-terminal pro-B-type natriuretic peptide) has predicted accelerated progression to HF. We sought to determine whether malignant LVH identified community-dwelling adults initially free of cardiovascular disease at high risk of asymptomatic decline in LV ejection fraction or a clinical cardiovascular event. Methods and Results--A total of 4985 of 6814 individuals without prevalent cardiovascular disease underwent baseline cardiac magnetic resonance for LVH in combination with measurement of plasma high-sensitivity cardiac troponin T and amino-terminal pro-B-type natriuretic peptide as part of MESA (Multi-Ethnic Study of Atherosclerosis) and were subsequently divided into 4 groups: (1) No LVH, no elevated biomarkers (n=2206; 44.3%); (2) No LVH, ≥1 elevated biomarkers (n=2275; 45.7%); (3) LVH, no elevated biomarkers (n=153; 3.0%); and (4) LVH, ≥1 elevated biomarkers (malignant LVH; n=351; 7.0%). Cardiac magnetic resonance was repeated 10 years later (n=2831) for assessment of LV ejection fraction < 50%. Median follow-up was 12.2 years. Malignant LVH was associated with 7.0-, 3.5-, and 2.6-fold adjusted increases in incidence of HF, cardiovascular death, and asymptomatic LV dysfunction, respectively, versus group 1. New-onset HF was predominately HF with reduced ejection fraction (9.5-fold increase). Conclusions--Malignant LVH is predictive of progression to asymptomatic LV dysfunction, HF (particularly HF with reduced ejection fraction), and cardiovascular death. Consequently, malignant LVH represents a high-risk phenotype among individuals without known cardiovascular disease, which should be targeted for increased surveillance and more-aggressive therapies.
AB - Background--As heart failure (HF)-associated morbidity and mortality continue to escalate, enhanced focus on prevention is increasingly important. "Malignant" left ventricular (LV) hypertrophy (LVH): LVH combined with an elevated cardiac biomarker reflecting either injury (high-sensitivity cardiac troponin T), or strain (amino-terminal pro-B-type natriuretic peptide) has predicted accelerated progression to HF. We sought to determine whether malignant LVH identified community-dwelling adults initially free of cardiovascular disease at high risk of asymptomatic decline in LV ejection fraction or a clinical cardiovascular event. Methods and Results--A total of 4985 of 6814 individuals without prevalent cardiovascular disease underwent baseline cardiac magnetic resonance for LVH in combination with measurement of plasma high-sensitivity cardiac troponin T and amino-terminal pro-B-type natriuretic peptide as part of MESA (Multi-Ethnic Study of Atherosclerosis) and were subsequently divided into 4 groups: (1) No LVH, no elevated biomarkers (n=2206; 44.3%); (2) No LVH, ≥1 elevated biomarkers (n=2275; 45.7%); (3) LVH, no elevated biomarkers (n=153; 3.0%); and (4) LVH, ≥1 elevated biomarkers (malignant LVH; n=351; 7.0%). Cardiac magnetic resonance was repeated 10 years later (n=2831) for assessment of LV ejection fraction < 50%. Median follow-up was 12.2 years. Malignant LVH was associated with 7.0-, 3.5-, and 2.6-fold adjusted increases in incidence of HF, cardiovascular death, and asymptomatic LV dysfunction, respectively, versus group 1. New-onset HF was predominately HF with reduced ejection fraction (9.5-fold increase). Conclusions--Malignant LVH is predictive of progression to asymptomatic LV dysfunction, HF (particularly HF with reduced ejection fraction), and cardiovascular death. Consequently, malignant LVH represents a high-risk phenotype among individuals without known cardiovascular disease, which should be targeted for increased surveillance and more-aggressive therapies.
KW - Heart failure
KW - Left ventricular dysfunction
KW - Left ventricular hypertrophy
KW - Mortality
KW - N-terminal pro-B-type
KW - Troponin T
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U2 - 10.1161/JAHA.117.006619
DO - 10.1161/JAHA.117.006619
M3 - Article
C2 - 29437599
AN - SCOPUS:85042159090
SN - 2047-9980
VL - 7
JO - Journal of the American Heart Association
JF - Journal of the American Heart Association
IS - 4
M1 - e006619
ER -