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      “Malignant” Left Ventricular Hypertrophy Identifies Subjects at High Risk for Progression to Asymptomatic Left Ventricular Dysfunction, Heart Failure, and Death: MESA (Multi‐Ethnic Study of Atherosclerosis)

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          Abstract

          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.

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          Most cited references13

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          Irbesartan in patients with heart failure and preserved ejection fraction.

          Approximately 50% of patients with heart failure have a left ventricular ejection fraction of at least 45%, but no therapies have been shown to improve the outcome of these patients. Therefore, we studied the effects of irbesartan in patients with this syndrome. We enrolled 4128 patients who were at least 60 years of age and had New York Heart Association class II, III, or IV heart failure and an ejection fraction of at least 45% and randomly assigned them to receive 300 mg of irbesartan or placebo per day. The primary composite outcome was death from any cause or hospitalization for a cardiovascular cause (heart failure, myocardial infarction, unstable angina, arrhythmia, or stroke). Secondary outcomes included death from heart failure or hospitalization for heart failure, death from any cause and from cardiovascular causes, and quality of life. During a mean follow-up of 49.5 months, the primary outcome occurred in 742 patients in the irbesartan group and 763 in the placebo group. Primary event rates in the irbesartan and placebo groups were 100.4 and 105.4 per 1000 patient-years, respectively (hazard ratio, 0.95; 95% confidence interval [CI], 0.86 to 1.05; P=0.35). Overall rates of death were 52.6 and 52.3 per 1000 patient-years, respectively (hazard ratio, 1.00; 95% CI, 0.88 to 1.14; P=0.98). Rates of hospitalization for cardiovascular causes that contributed to the primary outcome were 70.6 and 74.3 per 1000 patient-years, respectively (hazard ratio, 0.95; 95% CI, 0.85 to 1.08; P=0.44). There were no significant differences in the other prespecified outcomes. Irbesartan did not improve the outcomes of patients with heart failure and a preserved left ventricular ejection fraction. (ClinicalTrials.gov number, NCT00095238.) 2008 Massachusetts Medical Society
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            Natriuretic peptide-based screening and collaborative care for heart failure: the STOP-HF randomized trial.

            Prevention strategies for heart failure are needed. To determine the efficacy of a screening program using brain-type natriuretic peptide (BNP) and collaborative care in an at-risk population in reducing newly diagnosed heart failure and prevalence of significant left ventricular (LV) systolic and/or diastolic dysfunction. The St Vincent's Screening to Prevent Heart Failure Study, a parallel-group randomized trial involving 1374 participants with cardiovascular risk factors (mean age, 64.8 [SD, 10.2] years) recruited from 39 primary care practices in Ireland between January 2005 and December 2009 and followed up until December 2011 (mean follow-up, 4.2 [SD, 1.2] years). Patients were randomly assigned to receive usual primary care (control condition; n=677) or screening with BNP testing (n=697). Intervention-group participants with BNP levels of 50 pg/mL or higher underwent echocardiography and collaborative care between their primary care physician and specialist cardiovascular service. The primary end point was prevalence of asymptomatic LV dysfunction with or without newly diagnosed heart failure. Secondary end points included emergency hospitalization for arrhythmia, transient ischemic attack, stroke, myocardial infarction, peripheral or pulmonary thrombosis/embolus, or heart failure. A total of 263 patients (41.6%) in the intervention group had at least 1 BNP reading of 50 pg/mL or higher. The intervention group underwent more cardiovascular investigations (control, 496 per 1000 patient-years vs intervention, 850 per 1000 patient-years; incidence rate ratio, 1.71; 95% CI, 1.61-1.83; P<.001) and received more renin-angiotensin-aldosterone system-based therapy at follow-up (control, 49.6%; intervention, 56.5%; P=.01). The primary end point of LV dysfunction with or without heart failure was met in 59 (8.7%) of 677 in the control group and 37 (5.3%) of 697 in the intervention group (odds ratio [OR], 0.55; 95% CI, 0.37-0.82; P = .003). Asymptomatic LV dysfunction was found in 45 (6.6%) of 677 control-group patients and 30 (4.3%) of 697 intervention-group patients (OR, 0.57; 95% CI, 0.37-0.88; P = .01). Heart failure occurred in 14 (2.1%) of 677 control-group patients and 7 (1.0%) of 697 intervention-group patients (OR, 0.48; 95% CI, 0.20-1.20; P = .12). The incidence rates of emergency hospitalization for major cardiovascular events were 40.4 per 1000 patient-years in the control group vs 22.3 per 1000 patient-years in the intervention group (incidence rate ratio, 0.60; 95% CI, 0.45-0.81; P = .002). Among patients at risk of heart failure, BNP-based screening and collaborative care reduced the combined rates of LV systolic dysfunction, diastolic dysfunction, and heart failure. clinicaltrials.gov Identifier: NCT00921960.
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              Heart Failure Stages Among Older Adults in the Community: The Atherosclerosis Risk in Communities Study.

              Although heart failure (HF) disproportionately affects older adults, little data exist regarding the prevalence of American College of Cardiology/American Heart Association HF stages among older individuals in the community. Additionally, the role of contemporary measures of longitudinal strain and diastolic dysfunction in defining HF stages is unclear.
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                Author and article information

                Contributors
                christopher.defilippi@inova.org
                Journal
                J Am Heart Assoc
                J Am Heart Assoc
                10.1002/(ISSN)2047-9980
                JAH3
                ahaoa
                Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
                John Wiley and Sons Inc. (Hoboken )
                2047-9980
                08 February 2018
                February 2018
                : 7
                : 4 ( doiID: 10.1002/jah3.2018.7.issue-4 )
                : e006619
                Affiliations
                [ 1 ] Division of Cardiovascular Medicine University of Maryland School of Medicine Baltimore MD
                [ 2 ] Division of Nephrology University of Maryland School of Medicine Baltimore MD
                [ 3 ] Department of Pathology University of Maryland School of Medicine Baltimore MD
                [ 4 ] Division of Cardiology University of California at San Diego La Jolla CA
                [ 5 ] Division of Cardiology Johns Hopkins University Baltimore MD
                [ 6 ] Division of Cardiology University of Texas Southwestern Medical Center Dallas TX
                [ 7 ] Inova Heart and Vascular Institute Falls Church VA
                Author notes
                [*] [* ] Correspondence to: Christopher R. deFilippi, MD, Inova Heart and Vascular Institute, 3300 Gallows Road, Falls Church, VA 22042. E‐mail: christopher.defilippi@ 123456inova.org
                Article
                JAH32892
                10.1161/JAHA.117.006619
                5850178
                29437599
                60200e69-5a5e-463a-8605-ea24567bca1f
                © 2018 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

                This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                : 09 May 2017
                : 05 December 2017
                Page count
                Figures: 4, Tables: 2, Pages: 10, Words: 7177
                Funding
                Funded by: National Heart, Lung, and Blood Institute
                Award ID: HHSN268201500003I
                Award ID: N01‐HC‐95159
                Award ID: N01‐HC‐95160
                Award ID: N01‐HC‐95161
                Award ID: N01‐HC‐95162
                Award ID: N01‐HC‐95163
                Award ID: N01‐HC‐95164
                Award ID: N01‐HC‐95165
                Award ID: N01‐HC‐95166
                Award ID: N01‐HC‐95167
                Award ID: N01‐HC‐95168
                Award ID: N01‐HC‐95169
                Funded by: NCRR
                Award ID: UL1‐TR‐000040
                Award ID: UL1‐TR‐001079
                Funded by: Roche Diagnostics
                Categories
                Original Research
                Original Research
                Heart Failure
                Custom metadata
                2.0
                jah32892
                February 2018
                Converter:WILEY_ML3GV2_TO_NLMPMC version:version=5.3.2.2 mode:remove_FC converted:20.02.2018

                Cardiovascular Medicine
                heart failure,left ventricular dysfunction,left ventricular hypertrophy,mortality,n‐terminal pro‐b‐type,troponin t,hypertrophy,epidemiology,biomarkers

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