CLINICAL STUDIES
Increased left ventricular mass and hypertrophy are associated with increased risk for sudden death
Agha W. Haider, MD, PhD* ¶,
Martin G. Larson, ScD* ,
Emelia J. Benjamin, MD, ScM, FACC and
Daniel Levy, MD, FACC* ||
* National Heart, Lung, and Blood Institutes Framingham Heart Study, Framingham, Massachusetts, USA
National Heart, Lung, and Blood Institute, Bethesda, Maryland, USA
The Section of Epidemiology and Preventive Medicine, Boston University School of Medicine, Boston, Massachusetts, USA
Division of Cardiology, Boston Medical Center, Boston, Massachusetts, USA
¶ Massachusetts Veterans Epidemiology Research and Information Center, Harvard Medical School, Boston, Massachusetts, USA
|| Divisions of Cardiology and Clinical Epidemiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
Manuscript received February 10, 1998;
revised manuscript received May 20, 1998,
accepted June 22, 1998.
Address for correspondence: Dr. Daniel Levy, Framingham Heart Study, 5 Thurber Street, Framingham, Massachusetts 01702 dan{at}fram.nhlbi.nih.gov
Objectives. This study examined the relations of echocardiographically determined left ventricular (LV) mass and hypertrophy to the risk of sudden death.
Background. Echocardiographic LV hypertrophy is associated with increased risk for all-cause mortality and cardiovascular disease morbidity and mortality. However, little is known about the association of echocardiographic LV hypertrophy with sudden death.
Methods. We examined the relations of LV mass and hypertrophy to the incidence of sudden death in 3,661 subjects enrolled in the Framingham Heart Study who were 40 years of age. The baseline examination was performed from 1979 to 1983 and LV hypertrophy was defined as LV mass (adjusted for height) >143 g/m in men and >102 g/m in women. During up to 14 years of follow-up there were 60 sudden deaths. Cox models examined the relations of LV mass and LV hypertrophy to sudden death risk after adjusting for known risk factors.
Results. The prevalence of LV hypertrophy was 21.5%. The risk factoradjusted hazard ratio (HR) for sudden death was 1.45 (95% confidence interval [CI] 1.10 to 1.92, p = 0.008) for each 50-g/m increment in LV mass. For LV hypertrophy, the risk factoradjusted HR for sudden death was 2.16 (95% CI 1.22 to 3.81, p = 0.008). After excluding the first 4 years of follow-up, both increased LV mass and LV hypertrophy conferred long-term risk of sudden death (HR 1.53, 95% CI 1.01 to 2.28, p = 0.047 and HR 3.28, 95% CI 1.58 to 6.83, p = 0.002, respectively).
Conclusions. Increased LV mass and hypertrophy are associated with increased risk for sudden death after accounting for known risk factors.
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Abbreviations and Acronyms
| | CI | = confidence interval | | HR | = hazard ratio | | LV | = left ventricular |
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July 17, 2001;
104(3):
317 - 324.
[Abstract]
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D. Iarussi, A. Caruso, M. Galderisi, F. E. Covino, G. Dialetto, E. Bossone, O. de Divitiis, and M. Cotrufo
Association of Left Ventricular Hypertrophy and Aortic Dilation in Patients with Acute Thoracic Aortic Dissection
Angiology,
July 1, 2001;
52(7):
447 - 455.
[Abstract]
[PDF]
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S. C. Verduyn, C. Ramakers, G. Snoep, J. D. M. Leunissen, H. J. J. Wellens, and M. A. Vos
Time course of structural adaptations in chronic AV block dogs: evidence for differential ventricular remodeling
Am J Physiol Heart Circ Physiol,
June 1, 2001;
280(6):
H2882 - H2890.
[Abstract]
[Full Text]
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B. Biondi, E. A. Palmieri, S. Fazio, C. Cosco, M. Nocera, L. Saccà, S. Filetti, G. Lombardi, and F. Perticone
Endogenous Subclinical Hyperthyroidism Affects Quality of Life and Cardiac Morphology and Function in Young and Middle-Aged Patients
J. Clin. Endocrinol. Metab.,
December 1, 2000;
85(12):
4701 - 4705.
[Abstract]
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B. Kuch, H.-W. Hense, B. Gneiting, A. Doring, M. Muscholl, U. Brockel, and H. Schunkert
Body Composition and Prevalence of Left Ventricular Hypertrophy
Circulation,
July 25, 2000;
102(4):
405 - 410.
[Abstract]
[Full Text]
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B. H. Lorell and B. A. Carabello
Left Ventricular Hypertrophy : Pathogenesis, Detection, and Prognosis
Circulation,
July 25, 2000;
102(4):
470 - 479.
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T. Tamura, S. Said, J. Harris, W. Lu, and A. M. Gerdes
Reverse Remodeling of Cardiac Myocyte Hypertrophy in Hypertension and Failure by Targeting of the Renin-Angiotensin System
Circulation,
July 11, 2000;
102(2):
253 - 259.
[Abstract]
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R. Pedrinelli, G. Dell'Omo, G. Penno, S. Bandinelli, A. Bertini, V. Di Bello, and M. Mariani
Microalbuminuria and Pulse Pressure in Hypertensive and Atherosclerotic Men
Hypertension,
January 1, 2000;
35(1):
48 - 54.
[Abstract]
[Full Text]
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E. D. Frohlich
Risk Mechanisms in Hypertensive Heart Disease
Hypertension,
October 1, 1999;
34(4):
782 - 789.
[Abstract]
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B. D. Rosen, T. Edvardsen, S. Lai, E. Castillo, L. Pan, M. Jerosch-Herold, S. Sinha, R. Kronmal, D. Arnett, J. R. Crouse III, et al.
Left Ventricular Concentric Remodeling Is Associated With Decreased Global and Regional Systolic Function: The Multi-Ethnic Study of Atherosclerosis
Circulation,
August 16, 2005;
112(7):
984 - 991.
[Abstract]
[Full Text]
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