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Circulation. 1994;90:1786-1793

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Circulation, Vol 90, 1786-1793, Copyright © 1994 by American Heart Association


ARTICLES

Prognostic implications of baseline electrocardiographic features and their serial changes in subjects with left ventricular hypertrophy

D Levy, M Salomon, RB D'Agostino, AJ Belanger and WB Kannel
Framingham Heart Study, MA 01701.

BACKGROUND: During the past half-century, the ECG has been used extensively for the diagnosis of left ventricular hypertrophy. Persons with ECG evidence of left ventricular hypertrophy are at increased risk for the development of cardiovascular disease. METHODS AND RESULTS: Subjects from the Framingham Heart Study with ECG evidence of left ventricular hypertrophy were eligible for this investigation if they were free of cardiovascular disease and did not have complete bundle- branch block or Wolff-Parkinson-White syndrome. Logistic regression analyses of pooled biennial examinations were used to determine risk for cardiovascular disease as a function of baseline voltage (sum of R wave in aVL plus S wave in V3) and repolarization and as a function of serial changes in these ECG features of hypertrophy. The eligible sample consisted of 274 men (mean age, 60 years) and 250 women (mean age, 64 years) who contributed 2660 person-examinations. During follow- up, there were 269 new cardiovascular events. Compared with subjects in the first quartile of voltage at baseline, the age-adjusted odds ratio for cardiovascular disease among subjects in the fourth quartile was 3.08 (95% confidence interval [CI], 1.87 to 5.07) in men and 3.29 (95% CI, 1.78 to 6.09) in women. Compared with a normal repolarization pattern, the presence of severe repolarization abnormalities was associated with an age-adjusted odds ratio of 5.84 (95% CI, 3.55 to 9.62) in men and 2.47 (95% CI, 1.38 to 4.42) in women. Subjects with a serial decline in voltage were at lower risk for cardiovascular disease than were those with no serial change (men: odds ratio after adjusting for age and baseline voltage, 0.46; 95% CI, 0.26 to 0.84; women: odds ratio, 0.56; 95% CI, 0.30 to 1.04). In contrast, those with a serial increase in voltage were at greater risk for cardiovascular disease (men: odds ratio, 1.86; 95% CI, 1.14 to 3.03; women: odds ratio, 1.61; 95% CI, 0.91 to 2.84). Compared with those with no serial change, an improvement in repolarization was associated with a marginally significant reduction in cardiovascular risk in men (odds ratio after adjusting for age and baseline repolarization, 0.45; 95% CI, 0.20 to 1.01). Worsening of repolarization was associated with increased risk for cardiovascular disease in both sexes (men: odds ratio, 1.89; 95% CI, 1.05 to 3.40; women: odds ratio, 2.02; 95% CI, 1.07 to 3.81). CONCLUSIONS: The results of this investigation suggest that regression of ECG features of left ventricular hypertrophy confers an improvement in risk for cardiovascular disease, whereas serial worsening imposes increased risk. The benefits to be derived from regression of left ventricular hypertrophy must be confirmed in other clinical settings.


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Nephrol Dial TransplantHome page
A. U. Klingbeil and R. E. Schmieder
Not all left ventricular hypertrophy is created equal
Nephrol. Dial. Transplant., December 1, 1999; 14(12): 2803 - 2805.
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HypertensionHome page
M. G. Modena, N. Muia Jr, P. Aveta, R. Molinari, and R. Rossi
Effects of Transdermal 17{beta}-Estradiol on Left Ventricular Anatomy and Performance in Hypertensive Women
Hypertension, November 1, 1999; 34(5): 1041 - 1046.
[Abstract] [Full Text] [PDF]


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Eur Heart JHome page
E. Edmunds, C.G.C. Spencer, and G.Y.H. Lip
Left ventricular hypertrophy in the population.
Eur. Heart J., October 1, 1999; 20(20): 1514 - 1515.
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J Am Coll CardiolHome page
R. J. Gibbons, K. Chatterjee, J. Daley, J. S. Douglas, S. D. Fihn, J. M. Gardin, M. A. Grunwald, D. Levy, B. W. Lytle, R. A. O'Rourke, et al.
ACC/AHA/ACP-ASIM guidelines for the management of patients with chronic stable angina: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Patients With Chronic Stable Angina)
J. Am. Coll. Cardiol., June 1, 1999; 33(7): 2092 - 2197.
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NEJMHome page
A. Mosterd, R. B. D'Agostino, H. Silbershatz, P. A. Sytkowski, W. B. Kannel, D. E. Grobbee, and D. Levy
Trends in the Prevalence of Hypertension, Antihypertensive Therapy, and Left Ventricular Hypertrophy from 1950 to 1989
N. Engl. J. Med., April 22, 1999; 340(16): 1221 - 1227.
[Abstract] [Full Text] [PDF]


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NEJMHome page
F. G. Dunn and M. A. Pfeffer
Left Ventricular Hypertrophy in Hypertension
N. Engl. J. Med., April 22, 1999; 340(16): 1279 - 1280.
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CirculationHome page
P. A. Thurmann, P. Kenedi, A. Schmidt, S. Harder, and N. Rietbrock
Influence of the Angiotensin II Antagonist Valsartan on Left Ventricular Hypertrophy in Patients With Essential Hypertension
Circulation, November 10, 1998; 98(19): 2037 - 2042.
[Abstract] [Full Text] [PDF]


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J Am Coll CardiolHome page
A. W. Haider, M. G. Larson, E. J. Benjamin, and D. Levy
Increased left ventricular mass and hypertrophy are associated with increased risk for sudden death
J. Am. Coll. Cardiol., November 1, 1998; 32(5): 1454 - 1459.
[Abstract] [Full Text] [PDF]


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CirculationHome page
P. Verdecchia, G. Schillaci, C. Borgioni, A. Ciucci, R. Gattobigio, I. Zampi, G. Reboldi, and C. Porcellati
Prognostic Significance of Serial Changes in Left Ventricular Mass in Essential Hypertension
Circulation, January 13, 1998; 97(1): 48 - 54.
[Abstract] [Full Text] [PDF]


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Arterioscler. Thromb. Vasc. Bio.Home page
M. K. Hong, J. Vossoughi, G. S. Mintz, R. D. Kauffman, R. F. Hoyt Jr, J. F. Cornhill, E. E. Herderick, M. B. Leon, and J. M. Hoeg
Altered Compliance and Residual Strain Precede Angiographically Detectable Early Atherosclerosis in Low-Density Lipoprotein Receptor Deficiency
Arterioscler Thromb Vasc Biol, October 1, 1997; 17(10): 2209 - 2217.
[Abstract] [Full Text]


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J. Biol. Chem.Home page
D.-J. Choi, W. J. Koch, J. J. Hunter, and H. A. Rockman
Mechanism of beta -Adrenergic Receptor Desensitization in Cardiac Hypertrophy Is Increased beta -Adrenergic Receptor Kinase
J. Biol. Chem., July 4, 1997; 272(27): 17223 - 17229.
[Abstract] [Full Text] [PDF]


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CirculationHome page
R. B. Devereux
Do Antihypertensive Drugs Differ in Their Ability to Regress Left Ventricular Hypertrophy?
Circulation, April 15, 1997; 95(8): 1983 - 1985.
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CirculationHome page
J. S. Gottdiener, D. J. Reda, B. M. Massie, B. J. Materson, D. W. Williams, and R. J. Anderson
Effect of Single-Drug Therapy on Reduction of Left Ventricular Mass in Mild to Moderate Hypertension: Comparison of Six Antihypertensive Agents
Circulation, April 15, 1997; 95(8): 2007 - 2014.
[Abstract] [Full Text]


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HypertensionHome page
S. G. Sheps and E. D. Frohlich
Limited Echocardiography for Hypertensive Left Ventricular Hypertrophy
Hypertension, February 1, 1997; 29(2): 560 - 563.
[Full Text]


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J. Thorac. Cardiovasc. Surg.Home page
J. R. Gonzalez-Juanatey, J. M. Garca-Acuna, M. V. Fernandez, A. A. Cendon, V. C. Fuentes, J. B. Garcia-Bengoechea, and M. G. de la Pena
INFLUENCE OF THE SIZE OF AORTIC VALVE PROSTHESES ON HEMODYNAMICS AND CHANGE IN LEFT VENTRICULAR MASS: IMPLICATIONS FOR THE SURGICAL MANAGEMENT OF AORTIC STENOSIS
J. Thorac. Cardiovasc. Surg., August 1, 1996; 112(2): 273 - 280.
[Abstract] [Full Text]


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JAMAHome page
W. B. Kannel
Blood Pressure as a Cardiovascular Risk Factor: Prevention and Treatment
JAMA, May 22, 1996; 275(20): 1571 - 1576.
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JAMAHome page
R. B. Devereux
Regression of Left Ventricular Hypertrophy: How and Why?
JAMA, May 15, 1996; 275(19): 1517 - 1518.
[Abstract] [PDF]