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      Association between Electrocardiographic Left Ventricular Hypertrophy with Strain Pattern and Left Ventricular Structure and Function


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          Background and Purpose: Electrocardiographic left ventricular hypertrophy (LVH) with strain pattern has been documented as a marker for LVH. Its presence on the ECG of hypertensive patients is associated with poor prognosis. The study was carried out to assess the association of the electrocardiographic strain with left ventricular mass (LVM) and function in hypertensive Nigerians. Material and Methods: ECG as well as echocardiograms were performed in 64 hypertensive patients with ECG-LVH and strain pattern, 65 patients with ECG-LVH by Sokolow-Lyon (SL) voltage criteria and 62 normal controls. Results: The study showed that electrocardiographic left ventricular (LV) strain pattern is associated with dilated left atrium, larger LV internal dimensions and greater absolute and indexed LVM in hypertensive Nigerians compared with ECG-LVH by SL voltage criteria alone or normal controls. Conclusion: The findings of this study support the fact that the ECG strain pattern is associated with increased LVM and an increased risk of developing abnormal LV geometry.

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          Most cited references 14

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          Prognostic value of a new electrocardiographic method for diagnosis of left ventricular hypertrophy in essential hypertension.

          We tested the prognostic value of a new electrocardiographic (ECG) method (Perugia score) for diagnosis of left ventricular hypertrophy (LVH) in essential hypertension and compared it with five standard methods (Cornell voltage, Framingham criterion, Romhilt-Estes point score, left ventricular strain, Sokolow-Lyon voltage). Several standard ECG methods for assessment of LVH are used in the clinical setting, but a comparative prognostic assessment is lacking. A total of 1,717 white hypertensive subjects (mean age 52 years; 51% men) were prospectively followed up for up to 10 years (mean 3.3). At entry, the prevalence of LVH was 17.8% (Perugia score), 9.1% (Cornell), 3.9% (Framingham), 5.2% (Romhilt-Estes), 6.4% (strain) and 13.1% (Sokolow-Lyon). During follow-up there were 159 major cardiovascular morbid events (33 fatal). The event rate was higher in the subjects with than in those without LVH (all p < 0.001) according to all methods except the Sokolow-Lyon method. By multivariate analysis, an independent association between LVH and cardiovascular disease risk was maintained by the Perugia score (hazard ratio [HR] 2.04, 95% confidence interval [CI] 1.5 to 2.8) and the Framingham (HR 1.91, 95% CI 1.1 to 3.2), Romhilt-Estes (HR 2.63, 95% CI 1.7 to 4.1) and strain methods (HR 2.11, 95% CI 1.4 to 3.2). The Perugia score showed the highest population-attributable risk for cardiovascular events, accounting for 15.6% of all cases, whereas the Framingham, Romhilt-Estes and strain methods accounted for 3.0%, 7.4% and 6.8% of all events, respectively. LVH diagnosed by the Perugia score was also associated with an increased risk of cardiovascular mortality (HR 4.21, 95% CI 2.1 to 8.7), with a population-attributable risk of 37.0%. The Perugia score carried the highest population-attributable risk for cardiovascular morbidity and mortality compared with classic methods for detection of LVH. Traditional interpretation of standard electrocardiography maintains an important role for cardiovascular risk stratification in essential hypertension.
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            Prevalence and natural history of electrocardiographic left ventricular hypertrophy.

             W Kannel (1983)
            Left ventricular hypertrophy, particularly on the electrocardiogram, is an ominous, not an incidental accompaniment of hypertension and cardiovascular disease. The prevalence of electrocardiographic left ventricular hypertrophy increases with age with a slight male predominance, and one in 10 persons aged 30 to 62 can expect to have it within 12 years. At any age, cardiac enlargement on roentgenograms is twice as prevalent as electrocardiographic left ventricular hypertrophy, and in only 16 percent of those with x-ray evidence of cardiac enlargement does electrocardiographic left ventricular hypertrophy subsequently develop. Hypertension predisposes and at systolic pressures exceeding 180 mm Hg evidence of electrocardiographic left ventricular hypertrophy develops in 50 percent, with no closer relation to diastolic, than to systolic pressure. In addition to drastic curtailment of life expectancy, electrocardiographic left ventricular hypertrophy is a harbinger of serious cardiovascular disease. Definite electrocardiographic left ventricular hypertrophy is associated with an eightfold increase in cardiovascular mortality and a sixfold increase in coronary mortality. Electrocardiographic left ventricular hypertrophy with repolarization criteria more than doubles the risk of hypertension alone and carries a greater risk of cardiovascular morbidity and mortality than cardiac enlargement. It identifies hypertensive patients with a compromised coronary circulation and myocardial damage. Risk of stroke, cardiac failure, and every clinical manifestation of coronary heart disease is substantially increased. In those with electrocardiographic left ventricular hypertrophy risk of cardiac failure is three times that in those with hypertension alone. Electrocardiographic left ventricular hypertrophy based solely on voltage criteria reflects chiefly the severity and duration of associated hypertension, carrying only half the cardiovascular risk of electrocardiographic left ventricular hypertrophy with repolarization abnormality. The precise pathologic and anatomic meaning of electrocardiographic left ventricular hypertrophy is unclear in view of the modest correlations with anatomic, x-ray, ventriculographic, and electrocardiographic measures of cardiac hypertrophy. The electrocardiographic aberrations are as much a product of myocardial damage as hypertrophy, and their appearance must be regarded as a grave prognostic sign in the course of cardiovascular disease.
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              Prevalence of left ventricular hypertrophy in a general population; The Tromsø Study.

              Left ventricular hypertrophy has been shown to be an independent predictor of cardiovascular morbidity. Acknowledging the skewed distribution of left ventricular mass, we wanted to develop criteria for left ventricular hypertrophy based on percentiles of left ventricular mass, and observe the effect on estimates of left ventricular hypertrophy prevalences in different subgroups and on the relationship to cardiovascular risk factors in a general population. In a population-based sample of 3287 subjects aged 25-85 years, left ventricular mass was estimated using M-mode echocardiography. A 'healthy' subgroup was used as a reference sample to define sex-specific left ventricular hypertrophy criteria. Sex-specific 97.5 percentiles for left ventricular mass by height, based on the reference sample, were 145.5 and 125.4 g.m(-1), for men and women, respectively. The prevalences of left ventricular hypertrophy in the total population were 14.9% for men and 9.1% for women. The main independent predictors of left ventricular hypertrophy were male gender, body mass index, systolic blood pressure, valvular heart disease, cardiovascular disease and antihypertensive medication. Body mass index and systolic blood pressure had a strong synergistic association with left ventricular hypertrophy in men, but not in women. An alternative framework for defining left ventricular hypertrophy is provided. Body mass index is the culprit factor for risk of left ventricular hypertrophy. Our study indicates that weight reduction is a relevant measure for treatment and possibly prevention of left ventricular hypertrophy in a substantial part of the general population.

                Author and article information

                S. Karger AG
                June 2006
                03 July 2006
                : 106
                : 1
                : 14-21
                Department of Medicine, College of Medicine, University of Ibadan/University College Hospital, Ibadan, Nigeria
                92478 Cardiology 2006;106:14–21
                © 2006 S. Karger AG, Basel

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                Page count
                Tables: 4, References: 29, Pages: 8
                Original Research


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