Hypertension
Figure 1: Relationship Between Left Ventricular Mass and Left Ventricular Mass Measured at Subsequent Baseline Echocardiogram After 14 Days
600 ρ=0.93 500 400 300 200 100 100 200 300 400 LV mass (g) (first evaluation)
Left ventricular mass = horizontal axis; echocardiogram = vertical axis. Source: Palmieri et al., 1999.22
comparative agent (atenolol) or regression compared with persistence or progression of electrocardiographic LV hypertrophy.15–17
As part of the LIFE trial, >10% of study participants were enrolled in the LIFE echocardiography substudy in which echocardiograms were performed at study baseline and yearly thereafter.18
The
echocardiography population was representative of the main LIFE study in age, blood pressure and prevalences of cardiovascular diseases and diabetes at baseline, but differed from the remaining LIFE participants in being disproportionately male, due predominately to participation in the echocardiographic substudy of several Veterans’ Administration Hospitals in the US and a centre in Norway that recruited participants from the all-male Oslo Heart Study. Height and heart rate were higher and body mass index lower in the echocardiography substudy participants. A higher population of blacks were enrolled in the echocardiography substudy compared with the overall LIFE population to assess possible ethnic differences in LV geometry and the performance of electrocardiographic indices of LV hypertrophy.18
Assessment of Left Ventricular Hypertrophy Because of the importance of assessing LV hypertrophy as a marker of cardiac risk, several methods have been developed to estimate LV mass. Although electrocardiography carries independent prognostic information, echocardiography is more sensitive for assessing LV hypertrophy.19,20
Furthermore, to date, echocardiography remains the only modality that has been anatomically validated in humans for estimation of LV mass.21
Use of a standardised protocol and training of
sonographers are required to limit variability of echocardiographic measurements. Data from the Prospective Randomized Enalapril Study Evaluating Regression of Ventricular Enlargement (PRESERVE) documented excellent interstudy variability and show the ability to detect small changes of LV mass in modestly sized populations.22 Palmieri et al. reported that the short-term between-study variability had high interclass correlation (ρ=0.93; see Figure 1), an estimator of variability between replicate measurements, resulting in LV mass ±34g or ±18g in a single patient with ≥90 or ≥80% likelihood to be true changes, respectively.22
24 500 600
This has led to controversy in terms of image modality for detection of LV hypertrophy.26,27
The current data suggest that 41 patients are
needed per treatment arm to provide statistical power of 90% at an error level of 1% to detect a between-group difference of at least 10g/m2. Similarly, 3D echocardiography requires 15 patients per arm and magnetic resonance imaging requires 14 patients per arm. Thus, echocardiographic LV mass remains an excellent bioassay for clinical studies of LV hypertrophy that require moderate or large population sizes to obtain sufficient clinical end-points or to encompass participants with varied characteristics.22,23
Left Ventricular Mass Index and Left Ventricular Geometry Echocardiographic partition values for LV hypertrophy/body surface area were suggested by Hammond et al.28
suggest
Lately, both 3D echocardiography23 imaging24
and cardiac magnetic resonance have been shown to have lower variability than 2D
echocardiography, and magnetic resonance imaging has now been used in population-based studies.25
However, there are still no human necropsy comparison data to validate magnetic resonance imaging.
to be 134g/m2 for men and
110g/m2 for women. However, more recent data derived from the PRESERVE trial, using newer echocardiographs in reference populations that met more stringent criteria of normality,29,30
partition values of 116g/m2 for men and 104g/m2 for women or 115 and 96g/m2, respectively. A comparison of the LIFE echocardiography study participants versus apparently normal adults showed that indexation of LV mass for height2.7 avoided the underestimation of the prevalence of LV hypertrophy in overweight and obese patients that occurs with indexation of LV mass by body surface area. In addition, patients recruited by LV mass indexed for body surface area have higher blood pressure, whereas patients recruited by LV mass indexed for height2.7 have a higher prevalence of obesity (see Table 1). In view of increasing obesity worldwide, indexation by the allometric power of height becomes increasingly important.
The combination of LV mass index (LVMI) and relative wall thickness has been used to identify three abnormal LV geometrical patterns,4,31 known as concentric remodelling (normal LVMI with increased relative wall thickness), eccentric hypertrophy (increased LVMI and normal relative wall thickness) and concentric hypertrophy (increased LVMI and increased relative wall thickness). Relative wall thickness has been calculated either as the ratio of 2x posterior wall thickness/LV internal diameter32
posterior wall thickness)/LV internal diameter.33,34
or as the ratio of (interventricular septal + Analyses of data
from a working population from New York suggests the partition value of relative wall thickness to be 0.43.30,35
Different studies have shown quite different prevalences of LV hypertrophy depending on the population studied and the methods used for calculation of LVMI and relative wall thickness. Studies have used a variety of partition values for LV mass and relative wall thickness to identify LV hypertrophy and geometrical remodelling and therefore have arrived at very different prevalences of abnormal geometry.35
Concentricity, associated with low weight,36
i.e. increased relative wall thickness, is older age37
and black ethnicity,25,38
independent of body composition. However, it remains controversial whether higher relative wall thickness is a genetic variation or a reflection of the composite influence of greater pressure than volume–load and a response to offset increased wall stress.34
The EUROPEAN CARDIOLOGY
LV mass (g) (second evaluation)
Page 1 |
Page 2 |
Page 3 |
Page 4 |
Page 5 |
Page 6 |
Page 7 |
Page 8 |
Page 9 |
Page 10 |
Page 11 |
Page 12 |
Page 13 |
Page 14 |
Page 15 |
Page 16 |
Page 17 |
Page 18 |
Page 19 |
Page 20 |
Page 21 |
Page 22 |
Page 23 |
Page 24 |
Page 25 |
Page 26 |
Page 27 |
Page 28 |
Page 29 |
Page 30 |
Page 31 |
Page 32 |
Page 33 |
Page 34 |
Page 35 |
Page 36 |
Page 37 |
Page 38 |
Page 39 |
Page 40 |
Page 41 |
Page 42 |
Page 43 |
Page 44 |
Page 45 |
Page 46 |
Page 47 |
Page 48 |
Page 49 |
Page 50 |
Page 51 |
Page 52 |
Page 53 |
Page 54 |
Page 55 |
Page 56 |
Page 57 |
Page 58 |
Page 59 |
Page 60 |
Page 61 |
Page 62 |
Page 63 |
Page 64 |
Page 65 |
Page 66 |
Page 67 |
Page 68 |
Page 69 |
Page 70 |
Page 71 |
Page 72 |
Page 73 |
Page 74 |
Page 75 |
Page 76 |
Page 77 |
Page 78 |
Page 79 |
Page 80 |
Page 81 |
Page 82 |
Page 83 |
Page 84 |
Page 85 |
Page 86 |
Page 87 |
Page 88 |
Page 89 |
Page 90 |
Page 91 |
Page 92 |
Page 93 |
Page 94 |
Page 95 |
Page 96 |
Page 97 |
Page 98 |
Page 99 |
Page 100