Relationship Between On-Treatment Decreases in Inappropriate Versus Absolute or Indexed Left Ventricular Mass and Increases in Ejection Fraction in Hypertension

Abstract

Abstract-Although) LVMI decreased with treatment, treatment failed to increase EF in either group (1.2Ϯ10.8% and 2.7Ϯ10.7%, respectively). In contrast, in patients with inappropriate LV hypertrophy (LVM inappr Ͼ150%; nϭ33) LVM inappr decreased (Ϫ32Ϯ27%; PϽ0.0001) and EF increased (5.0Ϯ10.3%; PϽ0.05) after treatment, whereas in patients with an LVM inappr Յ150% (nϭ135), neither LVM inappr (Ϫ0.5Ϯ23%) nor EF (0.9Ϯ10.3%) changed with therapy. With adjustments for circumferential LV wall stress and other confounders, whereas on-treatment decreases in LVM or LVMI were weakly related to an attenuated EF (partial rϭ0.17; PϽ0.05), on-treatment decreases in LVM inappr were strongly related to increases in EF even after further adjustments for LVM or LVMI (partial rϭϪ0.63 [CI, Ϫ0.71 to Ϫ0.52]; PϽ0.0001). In conclusion, decreases in LVM inappr are strongly related to on-treatment increases in EF beyond changes in LVM and LVMI. LV hypertrophy can, therefore, be viewed as a compensatory change that preserves EF, but when in excess of that predicted by stroke work, it can be viewed as a pathophysiological process accounting for a reduced EF. 1-7 and the development of a reduced ejection fraction (EF) 8 independent of myocardial infarction. LV mass (LVM) may, therefore, determine the progression to heart failure with a reduced rather than a preserved EF. 9,10 However, in keeping with the classic tenet that LVH is a compensatory response to LV load, an increased LVM 11-13 or on-treatment decreases in LVM 14 have been associated with an unchanged EF. Moreover, LVH may even be associated with an enhanced EF for that predicted by wall stress, 15 and on-treatment decreases in LVM have been related to reductions rather than increases in indices of systolic LV chamber function. 16 There is, therefore, considerable uncertainty as to whether LVH contributes to decreases in systolic chamber function.One possibility that may explain discrepancies in the ability to show consistent relations between LVM or LVM index (LVMI) and a reduced systolic LV chamber function [11][12][13][14][15][16] is that absolute LVM and LVMI may incorporate a component of LVH considered compensatory in nature, whereas there may also be a component of LVH that contributes to decompensation. In this regard, LVM in excess of that predicted by workload (ie, stroke workϭblood pressure [BP]ϫstroke volume), termed "inappropriate LVM" (LVM inappr ), 17 is inversely associated with systolic LV chamber function.18-25 However, these relationships have largely been demonstrated in cross-sectional studies [18][19][20][21][22][23][24] and are at odds with on-treatment decreases in systolic LV chamber function associated with LVH regression. 16 Inverse LVM inappr ϪLV systolic chamber function relations 18-24 may, therefore, reflect compensatory increases in LVM as a consequence of systolic dysfunction or associated confounding effects. Although one previous study has reported that on-treatment regression but not persistence of LVM inappr is associated with an improved EF, 25 wh...

Independent associations between resistin and left ventricular mass and myocardial dysfunction in a community sample with prevalent obesity

“…Echocardiography was performed as previously described [20][21][22]. All measurements were recorded and analyzed off-line by experienced investigators whom were unaware of the clinical data of the participants.…”

“…Left ventricular hypertrophy was defined as an LVMI ≥ 60 g/m 1.7 in women and LVMI ≥ 80 g/m 1.7 in men [24]. Stroke volume was evaluated from the difference between LV end diastolic and systolic volumes determined using the Z-derived method [22]. Circumferential LV systolic wall stress was calculated as previously described [22].…”

“…Stroke volume was evaluated from the difference between LV end diastolic and systolic volumes determined using the Z-derived method [22]. Circumferential LV systolic wall stress was calculated as previously described [22]. The extent of LVM inappr was determined from predicted LVM [22], where predicted LVM was calculated as 55.37 + (6.64 × height 2.7 ) + (0.64 × [systolic BP × stroke volume × 0.014]) − (18.07 × gender), where male gender = 1 and female gender = 2, and where stroke volume was calculated from LV volumes assessed from the Z-derived method.…”

“…Circumferential LV systolic wall stress was calculated as previously described [22]. The extent of LVM inappr was determined from predicted LVM [22], where predicted LVM was calculated as 55.37 + (6.64 × height 2.7 ) + (0.64 × [systolic BP × stroke volume × 0.014]) − (18.07 × gender), where male gender = 1 and female gender = 2, and where stroke volume was calculated from LV volumes assessed from the Z-derived method. Inappropriate LVM was expressed either as actual-predicted LVM in grams, or % actual LVM/ predicted LVM.…”

“…Left ventricular ejection fraction (EF) (biplane Simpson) was calculated to determine LV chamber systolic function using a standard formula [22]. Endocardial (FSend) (LV systolic chamber function) and midwall (FSmid) (LV systolic myocardial function) fractional shortening was similarly determined as previously described [22].…”