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Objectives: This study sought to determine whether specific patterns of adverse left ventricular (LV) structural remodeling are associated with differential rates of cardiovascular (CV) outcomes., Background: It is not known whether a stepwise combinatorial assessment of LV volume, mass, and geometry done to define specific remodeling patterns provides incremental prognostic information., Methods: A total of 3,181 Cardiovascular Health Study participants (mean age, 73 years of age; 60% women, 5% African American) were categorized by LV remodeling patterns and related to a multivariate-adjusted (age, sex, race, ejection fraction, hypertension, myocardial infarction, diabetes mellitus, chronic kidney disease) analysis of CV outcomes (incident heart failure [HF], all-cause mortality, and a combined endpoint of HF and mortality) over a 13-year follow-up period., Results: Examined independently, either left ventricular enlargement (LVE) or left ventricular hypertrophy (LVH) was associated with a higher risk of HF (32%, 34%, respectively) than with normal geometry (17%; p < 0.001). When LV volume and mass were used in combination, important incremental prognostic information was achieved. In the absence of LVE, HF was more common in those with LVH than in those with normal mass (32% vs. 16%, respectively; p < 0.001). In the presence of LVE, HF was more common in those with LVH than in those with normal mass (37% vs. 29%, respectively; p = 0.021). The subgroup with normal volume and mass but relative wall thickness (RWT) >0.42 carried a higher risk of HF (21%) than those with normal geometry (15%; p = 0.011). Once LVH or LVE was present, the addition of RWT to this analysis did not affect HF rate. Similar results were obtained for the other CV outcomes., Conclusions: Stepwise combinatorial assessment of LV volume, mass, and geometry provides incremental prognostic information regarding CV outcomes., (Copyright © 2014 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Current noninvasive techniques used to evaluate left ventricular systolic function are limited by dependence on the angle of insonation (tissue Doppler imaging/TDI) or limited by availability (MRI tagging). We utilized 2-dimensional speckle strain (epsilon) imaging (1) to establish normal values for all three epsilon vectors; (2) to compare circumferential epsilon values with circumferential shortening (midwall fractional shortening (FS(mw)); (3) to examine the relationship between left ventricular epsilon and wall stress; and (4) to compare 2D echocardiographic characteristics by gender. Echocardiography was performed in 60 normal subjects (mean 39 +/- 15 years). Small, but significant regional heterogeneity was seen in circumferential epsilon, but not in radial or longitudinal epsilon. We found an inverse correlation between circumferential epsilon and stress (r =-0.29, p<0.05) as well as longitudinal epsilon and stress (r =-0.11, P < 0.05), though the relationships were not close. We also observed a linear relationship between mean circumferential epsilon and FS(mw) (r = 0.29, P < 0.05). In conclusion, (1) 2-dimensional epsilon imaging permits measurement of regional systolic epsilon values in the majority of normal individuals; (2) epsilon values furnished by this method obey expected stress-shortening relationships; (3) systolic epsilon displays minor regional heterogeneity in the circumferential direction; (4) for the first time, a close relationship between FS(mw) and mean circumferential epsilon was demonstrated; and (5) there are minor gender-related differences in LV geometry and function.

In aortic stenosis, gender and other differences in the adaptive remodeling of the left ventricle have been described, but the influence of left ventricular (LV) geometry on systolic function is not widely appreciated. This study tested the hypothesis that the increased ejection fraction seen in some elderly women with aortic stenosis is due to changes in LV geometry, not increased myocardial mass or enhanced myocardial function. We therefore investigated gender-related differences in LV and myocardial function by analysis of end-systolic circumferential stress versus shortening relations in 65 patients (29 men and 36 women) with aortic stenosis who underwent cardiac catheterization and echocardiography. Despite similar degrees of aortic stenosis, there were significant differences between men and women with regard to LV geometry and function. When compared with men, women had higher peak LV pressures (205 +/- 27 vs 188 +/- 27 mm Hg, p < 0.01), higher ejection fractions (66 +/- 14% vs 57 +/- 18%, p < 0.05), smaller LV end-diastolic dimensions (43 +/- 8 vs 51 +/- 6 mm, p < 0.01) and higher relative wall thickness (0.66 +/- 0.27 vs 0.50 +/- 0.10, p < 0.01). LV mass was similar in the 2 groups. Mean values for stress were lower in women and there was a predominance of women at extremely low levels of stress; this subgroup had very high values for relative wall thickness and endocardial shortening, but overall stress-shortening relations were normal.(ABSTRACT TRUNCATED AT 250 WORDS)

The time course of left ventricular (LV) circumferential stress and fiber shortening velocity (Vcf) were determined at 20 msec intervals in 30 patients from simultaneous recordings of LV pressure (micromanometer) and LV dimensions (echography). In 12 patients with normal LV function, endocardial and midwall maximal (max) Vcf, Vcf at peak stress, and endocardial mean Vcf were significantly greater than in eight patients with myocardial disease. Peak stress was less in the normal subjects (mean equal 241 gl/cm2, range 180 to 310 g/cm2) than in those with myocardial diseases (mean equals 371 g/cm2, range 280 to 513 g/cm2). Vcf was reduced in five out of seven patients with chronic LV volume overload, while peak stress ranged from normal in three to increased in four. Max Vcf, mean Vcf, and peak stress were normal in three patients with chronic LV pressure overload; Vcf at peak stress was normal in two. Good correlation was observed between angiographic determinations of mean Vcf and endocardial max Vcf, Vcf at peak stress and mean Vcf. Induced changes in preload in five patients (dextran infusion at constant heart rate) produced a 12.2 per cent increase in peak stress (P small than 0.05), and insignificant changes in max Vcf (3.7 per cent increase, P = NS), in Vcf at peak stress (5 per cent decrease, P smaller than 0.05), in mean Vcf (0.7 per cent increase, P = NS). Increasing afterload with angiotensin in seven patients (peak stress increased by 45 per cent, P smaller than 0.01) reduced max Vcf, Vcf at peak stress and mean Vcf by 33 per cent, 39 per cent respectively. Lowering afterload in one patient (amyl nitrite) produced an increase in Vcf. Improvement in Vcf was observed in all instances during positive inotropic stimulation (isoproterenol in three normals, digoxin in four with myocardial disease). Thre response of endocardial and midwall Vcf to loading and contractility were similar. In man Vcf is an index of myocardial contractility which is affected minimally by changes in preload but responds inversely to changes in afterload. Its sensitivity to acute afterload changes may, at times, limit its clinical applicability.

Left ventricular relative wall thickness, expressed as the ratio of end-diastolic radius to wall thickness (R/Th ratio), has a constant relation with left ventricular systolic pressure in children and adults with a normal heart, subjects with physiologic forms of cardiac hypertrophy (athletes) and patients with compensated chronic left ventricular volume overload (chronic aortic regurgitation). Greatly increased values for the radius/thickness ratio, suggesting inadequate hypertrophy, indicate a poor prognosis in patients with chronic aortic regurgitation and in those with congestive cardiomyopathy; decreased values for this ratio are found in patients with hypertrophic cardiomyopathy (inappropriate hypertrophy) and in patients with compensated aortic stenosis (appropriate hypertrophy). In patients with compensated aortic stenosis, echocardiographic measurement of the left ventricular end-diastolic radius/wall thickness ratio has been used to estimate left ventricular systolic pressure. Measurement of left ventricular relative wall thickness appears to provide diagnostic and prognostic data in patients with a broad variety of cardiac disorders.

Left ventricular (LV) diastolic pressure (P), volume (V), and rate of change of volume (dV/dt) were determined at 16.7 msec intervals in 17 patients (simultaneous micromanometer and single plane volume angiography). Four patients had mitral stenosis with atrial fibrillation and 13 patients (three normal, two congestive cardiomyophathy, three LV hypertrophy, and five coronary artery disease) were in normal sinus rhythm. Maximum early diastolic filling rates (max dV/dt) in the normal and cardiomyopathy patients were similar and ranged from 269 to 370 cc/m-2/sec; in coronary artery disease and LV hypertrophy, max dV/dt ranged from 197 to 290 cc/m-2/sec and 213 to 255 cc/m-2/sec respectively; in mitral stenosis, max dV/dt ranged from 215 to 270 cc/m-2 sec. The peak filling rate during atrial systole ranged form 60 to 240 cc/m-2/sec in the 13 patients with sinus rhythm. The instantaneous diastolic P-V data were fit by an exponential equation (P = be-kV) and the P-V relation throughout diastole was represented by the best fit line. The rate constant (k) in the equation was highest in the patient with IHSS and lowest in those with large dilated hearts. In mitral stenosis with atrial fibrillation the fit of the equation to the P-V data appeared better than in the patients with normal sinus rhythm. Peak ventricular filling rate during atrial systole varied directly with LV volume distensibility at the onset of atrial systole (r = 0.64). Data suggest that dynamic mechanical properties of the LV influence the diastolic P-V relations and that pressure "deviations" (deltaP) from the best fit line during atrial systole may be related to viscous drag. In a given ventricle the velocity dependence of deltaP appears to be modified by the volume distensibility of the ventricle. Variable rates of filling may preclude the assumption of an exponential relation between P and V throughout diastole and therefore may limit estimates of diastolic distensibility or compliance which rely on such an assumption.

Left ventricular diastolic compliance is determined by the level of operating pressure and the diastolic pressure-volume relation. This relation is curvillinear and the slope of a tangent (operative chamber stiffness) to the pressure-volume curve increases as the chamber progressively fills. Such preload-dependent changes in compliance occur during any acute alteration in ventricular volume. At a given diastolic pressure, operative chamber stiffness (or its reciprocal, operative chamber compliance) is determined by the relative values for ventricular volume and muscle mass and by the stiffness of a unit of myocardium. Thus, there may be a leftward shift of the diastolic pressure-volume curve (increase in the modulus of chamber stiffness) as a consequence of ventricular hypertrophy or an increase in the stiffness of heart muscle itself (increase in modulus of muscle stiffness). To distinguish between hypertrophy and stiff muscle, it is useful to examine the modulus of chamber stiffness, derived from pressure-volume data, together with the volume/mass ratio of the ventricle. In this fashion, changes in the modulus of chamber stiffness that are inappropriate for a given volume/mass ratio may be attributed to changes in the material properties of the heart muscle. Examples of clinical and experimental pressure-volume studies are presented to illustrate the variety of mechanisms by which acute and chronic changes in ventricular chamber compliance evolve during the course of clinical heart disease. The pathophysiology of pulmonary congestion is best understood by considering the factors responsible for producing changes in chamber stiffness of the ventricle, whereas an examination of muscle stiffness is likely to provide more insight into the extent of irreversible functional and structural defects of the myocardium.

This report presents a method for determining the time course of circumferential LV wall stress and fiber shortening velocity (endocardial as well as midwall) using simultaneous recordings of LV dimensions by echography and LV pressure (micromanometer). The values for max VCF, VCF at peak stress, mean VCF, and peak stress are in general agreement with those observed with previous methods; the separation between normal and abnormal LV function appears to be good. The method permits frequent observations to be performed in a single patient, which is of particular value during acute interventions. Data from a small number of interventions suggest that VCF in man is relatively insensitive to acute changes in preload, is inversely affected by changes in afterload and appears sensitive to inotropic stimulation. Although VCF seems to be a good index of LV performance, its sensitivity to afterload might, at times, limit its usefulness.

Observations that the inner (subendocardial) half of the left ventricular wall contributes more to total left ventricular wall thickening than the outer (subepicardial) half may have important implications in the analysis of myocardial fiber length transients. Accordingly, we measured endocardial and midwall shortening and lengthening rates in normal and hypertrophic heart and compared the results obtained with conventional methods of measurement with those obtained with a modified model that does not depend on use of conventional assumptions about the midwall. This modified (two-shell) cylindrical model) method considers the substantial contribution of inner wall thickening and thus does not require the assumption of a theoretical midwall fiber that remains at the midwall throughout the cardiac cycle. Echocardiographic data from six normal subjects and six patients with concentric left ventricular hypertrophy (LVH) were examined; left ventricular wall thickness ranged from 8 to 10 mm in normal subjects and from 11 to 16 mm in the patients with LVH. By design, the standard measurements of left ventricular size (diastolic and systolic dimensions) and systolic function (fractional shortening and endocardial fiber shortening velocities) were equal in the two groups. Endocardial, conventional midwall, and modified midwall methods all indicate reduced fiber lengthening rates in patients with LVH; peak fiber lengthening rates for normal and LVH groups were 4.5 +/- 0.7 vs 3.1 +/- 0.8 sec-1 (p less than .02) at the endocardium, 2.3 +/- 0.4 vs 1.6 +/- 0.4 sec-1 (p less than .02) at the midwall (conventional method), and 2.1 +/- 0.3 vs 1.4 +/- 0.3 sec-1 (p less than .01) at the midwall (modified method).(ABSTRACT TRUNCATED AT 250 WORDS)

Two coordinates of left ventricular end-diastolic pressure (P) and volume (V) were provided by the infusion of angiotensin in 22 patients. The slope (k) of the ln P-V relation, coupled with knowledge of the operating (end-diastolic) pressure allows determination of end-diastolic volume compliance (dV/VdP). Estimates of end-diastolic compliance from a single coordinate of pressure and volume compared well (r equals 0.90) with the two coordinate method, whereas for specific compliance (deltaV/V1 deltaP) appeared to be misleading in cases of idiopathic hypertrophic subaortic stenosis and congestive cardiomyopathy. Since volume compliance is determined in part by the operating pressure, compliance may be reduced in small, normal or enlarged ventricles. Left ventricular linear compliance was derived from volume compliance and was normalized for left ventricular wall thickness. The product of linear compliance and end-diastolic stress provides an index of myocardial strain, termed "muscle fiber stretch," which may be related to systolic performance and thus allow comparison of length-performance relations in ventricles with normal and abnormal compliance.