Left Ventricular Wall Volume Research Articles

Sex Differences in Left Ventricular Wall Stress in Apparently Healthy Adults with Similar Cuff-Measured Blood Pressure.

Outcome-based evidence shows that women have a higher risk of heart failure than men at a similar level of blood pressure. Left ventricular wall stress (Ó) or afterload is an important determinant of myocardial performance. Thus, it might play a key role in determining the sex differences in heart failure.The Ó at the beginning of aortic valve opening (Ó-AVO), the systolic peak value of the Ó (Ó-peak), and the Ó at the end systole (Ó-ES) were determined using transthoracic echocardiography combined with cuff-measured brachial blood pressure in 990 age- and heart rate- and cuff-measured blood pressure-matched apparently healthy adults (495 men). The sex differences in the aortic pressure, the ratio of left ventricular wall volume to cavity volume (VW/VC), and Ó were analyzed.Compared with men, women demonstrated higher aortic systolic blood pressure (106.7 versus 101.7 mmHg), smaller VW/VC (1.12 versus 1.25 for the end-diastole VW/VC, 3.49 versus 3.82 for the end-systole VW/VC), and greater Ó (340.0 versus 315.6 for Ó-AVO, 471.9 versus 412.5 for Ó-peak, and 256.2 versus 230.3 kdynes/cm2 for Ó-ES) (all P < 0.001).At the same level of cuff-measured blood pressure, women have a greater Ó or afterload than men in consequence of the sex differences in left ventricular geometry and pulse pressure amplification. The evidence indicates that non-sex-specific categories of blood pressure factitiously impose a relatively higher afterload on the left ventricle in women and may therefore increase potential risk of heart failure in women.

Hypertension Programmed in Adult Hens by Isolated Effects of Developmental Hypoxia In Ovo.

In mammals, pregnancy complicated by chronic hypoxia can program hypertension in the adult offspring. However, mechanisms remain uncertain because the partial contributions of the challenge on the placenta, mother, and fetus are difficult to disentangle. Here, we used chronic hypoxia in the chicken embryo-an established model system that permits isolation of the direct effects of developmental hypoxia on the cardiovascular system of the offspring, independent of additional effects on the mother or the placenta. Fertilized chicken eggs were exposed to normoxia (N; 21% O2) or hypoxia (H; 13.5%-14% O2) from the start of incubation (day 0) until day 19 (hatching, ≈day 21). Following hatching, all birds were maintained under normoxic conditions until ≈6 months of adulthood. Hypoxic incubation increased hematocrit (+27%) in the chicken embryo and induced asymmetrical growth restriction (body weight, -8.6%; biparietal diameter/body weight ratio, +7.5%) in the hatchlings (all P<0.05). At adulthood (181±4 days), chickens from hypoxic incubations remained smaller (body weight, -7.5%) and showed reduced basal and stimulated in vivo NO bioavailability (pressor response to NG-nitro-L-arginine methyl ester, -43%; phenylephrine pressor response during NO blockade, -61%) with significant hypertension (mean arterial blood pressure, +18%), increased cardiac work (ejection fraction, +12%; fractional shortening, +25%; enhanced baroreflex gain, +456%), and left ventricular wall thickening (left ventricular wall volume, +36%; all P<0.05). Therefore, we show that chronic hypoxia can act directly on a developing embryo to program hypertension, cardiovascular dysfunction, and cardiac wall remodeling in adulthood in the absence of any maternal or placental effects.

Excessive volume of hydrogel injectates may compromise the efficacy for the treatment of acute myocardial infarction.

Biomaterial injectates are promising as a therapy for myocardial infarction to inhibit the adverse ventricular remodeling. The current study explored interrelated effects of injectate volume and infarct size on treatment efficacy. A finite element model of a rat heart was utilized to represent ischemic infarcts of 10%, 20%, and 38% of left ventricular wall volume and polyethylene glycol hydrogel injectates of 25%, 50%, and 75% of the infarct volume. Ejection fraction was 49.7% in the healthy left ventricle and 44.9%, 46.4%, 47.4%, and 47.3% in the untreated 10% infarct and treated with 25%, 50%, and 75% injectate, respectively. Maximum end-systolic infarct fiber stress was 41.6, 53.4, 44.7, 44.0, and 45.3 kPa in the healthy heart, the untreated 10% infarct, and when treated with the three injectate volumes, respectively. Treating the 10% and 38% infarcts with the 25% injectate volume reduced the maximum end-systolic fiber stress by 16.3% and 34.7% and the associated strain by 30.2% and 9.8%, respectively. The results indicate the existence of a threshold for injectate volume above which efficacy does not further increase but may decrease. The efficacy of an injectate in reducing infarct stress and strain changes with infarct size. Copyright © 2016 John Wiley & Sons, Ltd.

Moderate Mitral Regurgitation Accelerates Left Ventricular Remodeling After Posterolateral Myocardial Infarction

Chronic ischemic mitral regurgitation (MR) is associated with poor outcome. However, the effect of chronic ischemic MR on left ventricular (LV) remodeling after posterolateral myocardial infarction (MI) remains controversial. We tested the hypothesis that moderate MR accelerates LV remodeling after posterolateral MI. Posterolateral MI was created in 10 sheep. Cardiac magnetic resonance imaging was performed 2 weeks before and 2, 8, and 16 weeks after MI. Left ventricular and right ventricular volumes were measured, and regurgitant volume was calculated as the difference between LV and right ventricle stroke volumes. Multivariate mixed effects regression showed that LV volumes at end diastole and end systole and LV sphericity were strongly correlated with both regurgitant volume (p < 0.0001, p = 0.0086, and p = 0.0007, respectively) and percent infarct area (p = 0.0156, p = 0.0307, and p < 0.0001, respectively). Conversely, whereas LV hypertrophy (LV wall volume) increased from 2 weeks to 16 weeks after MI, there was no effect of either regurgitant volume or percent infarct. Moderate MR accelerates LV remodeling after posterolateral MI. Further studies are needed to determine whether mitral valve repair is able to slow or reverse MI remodeling after posterolateral MI.

Respective impacts of aortic stenosis and systemic hypertension on left ventricular hypertrophy

It has been reported that 30–40% of patients with aortic stenosis are hypertensive. In such patients, the left ventricle faces a double (i.e. valvular and vascular) pressure overload, which results in subsequent wall volume hypertrophy. From a clinical standpoint, it is difficult to separate the respective contributions of aortic stenosis and systemic hypertension to left ventricular burden and patient's symptoms and thus to predict whether valve replacement would be beneficial. The objective of this theoretical study was therefore to investigate the relative effects of valvular and vascular afterloads on left ventricular hypertrophy. We used a ventricular–valvular–vascular mathematical model in combination with the Arts’ model describing the myofiber stress. Left ventricular wall volume was computed for different aortic blood pressure levels and different degrees of aortic stenosis severity. Our simulations show that the presence of concomitant systemic hypertension has a major influence on the development of left ventricular hypertrophy in patients with aortic stenosis. These results also suggest that mild-to-moderate aortic stenosis has a minor impact on left ventricular wall volume when compared with hypertension. On the other hand, when aortic stenosis is severe, wall volume increases exponentially with increasing aortic stenosis severity and the impact of aortic stenosis on left ventricular hypertrophy becomes highly significant.

Interdependence between measures of extent and severity of myocardial perfusion defects provided by automatic quantification programs

To evaluate the accuracy of the values of lesion extent and severity provided by the two automatic quantification programs AutoQUANT and 4D-MSPECT using myocardial perfusion images generated by Monte Carlo simulation of a digital phantom. The combination between a realistic computer phantom and an accurate scintillation camera simulation tool allows the generation of realistic single-photon emission computed tomography (SPECT) images similar to those obtained in clinical patient studies. The NCAT phantom and the SIMIND Monte Carlo program were used to simulate myocardial perfusion studies. Perfusion defects with sizes ranging from 5 to 17% of the left ventricular wall volume and reductions in tracer uptake of 20, 60 and 100% were simulated in three vascular territories. The values of the extent provided by the programs were dependent on the reduction in tracer uptake, i.e. the severity. Similarly, the measures of severity were dependent on the size of the lesions. The severity provided by AutoQUANT for different defects was not dependent on the location, whereas 4D-MSPECT presented different values depending on the location in the left ventricle. The measures of extent and severity of the defects with the same true extent and activity uptake reduction provided by the two programs were different. The NCAT phantom and the SIMIND Monte Carlo program were shown to be useful in simulating clinical myocardial SPECT studies. The quantification programs gave values of lesion extent that were dependent on the magnitude of the severity. Users should therefore consider this dependence when interpreting results from these programs.

Functional assessment of myoblast transplantation for cardiac repair with magnetic resonance imaging

Contraction of transplanted myoblasts and their effects on function and remodeling after myocardial infarction remain controversial. We used magnetic resonance imaging (MRI) to study wall thickening and left ventricular (LV) function and geometry after myoblast transplantation. Three weeks after cryo-infarction rabbits were randomized to receive an injection of approximately 2 x 10(8) myoblasts (n=8) or medium (n=9) into the scar. Cine MRI and contrast enhanced (ce) MRI images were acquired before injection (baseline) and 4 weeks later (endpoint). Regional wall thickening was measured at the site of transmural hyperenhancement. In the control group, regional wall thickening decreased to -15.3+/-8.6% at baseline, which further decreased to -18.3+/-5.7% at endpoint. Further, end-diastolic volume increased from 3.96+/-0.27 to 5.00+/-0.46 ml and end-systolic volume from 2.23+/-0.19 to 2.96+/-0.30 ml (both P<0.05 vs. baseline), which was accompanied by increased LV wall volumes (P<0.05 vs. baseline). In contrast, myoblast transplantation increased regional wall thickening from -11.9+/-15.9% at baseline to 26.9+/-17.0% (P<0.05 vs. control), which resulted in significantly improved two-dimensional ejection fractions at the infarct level and prevented the increase in end-diastolic and end-systolic volumes and wall volume. Intracardiac myoblast transplantation after myocardial infarction improves regional wall thickening and prevents progressive left ventricular remodeling.

Evaluation of left ventricular volumes and ejection fraction by automated gated myocardial SPECT versus cardiovascular magnetic resonance

Electrocardiogram-gated myocardial single-photon emission computed tomography (SPECT) with (99m)Tc-tetrofosmin allows simultaneous evaluation of myocardial perfusion and function. In this study, left ventricular volumes, ejection fraction (LVEF), and left ventricular wall volume (LVWV) derived from gated SPECT were compared with measurements from cardiovascular magnetic resonance (CMR), performed within a few hours. The study population included 55 patients with known or suspected coronary artery disease, including 13 patients with recent acute myocardial infarction. End-diastolic (EDV) and end-systolic (ESV) volumes, LVEF and LVWV were derived automatically from gated SPECT using commercially available software (QGS). In the CMR studies, manually delineated endocardial and epicardial borders on short-axis slices were used to calculate the volumes. Gated SPECT underestimated EDV by 35 +/- 14 ml (mean +/- SD) (P < 0.001), ESV by 10 +/- 13 ml (P < 0.001), and LVEF by 4 +/- 7 percentage points (P < 0.001). There were no systematic difference in EDV, ESV or LVEF between the methods. SPECT underestimated LVWV by 49 +/- 30 ml (P < 0.001), with a trend towards increasing underestimation by SPECT for larger wall volumes. These findings show that gated SPECT slightly underestimates EDV, ESV and LVEF compared with CMR. This underestimation is systematic, however, indicating that ventricular volumes derived from gated SPECT are robust enough to guide clinical management. Estimates of LVWV in patients with large wall volumes are less accurate.

Lazaroid (U74389G)-supplemented cardioplegia: results of a double-blind, randomized, controlled trial in a porcine model of orthotopic heart transplantation

Background: U74389G (16-desmethyl tirilazad), a 21-aminosteroid or “lazaroid,” inhibits lipid peroxidation, which is an important element of ischemia–reperfusion injury. The aim of this study was to determine whether the addition of U74389G to the cardioplegic preservation solution could improve early cardiac allograft function. Methods: A porcine model of donor brain death and orthotopic cardiac transplantation was used. Hearts were arrested and preserved for 6 hours in an aspartate-enriched extracellular cardioplegia that had been supplemented with either U74389G and its carrier ( n = 7) or the carrier alone ( n = 9). Epicardial sonomicrometry and transmyocardial micromanometry were used to obtain pressure–volume loops before and after transplantation. Left ventricular wall volume was measured by volume displacement. Results: A higher proportion of U74389G-treated hearts were weaned successfully from cardiopulmonary bypass, but this difference did not achieve statistical significance (86% [6 of 7] vs 56% [5 of 9]; p = 0.308). In the hearts that were weaned successfully, preservation of left ventricular contractility, as judged by the pre-load recruitable stroke work relationship, was significantly better in the U74389G-treated hearts ( p = 0.0271). In contrast, left ventricular compliance, as judged by the end-diastolic pressure–volume relationship, was significantly better preserved in the control group ( p < 0.0001). U74389G-treated hearts developed less myocardial edema, as judged by the post-transplant left ventricular wall volume/baseline steady-state epicardial end-diastolic volume ratio (64 ± 9% vs 76 ± 11%; p = 0.045). Conclusions: The benefit obtained from U74389G-supplemented cardioplegic preservation solution was marginal for hearts stored for 6 hours. After longer ischemic times, the benefit may be clearer.

Left ventricular adaptation to aortic regurgitation in conscious dogs

Objective: Cardiac failure as a result of valvular heart disease remains a major clinical problem that frequently leads to ventricular dysfunction, myocardial failure, and even death. The development of irreversible myocardial damage may be especially insidious in volume overload as a result of aortic or mitral regurgitation. Methods and results: Left ventricular wall volume, ventricular function, and myocardial performance were assessed in 10 chronically instrumented conscious dogs before and after creation of aortic regurgitation. Left ventricular wall volume was measured by serial echocardiography. Left ventricular function was assessed by total cardiac output, stroke work, the slope of the Frank-Starling relationship, and the slope of the end-systolic pressure-volume relationship. Myocardial performance was assessed by the slope of the myocardial power output versus end-diastolic strain relationship. End-diastolic wall stress and volume both increased acutely and remained elevated after creation of aortic regurgitation. Peak systolic wall stress increased initially (1 to 3 weeks) from 336 ± 30 to 369 ± 55 mm Hg but returned to control values as left ventricular wall volume increased from 78 ± 13 to 88 ± 16 ml after development of compensatory hypertrophy. Left ventricular systolic function remained constant or increased and was maintained initially by increased myocardial performance, which returned to baseline levels after the development of compensatory hypertrophy. Conclusions: Myocardial performance and ventricular function vary independently in aortic regurgitation. Measures of myocardial performance such as the myocardial power output versus end-diastolic strain relationship may be useful in clinical assessment of aortic regurgitation. (J Thorac Cardiovasc Surg 1997;113:149-58)

Quantitative relationships between left ventricular ejection and wall thickening and geometry

The quantitative relationships that exist between left ventricular (LV) wall shortening, wall thickening, and geometry during LV ejection are not well defined. We used a mathematical model to measure these parameters in 40 patients with various LV geometries studied by echocardiography. As opposed to wall shortening, the percent contribution of wall thickening to LV ejection (% delta Vh) was 25 +/- 2% in normal subjects; in all the patients, it varied from 18 to 45% and was inversely correlated (r = 0.94) to the midwall radius-to-wall thickness ratio (R/h) of the ventricle at end diastole. On the other hand, the ratio of the quantity of blood ejected per unit of LV wall volume magnitude of delta V/V omega magnitude of varied from 0.20 to 1.20 (normal subjects 0.83 +/- 0.11) and was directly correlated (r = 0.94) to R/h; using independent data in the literature, we also found a similar relationship (r = 0.80) between the ratio of quantity of blood ejected per unit of LV mass (magnitude of delta V/M omega magnitude of) and R/h. Patients with presumably abnormal myocardial function did not satisfy the relationship between magnitude of delta V/V omega magnitude of or magnitude of delta V/M omega magnitude of and R/h.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of coronary venous pressure on left ventricular diastolic distensibility.

Coronary arterial pressure and flow are known to influence left ventricular (LV) diastolic distensibility, but the influence of coronary venous pressure is unknown. To test the hypothesis that increased coronary venous pressure leads to an increase in LV wall volume and a decrease in LV diastolic distensibility, we studied excised, blood-perfused LV isovolumic dog hearts without the pericardium. In protocol I (n = 8), to raise coronary venous pressure the pressure of right atrium (RA) and right ventricle (RV) was increased by the height of a blood reservoir connected with a cannula that opened in both the RA and RV. In protocol II (n = 7), to isolate the effect of RV enlargement on LV diastolic distensibility (direct ventricular interaction), an isovolumic RV balloon was used with coronary venous pressure held constant at 0 mm Hg. Changes in LV diastolic distensibility were assessed by shifts of the LV end-diastolic pressure-volume relation. Changes in LV wall volume were detected by subepicardial segment length at end-diastole. The mean pressures of RA and RV (protocol I) and RV balloon only (protocol II) were increased from 0 to 15 and 30 mm Hg over a range of LV volume. In protocol I, when RA.RV pressure was increased from 0 to 30 mm Hg at three levels of LV volume (22 +/- 2, 31 +/- 3, and 40 +/- 3 ml), LV end-diastolic pressures increased significantly from 5.2 +/- 0.3 to 11.2 +/- 1.5, from 10.4 +/- 0.3 to 18.2 +/- 1.2, and from 20.2 +/- 1.0 to 28.8 +/- 1.2 mm Hg, respectively. In protocol II, when RV balloon pressure was increased from 0 to 30 mm Hg at the three LV volumes (21 +/- 3, 31 +/- 3, and 41 +/- 4 ml), LV end-diastolic pressures showed smaller increases from 5.2 +/- 0.2 to 6.6 +/- 0.2, from 9.8 +/- 0.3 to 11.6 +/- 0.6, and from 19.0 +/- 0.5 to 21.4 +/- 0.8 mm Hg, respectively. In both protocols, the LV end-diastolic pressure-volume relation shifted upward in a nearly parallel fashion, but the shift was much greater in protocol I than in protocol II. Despite constant LV volume, an increase in LV wall dimension in protocol I was significant and much greater than that in protocol II. From these results, we conclude that increased coronary venous pressure decreases LV diastolic distensibility with increasing LV wall volume, and this mechanism appears to act independently of diastolic ventricular interaction caused by RV enlargement.

Effects of standard mitral valve replacement on left ventricular function

Recent studies have suggested that excision of the mitral valve apparatus during mitral valve replacement impairs left ventricular performance. However, functional measurements in humans have been difficult to obtain in a load-independent fashion. To investigate this concept, 12 patients (mean age, 65 ± 8 years; mean New York Heart Association functional class, 3.3 ± 0.7) with 4+ mitral regurgitation (n = 8) or mitral stenosis (valve area, 1.2 ± 0.2 cm 2) (n = 4) underwent prosthetic valve replacement using crystalloid cardioplegia. No patient required therapeutic inotropic support, every patient had at least the anterior mitral leaflet excised, and paced heart rate was maintained constant throughout. Left ventricular volume was measured with radionuclide angiocardiography, left ventricular pressure with a 3F micromanometer, and left ventricular wall volume with two-dimensional transesophageal echocardiography. Left ventricular preload was varied over a mean enddiastolic pressure range of 9 to 20 mm Hg and an end-diastolic volume range of 134 to 170 mL to generate four to five steady-state pressure-volume loops before and ten minutes after cardiopulmonary bypass. Left ventricular performance was estimated with the stroke work/end-diastolic volume relationship, which is insensitive to load. After bypass, no significant change ( p > 0.1) was noted in wall volume for patients with mitral regurgitation or mitral stenosis (175 ± 68 to 189 ± 63 mL/m 2 and 130 ± 22 to 127 ± 19 mL/m 2, respectively). The stroke work/end-diastolic volume relationships were highly linear before and after bypass with a mean linear regression coefficient of 0.96 ± 0.03, and the slope and x-intercept were not changed after bypass ( p > 0.1). These data suggest that partial excision of the mitral apparatus does not significantly impair left ventricular performance during the early period after routine valve replacement.

In vivo estimation of left ventricular wall volume in volume-overloaded canine hearts.

Several geometric algorithms have been applied to estimate left ventricular wall volume (Vwall) from two-dimensional echocardiograms but have not been validated in eccentrically hypertrophied hearts. These algorithms can be fitted to the general formula: Vwall = k.Ao.Lo = k.Ai.Li, where Ao and Ai are the outer (epicardial) and inner (endocardial) short-axis areas, Lo and Li are the corresponding long-axis lengths, and k is a constant. The simplifying assumption that Lo and Li are equal yields Vwall = k.Awall.Lo, where Awall = Ao - Ai. In 20 unsedated dogs (10-30 kg), including 10 with aortic regurgitation of 1-18 wk duration, the relationship between actual Vwall (determined postmortem) and Awall.Lo was not significantly different from the line of identity (Vwall = 1.01 Awall.Lo + 0.5 ml, r = 0.98, SEE = 3.5 ml), indicating k was not significantly different from 1. There was no significant difference between predicted and actual Vwall over a range of 31-105 ml, and interobserver variability was 4.1%. The simple area-length product, Awall.Lo, accurately predicts Vwall of both normal and volume-overloaded hypertrophied canine left ventricles and is thus suitable for serial observations of hypertrophic adaptation to volume overload.

Estimation of human myocardial mass with MR imaging.

The accuracy and reproducibility of magnetic resonance (MR) imaging in the determination of left ventricular mass in humans was investigated. Left ventricular wall volume was measured from ten short-axis, end-diastolic MR images that spanned the left ventricle. Mass was estimated on the basis of average left ventricular wall volume and an assumed myocardial density. To establish the accuracy of the technique, the authors imaged ten cadaver hearts and compared true left ventricular weight with the mass estimate based on MR imaging findings. In vivo determination of left ventricular mass was evaluated in 40 subjects, with resultant calculated masses of 156.4-319.3 g. Intra- and interobserver variabilities of the technique were analyzed in ten subjects. Both the intra- (r = .96, standard error of estimate [SEE] = 11.1 g) and interobserver variabilities (r = .91, SEE = 17.8 g) were excellent. Eight subjects were imaged on two separate occasions to evaluate reproducibility of the technique and confidence limits for a given measurement. For these eight, there was good correlation between the two estimates (r = .93, SEE = 21 g). The authors conclude that MR imaging yields highly accurate and reproducible estimates of left ventricular mass in humans in vivo.

Test of reliability of echocardiographic estimation of left ventricular dimensions and volumes.

This test is based on the incompressibility of myocardium, which dictates that left ventricular wall volume remains constant throughout the cardiac cycle. The volumes occupied by the left ventricular cavity, by ventricular wall plus cavity, and hence by ventricular wall alone were estimated, both at end-systole and at end-diastole, from ecocardiographic measurements of cavity transverse dimension and wall thickness. Wall volumes were determined by assuming an ellipsoid shape (the major axis being predicted from aggression equations relating angiocardiographic and echocardiographic cavity dimensions) and also by the cube method. A discrepancy between systolic and diastolic wall volume estimates indicates either that the measurements of ventricular dimensions were unreliable or that the assumptions of ventricular geometry involved in the volume calculations were incorrect. Studies were made on 60 subjects. Using the ellipsoid formula, values for wall volume ranged from 66 to 719 ml; systolic and diastolic wall volumes correlated closely (r = 0-96, mean difference = 6-8 +/- 0-9 (SEM) %) supporting the reliability of the echocardiographic dimensions and estimates of cavity and wall volume. In the 12 patients with very large end-diastolic cavity transverse dimensions (6-5 to 8-6 cm) however, correlation was less good (r - 0-81, mean difference = 14-3 +/- 2-3 (SEM) 5). Using the cube method, which does not allow for the changing relation between minor and major cavity axes with increasing cavity size, wall volumes were greater (76 to 986 ml) but correlation was similar (r = 0-94, mean difference = 7-1 +/- 0-9 (SEM)%). Having established that it is possible to obtain close agreement between wall volumes determined at different points in the cardiac cycle, this test can be used to assess the reliability of echocardiographic left ventricular dimensions and volume estimates in individual subjects.