Left Ventricular Systolic Stiffness Research Articles

Age related structural and functional changes in left ventricular performance in healthy subjects: a 2D echocardiographic study

Left ventricular (LV) adaptation to aging is currently poorly understood. We aimed to characterize age related changes in LV structure and function by studying a large group of healthy subjects across a wide age range. Prospectively enrolled healthy volunteers (n = 778, 327 females; age 18 to 100years, mean age 49.8 ± 18.1years), were divided into 4 age groups: 18 to 34years (n = 165); 35 to 49years (n = 242), 50 to 79years (n = 334) and ≥ 80years (n = 40). All subjects underwent clinical examination, as well as comprehensive transthoracic echocardiogram [TTE]. Body mass index, systolic blood pressure (BP), and left atrial volume (p < 0.0001) increased with age while diastolic BP (p < 0.0001) decreased over time. LV mass/body surface area (BSA) and relative wall thickness increased with age (p < 0.0001) coincident with worsening parameters of diastolic function (E/A and E/Em, p < 0.0001). The ejection fraction and Sm did not change significantly. Stroke volume, ejection time index, flow rate and stroke work significantly increased with age (p < 0.01). The arterial elastance (Ea), a measure of ventricular afterload, and ventricular elastance (Ees), an index of LV systolic stiffness did not change with age nor did their ratio (Ees/Ea) the latter being an expression of ventricular-arterial coupling. Age, gender and LVM were the main independent variables associated with LV systolic function. In conclusion, LV adaptation to aging in a healthy cohort is characterized by concentric LV remodeling, increased contractility and preserved ventricular-arterial coupling.

Impact of Hypertension on Ventricular-Arterial Coupling and Regional Myocardial Work at Rest and during Isometric Exercise

To understand better the mechanism of left ventricular (LV) remodeling related to hypertension, it is important to evaluate LV function in relation to the changes in loading conditions. The aim of this study was to investigate changes in conventional ventricular-arterial coupling indexes, LV strain, and a new index reflecting regional myocardial work assessed noninvasively at rest and during isometric exercise in a random sample including participants with normal blood pressure and those with hypertension. A total of 148 participants (53.4% women; mean age, 52.0 years; 39.2% with hypertension) underwent simultaneous echocardiographic and arterial data acquisition at rest and during increased afterload (handgrip exercise). End-systolic pressure was determined from the carotid pulse wave. Arterial elastance (Ea) and LV elastance (Ees) were calculated as end-systolic pressure/stroke volume and end-systolic pressure/end-systolic volume. Doppler tissue imaging and two-dimensional speckle tracking were used to derive LV longitudinal strain. Regional myocardial work (ejection work density [EWD]) was the area of the pressure-strain loop during ejection. At rest, with adjustments applied, Ees (3.06 vs 3.71 mm Hg/mL, P = .0003), Ea/Ees (0.54 vs 0.47, P = .002) and EWD (670 vs 802 Pa/m(2), P = .0001) differed significantly between participants with normal blood pressure and those with hypertension. During handgrip exercise, Ea and Ea/Ees significantly increased (P < .0001) in both groups. Doppler tissue imaging and two-dimensional LV strain decreased in participants with hypertension (P ≤ .008). Only in subjects with normal blood pressure EWD significantly increased (+14.7%, P = .0009). Although patients with hypertension compared with those with normal blood pressure have increased LV systolic stiffness and regional myocardial work to match arterial load at rest, they might have diminished cardiac reserve to increase myocardial performance, as estimated by EWD during isometric exercise.

Resting global and regional left ventricular contractility in patients with heart failure and normal ejection fraction: insights from speckle-tracking echocardiography

ObejctiveTo compare left ventricular (LV) systolic performance and contractility in patients with heart failure and normal ejection fraction (HFNEF), compared with patients with heart failure and reduced ejection fraction (HFREF)...

Contractility and Ventricular Systolic Stiffening in Hypertensive Heart Disease: Insights Into the Pathogenesis of Heart Failure With Preserved Ejection Fraction

We sought to compare left ventricular (LV) systolic stiffness and contractility in normal subjects, hypertensive patients without heart failure, and patients with heart failure and preserved ejection fraction (HFpEF) and to determine whether LV systolic stiffness or myocardial contractility is associated with the rate of mortality in patients with HFpEF. Arterial load is increased in patients with hypertension and is matched by increased end-systolic LV stiffness (ventricular-arterial coupling). Increased end-systolic LV stiffness may be mediated by enhanced myocardial contractility or processes that increase passive myocardial stiffness. Healthy control patients (n = 617), hypertensive patients (no heart failure, n = 719), and patients with HFpEF (n = 244, 96% hypertensive) underwent echo-Doppler characterization of arterial (Ea) and LV end-systolic (Ees) stiffness (elastance), ventricular-arterial coupling (Ea/Ees ratio), and chamber-level and myocardial contractility (stress-corrected midwall shortening). We found that Ea and Ees were similarly increased in hypertensive patients with or without HFpEF compared with control patients, but ventricular-arterial coupling was similar across groups. In hypertensive patients, increased Ees was associated with enhanced chamber-level and myocardial contractility, whereas in patients with HFpEF, chamber and myocardial contractility were depressed compared with both hypertensive and control patients. Group differences persisted after adjusting for geometry. In patients with HFpEF, impaired myocardial contractility (but not Ees) was associated with increased age-adjusted mortality. Although arterial load is increased and matched by increased LV systolic stiffness in hypertensive patients with or without HFpEF, the mechanisms of systolic LV stiffening differ substantially. These data suggest that myocardial contractility increases to match arterial load in asymptomatic hypertensive heart disease, but that progression to HFpEF may be mediated by processes that simultaneously impair myocardial contractility and increase passive myocardial stiffness.

Effect of age on vascular function, LV structure and systolic and diastolic ventricular function in the adult population

Background: Aging may be associated with decreases in aortic compliance and/or increased arterial resistance, both factors which contribute to increased arterial stiffness (arterial elastance, Ea). Arterial stiffening may increase cardiac systolic load, result in left ventricular (LV) hypertrophy and alter LV systolic and diastolic function. Hypothesis: Aging is associated with increases in arterial stiffness, LV hypertrophy, increased LV systolic stiffness and diastolic dysfunction in the population independent of sex, body size (body surface area, BSA) or the presence of cardiovascular disease. Methods: Medical record review and Doppler echocardiography were performed in a cross sectional sample of Olmsted County, MN residents (age ≥ 45). Ea (end systolic pressure/stroke volume), LV mass, a load independent index of systolic function (end systolic stress-shortening relationship, σes-FS) and a pre-load independent index of diastolic relaxation (tissue Doppler early diastolic annular velocity, E') were measured. A positive (up/rightward) shift in the σes-FS relationship is indicative of increased LV systolic stiffness and may reflect enhanced contractility and/or LV structural changes (hypertrophy or fibrosis). Multivariate analysis defined the relative effect of Age controlling for sex and BSA on these parameters in the population (n = 2042) and in the subset free from known cardiovascular disease or diabetes (No CV dis) (n = 1047). Results: See Table. Controlling for sex and BSA, Ea and LV mass increased while E' decreased with increasing Age, both in the entire population and in those with No CV dis. The σes-FS relationship was shifted up/rightward with increasing Age, both in the entire population and more dramatically so in those with No CV dis. Conclusions: Aging is associated with arterial stiffening, LV hypertrophy, increased LV systolic stiffness and diastolic dysfunction. These effects are independent of the presence of known cardiovascular disease and may explain, in part, increasing cardiovascular events with advanced age. Tabled 1 SC - Population P - Population SC - No CV dis P - No CV dis Ea 0.115 <0.0001 0.135 <0.0001 LV mass 0.117 <0.0001 0.142 <0.0001 σes-FS relationship 0.116 0.007 0.324 0.0003 E' −0.409 <0.0001 −0.286 <0.0001 SC - standardized coefficient reflects relative effect of age in multivariate analysis controlling for sex and body size Open table in a new tab SC - standardized coefficient reflects relative effect of age in multivariate analysis controlling for sex and body size

Left ventricular active stiffness: dependency on time and inotropic state.

Left ventricular systolic stiffness was measured by rapidly changing ventricular volume (within 7 ms) of isovolumically contracting isolated rabbit hearts. Instantaneous pressure-volume relations were found to be linear with slopes that depended upon the moment during contraction at which the volume change was induced. These slopes were proportional to the total pressure developed in the ventricle just prior to the volume change. The same was found when the time course of pressure was influenced by changing the Ca++ content of the perfusate. An influence, however, also could be detected when end-diastolic volume was changed. At the same pre-release pressure a greater volume caused a decrease of active stiffness. The results indicate the possibility of an active component in ventricular systolic stiffness.