Long-term left ventricular echocardiographic follow-up of SHR and WKY rats: effects of hypertension and age

Long-term follow-up of left ventricular (LV) function using echocardiography has not been reported and, in this study, was carried out in normotensive (WKY) rats and spontaneously hypertensive rats (SHR). In 10 WKY rats and SHR, LV diastolic and systolic diameter (LVEDD and LVSD), shortening fraction (SF), and weight (LVW) were determined at 8, 15, 20, 35, and 80 wk of age. The ratio of early to late mitral flow and mitral annulus velocity (VE/VA and Em/Am), isovolumic relaxation time (IVRT), deceleration time of the E wave (DTE), Tei index, and mitral flow propagation velocity (Vp) were measured. No difference in LVEDD was found between SHR and WKY rats; however, LVEDD was increased at 80 wk in both strains. SF decreased slightly in old WKY rats. LVW progressively increased from 20 to 80 wk in both strains and was greater in SHR. VE/VA and Em/Am decreased at 80 wk in WKY rats. LV relaxation (IVRT, Tei index, and Vp) was progressively impaired in SHR compared with WKY rats. LV compliance (DTE) was altered in old SHR. Echocardiography permitted a long follow-up of LV function in SHR and WKY rats. Ventricular relaxation was impaired early in the life of SHR and progressed with aging. Furthermore, LV compliance was altered, but systolic function remained unchanged, in old SHR. In contrast, relaxation and SF were only slightly altered in old WKY rats, suggesting that pressure-related changes in LV function were the dominant features in the SHR.     

Abnormal cardiac inflow patterns during postnatal development in a mouse model of Holt-Oram syndrome

Tbx5(del/+) mice provide a model of human Holt-Oram syndrome. In this study, the cardiac functional phenotypes of this mouse model were investigated with 30-MHz ultrasound by comparing 12 Tbx5(del/+) mice with 12 wild-type littermates at 1, 2, 4, and 8 wk of age. Cardiac dimensions were measured with two-dimensional and M-mode imaging. The flow patterns in the left and right ventricular inflow channels were evaluated with Doppler flow sampling. Compared with wild-type littermates, Tbx5(del/+) mice showed significant changes in the mitral flow pattern, including decreased peak velocity of the left ventricular (LV) early filling wave (E wave), increased peak velocity of the late filling wave (A wave), and decreased or even reversed peak E-to-A ratio. The prolongation of LV isovolumic relaxation time was detected in Tbx5(del/+) neonates as early as 1 wk of age. In Tbx5(del/+) mice, LV wall thickness appeared normal but LV chamber dimension was significantly reduced. LV systolic function did not differ from that in wild-type littermates. In contrast, the Doppler flow spectrum in the enlarged tricuspid orifice of Tbx5(del/+) mice demonstrated increased peak velocities of both E and A waves and increased total time-velocity integral but unchanged peak E/A. In another 13 mice (7 Tbx5(del/+), 6 wild-type) at 2 wk of age, significant correlation was found between Tbx5 gene expression level in ventricular myocardium and LV filling parameters. In conclusion, the LV diastolic function of Tbx5(del/+) mice is significantly deteriorated, whereas the systolic function remains normal.     

Heterogeneity of the myocardium. Function of the left and right ventricle under normal and pathological conditions

A number of important differences can be found between the left ventricle (LV) and right ventricle (RV) of the heart under physiological conditions. In anatomy, the most important is probably the architecture of the atrioventricular valve and its annulus. The LV has a mitral valve (with two cusps) and a firm annulus, while the RV has a tricuspid valve with a greater total area, but relatively small cuspid areas, and an elastic annulus. The difference in the blood supply is important. Owing to high intramural pressure, the coronary flow in the wall of the LV occurs only during the diastole; in the RV it is limited only in the presence of a significant increase in intracavitary pressure. The LV myocardium is functionally "accustomed" to short-term marked changes in the systolic load (in extreme static exercise the arterial pressure rises for a short time to three times the normal value), while the RV is adapted to changes in the diastolic load (marked filling changes associated with deep breathing, for instance). The difference in the response to a long-term volume load is difficult to evaluate: between a defect of the interatrial septum and aortic insufficiency there are too many differences. A long-term pressure load seems to be tolerated better by the right ventricle: patients with severe pulmonary stenosis and a pressure six times higher than the physiological value have lived 25 years and patients with isolated corrected L-transposition of the great arteries can reach 35 years without any signs of impaired RV function.(ABSTRACT TRUNCATED AT 250 WORDS)     

Echocardiographic assessment of age-associated changes in systolic and diastolic function of the female F344 rat heart.

Aging is associated with hypertrophy, dilatation, and fibrosis of the left ventricle (LV) of the heart. Advances in echocardiographic assessment have made it possible to follow changes in cardiac function in a serial, noninvasive manner. The purpose was to determine whether there is echocardiographic evidence of age-associated changes in chamber dimensions and systolic and diastolic properties of the female Fischer 344 (F344) rat heart. On the basis of previous invasive studies, it was predicted that echocardiographic assessment would detect age-associated changes in indexes of systolic and diastolic function. Rats were sedated with 1.5% isoflurane and placed in the supine position. Two-dimensional images and two-dimensionally guided M-mode, Doppler M mode, Doppler tissue, and pulsed-wave Doppler recordings were obtained from the parasternal long axis, parasternal short axis, and/or apical four-chamber views as per convention by using a 15-MHz linear array or 8-MHz phased-array transducer or a GE S10-MHz phased-array transducer. Compared with young adult 4-mo-old rats, there is a significant decrement in the resting systolic function of the LV in 30-mo-old female F344 rats as evidenced by declines in LV ejection fraction (80 +/- 9 vs. 89 +/- 5%; mean +/- SD), fractional shortening (43 +/- 9 vs. 54 +/- 8%) and velocity of circumferential fiber shortening (2.43 +/- 0.53 vs. 2.99 +/- 0.50 circ/s). Evidence for age-associated differences in diastolic function included an increase in isovolumic relaxation time (25.0 +/- 7.6 vs. 17.2 +/- 4.4 ms) and decreases in the tissue Doppler peak E waves at the septal annulus and at the lateral annulus of the mitral valve. The modest changes in systolic and diastolic LV function that occur with advancing age in the female F344 rat are likely to reduce the capacity of the heart to respond to hemodynamic challenges.     

胸内正压对正常人左室功能影响及其力学原理

目的：探讨胸内正压对正常人左室射血及充盈的影响及其力学原理。方法：超声心动图观测30例正常人初始时与标准乏氏动作张力期10s时左室舒张末容积（LVEDV）、左室收缩末容积（LVESV）、每搏量（SV）、射血分值（EF）、流入道血流速度（E峰、A峰）、E／A值、二尖瓣环舒张早期运动速度（e）及舒张早期充盈压（E/e）的变化。结果：与初始时比较,标准乏氏动作张力期LVEDV、LVESV及SV减低而心率（陬）增快（P均〈0．001）,EF值增加,但无统计学意义（P〉0．05）;E峰与E／A值减低（P均〈O．05）;e没有变化（P〉0．05）．E／e值减低（P〈O．05）。结论：胸内正压对左室游离壁的力学作用促进了左室收缩运动而阻碍了左室舒张运动,会引起EF值增加,E峰及E／A值减低;2,胸内正压降低了肺静脉系统与心脏的跨壁压力,增加了血流阻力也是导致肺静脉系统与左室血液回流减少．E峰减低．E／e值减低的一个原因。     

Validation of echocardiographic and Doppler indexes of left ventricular relaxation in adult hypertensive and normotensive rats

This study was performed to validate echocardiographic and Doppler techniques for the assessment of left ventricular (LV) diastolic function in spontaneously hypertensive rats (SHR) and normotensive Wistar rats. In 11 Wistar rats and 20 SHR, we compared 51 sets of invasive and Doppler LV diastolic indexes. Noninvasive indexes of LV relaxation were related to the minimal rate of pressure decline (-dP/dt(min)), particularly isovolumic relaxation time (IVRT), the Tei index, the early velocity of the mitral annulus (E(m)) using Doppler tissue imaging, and early mitral flow propagation velocity using M-mode color (r = 0.28-0.56 and P < 0.05-0.0001). When the role of systolic load was considered, the correlation between Doppler indexes of LV diastolic function and relaxation rate [(-dP/dt(min))/LV systolic pressure] improved (r = 0.48-0.86 and P = 0.004-0.0001, respectively). Similarly, Doppler indexes of LV diastolic function and the time constant of isovolumic LV relaxation (tau) correlated well (r = 0.50-0.84 and P = 0.0002-0.0001, respectively). In addition, eight SHR and eight Wistar rats were compared; their LV end-diastolic diameters were similar, whereas the SHR LV mass was greater. Furthermore, IVRT and Tei index were significantly higher and E(m) was lower in SHR. Moreover, tau was higher in SHR, demonstrating impaired LV relaxation. In conclusion, LV relaxation can be assessed reliably using echocardiographic and Doppler techniques, and, using these indexes, impaired relaxation was demonstrated in SHR.     

Right Ventricular Systolic Dysfunction Is Common in Hypertensive Heart Failure: A Prospective Study in Sub-Saharan Africa

IntroductionRight ventricular (RV) systolic dysfunction is now recognized widely as a strong and independent predictor of adverse outcomes in patients with heart failure (HF). Reduction of RV systolic function more closely predicts impaired exercise tolerance and poor survival than does left ventricular (LV) systolic function. In spite of this, there is a dearth of data on RV function in hypertensive HF which is the commonest form of HF in sub-Saharan Africa. We therefore conducted a prospective cohort study of hypertensive HF patients presenting to the University of Abuja Teaching Hospital, Abuja, Nigeria over an 8 year period.MethodsEach subject had transthoracic echocardiography performed on them according to the guidelines of American Society of Echocardiography. RV systolic function was defined as a tricuspid annular plane systolic excursion (TAPSE) <15mm using M-mode echocardiography.ResultsRV systolic dysfunction was identified in 272 (44.5%) of the 611 subjects that were studied. Subjects with TAPSE less than 15mm had worse prognosis compared to those with TAPSE ≥15mm.There was a significant correlation between TAPSE and other adverse prognostic markers including left and right atrial area, LV size, LV mass, LV ejection fraction, restrictive mitral inflow and RV systolic pressure (RVSP). However, LV ejection fraction and right atrial area were the only independent determinants of RV systolic dysfunction.ConclusionsHypertensive HF is a major cause of RV systolic dysfunction even in a population with a low prevalence of coronary artery disease, and RV systolic dysfunction is associated with poor prognosis in hypertensive HF. Detailed assessment of RV function should therefore be part of the echocardiography evaluation of patients with hypertensive HF.     

Modeling left ventricular diastolic dysfunction: classification and key indicators

Background

Mathematical modeling can be employed to overcome the practical difficulty of isolating the mechanisms responsible for clinical heart failure in the setting of normal left ventricular ejection fraction (HFNEF). In a human cardiovascular respiratory system (H-CRS) model we introduce three cases of left ventricular diastolic dysfunction (LVDD): (1) impaired left ventricular active relaxation (IR-type); (2) increased passive stiffness (restrictive or R-type); and (3) the combination of both (pseudo-normal or PN-type), to produce HFNEF. The effects of increasing systolic contractility are also considered. Model results showing ensuing heart failure and mechanisms involved are reported.

Methods

We employ our previously described H-CRS model with modified pulmonary compliances to better mimic normal pulmonary blood distribution. IR-type is modeled by changing the activation function of the left ventricle (LV), and R-type by increasing diastolic stiffness of the LV wall and septum. A 5^th-order Cash-Karp Runge-Kutta numerical integration method solves the model differential equations.

Results

IR-type and R-type decrease LV stroke volume, cardiac output, ejection fraction (EF), and mean systemic arterial pressure. Heart rate, pulmonary pressures, pulmonary volumes, and pulmonary and systemic arterial-venous O₂ and CO₂ differences increase. IR-type decreases, but R-type increases the mitral E/A ratio. PN-type produces the well-described, pseudo-normal mitral inflow pattern. All three types of LVDD reduce right ventricular (RV) and LV EF, but the latter remains normal or near normal. Simulations show reduced EF is partly restored by an accompanying increase in systolic stiffness, a compensatory mechanism that may lead clinicians to miss the presence of HF if they only consider LVEF and other indices of LV function. Simulations using the H-CRS model indicate that changes in RV function might well be diagnostic. This study also highlights the importance of septal mechanics in LVDD.

Conclusion

The model demonstrates that abnormal LV diastolic performance alone can result in decreased LV and RV systolic performance, not previously appreciated, and contribute to the clinical syndrome of HF. Furthermore, alterations of RV diastolic performance are present and may be a hallmark of LV diastolic parameter changes that can be used for better clinical recognition of LV diastolic heart disease.     

Doppler echocardiographic estimation of left ventricular end-diastolic pressure after MI in rats

The spectral Doppler mitral flow pattern, alone or combined with tissue Doppler mitral annulus velocity, can be used to predict left ventricular (LV) filling pressure in humans, whereas invasive hemodynamic measurements are still required in the rat. This study was undertaken to assess whether LV end-diastolic pressure (LVEDP) can be estimated using Doppler echocardiography in the rat after myocardial infarction (MI). Thirty-seven rats (23 rats with MI after left coronary artery ligation and 14 sham-operated rats) were evaluated 3 mo after surgery with echo-Doppler and invasive hemodynamic measurements. Pulse wave spectral Doppler at the mitral valve tip was used to measure the E wave, the E wave deceleration time (DT), and the A wave; spectral Doppler tissue imaging was used to measure the early diastolic lateral mitral annulus velocity (E(a)). We found weak correlations between LVEDP and the peak velocity of the early mitral inflow (E), E/peak velocity of the late mitral inflow, and DT, and strong correlations with E(a) and especially with E/E(a) [R(2) = 0.89, LVEDP (in mmHg) = 0.987E/E(a) - 4.229]. Longitudinal followup of a subgroup of rats with MI revealed a marked rise of E/E(a) between days 7 and 21 in rats with heart failure only. We conclude that Doppler echocardiography can be used for serial assessment of LV diastolic function in rats with MI.     

Combined pulmonary stenosis and insufficiency preserves myocardial contractility in the developing heart of growing swine at midterm follow-up.

This study was conducted to determine the effects of chronic combined pulmonary stenosis and pulmonary insufficiency (PSPI) on right (RV) and left ventricular (LV) function in young, growing swine. Six pigs with combined PSPI were studied, and data were compared with previously published data of animals with isolated pulmonary insufficiency and controls. Indexes of systolic function (stroke volume, ejection fraction, and cardiac functional reserve), myocardial contractility (slope of the end-systolic pressure-volume and change in pressure over time-end-diastolic volume relationship), and diastolic compliance were assessed within 2 days of intervention and 3 mo later. Magnetic resonance imaging was used to quantify pulmonary insufficiency and ventricular volumes. The conductance catheter was used to obtain indexes of the cardiac functional reserve, diastolic compliance, and myocardial contractility from pressure-volume relations acquired at rest and under dobutamine infusion. In the PSPI group, the pulmonary regurgitant fraction was 34.3 +/- 5.8%, the pressure gradient across the site of pulmonary stenosis was 20.9 +/- 20 mmHg, and the average RV peak systolic pressure was 70% systemic at 12 wk follow-up. Biventricular resting cardiac outputs and cardiac functional reserves were significantly limited (P < 0.05), LV diastolic compliance significantly decreased (P < 0.05), but RV myocardial contractility significantly enhanced (P < 0.05) compared with control animals at 3-mo follow-up. In the young, developing heart, chronic combined PSPI impairs biventricular systolic pump function and diastolic compliance but preserves RV myocardial contractility.     

Alveolar hypoxia induces left ventricular diastolic dysfunction and reduces phosphorylation of phospholamban in mice

Chronic obstructive pulmonary disease (COPD) may lead to pulmonary hypertension (PH) and reduced function of the right ventricle (RV). However, COPD patients may also develop left ventricular (LV) diastolic dysfunction. We hypothesized that alveolar hypoxia induces LV diastolic dysfunction and changes in proteins governing Ca(2+) removal from cytosol during diastole. Mice exposed to 10% oxygen for 1, 2, or 4 wk were compared with controls. Cardiac hemodynamics were assessed with Doppler echocardiography and a microtransducer catheter under general anesthesia. The pulmonary artery blood flow acceleration time was shorter and RV pressure was higher after 4 wk of hypoxia compared with controls (both P < 0.05). In the RV and LV, 4 wk of hypoxia induced a prolongation of the time constant of isovolumic pressure decay (51% RV, 43% LV) and a reduction in the maximum rate of decline in pressure compared with control (42% RV, 42% LV, all P < 0.05), indicating impaired relaxation and diastolic dysfunction. Alveolar hypoxia induced a 38%, 47%, and 27% reduction in Ser16-phosphorylated phospholamban (PLB) in the RV after 1, 2, and 4 wk of hypoxia, respectively, and at the same time points, Ser16-phosphorylated PLB in the LV was downregulated by 32%, 34%, and 25% (all P < 0.05). The amounts of PLB and sarco(endo)plasmic reticulum Ca(2+) ATPase (SERCA2a) were not changed. In conclusion, chronic alveolar hypoxia induces hypophosphorylation of PLB at Ser16, which might be a mechanism for impaired relaxation and diastolic dysfunction in both the RV and LV.     

Absence of diastolic mitral annular oscillations is a marker for relaxation-related diastolic dysfunction

Although Doppler tissue imaging frequently indicates the presence of mitral annular oscillations (MAO) following the E' wave (E' wave, etc.), only recently was it shown that annular "ringing" follows the rules of damped harmonic oscillatory motion. Oscillatory model-based analysis of E' and E' waves provides longitudinal left ventricular (LV) stiffness (k'), relaxation/viscoelasticity (c'), and stored elastic strain (x(o)') parameters. We tested the hypothesis that presence (MAO(+)) vs. absence (MAO(-)) of diastolic MAO is an index of superior LV relaxation by analyzing simultaneous echocardiographic-hemodynamic data from 35 MAO(+) and 20 MAO(-) normal ejection fraction (EF) subjects undergoing cardiac catheterization. Echocardiographic annular motion and transmitral flow data were analyzed with a previously validated kinematic model of filling. Invasive and noninvasive diastolic function (DF) indexes differentiated between MAO(+) and MAO(-) groups. Specifically, the MAO(+) group had a shorter time constant of isovolumic relaxation [tau; 51 (SD 13) vs. 67 (SD 27) ms; P<0.01] and isovolumic relaxation time [63 (SD 16) vs. 82 (SD 17) ms; P<0.001] and greater ratio of peak E-wave to peak A-wave velocity [1.19 (SD 0.31) vs. 0.97 (SD 0.31); P<0.05]. The MAO(+) group had greater peak lateral mitral annulus velocity [E'; 17.5 (SD 3.1) vs. 13.5 (SD 3.8) cm/s; P<0.001] and LVEF [71.2 (SD 7.5)% vs. 65.4 (SD 9.1)%; P<0.05] and lower heart rate [65 (SD 9) vs. 74 (SD 9) beats/min, P<0.001]. Additional conventional and kinematic modeling-derived indexes were highly concordant with these findings. We conclude that absence of early diastolic MAO is an easily discernible marker for relaxation-related diastolic dysfunction. Quantitation of MAO via stiffness and relaxation/viscoelasticity parameters facilitates quantitative assessment of regional (i.e., longitudinal) DF and may improve diagnosis of diastolic dysfunction.     

组织多普勒成像对射血分数正常的心衰患者左心功能评价

目的:探讨组织多普勒成像(TDI)技术评价射血分数正常的心衰患者左室长轴功能特点。方法:选取30名健康人(Ⅰ组)、EF>50%的心衰患者30名(Ⅱ组)和EF<50%的心衰患者30名(Ⅲ组)作为研究对象,采用TDI在二尖瓣环室间隔(ivs)、侧壁(l)、前壁(a)、后壁(p)、下壁(d)测量其Sm、DSm、IVCTm、TSm、Em、Am、IVRTm、TEm等指标。结果:Ⅰ组、Ⅱ组、Ⅲ组DSm、Sm逐渐减低,(P<0.05);而IVCTm、TSm逐渐升高(P<0.05);IVRTm、TEm在Ⅰ组、Ⅲ组、Ⅱ组逐渐升高(P<0.05);DSm及TEm在诊断EF>50%心衰患者心功能的指标中ROC曲线下面积最大,同样DSp及TEp在五个位点中ROC曲线下面积最大。结论:射血分数正常的心衰患者存在收缩减低;DSm及TEm是诊断EF>50%心衰患者心功能比较有效的指标;后壁是诊断的最佳位点。     

Left ventricular endocardial longitudinal and transverse changes during isovolumic contraction and relaxation: a challenge

Left ventricular (LV) longitudinal and transverse geometric changes during isovolumic contraction and relaxation are still controversial. This confusion is compounded by traditional definitions of these phases of the cardiac cycle. High-resolution sonomicrometry studies might clarify these issues. Crystals were implanted in six sheep at the LV apex, fibrous trigones, lateral and posterior mitral annulus, base of the aortic right coronary sinus, anterior and septal endocardial wall, papillary muscle tips, and edge of the anterior and posterior mitral leaflets. Changes in distances were time related to LV and aortic pressures and to mitral valve opening. At the beginning of isovolumic contraction, while the mitral valve was still open, the LV endocardial transverse diameter started to shorten while the endocardial longitudinal diameter increased. During isovolumic relaxation, while the mitral valve was closed, LV transverse diameter started to increase while the longitudinal diameter continued to decrease. These findings are inconsistent with the classic definitions of the phases of the cardiac cycle.     

The impact of endurance exercise training on left ventricular systolic mechanics

Although exercise training-induced changes in left ventricular (LV) structure are well characterized, adaptive functional changes are incompletely understood. Detailed echocardiographic assessment of LV systolic function was performed on 20 competitive rowers (10 males and 10 females) before and after endurance exercise training (EET; 90 days, 10.7 +/- 1.1 h/wk). Structural changes included LV dilation (end-diastolic volume = 128 +/- 25 vs. 144 +/- 28 ml, P < 0.001), right ventricular (RV) dilation (end-diastolic area = 2,850 +/- 550 vs. 3,260 +/- 530 mm2, P < 0.001), and LV hypertrophy (mass = 227 +/- 51 vs. 256 +/- 56 g, P < 0.001). Although LV ejection fraction was unchanged (62 +/- 3% vs. 60 +/- 3%, P = not significant), all direct measures of LV systolic function were altered. Peak systolic tissue velocities increased significantly (basal lateral S'Delta = 0.9 +/- 0.6 cm/s, P = 0.004; and basal septal S'Delta = 0.8 +/- 0.4 cm/s, P = 0.008). Radial strain increased similarly in all segments, whereas longitudinal strain increased with a base-to-apex gradient. In contrast, circumferential strain (CS) increased in the LV free wall but decreased in regions adjacent to the RV. Reductions in septal CS correlated strongly with changes in RV structure (DeltaRV end-diastolic area vs. DeltaLV septal CS; r2 = 0.898, P < 0.001) and function (Deltapeak RV systolic velocity vs. DeltaLV septal CS, r2 = 0.697, P < 0.001). EET leads to significant changes in LV systolic function with regional heterogeneity that may be secondary to concomitant RV adaptation. These changes are not detected by conventional measurements such as ejection fraction.     

Relationship between tissue Doppler-derived RV systolic function and invasive hemodynamic measurements

Tissue Doppler imaging (TDI) is effective in assessing right ventricular (RV) function, but the relationship between invasive measurements and RV-TDI remains unclear. We investigated the RV systolic function by using the TDI-derived systolic myocardial (Sa) velocity and myocardial performance index (MPI). Beagles (n = 7) were anesthetized in the right lateral recumbent position. A 3.5-Fr micromanometer-tipped catheter was placed in the RV to determine the hemodynamic changes. Dobutamine (5.0 and 10 microg.kg(-1).min(-1)) and esmolol (50 and 100 microg.kg(-1).min(-1)) were infused intravenously. Pulsed Doppler (PD) and TDI measurements were performed in the apical four-chamber view. Compared with baseline, the PD-MPI decreased significantly with the dobutamine infusion at 5 microg.kg(-1).min(-1) (P < 0.05). Both dobutamine infusions significantly decreased the TDI-MPI (P < 0.01, P < 0.05). Esmolol increased the PD- and TDI-MPI but not significantly. Dobutamine significantly increased the Sa velocity (both P < 0.001), whereas esmolol had no effect. The Sa velocity was strongly correlated with the peak positive derivative of the RV pressure (+dP/dt; r = 0.93). The negative correlation between the +dP/dt and TDI-MPI (r = -086) was greater that with the PD-MPI (r = -0.54). Stepwise regression analysis showed that the Sa velocity and PD-derived isovolumic contraction time were identified to predict the +dP/dt (r = 0.94, r(2) = 0.89; P < 0.001). We determined that the systolic myocardial velocity and TDI-MPI were strongly correlated with the RV contractility. These results suggest that the TDI-derived systolic myocardial velocity and MPI predict RV systolic function.     

MRI assessment of LV relaxation by untwisting rate: a new isovolumic phase measure of tau

Most noninvasive measures of diastolic function are made during left ventricular (LV) filling and are therefore subject to "pseudonormalization," because variation in left atrial (LA) pressure may confound the estimation of relaxation rate. Counterclockwise twist of the LV develops during ejection, but untwisting occurs rapidly during isovolumic relaxation, before mitral opening. We hypothesized that the rate of untwisting might reflect the process of relaxation independent of LA pressure. Recoil rate (RR), the velocity of LV untwisting, was measured by tagged magnetic resonance imaging and regressed against the relaxation time constant (tau), recorded by catheterization, in 10 dogs at baseline and after dobutamine, saline, esmolol, and methoxamine treatment. RR correlated closely (average r = -0.86) with tau and was unaffected by elevated LA pressure. Multiple regression showed that tau, but not LA or aortic pressure, was an independent predictor of RR (P < 0.0001, P = 0.99, and P = 0.18, respectively). The rate of recoil of torsion, determined wholly noninvasively, provides an isovolumic phase, preload-independent assessment of LV relaxation. Use of this novel parameter should allow the detailed study of diastolic function in states known to affect filling rates, such as aging, hypertension, and congestive heart failure.     

A diastolic dysfunction model in non-human primates with transverse aortic constriction

Transverse aortic constriction (TAC) has been widely used to study cardiac hypertrophy, fibrosis, diastolic dysfunction, and heart failure in rodents. Few studies have been reported in preclinical animal models. The similar physiology and anatomy between non-human primates (NHPs) and humans make NHPs valuable models for disease modeling and testing of drugs and devices. In the current study, we aimed to establish a TAC model in NHPs and characterize the structural and functional profiles of the heart after TAC. A non-absorbable suture was placed around the aorta between the brachiocephalic artery and left common carotid artery to create TAC. NHPs were divided into 2 groups according to pressure gradient (PG): the Mild Group (PG=31.01 ± 12.40 mmHg, n=3) and the Moderate Group (PG=53.00 ± 9.37 mmHg, n=4). At 4 weeks after TAC, animals in both TAC groups developed cardiac hypertrophy: enlarged myocytes and increased wall thickness of the left ventricular (LV) anterior wall. Although both TAC groups had normal systolic function that was similar to a Sham Group, the Moderate Group showed diastolic dysfunction that was associated with more severe cardiac fibrosis, as evidenced by a reduced A wave velocity, large E wave velocity/A wave velocity ratio, and short isovolumic relaxation time corrected by heart rate. Furthermore, no LV arrhythmia was observed in either animal group after TAC. A diastolic dysfunction model with cardiac hypertrophy and fibrosis was successfully developed in NHPs.     

Cardiac structural and functional responses to salt loading in SHR

Increased dietary salt intake induces cardiac fibrosis in the spontaneously hypertensive rat (SHR), yet little information details its effects on left ventricular (LV) function. Additionally, young normotensive rats are more sensitive to the trophic effect of dietary sodium than older rats. Thus cardiac responses to salt loading were evaluated at two ages in the SHR; LV collagen content was also examined. SHR (8 or 20 wk of age) were given an 8% salt diet; their age-matched controls received standard chow. Echocardiographic indexes, arterial pressure, and LV hydroxyproline concentration were measured at 16 and 52 wk in the younger and older SHR groups, respectively. In most SHR, salt excess increased arterial pressure, LV mass, and hydroxyproline concentration and impaired LV relaxation manifested by prolonged isovolumic relaxation time, decreased early and atrial filling velocity ratio (V(E)/V(A)), and slower propagation velocity of E wave (V(P)). LV systolic function remained normal. However, one-quarter of the young salt-loaded SHR developed cardiac failure with systolic and diastolic dysfunction associated with greater LV mass and ventricular fibrosis. They also had lower arterial pressure, decreased fractional shortening, and a restrictive pattern of mitral flow. Moreover, the shorter deceleration time of the E wave and increased V(E)/V(P), an index of LV filling pressure, indicated increased LV stiffness in these rats. These findings demonstrated that sodium sensitivity in SHR is manifested not only by further pressure elevation but also by significant LV functional impairment that most likely is related to enhanced ventricular fibrosis. Moreover, the SHR are more susceptible to cardiac damage when high dietary salt is introduced earlier in life.     

Assessment of Left and Right Ventricular Diastolic and Systolic Functions Using Two-Dimensional Speckle-Tracking Echocardiography in Patients with Coronary Slow-Flow Phenomenon

ObjectiveCoronary slow-flow phenomenon (CSFP) is an angiographic diagnosis characterised by a low rate of flow of contrast agent in the normal or near-normal epicardial coronary arteries. Many of the patients with CSFP may experience recurrent acute coronary syndromes. However, current clinical practice tends to underestimate the impact of CSFP due to the yet unknown effect on the cardiac function. This study was performed to evaluate left ventricular (LV) and right ventricular (RV) diastolic and systolic functions, using two-dimensional (2D) longitudinal strain and strain rate, in patients with CSFP, and to determine the relationships between the thrombolysis in myocardial infarction (TIMI) frame count (TFC) and LV and RV diastolic and systolic functions.MethodsSixty-three patients with CSFP and 45 age- and sex-matched controls without CSFP were enrolled in the study. Diagnosis of CSFP was made by TFC. LV and RV diastolic and systolic functions were assessed by 2D speckle-tracking echocardiography.ResultsLV peak early diastolic longitudinal strain rate (LSRe) was lower in patients with CSFP than in controls (P = 0.01). LV peak systolic longitudinal strain (LS) and LV peak systolic longitudinal strain rate (LSRs) were lower in patients with CSFP than in controls (P = 0.004 and P = 0.03, respectively). There was no difference in LV ejection fraction. RV peak early diastolic longitudinal strain rate (RSRe) was lower in patients with CSFP than in controls (P = 0.03). There were no differences in RV peak systolic longitudinal strain (RS), RV peak systolic longitudinal strain rate (RSRs), or RV fractional area change among the groups. The mean TFC correlated negatively with LSRe and RSRe in patients with CSFP (r = −0.26, P = 0.04 and r = −0.32, P = 0.01, respectively).ConclusionsLV diastolic and systolic functions were impaired in patients with CSFP. CSFP also affected RV diastolic function, but not RV systolic function.