Torsional motion of the left ventricle does not affect ventricular fluid dynamics of both foetal and adult hearts

Left ventricular torsion is caused by shortening and relaxation of the helical fibres in the myocardium, and is thought to be an optimal configuration for minimizing myocardial tissue strains. Characteristics of torsional motion has also been proposed to be markers for cardiac dysfunction. However, its effects on fluid and energy dynamics in the left ventricle have not been comprehensively investigated. To investigate this, we performed image-based flow simulations on five healthy adult porcine and two healthy human foetal left ventricles (representing two different length scales) at different degrees of torsional motions. In the adult porcine ventricles, cardiac features such as papillary muscles and mitral valves, and cardiac conditions such as myocardial infarctions, were also included to investigate the effect of twist. The results showed that, for all conditions investigated, ventricular torsional motion caused minimal changes to flow patterns, and consistently accounted for less than 2% of the energy losses, wall shear stresses, and ejection momentum energy. In contrast, physiological characteristics such as chamber size, stroke volume and heart rate had a much greater influence on flow patterns and energy dynamics. The results thus suggested that it might not be necessary to model the torsional motion to study the flow and energy dynamics in left ventricles.     

Quantification of left and right ventricular kinetic energy using four-dimensional intracardiac magnetic resonance imaging flow measurements

We aimed to quantify kinetic energy (KE) during the entire cardiac cycle of the left ventricle (LV) and right ventricle (RV) using four-dimensional phase-contrast magnetic resonance imaging (MRI). KE was quantified in healthy volunteers (n = 9) using an in-house developed software. Mean KE through the cardiac cycle of the LV and the RV were highly correlated (r(2) = 0.96). Mean KE was related to end-diastolic volume (r(2) = 0.66 for LV and r(2) = 0.74 for RV), end-systolic volume (r(2) = 0.59 and 0.68), and stroke volume (r(2) = 0.55 and 0.60), but not to ejection fraction (r(2) < 0.01, P = not significant for both). Three KE peaks were found in both ventricles, in systole, early diastole, and late diastole. In systole, peak KE in the LV was lower (4.9 ± 0.4 mJ, P = 0.004) compared with the RV (7.5 ± 0.8 mJ). In contrast, KE during early diastole was higher in the LV (6.0 ± 0.6 mJ, P = 0.004) compared with the RV (3.6 ± 0.4 mJ). The late diastolic peaks were smaller than the systolic and early diastolic peaks (1.3 ± 0.2 and 1.2 ± 0.2 mJ). Modeling estimated the proportion of KE to total external work, which comprised ～0.3% of LV external work and 3% of RV energy at rest and 3 vs. 24% during peak exercise. The higher early diastolic KE in the LV indicates that LV filling is more dependent on ventricular suction compared with the RV. RV early diastolic filling, on the other hand, may be caused to a higher degree of the return of the atrioventricular plane toward the base of the heart. The difference in ventricular geometry with a longer outflow tract in the RV compared with the LV explains the higher systolic KE in the RV.     

Three-dimensional diastolic blood flow in the left ventricle

Three-dimensional blood flow in a human left ventricle is studied via a computational analysis with magnetic resonance imaging of the cardiac motion. Formation, growth and decay of vortices during the myocardial dilation are analyzed with flow patterns on various diametric planes. They are dominated by momentum transfer during flow acceleration and deceleration through the mitral orifice. The posterior and anterior vortices form an asymmetric annular vortex at the mitral orifice, providing a smooth transition for the rapid inflow to the ventricle. The development of core vortex accommodates momentum for deceleration and for acceleration at end diastolic atrial contraction. The rate of energy dissipation and that of work done by viscous stresses are small; they are approximately balanced with each other. The kinetic energy flux and the rate of work done by pressure delivered to blood from ventricular dilation is well balanced by the total energy influx at the mitral orifice and the rate change of kinetic energy in the ventricle.     

Right and left ventricular adaptation to hypoxia: a tissue Doppler imaging study

Hypoxia has been reported to alter left ventricular (LV) diastolic function, but associated changes in right ventricular (RV) systolic and diastolic function remain incompletely documented. We used echocardiography and tissue Doppler imaging to investigate the effects on RV and LV function of 90 min of hypoxic breathing (fraction of inspired O(2) of 0.12) compared with those of dobutamine to reproduce the same heart rate effects without change in pulmonary vascular tone in 25 healthy volunteers. Hypoxia and dobutamine increased cardiac output and tricuspid regurgitation velocity. Hypoxia and dobutamine increased LV ejection fraction, isovolumic contraction wave velocity (ICV), acceleration (ICA), and systolic ejection wave velocity (S) at the mitral annulus, indicating increased LV systolic function. Dobutamine had similar effects on RV indexes of systolic function. Hypoxia did not change RV area shortening fraction, tricuspid annular plane systolic excursion, ICV, ICA, and S at the tricuspid annulus. Regional longitudinal wall motion analysis revealed that S, systolic strain, and strain rate were not affected by hypoxia and increased by dobutamine on the RV free wall and interventricular septum but increased by both dobutamine and hypoxia on the LV lateral wall. Hypoxia increased the isovolumic relaxation time related to RR interval (IRT/RR) at both annuli, delayed the onset of the E wave at the tricuspid annulus, and decreased the mitral and tricuspid inflow and annuli E/A ratio. We conclude that hypoxia in normal subjects is associated with altered diastolic function of both ventricles, improved LV systolic function, and preserved RV systolic function.     

Flow patterns in three-dimensional left ventricular systolic and diastolic flows determined from computational fluid dynamics

A realistic model of the left ventricle of the heart was previously constructed, using a cast from a dog heart which was in diastole. Previous studies of the three-dimensional heart model were conducted in systole only. The purpose of this investigation was to extend the model to both systole and diastole, and to determine what the effect of a previous cardiac cycle was on the next cardiac cycle. The 25.8 cc ventricular volume was reduced by 40% in 0.25 seconds, then increased to the original volume in another 0.25 seconds and then allowed to rest for 0.25 seconds. Runs done with an ejection fraction of 60% showed little variation from one cardiac cycle to another after the third cardiac cycle was completed; the maximum velocity could vary by over 30% between the first and second cardiac cycles. In systole, centerline and cross-sectional velocity vectors greatly increased in magnitude at the aortic outlet. Most of the pressure drop occurred in the top 15% of the heart. The diastolic phase showed complex vortex formation not seen in the systolic contractions; these complex vortices could account for experimentally observed turbulent blood flow fluctuations in the aorta.     

Fluid mechanics of blood flow in human fetal left ventricles based on patient-specific 4D ultrasound scans

The mechanics of intracardiac blood flow and the epigenetic influence it exerts over the heart function have been the subjects of intense research lately. Fetal intracardiac flows are especially useful for gaining insights into the development of congenital heart diseases, but have not received due attention thus far, most likely because of technical difficulties in collecting sufficient intracardiac flow data in a safe manner. Here, we circumvent such obstacles by employing 4D STIC ultrasound scans to quantify the fetal heart motion in three normal 20-week fetuses, subsequently performing 3D computational fluid dynamics simulations on the left ventricles based on these patient-specific heart movements. Analysis of the simulation results shows that there are significant differences between fetal and adult ventricular blood flows which arise because of dissimilar heart morphology, E/A ratio, diastolic–systolic duration ratio, and heart rate. The formations of ventricular vortex rings were observed for both E- and A-wave in the flow simulations. These vortices had sufficient momentum to last until the end of diastole and were responsible for generating significant wall shear stresses on the myocardial endothelium, as well as helicity in systolic outflow. Based on findings from previous studies, we hypothesized that these vortex-induced flow properties play an important role in sustaining the efficiency of diastolic filling, systolic pumping, and cardiovascular flow in normal fetal hearts.     

The echocardiographic study of the rabbit heart left ventricle morpho-functional parameters

Morphometric and functional parameters of the heart left ventricle in rabbits during systole and diastole were investigated by the method of echocardiography. Morphometric parameters were studied on three levels: the mitral valve, the papillary muscles and the apical level. The internal dimension of the left ventricle uniformly decreases in three parallel planes during systole, its maximal reduction being observed on the apical level. During the contraction phase, the posterior wall thickness of the left ventricular and the interventricular septum thickness increases on the basal level to a greater extent than on the apical one. During systole, the interventricular septum movement is greater than the left ventricular posterior wall motion. During the heart cycle, the form of the left ventricular cavity changes from an ellipsoid in diastole to elliptic paraboloid in systole.     

Cardiac function of the leopard shark,Triakis semifasciata

Summary The pressure difference between the cardinal sinus and the pericardium, and the transmural ventricular diastolic pressure at rest and during swimming in the leopard shark, Triakis semifasciata, was measured to characterize the mechanism of cardiac filling in chronically-instrumented fish and to evaluate cardiac responses to swimming. Echo-Doppler and radiographic imaging were also used to fully describe the cardiac cycle. Swimming induces an increase in preload as manifested by a large increment of cardinal sinus pressure (0.26/0.20 [systolic/diastolic] to 0.49/0.32 kPa) which always exceeds pericardial pressure. Increases in both mean ventricular diastolic transmural pressure (0.30–0.77 kPa) and cardinal sinus pressure during swimming suggest increased cardiac filling by vis a tergo as the mechanism for augmenting cardiac output. In contrast to mammals, the fluid-filled pericardial space of elasmobranchs is considerably larger and the pericardium itself does not move in concert with the heart throughout the cardiac cycle. Also, modest increases in heart rate drastically curtail the duration of diastole, which becomes much less than that of systole, a phenomenon not found in mammals. In the absence of tachycardia (<40 bpm), ventricular filling is characterized by a period of early rapid filling, and a late period of filling owing to atrial systole, separated by a period of diastasis. Ventricular filling in elasmobranchs is thus biphasic and is not solely dependent on atrial systole. Atrial diastole is characterized by three filling periods associated with atrial relaxation, ventricular ejection, and sinus venosus contraction. The estimated ventricular ejection fraction of Triakis (80%) exceeds that of the mammalian left ventricle.     

Left atrial conduit volume is generated by deviation from the constant-volume state of the left heart: a combined MRI-echocardiographic study

Although modeling the four-chambered heart as a constant-volume pump successfully predicts causal physiological relationships between cardiac indexes previously deemed unrelated, the real four-chambered heart slightly deviates from the constant-volume state by ventricular end systole. This deviation has consequences that affect chamber function, specifically, left atrial (LA) function. LA attributes have been characterized as booster pump, reservoir, and conduit functions, yet characterization of their temporal occurrence or their causal relationship to global heart function has been lacking. We investigated LA function in the context of the constant-volume attribute of the left heart in 10 normal subjects using cardiac magnetic resonance imaging (MRI) and contemporaneous Doppler echocardiography synchronized via ECG. Left ventricular (LV) and LA volumes as a function of time were determined via MRI. Transmitral flow, pulmonary vein (PV) flow, and lateral mitral annular velocity were recorded via echocardiography. The relationship between the MRI-determined diastolic LA conduit-volume (LACV) filling rate and systolic LA filling rate correlate well with the relationship between the echocardiographically determined average flow rate during the early portion of the PV D wave and the average flow rate during the PV S wave (r = 0.76). We conclude that the end-systolic deviation from constant volume for the left heart requires the generation of the LACV during diastole. Because early rapid filling of the left ventricle is the driving force for LACV generation while the left atrium remains passive, it may be more appropriate to consider LACV to be a property of ventricular diastolic rather than atrial function.     

Coronary circulatory pressure gradients

The pressure gradients of the canine coronary circulation were measured in 37 dogs during control and following eight interventions: left stellate ganglion or left vagosympathetic trunk stimulation, as well as isoproterenol, acetylcholine, noradrenaline, adenosine, phenylephrine, or adrenaline infusions. During control, pressure gradients in the epicardial coronary arteries (measured from the aorta to coronary artery branch) were 15.2 +/- 1 mmHg (1 mmHg (1 mmHg = 133.32 Pa) during systole and 10.6 +/- 1.5 mmHg during diastole. Adrenaline increased this systolic gradient, while acetylcholine and phenylephrine decreased it. In contrast, the pressure gradients in the small coronary arteries (from the branch of an epicardial artery to the pressure in an obstructed coronary artery) were 56 +/- 1.3 mmHg during systole and 63.7 +/- 1.3 mmHg during diastole. These gradients were increased by phenylephrine during both systole and diastole, noradrenaline and adrenaline during diastole and decreased by isoproterenol (systolic), left vagosympathetic trunk stimulation (diastolic), acetylcholine (systolic and diastolic), and adenosine (diastolic). The microcirculation and small vein gradients during control were 16.4 +/- 1.2 mmHg during systole and 8.5 +/- 0.8 mmHg during diastole. Decreases in this gradient were produced by isoproterenol, acetylcholine, and adenosine during systole and adenosine during diastole. These observations are consistent with the concept that the coronary circulation has considerable regulatory capacity in all of its component parts. Specifically, epicardial arteries appear to function as both conduits and as resistance vessels, small arteries as major resistance vessels, and the microcirculation and small veins as both capacitors and resistors.     

Subendocardial and subepicardial pressure-flow relations in the rat heart in diastolic and systolic arrest

Ischemic heart disease is more apparent in the subendocardial than in subepicardial layers. We investigated coronary pressure-flow relations in layers of the isolated rat left ventricle, using 15 microm microspheres during diastolic and systolic arrest in the vasodilated coronary circulation. A special cannula allowed for selective determination of left main stem pressure-flow relations. Arterio-venous shunt flow was derived from microspheres in the venous effluent. We quantitatively investigated the pressure-flow relations in diastolic arrest (n=8), systolic arrest at normal contractility (n=8) and low contractility (n=6). In all three groups normal and large ventricular volume was studied. In diastolic arrest, at a perfusion pressure of 90 mmHg, subendocardial flow is larger than subepicardial flow, i.e., the endo/epi ratio is approximately 1.2. In systolic arrest the endo/epi ratio is approximately 0.3, and subendocardial flow and subepicardial flow are approximately 12% and approximately 55% of their values during diastolic arrest. The endo/epi ratio in diastolic arrest decreases with increasing perfusion pressure, while in systole the ratio increases. The slope of the pressure-flow relations, i.e., inverse of resistance, changes by a factor of approximately 5.3 in the subendocardium and by a factor approximately 2.2 in the subepicardium from diastole to systole. Lowering contractility affects subendocardial flow more than subepicardial flow, but both contractility and ventricular volume changes have only a limited effect on both subendocardial and subepicardial flow. The resistance (inverse of slope) of the total left main stem pressure-flow relation changes by a factor of approximately 3.4 from diastolic to systolic arrest. The zero-flow pressure increases from diastole to systole. Thus, coronary perfusion flow in diastolic arrest is larger than systolic arrest, with the largest difference in the subendocardium, as a result of layer dependent increases in vascular resistance and intercept pressure. Shunt flow is larger in diastolic than in systolic arrest, and increases with perfusion pressure. We conclude that changes in contractility and ventricular volume have a smaller effect on pressure-flow relations than diastolic-systolic differences. A synthesis of models accounting for the effect of cardiac contraction on perfusion is suggested.     

Elucidation of spatially distinct compensatory mechanisms in diastole: radial compensation for impaired longitudinal filling in left ventricular hypertrophy.

Cardiac output maintenance is so fundamental that, when regional systolic function is impaired, as during ischemia, nonischemic segments compensate by becoming hypercontractile. By analogy, diastolic compensatory mechanisms that maintain filling volume must exist but remain to be fully elucidated. Viewing filling in spatially distinct (longitudinal, radial) mechanistic terms facilitates elucidation of diastolic compensatory mechanisms. Because impairment of longitudinal (long axis) diastolic function (DF) in left ventricular hypertrophy (LVH) is established, we hypothesized that to maintain filling volume, radial (short-axis) filling function would compensate. In 20 normal left ventricular ejection fraction (LVEF) subjects (10 with LVH, 10 without LVH), we analyzed longitudinal function via Doppler tissue imaging of mitral annular motion and radial function as change in short-axis endocardial dimension via M-mode. The spatial (long axis, short axis) endocardial LV dimensions and their changes allowed assignment of E-wave filling volume into (cylindrical geometry-based) longitudinal and radial components. Despite indistinguishable (P = 0.70) E-wave velocity-time integrals (E-wave filling volume surrogate), systolic stroke volumes, and end-diastolic volumes in the LVH and control groups, longitudinal volume in absolute terms and the percent of E-wave volume accommodated longitudinally were reduced in the LVH group (P < 0.05 and P < 0.01, respectively), whereas the percent of E-wave volume accommodated radially was enhanced (P < 0.01). We conclude that, in normal LVEF (decreased longitudinal volume accommodation) LVH subjects vs. controls, spatially distinct compensatory mechanisms in diastole manifest as increased radial volume accommodation per unit of E-wave filling volume. Assessment of spatially distinct diastolic compensatory mechanisms in other pathophysiological subsets is warranted.     

α-酮酸片对维持性血液透析患者心脏功能和结构的影响

目的：探讨α-酮酸片（α-KA）对维持性血液透析（MHD）患者心脏功能和结构的影响。方法：观察30例α-酮酸片（商品名：开同）治疗组维持性血液透析患者与30例对照组患者,分别在治疗前及治疗6个月后超声心动图测定心脏结构指标：左房收缩末期内径（LADs）、左室舒张末期内径（LVEDd）、室间隔舒张末期厚度（IVSTd）、左室后壁舒张末期厚度（LVPWTd）,左房内径指数（LAI）、左心室心肌重量指数（LVMI）、相对室壁厚度（RWT）,心脏功能指标：左室射血分数（LVEF）,左室短轴缩短率（FS）,二尖瓣口舒张早期和晚期最大血流速度比（E/A）各项指标等检测,比较治疗前后各指标变化。结果：治疗组MHD患者心脏结构指标：左房收缩末期内径（LADs）、左室舒张末期内径（LVEDd）、室间隔舒张末期厚度（IVSTd）、左室后壁舒张末期厚度（LVPWTd）,左房内径指数（LAI）、左心室心肌重量指数（LVMI）值均明显低于对照组,二者差异有显著性（P〈0.05）,两组相对室壁厚度（RWT）相比没有明显的差异（P〉0.05）。心脏功能指标：左室射血分数（LVEF）,左室短轴缩短率（FS）,二尖瓣口舒张早期和晚期最大血流速度比（E/A）值较对照组明显增高（P〈0.05）,有统计学意义。结论：α-酮酸片可以改善MHD患者的心脏结构和功能,其对MHD患者心血管并发症的预防和治疗有一定临床指导意义。     

Coupling of left ventricular and aortic volume elasticity in the rabbit

Changes in volume elasticity (VE) of the left ventricle and aorta could be important for blood flow. A procedure is presented to rapidly assess VE of the left ventricle and aorta by analyzing changes in the eigenfrequency. Six control rabbits and 11 rabbits with atheromatosis (12 wk of high-cholesterol feeding) were studied. In control rabbits, during the first half of the systole, left ventricular VE continuously increased to +43% (P < 0.05). Then VE gradually declined to an end-diastolic minimum (20% of the average systolic levels, P < 0.05). Aortic VE changes were in the opposite direction to the ventricle. Aortic VE continuously decreased throughout the systole; the last value was 20% lower than at the beginning of the systole (P < 0.05). Conversely, diastolic VE of the aorta took on greater values. This inverse time course between ventricle and aorta may reduce energy requirements for conveying blood. High cholesterol-fed rabbits did not reveal the inverse behavior of ventricular and aortic VE, e.g., aortic VE increased during the systole (119%, P < 0.05).     

4-D blood flow in the human right ventricle

Right ventricular (RV) function is a powerful prognostic indicator in many forms of heart disease, but its assessment remains challenging and inexact. RV dysfunction may alter the normal patterns of RV blood flow, but those patterns have been incompletely characterized. We hypothesized that, based on anatomic differences, the proportions and energetics of RV flow components would differ from those identified in the left ventricle (LV) and that the portion of the RV inflow passing directly to outflow (Direct Flow) would be prepared for effective systolic ejection as a result of preserved kinetic energy (KE) compared with other RV flow components. Three-dimensional, time-resolved phase-contrast velocity, and balanced steady-state free-precession morphological data were acquired in 10 healthy subjects using MRI. A previously validated method was used to separate the RV and LV end-diastolic volumes into four flow components and measure their volume and KE over the cardiac cycle. The RV Direct Flow: 1) followed a smoothly curving route that did not extend into the apical region of the ventricle; 2) had a larger volume and possessed a larger presystolic KE (0.4 ± 0.3 mJ) than the other flow components (P < 0.001 and P < 0.01, respectively); and 3) represented a larger part of the end-diastolic blood volume compared with the LV Direct Flow (P < 0.01). These findings suggest that diastolic flow patterns distinct to the normal RV create favorable conditions for ensuing systolic ejection of the Direct Flow component. These flow-specific aspects of RV diastolic-systolic coupling provide novel perspectives on RV physiology and may add to the understanding of RV pathophysiology.     

Effects of glossopharyngeal insufflation on cardiac function: an echocardiographic study in elite breath-hold divers.

Glossopharyngeal insufflation (GI), a technique used by breath-hold divers to increase lung volume and augment diving depth and duration, is associated with untoward hemodynamic consequences. To study the cardiac effects of GI, we performed transthoracic echocardiography, using the subcostal window, in five elite breath-hold divers at rest and during GI. During GI, heart rate increased in all divers (mean of 53 beats/min to a mean of 100 beats/min), and blood pressure fell dramatically (mean systolic, 112 to 52 mmHg; mean diastolic, 75 mmHg to nondetectable). GI induced a 46% decrease in mean left ventricular end-diastolic area, 70% decrease in left ventricular end-diastolic volume, 49% increase in mean right ventricular end-diastolic area, and 160% increase in mean right ventricular end-diastolic volume. GI also induced biventricular systolic dysfunction; left ventricular ejection fraction decreased from 0.60 to a mean of 0.30 (P = 0.012); right ventricular ejection fraction, from 0.75 to a mean of 0.39 (P < 0.001). Wall motion of both ventricles became significantly abnormal during GI; the most prominent left ventricular abnormalities involved hypokinesis or dyskinesis of the interventricular septum, while right ventricular wall motion abnormalities involved all visible segments. In two divers, the inferior vena cava dilated with the appearance of spontaneous contrast during GI, signaling increased right atrial pressure and central venous stasis. Hypotension during GI is associated with acute biventricular systolic dysfunction. The echocardiographic pattern of right ventricular systolic dysfunction is consistent with acute pressure overload, whereas concurrent left ventricular systolic dysfunction is likely due to ventricular interdependence.     

Echocardiographic features of pigs with spontaneous hypertrophic cardiomyopathy

Ultrasonography is one of the most common, noninvasive techniques used for cardiovascular diagnosis because it provides reliable information and enhances patient safety. Two-dimensional (2-D) and M-mode echocardiography is conducted to assess the severity and distribution of myocardial hypertrophy. Hypertrophic cardiomyopathy (HCM) is a primary myocardial disease that has variable manifestations because interactions between the many facets of systolic and diastolic dysfunction of the heart are complex. The objective of the study reported here was to characterized clinical HCM in pigs. A commercial Vingmed (CFM-800) 3.25 MHz transducer was used to perform 2-D and M-mode echocardiography. Experimental pigs (about 100 kg in body weight) were anesthetized and positioned in left lateral recumbency. Echocardiographic images (2-D) were acquired in parasternal short-axis and long-axis views. The 2-D images provided M-mode under direct anatomic visualization. The pigs were sacrificed for pathologic study after echocardiographic examination. In typical HCM cases (n = 8), the interventricular septum thickness increased, the left ventricular (LV) end-systolic and end-diastolic dimensions decreased, and the left atrial dimensions and the indexes of systolic function, such as ejection fraction and velocity of fiber shortening, increased. The LV outflow tract narrowed, particularly when gross upper septal hypertrophy was evident. Moreover, systolic cranial motion (SCM) of the septal leaflet of the mitral valve was observed. Doppler evidence of mitral regurgitation often was associated with SCM. The echocardiographic findings from pigs with HCM resembled those from humans. Thus, porcine HCM may serve as a spontaneous animal model for the study of HCM in humans.     

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。     

Modified heart-lung preparation for the evaluation of systolic and diastolic coronary flow in rats

A modified heart-lung preparation of the rat, which permits measuring systolic and diastolic coronary flow separately and enables coronary compliance to be evaluated, is described. The systemic circulation was substituted by a shunt circuit, and the elastic properties of the arterial tree were mimicked by a rubber balloon. Systolic and diastolic coronary flow was evaluated from the pulmonary and aortic flow signal. Integrated phasic pulmonary flow represented right ventricular stroke volume. Integrated phasic systolic aortic flow represented left ventricular stroke volume minus that volume flowing into the coronary arteries during systole, because the aortic flow probe had to be inserted distal to the origin of the coronary vessels. Because right and left ventricular stroke volume was identical under steady-state conditions, the difference between systolic pulmonary and systolic aortic flow resulted in systolic coronary flow. Diastolic coronary flow was measured by means of the retrograde flow through the aortic flow probe. Coronary compliance was calculated according to Frank's windkessel model from coronary resistance and from central diastolic aortic pressure, which decayed exponentially after switching out the rubber balloon and the shunt circuit. It could be shown that the proportion of systolic to diastolic coronary flow depends on coronary compliance.     

The Nature of the Disorder of Function in Chronic Postinfarction Aneurysm of the Left Ventricle

Assessment of left ventricular function in five patients with chronic postinfarction left ventricular aneurysm was carried out at the time of left heart catheterization and compared with that in six normal subjects. One patient was investigated before and after surgical resection of the aneurysm. The presence of the aneurysm placed the left ventricle at a mechanical disadvantage in systole and increased the resistance to diastolic filling (impedance). This was true even in patients with normal cardiac indices who were not badly disabled. Resection of the aneurysm corrected both these abnormalities, and, as well, lowered the time-tension index at a time when calculated left ventricular work was much increased. These differences between normals and patients with aneurysms, and the changes occurring as a result of resection of an aneurysm, show that the presence of the aneurysm places the left ventricle at a mechanical disadvantage in systole as well as altering its diastolic filling characteristics.