Effect of ectopic excitation on the ventricular pump function in chicken

The pump function of the heart ventricles was studied in chest-open anaesthetized adult female chickens under sinus rhythm and ectopic excitation of different localization. The intraventricular pressure in the right and left heart ventricles was measured by insertion of catheters through the ventricular free walls. Maximum systolic pressure, end-diastolic pressure, contractility (dP/dtmax) and relaxation (dP/dtmin) of both heart ventricles, and duration of the asynchronous contraction time of the left ventricle were analyzed. It was revealed that reduction of the pump function of the left ventricle tends to be greater under right ventricular ectopic excitation compared with left ventricular one. In comparison with the sinus rhythm, the pump function of the right ventricle was preserved to a greater extent under stimulation of the left ventricular apex and was significantly impaired under right ventricular ectopic excitation. Relaxation of both heart ventricles was more susceptible to ventricular ectopic excitation than contractility, and was more vulnerable in the right ventricle than in the left one. The direction of changes of the pump function of the heart ventricles in chickens under ventricular ectopic excitation was similar to changes of the pump function of mammalian hearts.     

p53 Gene deficiency promotes hypoxia-induced pulmonary hypertension and vascular remodeling in mice

Chronic hypoxia induces pulmonary arterial remodeling, resulting in pulmonary hypertension and right ventricular hypertrophy. Hypoxia has been implicated as a physiological stimulus for p53 induction and hypoxia-inducible factor-1α (HIF-1α). However, the subcellular interactions between hypoxic exposure and expression of p53 and HIF-1α remain unclear. To examine the role of p53 and HIF-1α expression on hypoxia-induced pulmonary arterial remodeling, wild-type (WT) and p53 knockout (p53KO) mice were exposed to either normoxia or hypoxia for 8 wk. Following chronic hypoxia, both genotypes demonstrated elevated right ventricular pressures, right ventricular hypertrophy as measured by the ratio of the right ventricle to the left ventricle plus septum weights, and vascular remodeling. However, the right ventricular systolic pressures, the ratio of the right ventricle to the left ventricle plus septum weights, and the medial wall thickness of small vessels were significantly greater in the p53KO mice than in the WT mice. The p53KO mice had lower levels of p21 and miR34a expression, and higher levels of HIF-1α, VEGF, and PDGF expression than WT mice following chronic hypoxic exposure. This was associated with a higher proliferating cell nuclear antigen expression of pulmonary artery in p53KO mice. We conclude that p53 plays a critical role in the mitigation of hypoxia-induced small pulmonary arterial remodeling. By interacting with p21 and HIF-1α, p53 may suppress hypoxic pulmonary arterial remodeling and pulmonary arterial smooth muscle cell proliferation under hypoxia.     

慢性缺氧对大鼠左右心室功能、心肌肌原纤维Ca~（2＋），Mg~（2＋）－ATP

模拟５０００ｍ中度缺氧时,大鼠右室功能显著加强,而左室功能加强不显著;左右心室肌原纤维Ｃａ２＋,Ｍｇ２＋－ＡＴＰ酶活性下降,肌球蛋白同功酶Ｖ２和Ｖ３百分含量增加,Ｖ１百分含量减少。８０００ｍ重度缺氧时,右室功能减弱,但无统计学意义,左室功能减弱有显著性;ＡＴＰ酶活性和同功酶的变化超过５０００ｍ组。此外,右室ＡＴＰ酶活性与ＰＡＰ呈反比且有显著性,左室ＡＴＰ酶活性与ＣＡＳＰ虽也呈反比但无显著性;右室同功酶Ｖ３百分含量与ＰＡＰ呈正比,左室同功酶Ｖ３百分含量与ＣＡＳＰ不呈比例。上述结果表明,因短期突发严重缺氧引起的心肌供氧不足对左心室心肌的直接损伤作用大于右心室心肌。     

Effect of right ventricular hypertrophy on cardiac performance and the relation between right ventricular systolic peak pressure and end-systolic volume

To investigate the role of hypertrophy of the right ventricle upon right heart performance and the significance of the peak systolic pressure/end-systolic volume (P/V) ratio in terms of right ventricular systolic performance, simultaneous measurements of radionuclide ventriculograms and central hemodynamics were done in 32 patients with chronic obstructive pulmonary disease. In 26 of the patients (80%) technically adequate two-dimensional echocardiograms could be performed. In the subset of patients with increased (greater than or equal to 6 mm) right ventricular end-diastolic wall thickness no relationship between pulmonary artery pressure and right ventricular ejection fraction (RVEF) existed in comparison with the remaining patients. P/V indices and cardiac output were not decreased. Considering the patients, whose P/V ratio did not increase from rest to exercise, RVEF decreased highly significantly more than in the remaining patients. The ratio of wall thickness and end-diastolic radius as determinant of peak systolic stress was significantly decreased in these patients compared with the remaining patients. In the patients with right ventricular hypertrophy despite significantly higher values of pulmonary artery pressures and resistances, the afterload in terms of systolic wall stress is markedly reduced. We conclude that in the hypertrophic state, right ventricular performance is not impaired despite decreased RVEF values. In the patients whose P/V ratio does not increase from rest to exercise, an inappropriate high peak systolic wall stress may exist both due to inadequate wall thickness and increased diameter of the right ventricle. The role of P/V in terms of prognosis and development of decompensated right heart failure remains undetermined.     

Right ventricular TNF resistance during endotoxemia: the differential effects on ventricular function

Right and left ventricular myocytes originate from different cellular progenitors; however, it is unknown whether these cells differ in their response to endotoxemia. We hypothesized that 1) the percentage of endotoxemic functional depression within the right ventricle (RV) would be smaller than that of the left ventricle; and 2) that better RV function would correlate with lower levels of right ventricular TNF production. Adult Sprague-Dawley rats were divided into right and left control and endotoxin groups. Controls received vehicle, while endotoxin groups received LPS at 20 mg/kg ip. Hearts were excised either 2 or 6 h after injection. Hearts excised at 2 h were assayed for TNF, IL-6, TNF receptor 1 (TNFR1), TNFR2, and via ELISA, while hearts excised at 6 h were assayed via the Langendorff model. The percentage of cardiac functional depression, exhibited as developed pressure, contractility, and rate of relaxation (expressed as a percentage of control) was significantly smaller in right ventricles compared with left ventricles following endotoxin exposure. Tissue levels of TNF were significantly elevated in both right and left ventricles 2 h after endotoxin exposure, and right ventricular endotoxin groups expressed higher levels of TNF compared with their left ventricular counterparts. No significant differences in IL-6, TNFR1, or TNFR2 levels were noted between endotoxin-exposed ventricles. This is the first study to demonstrate that right and left ventricular function differs after endotoxin exposure.     

Factors influencing left-ventricular stiffness

The aim of the study was to investigate the relative contributions of geometrical and material factors to overall left-ventricular cavity stiffness. Left-ventricular cavity shapes were reconstructed using a computer and the variation of myocardial elastic modulus was calculated, by the finite element method, through the passive phase of diastole when rising volume coincided with rising pressure. Geometric data were obtained from biplane cineangiography, with micromanometer pressure measurements, for ten patients with left ventricular disease. Dimensional analysis was applied to the initial and derived data from which the influences of myocardial compliance, wall thickness-to-long dimension ratio, and aspect ratio (long-to-short axes) were determined. The ratio between the volume elasticity and the myocardial modulus of elasticity, the normalized stiffness ratio (NSR), is proposed as a useful index of left ventricular mechanical behaviour in diastole. The volume elasticity of the chamber is dependent not only upon the myocardium elastic modulus and the wall thickness ratio, but also on the shape of the chambe. Changes in the thickness/radius ratio of the ventricle have less effect upon its distention than those in the long dimension/radius ratio. The left ventricle becomes more spherical in shpae through diastole and hence becomes stiffer by this geometric mechanism.     

Cardiac remodelling: concentric versus eccentric hypertrophy in strength and endurance athletes

Cardiac remodelling is commonly defined as a physiological or pathological state that may occur after conditions such as myocardial infarction, pressure overload, idiopathic dilated cardiomyopathy or volume overload. When training excessively, the heart develops several myocardial adaptations causing a physiological state of cardiac remodelling. These morphological changes depend on the kind of training and are clinically characterised by modifications in cardiac size and shape due to increased load. Several studies have investigated morphological differences in the athlete’s heart between athletes performing strength training and athletes performing endurance training. Endurance training is associated with an increased cardiac output and volume load on the left and right ventricles, causing the endurance-trained heart to generate a mild to moderate dilatation of the left ventricle combined with a mild to moderate increase in left ventricular wall thickness. Strength training is characterised by an elevation of both systolic and diastolic blood pressure. This pressure overload causes an increase in left ventricular wall thickness. This may or may not be accompanied by a slight raise in the left ventricular volume. However, the development of an endurancetrained heart and a strength-trained heart should not be considered an absolute concept. Both forms of training cause specific morphological changes in the heart, dependent on the type of sport. (Neth Heart J 2008;16:129-33.)     

Effects of training and anabolic steroids on collagen synthesis in dog heart.

The effects of endurance training and anabolic steroid (Methandienone 1.5 mg.kg-1 p. o. daily) and their combination on regional collagen biosynthesis and concentration in the hearts of male beagle dogs were studied by measuring prolyl 4-hydroxylase (PH) activity and hydroxyproline (HYP) concentration. The PH (P less than 0.05) and HYP (P less than 0.05) were both greater in the subendocardinal layer than in the subepicardium (EPI) of the left ventricular wall in controls, whereas opposite gradients (P less than 0.05) were observed in the right ventricle. Endurance exercise caused an increase of PH activity in EPI of the left ventricular wall (P less than 0.01). The HYP concentration increased in both layers of the right ventricle in the exercise plus steroid group (P less than 0.05). The results suggest that transmural differences exist in the rate of collagen synthesis and concentration in canine cardiac ventricles and that endurance exercise may accelerate collagen synthesis in EPI of the left ventricle and the combination of exercise and anabolic steroid causes an increase in collagen concentration in the right ventricular wall.     

三种正常大鼠磁共振成像心功能基础数据采集和分析

目的大鼠是常用的制备心脏病模型的实验动物,而磁共振成像（MRI）技术已经成为评价心脏病模型病理进程和药效的重要技术手段,但是目前国内外没有正常大鼠心脏的磁共振成像技术参数,影响了这一技术的应用。本文利用磁共振成像技术,采集和定量分析Wistar、Sprague-Dawley和Lewis三种常用大鼠的左、右心室功能参数,为心脏病模型制备和分析提供参考数据。方法利用7．0T高场强MRI心脏电影（CINE）序列,分析这三种常用大鼠活体心脏组织的左、右心室心功能参数。结果获得三种大鼠左、右心室的8—9周龄功能参数,包括：左、右心室的舒张末容积（EDV）、收缩末容积（ESV）、射血分数（EF）;左心室乳头肌层面舒张末期内径（EDD）、收缩末期内径（ESD）、短轴缩短率（Fs）、舒张末前后室壁厚度（EDAWT,EDPWT）、收缩末前后室壁厚度（ESAWT,ESPWT）、前室壁增厚率（AWT）和后室壁增厚率（PwT）;右心室乳头肌层面舒张末室壁厚度（EDWT）、收缩末室壁厚度（ESWT）和室壁增厚率（WT）等十八项心脏主要功能和结构的正常值。结论本研究获得的三种大鼠十八项心脏主要功能和结构的正常值,可作为心脏病模型制备成模判定和病理进程、药物评价的参考数据。     

犬心右室,左室大面积梗塞时的容量负荷评价

在１２只犬,结扎四支冠脉,造成犬心右室、左室大面积梗塞和心源性休克时,左室收缩压（ＬＶＳＰ）及最大正负压力阶差（±ｄｐ／ｄｔｍａｘ．）分别下降５４％、５１％和４７％,而右室收缩压（ＲＶＳＰ）及±ｄｐ／ｄｔｍａｘ．仅降低９％、２５％和２７％。组Ⅰ（６只犬）快速扩容（低分子右旋糖酐３０ｍｌ／ｋｇ,２０ｍｉｎ内静脉输入）,结果右室反向搏动增强,双心室±ｄｐ／ｄｔｍａｘ．进一步降低,右房压（ＲＡＰ）及左室舒张末压（ＬＶＥＤＰ）极度升高达２．９±０．２ｋＰａ和５．０±０．３ｋＰａ（Ｐ均＜０．０１）,甚至诱发室颤。组Ⅱ缓慢静点多巴胺（１０μｇ／ｋｇ·ｍｉｎ）和硝酸甘油（１μｇ／ｋｇ·ｍｉｎ）３０ｍｉｎ,有效提高了动脉压（ＡＰ）,心输出量（ＣＯ）,ＬＶＳＰ及左室±ｄｐ／ｄｔｍａｘ．使休克逆转。结果表明,大面积左、右室梗塞伴休克时,右室残余心肌的代偿性收缩仍能造成ＲＶＳＰ与右室泵功能呈分离状态;此时快速扩容将进一步损害左、右室功能,而联合使用硝酸甘油和多巴胺能有效纠正休克同时不造成ＲＡＰ和ＬＶＥＤＰ的升高。     

缺氧对右心室最大心肌心血流量的影响

为了探讨氧对冠状血管贮备方法的影响,我们观察了缺氧对血流动力学及右心室最大心肌血汉量的变化。结果表明,急性缺氧引起的ＰａＯ２、心输出量及氧运送量降低,但右心室心肌血流量增加,右心室最大与安静血流量比值降低,生缺氧时ＰａＯ２降低,血球比积和右心室生理指数增加,氧运送量和右心室血流量正常,但最大血流量降低,小动脉增厚、外胶元增加,以上结果提示,慢性缺氧对冠状血管贮备减少可能是小动脉壁增厚、外胶元增加和     

Time course sequences of angiotensin converting enzyme and chymase-like activities during development of right ventricular hypertrophy induced by pulmonary artery constriction in dogs

ACE and chymase play crucial roles in the establishment of pressure overload-induced cardiac hypertrophy. In the present study, time sequences of ACE and chymase-like activities, and their correlation with hypertrophic changes including free wall thickness and cardiac fibrosis, were elucidated in dogs with constant pressure overload to the right ventricle. Pulmonary artery banding (PAB) was applied so that the diameter of the main pulmonary artery was reduced to 60% of the original size, right ventricular pressure was elevated by about 70%, and pulmonary artery flow was increased by about three times of that in sham operation groups. These increases remained unchanged 15, 60, and 180 days after PAB, suggesting that constant right ventricular pressure overload was obtained, at least during this period. The diameter of the right ventricular myocyte was slightly increased and the percentage of fractional shortening was decreased 15 days after PAB. Right ventricular wall thickness and interstitial collagenous fiber were, however, not different from those of sham-operated dogs, suggesting that this period is a period of adaptation to the overload. Sixty days after PAB, the diameter of the right ventricular myocyte was further increased, and right ventricular wall thickness and interstitial collagenous fiber were also increased. These changes were almost identical even 180 days after PAB. Thus, stable hypertrophy was elicited from 60 through 180 days after PAB. ACE activity was facilitated at the adaptation period to the overload (15 days after PAB), but chymase activity was not facilitated at this period. On the other hand, both ACE and chymase-like activities were unchanged in the earlier phase (60 days after PAB) of stable hypertrophy, but facilitated in the latter phase (180 days after PAB). These findings suggest the pathophysiologic roles of these enzymes may be different over the time course of pressure overload-induced hypertrophy.     

缺氧对右心室最大心肌血流量的影响

为了探讨缺氧对冠状血管贮备力的影响,我们观察了缺氧时大鼠血流动力学及右心室最大心肌血流量的变化。结果表明,急性缺氧引起ＰａＯ２、心输出量及氧运送量降低,但右心室心肌血流量增加,右心室最大与安静血流量比值降低。慢性缺氧时ＰａＯ２降低,血球比积和右心室重量指数增加,氧运送量和右心室血流量正常,但最大血流量降低,小动脉增厚、外膜胶元增加。以上结果提示,慢性缺氧对冠状血管贮备减少可能是小动脉壁增厚、外膜胶元增加和血液粘滞性增加及右心室肥大的结果。     

Left ventricular hypertrophy in chronically hypertensive ponies

Systemic arterial hypertension is associated with equine laminitis, a disease precipitated by gross over-ingestion of carbohydrates. We examined the hearts from nine chronically hypertensive (161 +/- 11/99 +/- 6 mmHg) laminitic ponies and nine normotensive (128 +/- 2/76 +/- 3 mmHg) ponies postmortem for signs of left ventricular hypertrophy. The hypertensive ponies had hearts which were significantly larger (7.77 +/- 0.26 g/kg bodyweight (BW) vs. 5.67 +/- 0.22 g/kg BW), as well as increased combined left ventricle and septum weight (4.99 +/- 0.21 g/kg BW vs. 3.67 +/- 0.20 g/kg BW) and left ventricular free wall weight (3.71 +/- 0.23 g/kg BW vs. 2.62 +/- 0.19 g/kg BW) (p less than 0.05). The right ventricular free wall weights were not significantly different. Mean left ventricular free wall thickness was increased significantly in the hypertensive ponies compared to the normotensive group (26.1 +/- 0.4 mm and 22.5 +/- 1 mm, respectively), but neither septal nor right ventricular free wall thickness was different. These findings demonstrate that left ventricular hypertrophy accompanies equine laminitis-induced hypertension.     

Normal myocardial function in severe right ventricular volume overload hypertrophy

Severe left ventricular volume overloading causes myocardial and cellular contractile dysfunction. Whether this is also true for severe right ventricular volume overloading was unknown. We therefore created severe tricuspid regurgitation percutaneously in seven dogs and then observed them for 3.5-4.0 yr. All five surviving operated dogs had severe tricuspid regurgitation and right heart failure, including massive ascites, but they did not have left heart failure. Right ventricular cardiocytes were isolated from these and from normal dogs, and sarcomere mechanics were assessed via laser diffraction. Right ventricular cardiocytes from the tricuspid regurgitation dogs were 20% longer than control cells, but neither the extent (0.171 +/- 0.005 microm) nor the velocity (2.92 +/- 0.12 microm/s) of sarcomere shortening differed from controls (0.179 +/- 0.005 microm and 3.09 +/- 0.11 microm/s, respectively). Thus, despite massive tricuspid regurgitation causing overt right heart failure, intrinsic right ventricular contractile function was normal. This finding for the severely volume-overloaded right ventricle stands in distinct contrast to our finding for the left ventricle severely volume overloaded by mitral regurgitation, wherein intrinsic contractile function is depressed.     

Plasma atrial natriuretic factor and atrial wall stress in hypertensive and normotensive rabbits after pacing and volume expansion.

Atrial natriuretic factor (ANF) is present in high concentration in atria but in very low concentration in the ventricles. Under conditions of haemodynamic overload ventricular gene expression may become activated, but it is not clear if ventricular ANF can be released through a regulated or constitutive pathway. The purpose of this study was to determine whether basal and stimulated release of ANF are increased in perinephritic rabbits with mild hypertension. Six rabbits were rendered hypertensive by wrapping both kidneys in cellophane, and six sham-operated rabbits were used as controls. Eight weeks after renal wrapping, mean arterial pressure was approximately 20 mmHg higher in the experimental group. After anaesthesia, the renal-wrapped group had a higher vascular resistance. Right and left atrial wall stress was measured using sonomicrometry. Volume expansion by 30% of blood volume, using donor blood, caused a small increase in right and left atrial diastolic and systolic wall stress but did not significantly increase plasma ANF. Pacing the heart at 6 Hz caused increases in systolic but not diastolic wall stress and caused a significant increase in plasma ANF; the increase was larger after volume expansion. There were no significant differences between the responses of the experimental and control groups. It is concluded that mild hypertension, in the rabbit, does not lead to changes in atrial wall stress or either basal or stimulated release of ANF.     

Influence of left-ventricular shape on passive filling properties and end-diastolic fiber stress and strain

Passive filling is a major determinant for the pump performance of the left ventricle and is determined by the filling pressure and the ventricular compliance. In the quantification of the passive mechanical behaviour of the left ventricle and its compliance, focus has been mainly on fiber orientation and constitutive parameters. Although it has been shown that the left-ventricular shape plays an important role in cardiac (patho-)physiology, the dependency on left-ventricular shape has never been studied in detail. Therefore, we have quantified the influence of left-ventricular shape on the overall compliance and the intramyocardial distribution of passive fiber stress and strain during the passive filling period. Hereto, fiber stress and strain were calculated in a finite element analysis of passive inflation of left ventricles with different shapes, ranging from an elongated ellipsoid to a sphere, but keeping the initial cavity volume constant. For each shape, the wall volume was varied to obtain ventricles with different wall thickness. The passive myocardium was described by an incompressible hyperelastic material law with transverse isotropic symmetry along the muscle fiber directions. A realistic transmural distribution in fiber orientation was assumed. We found that compliance was not altered substantially, but the transmural distribution of both passive fiber stress and strain was highly dependent on regional wall curvature and thickness. A low curvature wall was characterized by a maximum in the transmural fiber stress and strain in the mid-wall region, while a steep subendocardial transmural gradient was present in a high curvature wall. The transmural fiber stress and strain gradients in a low and high curvature wall were, respectively, flattened and steepened by an increase in wall thickness.     

Ventricular weights in guinea pigs acclimated to cold plus hypoxia

Weanling male guinea pigs (Cavia porcellus), 2-3 weeks of age, with initial body weights of 207-271 g were exposed for 2-16 weeks to constant cold (6 degrees C) and hypoxia (PO2 = 85 Torr) equivalent to 4800 m above sea level. Their growth rates and body weights did not differ from those of control animals of the same age maintained under normoxic conditions (22 degrees C, PO2 = 133 Torr). After 2, 3, 4, 6, 10, or 16 weeks exposure the animals were sacrificed, the hearts were removed, the ventricles were separated and weighed, and myoglobin concentrations were determined. Total heart weight as well as both right and left ventricular weights increased linearly with age. By the second week of exposure of the guinea pigs to cold plus hypoxia the total heart and right ventricular weights were 25 and 50% greater than those of the normoxic control animals. Both weights increased at greater rates than those of the controls until Week 6 and then remained at 30 and 80% throughout the 16th week. The weights of the left ventricles in these animals were only slightly greater than those of the controls. In spite of the severe right ventricular hypertrophy these animals showed no clinical signs of right heart failure. Myoglobin concentrations were significantly greater in both ventricles for the cold-plus-hypoxic animals than for the controls.     

Mechanisms of oxygen demand/supply balance in the right ventricle

Few studies have investigated factors responsible for the O2 demand/supply balance in the right ventricle. Resting right coronary blood flow is lower than left coronary blood flow, which is consistent with the lesser work of the right ventricle. Because right and left coronary artery perfusion pressures are identical, right coronary conductance is less than left coronary conductance, but the signal relating this conductance to the lower right ventricular O2 demand has not been defined. At rest, the left ventricle extracts approximately 75% of the O2 delivered by coronary blood flow, whereas right ventricular O2 extraction is only ~50%. As a result, resting right coronary venous PO2 is approximately 30 mm Hg, whereas left coronary venous PO2 is approximately 20 mm Hg. Right coronary conductance does not sufficiently restrict flow to force the right ventricle to extract the same percentage of O2 as the left ventricle. Endogenous nitric oxide impacts the right ventricular O2 demand/supply balance by increasing the right coronary blood flow at rest and during acute pulmonary hypertension, systemic hypoxia, norepinephrine infusion, and coronary hypoperfusion. The substantial right ventricular O2 extraction reserve is used preferentially during exercise-induced increases in right ventricular myocardial O2 consumption. An augmented, sympathetic-mediated vasoconstrictor tone blunts metabolically mediated dilator mechanisms during exercise and forces the right ventricle to mobilize its O2 extraction reserve, but this tone does not limit resting right coronary flow. During exercise, right coronary vasodilation does not occur until right coronary venous PO2 decreases to approximately 20 mm Hg. The mechanism responsible for right coronary vasodilation at low PO2 has not been delineated. In the poorly autoregulating right coronary circulation, reduced coronary pressure unloads the coronary hydraulic skeleton and reduces right ventricular systolic stiffness. Thus, normal right ventricular external work and O2 demand/supply balance can be maintained during moderate coronary hypoperfusion.     

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.