The purpose of the present study was to explore aging-associated cardiac dysfunction and the possible mechanism by which swimming exercise modulates cardiac dysfunction in aged mice. Aged mice were divided into two groups: i) Aged mice; and ii) aged mice subjected to swimming exercises. Another cohort of 4-month-old male mice served as the control group. Cardiac structure and function in mice were analyzed using hematoxylin and eosin staining, and echocardiography. The levels of oxidative stress were determined by measuring the levels of superoxide dismutase, malondialdehyde and reactive oxygen species (ROS). Levels of the endoplasmic reticulum (ER) stress-related protein PKR-like ER kinase, glucose-regulated protein 78 and C/EBP homologous protein were determined to evaluate the level of ER stress. The aged group exhibited an abnormal cardiac structure and decreased cardiac function, both of which were ameliorated by swimming exercise. The hearts of the aged mice exhibited pronounced oxidative and ER stress, which were ameliorated by exercise, and was accompanied by the reactivation of myocardial cGMP and suppression of cGMP-specific phosphodiesterase type 5 (PDE5). The inhibition of PDE5 attenuated age-induced cardiac dysfunction, blocked ROS production and suppressed ER stress. An ER stress inducer abolished the beneficial effects of the swimming exercise on cardiac function and increased ROS production. The present study suggested that exercise restored cardiac function in mice with age-induced cardiac dysfunction by inhibiting oxidative stress and ER stress, and increasing cGMP-protein kinase G signaling.

目的:探讨阿托伐他汀对2型糖尿病心肌病心功能、脑钠肽(BNP)及超敏C反应蛋白(hs-CRP)的影响.方法:将59例2型糖尿病心肌病患者随机分为一般治疗组(n=29例)和阿伐他汀治疗组(n=30例),一般治疗组和阿伐他汀治疗组在治疗中严格控制血糖及给予抗心衰规范化治疗,阿伐他汀治疗组在此治疗基础上,加用阿伐他汀(20 mg/d)治疗.所有患者在治疗前和治疗8周后,左室射血分数(LVEF)、检测左室舒张末期内径(LVDd)、血浆脑钠肽前体检氨基端片段(BNP)和血清超敏C反应蛋白(hs-CRP).结果:两组患者在治疗前LVEF、LVDd、BNP及hs-CRP差异均无统计学意义(P>0.05),经8周治疗后,一般治疗组和阿托伐他汀治疗组,LVEF较治疗前明显改善(P<0.05),BNP及HS-CRP水平较治疗前明显降低(P<0.05),但LVDd未见明显改善(P>0.05),两组患者在治疗后,阿托伐他汀治疗组较一般治疗组BNP及hs-CRP明显降低(P<0.05),但LVEF和LVDd没有显著变化(P>0.05).结论:阿托伐他汀改善糖尿病心肌病心功能,可能与降低血浆中脑钠肽水平及炎症因子相关.

Exogenously administered B-type natriuretic peptide (BNP) has been shown to provide cardioprotection against various heart diseases. However, the underlying mechanisms remain elusive. This study explores whether BNP exerts its cardioprotection against hypoxia/reoxygenation (H/R) injury under high glucose/high fat (HG/HF) conditions in cardiac H9c2 cells and uncovers the underlying mechanisms. Our data revealed that BNP significantly increased the cell viability and decreased the release of lactate dehydrogenase (LDH) and creatine kinase (CK), with a maximal effect at the BNP concentration of 10(-7) mol/L. In addition, by analyzing the activation of cleaved caspase-3 and by Annexin V-FITC/PI staining, we showed that BNP attenuated H/R-induced cell apoptosis in HG/HF conditions. Western blot analysis showed enhanced phosphorylation of protein kinase RNA (PKR)-like endoplastmic reticulum (ER) kinase (PERK) and eukaryotic initiation factor 2 alpha (eIF2 alpha) (one of the three main signaling pathways in endoplastmic reticulum (ER) stress), and increased expression of GRP78 and CHOP proteins (ER stress-related proteins) in H9c2 cells which underwent H/R in HG/HF conditions. Treatment with BNP or 8-Br-cGMP (an analog of cGMP) reversed this activation. However, this effect was significantly weakened by KT-5823, a selective cGMP-dependent protein kinase G (PKG) inhibitor. In addition, similar to BNP, treatment with a specific inhibitor of ER stress tauroursodeoxycholic acid (TUDCA) protected the cells against H/R injury exposed to HG/HF conditions. In conclusion, these findings demonstrated that BNP effectively protected cells against H/R injury under HG/HF conditions by inhibiting the ER stress via activation of the cGMP-PKG signaling pathway.

Cannabinoid type 2 receptor (CB2R) agonist AM1241 induces anti-inflammation by ameliorating microglial phenotypes, the mechanism, however, is still unknown. Peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) is a transcription protein which can regulate mitochondrial biogenesis, and the aim of this study is to investigate whether PGC-1α is involved in AM1241-induced anti-inflammation in N9 microglial cells. We used 10 ng/ml lipopolysaccharide (LPS) plus 10 U/ml interferon γ (IFNγ) to activate microglia into classic activated phenotype (M1 phenotype), and found that co-administration of 10 µM AM1241 increased the expressions of mitochondria biogenesis-associated proteins, including nuclear respiratory factor 1 (NRF-1), mitochondrial transcription factor A (TFAM) and COX IV, and up-regulated the biomarker levels of microglial M2 phenotype, including arginase 1 (Arg-1) and brain-derived neurotrophic factor (BDNF), and down-regulated biomarker levels of M1 phenotype, including inducible nitric oxide synthase (iNOS) and tumor necrosis factor α (TNF-α), compared to the cells treated with LPS plus IFNγ only (P < 0.05). By using PGC-1α-siRNA, however, we found that down-regulation of PGC-1α significantly reversed the AM1241-induced effects above (P < 0.05). According to the results in this study, we found that PGC-1α may mediate CB2R agonist AM1241-induced anti-inflammation in N9 microglial cells, and the mechanism might be associated with the enhancement of mitochondria biogenesis.

Deep venous thrombosis (DVT) is a common critical emergency with an increasing incidence during recent years.Sluggish venous blood,vein wall damage and high blood coagulation contribute tothe formation of DVT after orthopedic surgery.Therefore,if any one of the above three factors is diminished,the incidence of DVT will be reduced.Based on a domestic and foreign country analysis,the interventional strategy of DVT is briefly reviewed.

目的:探讨钠尿肽极化液(N P-GIK)的抗心力衰竭作用.方法:采用冠状动脉左前降支结扎术复制大鼠缺血性心力衰竭模型,并随机分为三组(n=10):生理盐水组于心梗后1 ml/(kg ·d)静脉滴注生理盐水;NP-GIK组于心梗后1 ml/(kg·d)静脉滴注NP-GIK;假手术组不结扎冠脉作为对照.4周后,检测各组大鼠的全心重量(HW)、体质量(BW),测量全心长度(HL),计算HL/HW、全心肥厚指数(HW/BW),检测心率(HR)、左室发展压(LVDevP)和左室内压微分(± LV dp/dtmax)等血流动力学指标.结果:心梗后NP-GIK治疗4周显著降低HL/HW、HW/BW,增加LVDevP和± LV dp/dtmax,对于心率无显著影响.结论:NP-GIK 通过抑制心肌肥厚,改善心脏缺血后的血流动力学,延缓缺血性心力衰竭的进程.

Proximal resistance vessels, such as the mesenteric arteries, contribute substantially to the peripheral resistance. The reactivity of resistance vessels to vasoactive substance like natriuretic peptides plays an important role in the regulation of blood pressure. In current study, we investigated the reactivity of mesenteric arteries to atrial natriuretic peptide (ANP), a well known vasodilating factor, in spontaneously hypertensive rats (SHR), as well as the effects of exercise training on it. As a result, ANP-induced vasorelaxation was attenuated in SHR with significantly increased phosphodiesterase type 5 (PDE5), and decreased cGMP/ANP ratio, compared with WKY rats as control. Intriguingly, the decreased reactivity to ANP in SHR was markedly reversed by exercise training. In addition, ANP resistance of in vitro mesenteric arteries was diminished by sildenafil a potent selective inhibitor of PDE5. In conclusion, ANP resistance occurs in resistance vessels of SHR, suggesting predisposition to hypertension, which can be reversed by exercise.

目的 研究程序性坏死的特异性抑制剂Nec-1对小鼠脑出血神经功能的保护作用,并探讨其机制.方法 选取健康雄性ICR小鼠,体重25～ 30 g,采用在纹状体部位注射胶原酶Ⅳ或生理盐水的方法建立小鼠脑出血组或者脑出血对照组,在脑出血前15 min分别在侧脑室注射Nec-1溶液或vehicle溶液.将实验随机分为:对照组、脑出血+ vehicle处理组、脑出血+Nec-1处理组.分别利用干湿重法测定脑水肿程度,神经功能评分检测神经运动功能,Western blotting检测cleaved caspase-3,Bcl-2蛋白表达情况.结果 脑出血加剧脑水肿程度,而Nec-1处理组减轻脑水肿程度(P＜0.05).经Nec-1处理后,可以提高小鼠脑出血神经运动功能(P＜0.05).脑出血可以增加cleaved caspase-3蛋白表达,抑制Bcl-2蛋白表达,经Nec-1处理后,抑制cleaved caspase-3的表达水平(P＜0.05),增加Bcl-2的表达(P＜0.05).结论 Nec-1对脑出血发挥重要神经保护作用,这种保护作用可能是通过抑制凋亡通路实现的,提示程序性坏死在脑出血中具有重要作用,将为脑出血的治疗提供新的思路.

目的 观察人工合成的钠尿肽——血管钠肽(VNP)对糖尿病(DM)大鼠心肌缺血/再灌注(MI/R)损伤的影响及机制.方法 高脂饲料喂养SD大鼠4周后,注射链脲霉素STZ (25 mg/kg,i.p.),1周后随机血糖≥11.1mmol/L为DM模型构建成功,常规制备MI/R(30 min/4 h)模型.将大鼠随机分为4组:假手术组、MI/R组、DM+假手术组、DM+ MI/R组.多导生理记录仪检测左室压上升/下降最大速率(±LVdP/dtmax),Evans blue-TTC双染色法检测心肌梗死面积,TUNEL法进行心肌细胞凋亡测试、试剂盒检测caspase-3活性,Western blot检测GRP78、Chop和PKG等蛋白表达.结果 与对照组相比,DM大鼠MI/R心肌损伤加重.VNP治疗(再灌前10 min,给予100 μg/kg,i.v)可显著减轻DM大鼠MI/R损伤,包括增强±LVdP/dtmax,降低心梗范围、死亡率与Caspase-3活性(n=8,P＜0.05).此外,VNP可降低内质网应激相关蛋白GRP78、CHOP表达(n=3,P＜0.01).VNP上述效应可同时被PKG阻断剂KT-5823(再灌前20 min,给予0.5 mg/kg,i.p)抑制、并被cGMP衍生物8-Br-cGMP(1 mg/kg)模拟(P＜0.05,P＜0.01).用内质网应激抑制剂TUDCA(50 mg/kg)预处理DM大鼠,并不能增强VNP的心肌保护作用.结论 VNP治疗可减轻DM性MI/R损伤,其机制可能与通过cGMP-PKG信号抑制内质网应激有关,提示VNP对DM性缺血性心脏病具有潜在治疗价值.

目的 明确AC-NP(一种新型的钠尿肽分子)对于低氧性肺动脉高压的在体效应.方法 采用间断性减压低氧的方法复制低氧性肺动脉高压(HPH)大鼠模型,以AC-NP[50 μg/(kg ·d)]治疗HPH大鼠1周.检测分析血流动力学指标,以及右心室和肺动脉的重构情况.结果 低氧可致大鼠肺动脉压异常升高.AC-NP治疗1周显著降低HPH大鼠的肺动脉压、肺血管阻力、右心室肥厚和肺动脉的肌化,同时肺血流量显著增加.另外,静脉急性给予AC-NP可以显著改善HPH大鼠的血流动力学指标.结论 AC-NP对HPH具有一定的治疗作用.

目的:探讨吡格列酮(PIO)减轻内皮素-1(ET-1)引起大鼠心肌细胞损伤的作用及其机制.方法:将原代培养的大鼠心肌细胞分为5组:DMEM组(对照组)、ET-1组、ET-1+ PIO(1×10-9 mol/L)组、ET-1+ PIO(1×10-8mol/L)组及ET-1+ PIO(1×10-7 mol/L)组.将大鼠心肌细胞培养24 h后,吸取培养液,按试剂盒说明书测定心肌细胞培养液中乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)的活性及丙二醛(MDA)的含量.结果:药物干预24h,培养液中LDH的活性ET-1组明显高于对照组(P＜0.01),而ET-1+ PIO组LDH的活性低于ET-1组,其中1×10-8mol/L和1×10-7mol/L PIO+ ET-1组较ET-1组明显降低(分别为P＜0.05,P＜0.01).SOD的活性:ET-1组明显低于对照组(P＜0.01),ET-1+ PIO组高于ET-1组,其中1×10-8 mol/L和1×10-7 mol/L PIO+ ET-1组较ET-1组明显升高(分别为P ＜0.05,P＜0.01).MDA的含量:ET-1组明显高于对照组(P＜0.01),ET-1+ PIO组低于ET-1组,其中1×10-8 mol/L和1×10-7 mol/L PIO+ ET-1组较ET-1组明显降低(分别为P＜0.05,P＜0.01).结论:PIO可保护ET-1引起损伤的心肌细胞,机制可能与抑制脂质过氧化有关.

Objective:To modify the structure and evaluate the vasorelaxing function of natriuretic peptides . Methods :According to the structure‐activity relationship of natural natriuretic peptides (NPs) ,7 kinds of novel NPs (CNAAC 、BNAAC 、BNBAC 、ANCAC 、ANBAC 、BNCAC 、CNBAC) were artificially designed and engineered .Furthermore , perfusion experiments of in vitro blood vessels were performed to evaluate the vasorelaxing effects of these novel NPs ,com‐pared with the natural NPs including atrial natriuretic peptide (ANP) ,brain natriuretic peptide (BNP) ,and C type natri‐uretic peptide(CNP) .Results :Vasorelaxing effects were ranked as :CNP > CNAAC > BNAAC > BNBAC > ANCAC > ANP> BNP > ANBAC > BNCAC > CNBAC .Conclusion :Innovative designed NPs have the activity of their parent molecules ,and might be new candidate drugs against cardiovascular diseases .

目的 观察血管钠肽(VNP)对大鼠腹主动脉的舒张作用及对ATP敏感性钾通道(ATP-sensitive potassium channel,KATP)的作用.方法 采用离体血管灌流方法,测定VNP对血管环张力的影响.采用膜片钳方法观察VNP对KATP通道的影响.结果 VNP对大鼠的腹主动脉具有浓度依赖性舒张作用,该作用无内皮依赖性:VNP对内皮完整的腹主动脉最大舒张率(E max)为(81±8)％,对内皮缺失腹主动脉Emax为(74±6)％.在浴槽内预先孵育优降糖(1×10-6 mol/L)可降低血管对VNP的舒张效应.VNP可增强腹主动脉血管平滑肌细胞KATP通道电流:VNP(1 ×10-6 M)增强KATP通道Emax为(112±24)％,优降糖(1×10-6 mol/L)可消除这一作用.结论 VNP有舒张血管作用,这一作用与增强KATP通道电流有关.

Background/Aims: Neuronostatin, derived from the somatostatin preprohormone, was recently identified to be produced by several tissues exerting a role in cardiovascular regulation and metabolism. Nonetheless, the precise mechanism behind neuronostatin-elicited myocardial responses remains elusive. Methods: This study was designed to elucidate the impact of neuronostatin on cardiac contractile function and the underlying mechanism of action involved. Adult male C57 BL/6 mice were subjected to a bolus injection of neuronostatin (50 μg/kg, i.p.). Echocardiographic, cardiomyocyte contractile and intracellular Ca2+ handling properties were monitored to evaluate the effect of neuronostatin on cardiac function. Western blot analysis was used to examine potential signaling mechanisms involved. Results: Neuronostatin administration suppressed myocardial and cardiomyocyte contractile function and disturbed intracellular Ca2+ homeostasis. We observed enlarged LVESD (with unchanged LVEDD), reduced fractional shortening, depressed peak shortening, maximal velocity of shortening/relengthening, resting and electrically-stimulated rise in intracellular Ca2+, and prolonged relengthening duration in hearts from neuronostatin-treated mice. These effects were accompanied by downregulation of phosphorylation of sarcoplasmic reticulum Ca2+-ATPase (SERCA) and phospholamban (PLB) and activation of AMPK. Conclusion: Our data suggest that the cardiac depressant properties of neuronostatin possibly associated with loss of SERCA phosphorylation and AMPK activation. These findings revealed a potent inhibitory capacity for neuronostatin on cardiac function, the physiological relevance of which deserves further study.

Achyranthes bidentata, a Chinese medicinal herb, is reported to be neuroprotective. However, its role in cardioprotection remains largely unknown. Our present study aimed to investigate the effects of Achyranthes bidentata polypeptides (ABPP) preconditioning on myocardial ischemia/reperfusion (MI/R) injury and to test the possible mechanisms. Rats were treated with ABPP (10 mg/kg/d, i.p.) or saline once daily for one week. Afterward, all the animals were subjected to 30 min of myocardial ischemia followed by 4 h of reperfusion. ABPP preconditioning for one week significantly improved cardiac function following MI/R. Meanwhile, ABPP reduced infarct size, plasma creatine kinase (CK)/lactate dehydrogenase (LDH) activities and myocardial apoptosis at the end of reperfusion in rat hearts. Moreover, ABPP preconditioning significantly inhibited superoxide generation, gp91phox expression, malonaldialdehyde formation and enhanced superoxide dismutase activity in I/R hearts. Furthermore, ABPP treatment inhibited PTEN expression and increased Akt phosphorylation in I/R rat heart. PI3K inhibitor wortmannin blocked Akt activation, and abolished ABPP-stimulated anti-oxidant effect and cardioprotection. Our study demonstrated for the first time that ABPP reduces oxidative stress and exerts cardioprotection against MI/R injury in rats. Inhibition of PTEN and activation of Akt may contribute to the anti-oxidant capacity and cardioprotection of ABPP.

The spiral ganglion, which is primarily composed of spiral ganglion neurons and satellite glial cells, transmits auditory information from sensory hair cells to the central nervous system. Atrial natriuretic peptide (ANP), acting through specific receptors, is a regulatory peptide required for a variety of cardiac, neuronal and glial functions. Although previous studies have provided direct evidence for the presence of ANP and its functional receptors (NPR-A and NPR-C) in the inner ear, their presence within the cochlear spiral ganglion and their regulatory roles during auditory neurotransmission and development is not known. Here we investigated the expression patterns and levels of ANP and its receptors within the cochlear spiral ganglion of the postnatal rat using immunofluorescence and immunoelectron microscopy techniques, reverse transcription-polymerase chain reaction and Western blot analysis. We have demonstrated that ANP and its receptors colocalize in both subtypes of spiral ganglion neurons and in perineuronal satellite glial cells. Furthermore, we have analyzed differential expression levels associated with both mRNA and protein of ANP and its receptors within the rat spiral ganglion during postnatal development. Collectively, our research provides direct evidence for the presence and synthesis of ANP and its receptors in both neuronal and non-neuronal cells within the cochlear spiral ganglion, suggesting possible roles for ANP in modulating neuronal and glial functions, as well as neuron–satellite glial cell communication, within the spiral ganglion during auditory neurotransmission and development.

AIM: To study the effect of ambrisentan and bosentan on pulmonary vascular remodeling in rats with hypoxic pulmonary hypertension(HPH) and to compare the effect of the two drugs.METHODS: Forty Sprague Dawley rats were randomly divided into five groups: control group,model group,ambrisentan group,bosentan group and placebo group(eight rats in each group).Rats in the control group were kept under a normal environment for 4 weeks and rats in other groups were kept under hypobaric hypoxia environment(8 h/day) for 4 weeks.For placebo group,ambrisentan group and bosentan group,sodium choride(2 ml),ambrisentan(5 mg/kg) and bosentan(125 mg/kg) were given,respectively,during the third week.After 4 weeks,mean pulmonary arterial pressure(mPAP) and right ventricular systoic pressure(RVSP) were measured.Indexes of wall thickness of pulmonary arterioles including the percentage of vascular wall thickness/vascular external diameter(WT%) and the percentage of vascular wall area/total vascular area(WA%) were determined by a computerized image analyzer.α-SMA protein expression in pulmonary arteriole was observed by immunohistochemistry.RESULTS: H/E staining revealed that the pulmonary vessel wall was thickened and the vessel lumina decreased in the model and placebo groups.Ambrisentan and bosentan reversed this change.Compared with those in the control group,mPAP,WT%,WA% and protein expression of α-SMA increased significantly in the model and placebo groups.No significant difference was observed in the expression of α-SMA and indexes between ambrisentan group and bosentan group.CONCLUSION: Ambrisentan and bosentan significantly decrease pulmonary artery pressure and reverse pulmonary vessel remodeling in rats with HPH.No significant difference has been found in the curative effect between ambrisentan and bosentan.

AIM: To establish the rat model of high-altitude environment-induced pulmonary hypertension,observe proliferative changes in pulmonary arterial smooth muscle of hypoxic pulmonary vascular remodeling and to explore the effect of bosentan on high-altitude environment-induced pulmonary hypertension in rats and on the expression of platelet-derived growth factor(PDGF) in pulmonary artery in rats with high-altitude environment-induced pulmonary hypertension.METHODS: Rats were exposed to low-pressure and low-oxygen conditions in a self-modulating hypobaric and hypoxic cabin(air pressure 50 kPa,oxygen concentration 10%) to establish the high-altitude environment-induced pulmonary hypertension animal model.Forty male Sprague Dawley rats were randomly divided into four groups: control group,hypoxia group,placebo group and bosentan group.Rats in the control group remained in an orthobaric environment while rats in other groups were kept in hypobaric chamber for 8 h,1 day for 3 weeks,6 weeks and 6 weeks.After 3 weeks' exposure to hypobaric hypoxic environment,sodium chloride(2 ml) or bosentan(100 mg/kg) was administrated to placebo group and bosentan group for another 3 weeks.To observe the morphological changes of pulmonary vessels in rats,immunohistochemical technique was used to assess the abundance and localization of platelet-derived growth factor in pulmonary arteries.RESULTS: Thickening and stenosis of pulmonary arteries were observed in placebo group and bosentan reversed the changes.PDGF was expressed in pulmonary arteries in all four groups and the expression of PDGF increased with the increasing time of hypoxia.CONCLUSION: Bosentan successfully reversed hypoxic pulmonary vascular remodeling,suggesting that bosentan may be used to treat high-altitude environment-induced pulmonary hypertension.Bosentan may have a suppressible effect on the expression of PDGF in rats with high-altitude environment-induced pulmonary hypertension.

Spiral ganglion neurons (SGNs) are the primary auditory neurons in the inner ear, conveying auditory information between sensory hair cells and the central nervous system. Atrial natriuretic peptide (ANP), acting through specific receptors, is a regulatory peptide required for a variety of cardiac and neuronal functions. While the localization of ANP and its receptors (NPR-A and NPR-C) in the inner ear has been widely studied, there is only limited information regarding their localization in cochlear SGNs and their regulatory roles during primary auditory neurotransmission. Here we have investigated the presence of ANP and its receptors in the cochlear spiral ganglion of the postnatal rat using immunohistochemistry, reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analysis. ANP and its receptors are expressed in the cochlear SGNs at both the mRNA and protein level, and co-localize in the cochlear SGNs as shown by immunofluorescence. Our research provides a direct evidence for the presence and synthesis of ANP as well as its receptors in the cochlear SGNs, suggesting a possible role for ANP in modulating the neuronal functions of SGNs via its receptors.

Aims: The purpose of this study was to characterize left ventricular (LV) intracavitary flow during the isovolumic contraction (IVC) period in humans using vector flow mapping. Methods: Color flow Doppler imaging was performed from the apical long‐axis view in 61 patients with heart failure and 58 healthy volunteers. Doppler flow data obtained during IVC were analyzed offline with vector flow mapping. Results: A large vortex was formed from the LV inflow toward the outflow during IVC. In normal subjects, the area of the vortex was sustained, but the flow volume decreased significantly during IVC (P < 0.001). A significant apex‐to‐base flow velocity gradient was shown along the outflow axis on aortic valve opening. However, both the area and flow volume of the vortex decreased more severely during IVC in the patients (P < 0.001). The apex‐to‐base flow velocity gradient along the outflow axis disappeared and a reversed velocity gradient was observed at the basal‐mid level on aortic valve opening. In multivariate models, a decreased LV ejection fraction was the only independent predictor of the percentage decrease in area of the vortex during the IVC (P < 0.001), and a larger QRS width (P = 0.028) and LV end‐systolic long diameter (P = 0.002) were independent predictors of the percentage decrease in flow volume of the vortex. Conclusions: The vortex across the LV inflow–outflow region during IVC facilitates the ejection of blood during early systole, and an unsustained vortex may be associated with impaired cardiac function. (Echocardiography 2012;29:579‐587)