Intraventricular flow visualization in different heart failure stages with blood pump support in a mock circulatory loop

2021 ◽  
pp. 039139882110214
Author(s):  
Guang-Mao Liu ◽  
Fu-Qing Jiang ◽  
Jiang-Ping Song ◽  
Sheng-Shou Hu
Keyword(s):  
Heart Failure ◽  
Standard Deviation ◽  
Aortic Valve ◽  
Left Ventricle ◽  
Left Ventricular ◽  
Blood Pump ◽  
Blood Damage ◽  
Intraventricular Flow ◽  
Pump Inlet ◽  
Strong Vorticity

The intraventricular blood flow changed by blood pump flow dynamics may correlate with thrombosis and ventricular suction. The flow velocity, distribution of streamlines, vorticity, and standard deviation of velocity inside a left ventricle failing to different extents throughout the cardiac cycle when supported by an axial blood pump were measured by particle image velocimetry (PIV) in this study. The results show slower and static flow velocities existed in the central region of the left ventricle near the mitral valve and aortic valve and that were not sensitive to left ventricular (LV) failure degree or LV pressure. Strong vorticity located near the inner LV wall around the LV apex and the blood pump inlet was not sensitive to LV failure degree or LV pressure. Higher standard deviation of the blood velocity at the blood pump inlet decreased with increasing LV failure degree, whereas the standard deviation of the velocity near the atrium increased with increasing intraventricular pressure. The experimental results demonstrated that the risk of thrombosis inside the failing left ventricle is not related to heart failure degree. The “washout” performance of the strong vorticity near the inner LV wall could reduce the thrombotic potential inside the left ventricle and was not related to heart failure degree. The vorticity near the aortic valve was sensitive to LV failure degree but not to LV pressure. We concluded that the risk of blood damage caused by adverse flow inside the left ventricle decreased with increasing LV pressure.

The Results of the Use of Angiotensin Receptor Inhibitors and Neprilisin in Secondary Functional Mitral Regurgitation in Outpatient Practice

2020 ◽  
Vol 75 (5) ◽  
pp. 514-522
Author(s):  
Alexey S. Ryazanov ◽  
Konstantin I. Kapitonov ◽  
Mariya V. Makarovskaya ◽  
Alexey A. Kudryavtsev
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Mitral Regurgitation ◽  
Effective Area ◽  
Left Ventricular ◽  
Functional Mitral Regurgitation ◽  
Angiotensin Receptor ◽  
Optimal Drug ◽  
Patients With Heart Failure ◽  
Valsartan Group

Background. Morbidity and mortality in patients with functional mitral regurgitation (FMR) remains high, however, no pharmacological therapy has been proven to be effective.Aimsto study the effect of sacubitrile/valsartan and valsartan on functional mitral regurgitation in chronic heart failure.Methods.This double-blind study randomly assigned sacubitrile/valsartan or valsartan in addition to standard drug therapy for heart failure among 100 patients with heart failure with chronic FMR (secondary to left ventricular (LV) dysfunction). The primary endpoint was a change in the effective area of the regurgitation hole during the 12-month follow-up. Secondary endpoints included changes in the volume of regurgitation, the final systolic volume of the left ventricle, the final diastolic volume of the left ventricle, and the area of incomplete closure of the mitral valves.Results.The decrease in the effective area of the regurgitation hole was significantly more pronounced in the sacubitrile/valsartan group than in the valsartan group (0.070.066against0.030.058sm2; p=0.018)in the treatment efficacy analysis, which included 100patients (100%). The regurgitation volume also significantly decreased in the sacubitrile/valsartan group compared to the valsartan group (mean difference:8.4ml; 95%CI, from 13.2 until 1.9;р=0.21). There were no significant differences between the groups regarding changes in the area ofincomplete closure of the mitral valves and LV volumes, with the exception of the index of the final LV diastolic volume (p=0.07).Conclusion.Among patients with secondary FMR, sacubitril/valsartan reduced MR more than valsartan. Thus, angiotensin receptor inhibitors and neprilysin can be considered for optimal drug treatment of patients with heart failure and FMR.

Estimation of Left Ventricular Wall Stiffness by Analysis of Late Diastolic Pressure Components

2011 ◽  
Author(s):  
Casandra L. Niebel ◽  
Kelley C. Stewart ◽  
Takahiro Ohara ◽  
John J. Charonko ◽  
Pavlos P. Vlachos ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Diastolic Dysfunction ◽  
Diastolic Pressure ◽  
Left Ventricular Diastolic Dysfunction ◽  
Left Ventricular ◽  
Ventricular Wall ◽  
Ventricular Relaxation ◽  
Wall Stiffness ◽  
Ventricular Diastolic Dysfunction

Left ventricular diastolic dysfunction (LVDD) is any abnormality in the filling of the left ventricle and is conventionally evaluated by analysis of the relaxation driven phase, or early diastole. LVDD has been shown to be a precursor to heart failure and the diagnosis and treatment for diastolic failure is less understood than for systolic failure. Diastole consists of two filling waves, early and late and is primarily dependent on ventricular relaxation and wall stiffness.

Echocardiographic assessment of the aortic valve and left ventricular outflow tract

2005 ◽  
Vol 15 (S1) ◽  
pp. 27-36 ◽  
Author(s):  
Alfred Asante-Korang ◽  
Robert H. Anderson
Keyword(s):  
Aortic Valve ◽  
Left Ventricle ◽  
Left Ventricular Outflow Tract ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Outflow Tract ◽  
Left Heart ◽  
Transesophageal Echocardiogram ◽  
Left Ventricular Outflow ◽  
Echocardiographic Assessment

The previous reviews in this section of our Supplement1,2 have summarized the anatomic components of the ventriculo-arterial junctions, and then assessed the echocardiographic approach to the ventriculo-arterial junction or junctions as seen in the morphologically right ventricle. In this complementary review, we discuss the echocardiographic assessment of the comparable components found in the morphologically left ventricle, specifically the outflow tract and the arterial root. We will address the echocardiographic anatomy of the aortic valvar complex, and we will review the causes of congenital arterial valvar stenosis, using the aortic valve as our example. We will also review the various lesions that, in the outflow of the morphologically left ventricle, can produce subvalvar and supravalvar stenosis. We will then consider the salient features of the left ventricular outflow tract in patients with discordant ventriculo-arterial connections, and double outlet ventricles. To conclude the review, we will briefly address some rarer anomalies that involve the left ventricular outflow tract, showing how the transesophageal echocardiogram is used to assist the surgeon preparing for repair. The essence of the approach will be to consider the malformations as seen at valvar, subvalvar, or supravalvar levels,1 but we should not lose sight of the fact that aortic coarctation or interruption, hypoplasia of the left heart, and malformations of the mitral valve are all part of the spectrum of lesions associated with obstruction to the left ventricular outflow tract. These additional malformations, however, are beyond the scope of this review.

scholarly journals Left ventricular noncompaction—a rare cause of triad: heart failure, ventricular arrhythmias, and systemic embolic events: a case report 

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Despina Toader ◽  
Alina Paraschiv ◽  
Petrișor Tudorașcu ◽  
Diana Tudorașcu ◽  
Constantin Bataiosu ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Magnetic Resonance ◽  
Magnetic Resonance ◽  
Left Ventricle ◽  
Ventricular Arrhythmias ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Left Ventricular Noncompaction ◽  
Ventricular Noncompaction ◽  
The Right

Abstract Background Left ventricular noncompaction is a rare cardiomyopathy characterized by a thin, compacted epicardial layer and a noncompacted endocardial layer, with trabeculations and recesses that communicate with the left ventricular cavity. In the advanced stage of the disease, the classical triad of heart failure, ventricular arrhythmia, and systemic embolization is common. Segments involved are the apex and mid inferior and lateral walls. The right ventricular apex may be affected as well. Case presentation A 29-year-old Caucasian male was hospitalized with dyspnea and fatigue at minimal exertion during the last months before admission. He also described a history of edema of the legs and abdominal pain in the last weeks. Physical examination revealed dyspnea, pulmonary rales, cardiomegaly, hepatomegaly, and splenomegaly. Electrocardiography showed sinus rhythm with nonspecific repolarization changes. Twenty-four-hour Holter monitoring identified ventricular tachycardia episodes with right bundle branch block morphology. Transthoracic echocardiography at admission revealed dilated left ventricle with trabeculations located predominantly at the apex but also in the apical and mid portion of lateral and inferior wall; end-systolic ratio of noncompacted to compacted layers > 2; moderate mitral regurgitation; and reduced left ventricular ejection fraction. Between apical trabeculations, multiple thrombi were found. The right ventricle had normal morphology and function. Speckle-tracking echocardiography also revealed systolic left ventricle dysfunction and solid body rotation. Abdominal echocardiography showed hepatomegaly and splenomegaly. Abdominal computed tomography was suggestive for hepatic and renal infarctions. Laboratory tests revealed high levels of N-terminal pro-brain natriuretic peptide and liver enzymes. Cardiac magnetic resonance evaluation at 1 month after discharge confirmed the diagnosis. The patient received anticoagulants, antiarrhythmics, and heart failure treatment. After 2 months, before device implantation, he presented clinical improvement, and echocardiographic evaluation did not detect thrombi in the left ventricle. Coronary angiography was within normal range. A cardioverter defibrillator was implanted for prevention of sudden cardiac death. Conclusions Left ventricular noncompaction is rare cardiomyopathy, but it should always be considered as a possible diagnosis in a patient hospitalized with heart failure, ventricular arrhythmias, and systemic embolic events. Echocardiography and cardiac magnetic resonance are essential imaging tools for diagnosis and follow-up.

Regulation of K+ and Ca2+ channels in experimental cardiac failure

1991 ◽  
Vol 261 (6) ◽  
pp. H1979-H1987 ◽  
Author(s):  
M. Gopalakrishnan ◽  
D. J. Triggle ◽  
A. Rutledge ◽  
Y. W. Kwon ◽  
J. A. Bauer ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Cardiac Failure ◽  
Radioligand Binding ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
The Right

To examine the status of ATP-sensitive K+ (K+ATP) channels and 1,4-dihydropyridine-sensitive Ca2+ (Ca2+DHP) channels during experimental cardiac failure, we have measured the radioligand binding properties of [3H]glyburide and [3H]PN 200 110, respectively, in tissue homogenates from the rat cardiac left ventricle, right ventricle, and brain 4 wk after myocardial infarction induced by left coronary artery ligation. The maximal values (Bmax) for [3H]glyburide and [3H]PN 200 110 binding were reduced by 39 and 40%, respectively, in the left ventricle, and these reductions showed a good correlation with the right ventricle-to-body weight ratio in heart-failure rats. The ligand binding affinities were not altered. In the hypertrophied right ventricle, Bmax values for both the ligands were not significantly different when data were normalized to DNA content or right ventricle weights but showed an apparent reduction when normalized to unit protein or tissue weight. Moderate reductions in channel densities were observed also in whole brain homogenates from heart failure rats. Assessment of muscarinic receptors, beta-adrenoceptors and alpha 1-adrenoceptors by [3H]quinuclidinyl benzilate, [3H]dihydroalprenolol, and [3H]prazosin showed reductions in left ventricular muscarinic and beta-adrenoceptor densities but not in alpha 1-adrenoceptor densities, consistent with earlier observations. It is suggested that these changes may in part contribute to the pathology of cardiac failure.

scholarly journals An Echocardiographic Evaluation of Dilated Cardiomyopathy in a Tertiary Care Hospital

2019 ◽  
Vol 57 (215) ◽  
Author(s):  
Raj Kumar Thapa ◽  
Kanchan K.C ◽  
Rishi Khatri ◽  
Devendra Khatri ◽  
Rajeeb Kumar Deo ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Left Ventricle ◽  
Ejection Fraction ◽  
Dilated Cardiomyopathy ◽  
Tertiary Care ◽  
Left Ventricular ◽  
Care Hospital ◽  
Echocardiographic Evaluation ◽  
Significant Difference

Introduction: Cardiomyopathies are diseases of heart muscle that may originate from genetic defects, cardiac myocyte injury or infiltration of myocardial tissues. Dilated cardiomyopathy is the most common phenotype and is often a final common pathway of numerous cardiac insults. Mostly it remains unknown in the absence of echocardiography, histopathology and genetic evaluation. Though common it is underdiagnosed with not much of data available in our setup.Methods: This study was analytical cross-sectional study of hospital data on Echocardiographic findings in 65 patients of DCM visiting cardiology unit for Echocardiographic evaluation from 1st of February to 31st July 2018 for the period of six months in Shree Birendra Hospital, a tertiary care military hospital at Chhauni, Kathmandu. Pediatric age group patients and those who refused to give consent were excluded. Data obtained were entered in Microsoft Excel 2010 and analyzed by IBM SPSS 21.Results: Among 65 patients enrolled 40 (61%) were male and 25 (39%) female with male to female ratio of 1.6:1. Elderly people (61-75 years) with an average age of 65 were commonly involved and they presented mostly with congestive heart failure, 32 (49%). Echocardiographic evaluation showed 36 (55%) with mildly dilated Left Ventricle (5.6-6.0cm). Majority had reduced Left ventricular systolic function with an average Ejection fraction (EF) of 39.6%. No significant difference between male and female with the average EF% (P=0.990) and there was no significant relation between age and average EF% (P=0.091).Conclusions: Dilated Cardiomyopathy is the commonest cardiomyopathy phenotype mostly presenting with congestive heart failure. It is often underdiagnosed in our part of the world, however echocardiography will easily detect the condition. Keywords: dilated cardiomyopathy; echocardiography; ejection fraction; left ventricle.

In the Loop—Left Ventricular Pressures

2011 ◽  
pp. 42-47
Author(s):  
James R. Munis
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Aortic Valve ◽  
Left Ventricle ◽  
Stroke Volume ◽  
Cardiovascular System ◽  
Aortic Root ◽  
Left Ventricular ◽  
Root Pressure ◽  
The Third

We've already looked at 2 types of pressure that affect physiology (atmospheric and hydrostatic pressure). Now let's consider the third: vascular pressures that result from mechanical events in the cardiovascular system. As you already know, cardiac output can be defined as the product of heart rate times stroke volume. Heart rate is self-explanatory. Stroke volume is determined by 3 factors—preload, afterload, and inotropy—and these determinants are in turn dependent on how the left ventricle handles pressure. In a pressure-volume loop, ‘afterload’ is represented by the pressure at the end of isovolumic contraction—just when the aortic valve opens (because the ventricular pressure is now higher than aortic root pressure). These loops not only are straightforward but are easier to construct just by thinking them through, rather than by memorization.

scholarly journals Stochastic Modeling and Dynamic Analysis of the Cardiovascular System with Rotary Left Ventricular Assist Devices

2019 ◽  
Vol 2019 ◽  
pp. 1-18 ◽  
Author(s):  
Jeongeun Son ◽  
Dongping Du ◽  
Yuncheng Du
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Pump Power ◽  
Aortic Valve ◽  
Cardiovascular System ◽  
Left Ventricular ◽  
Ventricular Assist Devices ◽  
Left Ventricular Assist Devices ◽  
Ventricular Assist ◽  
Left Ventricular Assist

Left ventricular assist devices (LVADs) have been used for end-stage heart failure patients as a therapeutic option. The aortic valve plays a critical role in heart failure and its treatment with a LVAD. The cardiovascular-LVAD model is often used to investigate the physiological demands required by patients and predict the hemodynamic of the native heart supported with a LVAD. As it is a “bridge-to-recovery” treatment, it is important to maintain appropriate and active dynamics of the aortic valve and the cardiac output of the native heart, which requires that the LVAD pump be adjusted so that a proper balance between the blood contributed through the aortic valve and the pump is maintained. In this paper, we investigate how the pump power of the LVAD pump can affect the dynamic behaviors of the aortic valve for different levels of activity and different severities of heart failure. Our objective is to identify a critical value of the pump power (i.e., breakpoint) to ensure that the LVAD pump does not take over the pumping function in the cardiovascular-pump system and share the ejected blood with the left ventricle to help the heart to recover. In addition, the hemodynamic often involves variability due to patients’ heterogeneity and the stochastic nature of the cardiovascular system. The variability poses significant challenges to understanding dynamic behaviors of the aortic valve and cardiac output. A generalized polynomial chaos (gPC) expansion is used in this work to develop a stochastic cardiovascular-pump model for efficient uncertainty propagation, from which it is possible to rapidly calculate the variance in the aortic valve opening duration and the cardiac output in the presence of variability. The simulation results show that the gPC-based cardiovascular-pump model is a reliable platform that can provide useful information to understand the effect of the LVAD pump on the hemodynamic of the heart.

scholarly journals Use of Sacubitril/valsartan in patients with cardio toxicity and heart failure due to chemotherapy

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Vanesa Gregorietti ◽  
Teresa Lopez Fernandez ◽  
Diego Costa ◽  
Elías Ortega Chahla ◽  
Andrés J. Daniele
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Serum Creatinine ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Internal Diameter ◽  
Walk Test ◽  
Aldosterone Antagonists ◽  
Treatment Standard

Abstract Background Cancer therapy-related cardiac dysfunction (CTRCD) is a critical problem with an impact on both oncological and cardiovascular prognosis, especially when it prevents patients from receiving cancer treatment. Standard therapy for heart failure (HF) is recommended for CTRCD, but there is no well-established evidence on how sacubitril/valsartan may help cancer patients with cardiotoxicity. Objectives The aim of this trial was to study the effectiveness of sacubitril-valsartan in patients with CTRCD treated in cardio-oncology units. Methods We enrolled 635 patients with breast cancer and followed them with echocardiography and NT- proBNP. Patients who developed left ventricular dysfunction and heart failure were treated with angiotensin-converting enzyme inhibitors (ACEI) (enalapril) or angiotensin receptor blockers (ARB) (valsartan), aldosterone antagonists (eplerenone), digitalis and diuretics (furosemide), as needed. When patients remained symptomatic and met the PARADIGM-HF inclusion criteria, sacubitril/valsartan was started instead of enalapril or valsartan. We analyzed clinical, laboratory and echocardiographic variables to determine the beneficial effects of sacubitril/valsartan on left ventricular remodeling (improvement of left ventricular ejection fraction (LVEF), left ventricle internal diameter in diastole), diastolic dysfunction (E/e’ ratio), reduction in NT-proBNP levels, New York Heart Association (NHYA) class and improvement in the 6-min walk test. Also, we analyzed serum creatinine and potassium levels to determine treatmentsafety in this population. Median follow-up was 20 months. Results Twenty-eight patients developed cardiotoxicity and were treated with sacubitril/valsartan. The sacubitril/valsartan dose was 100 mg (sacubitril 49 mg/valsartan 51 mg) in 12 patients (42.85%) and 200 mg (sacubitril 97 mg/valsartan 103 mg) in 16 patients (57.15%). No deaths were reported, and one patient underwent heart transplantation. Baseline median NT-proBNP was 997.5 pg/ml (IQR 663.8 — 2380.8), which decreased to a median of 416.5 pg/ml (IQR 192.0–798.2) on follow-up with p < 0.001. Baseline NYHA functional class was III (78.6%) or IV (21.4%), and it improved to I (57.1%) or II (42.9%) on follow-up. LVEF increased with treatment from 26.7 ± 5.4% to 32.3 ± 5.5% (p < 0.001). There were also significant improvements in left ventricle internal diameter in diastole (LVIDD), diastolic function, 6-min walk test, and mitral valve regurgitation. There were no differences between basal and follow-up levels of serum creatinine or potassium. Conclusion Sacubitril/valsartan might be a promising treatment option in patients with refractory CTRCD.

Congestive Heart Failure in Copper-Deficient Mice

2003 ◽  
Vol 228 (7) ◽  
pp. 811-817 ◽  
Author(s):  
Laila Elsherif ◽  
Raymond V. Ortines ◽  
Jack T. Saari ◽  
Y. James Kang
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Left Ventricle ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Experimental Models ◽  
Left Ventricular ◽  
Mouse Heart ◽  
Total Period

Copper Deficiency (CuD) leads to hypertrophic cardiomyopathy in various experimental models. The morphological, electrophysiological, and molecular aspects of this hypertrophy have been under investigation for a long time. However the transition from compensated hypertrophy to decompensated heart failure has not been investigated in the study of CuD. We set out to investigate the contractile and hemodynamic parameters of the CuD mouse heart and to determine whether heart failure follows hypertrophy in the CuD heart. Dams of FVB mice were fed CuD or copper-adequate (CuA) diet starting from the third day post delivery and the weanling pups were fed the same diet for a total period of 5 weeks (pre- and postweanling). At week 4, the functional parameters of the heart were analyzed using a surgical technique for catheterizing the left ventricle. A significant decrease in left ventricle systolic pressure was observed with no significant change in heart rate, and more importantly contractility as measured by the maximal rate of left ventricular pressure rise (+dP/dt) and decline (−dP/dt) were significantly depressed in the CuD mice. However, left ventricle end diastolic pressure was elevated, and relaxation was impaired in the CuD animals; the duration of relaxation was prolonged. In addition to significant changes in the basal level of cardiac function, CuD hearts had a blunted response to the stimulation of the β-adrenergic agonist isoproterenol. Furthermore, morphological analysis revealed increased collagen accumulation in the CuD hearts along with lipid deposition. This study shows that CuD leads to systolic and diastolic dysfunction in association with histopathological changes, which are indices commonly used to diagnose congestive heart failure.

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