Measurement of deformation of canine epicardium in vivo during cardiac cycle

1980 ◽  
Vol 239 (3) ◽  
pp. H432-H437 ◽  
Author(s):  
T. Arts ◽  
R. S. Reneman
Keyword(s):  
Magnetic Field ◽  
Cardiac Cycle ◽  
Experimental Situation ◽  
Accurate Method ◽  
Left Ventricular ◽  
Shear Angle ◽  
Left Ventricular Ejection ◽  
Natural Strain ◽  
The Right

A new accurate method to determine the deformation of the epicardial surface during the cardiac cycle in vivo is described. Epicardial deformation is determined by a circumferential strain, a base-to-apex strain, and a shear angle. In the measuring setup, one magnetic field-generating coil (MFGC) and two sensor coils are attached to the epicardium, thus forming an approximately right-angled triangle with the MFGC at the right-angled corner and the sides containing the right angle, parallel to the circumferential and base-to-apex direction, respectively. The MFGC generates a magnetic field that rotates around the axis of the coil. The strength of that field decreases with increasing distance. Both strains and the shear angle are derived from the amplitudes of the voltages induced in the sensor coils and their phase difference. In the experimental situation the accuracy of the measurement of strain and shear angle is +/- 0.005 and +/- 1 degree, respectively. The device has a frequency response of 100 Hz (-3 dB) and practically no zero drift. In four open-chest dogs during left ventricular ejection, circumferential natural strain, base-to-apex natural strain, and shear angle at the epicardium of the left ventricular free wall ranged from -0.06 to -0.13, from -0.02 to -0.08, and from 6.8 degrees to 11.5 degrees, respectively.

scholarly journals Adropin-based dual treatment enhances the therapeutic potential of mesenchymal stem cells in rat myocardial infarction

2021 ◽  
Vol 12 (6) ◽  
Author(s):  
HuiYa Li ◽  
DanQing Hu ◽  
Guilin Chen ◽  
DeDong Zheng ◽  
ShuMei Li ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Therapeutic Potential ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Paracrine Factors ◽  
Dual Treatment

AbstractBoth weak survival ability of stem cells and hostile microenvironment are dual dilemma for cell therapy. Adropin, a bioactive substance, has been demonstrated to be cytoprotective. We therefore hypothesized that adropin may produce dual protective effects on the therapeutic potential of stem cells in myocardial infarction by employing an adropin-based dual treatment of promoting stem cell survival in vitro and modifying microenvironment in vivo. In the current study, adropin (25 ng/ml) in vitro reduced hydrogen peroxide-induced apoptosis in rat bone marrow mesenchymal stem cells (MSCs) and improved MSCs survival with increased phosphorylation of Akt and extracellular regulated protein kinases (ERK) l/2. Adropin-induced cytoprotection was blocked by the inhibitors of Akt and ERK1/2. The left main coronary artery of rats was ligated for 3 or 28 days to induce myocardial infarction. Bromodeoxyuridine (BrdU)-labeled MSCs, which were in vitro pretreated with adropin, were in vivo intramyocardially injected after ischemia, following an intravenous injection of 0.2 mg/kg adropin (dual treatment). Compared with MSCs transplantation alone, the dual treatment with adropin reported a higher level of interleukin-10, a lower level of tumor necrosis factor-α and interleukin-1β in plasma at day 3, and higher left ventricular ejection fraction and expression of paracrine factors at day 28, with less myocardial fibrosis and higher capillary density, and produced more surviving BrdU-positive cells at day 3 and 28. In conclusion, our data evidence that adropin-based dual treatment may enhance the therapeutic potential of MSCs to repair myocardium through paracrine mechanism via the pro-survival pathways.

scholarly journals Assessment of aortic and mitral annuli dynamics during the cardiac cycle using speckle tracking echocardiography

2014 ◽  
Vol 1 (1) ◽  
pp. 11-16 ◽  
Author(s):  
Wenjuan Bai ◽  
Hui Li ◽  
Hong Tang ◽  
Qing Zhang ◽  
Ye Zhu ◽  
...  
Keyword(s):  
Left Ventricular Function ◽  
Ventricular Function ◽  
Speckle Tracking ◽  
Cardiac Cycle ◽  
Speckle Tracking Echocardiography ◽  
Left Ventricular ◽  
Healthy Adults ◽  
Aortic Annulus ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction

The aims of this study were i) to evaluate mitral and aortic annuli excursion, and aortomitral angle (AMA) during the cardiac cycle in healthy adults using two-dimensional speckle tracking echocardiography, ii) to assess two annuli dynamics and coupling behaviors as an integral, and iii) to detect the relation between two annuli and left ventricular ejection fraction (LVEF). A total of 74 healthy adults underwent transthoracic echocardiography. In the parasternal long-axis view, a number of points were extracted, including right coronary aortic annular, aortomitral fibrous junction, and posterior mitral annular points. The annuli excursion and AMA were measured using a speckle tracking-derived software during the cardiac cycle. During the isovolumic contraction and the isovolumic relaxation phase, annuli excursion and AMA remain stable for a short time. During the systole, annuli excursion increased sharply to the maximum, while AMA narrowed quickly to the minimum value. During the diastole, there are three patterns of decrease in annuli excursion and AMA expansion in different phases. The annuli excursion of three points correlates well with the LVEF (right coronary aortic annulus excursion, r=0.71, P<0.05; non-coronary aortic annulus excursion, r=0.70, P<0.05; posterior mitral annulus excursion, r=0.82, P<0.05). Moreover, there are positive correlations between annuli excursion and the variation of AMA (r=0.60, P<0.05). The annuli excursion and AMA have various regular patterns in healthy adults. The interactions of mitral and aortic annuli correlate with the left ventricular function. Our findings may have relevance to the evaluation of left ventricular function and presurgical planning of patients with valvular diseases.

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.

Activity of in vivo canine cardiac plexus neurons

1988 ◽  
Vol 255 (4) ◽  
pp. H789-H800 ◽  
Author(s):  
M. Gagliardi ◽  
W. C. Randall ◽  
D. Bieger ◽  
R. D. Wurster ◽  
D. A. Hopkins ◽  
...  
Keyword(s):  
Cardiac Cycle ◽  
Pulmonary Veins ◽  
Systolic Pressure ◽  
Identified Neurons ◽  
Fat Pad ◽  
Respiratory Dynamics ◽  
The Right ◽  
Ganglion Neurons ◽  
Ganglionated Plexus

The activity of 394 spontaneously active neurons located in the ganglionated plexus of the ventral epicardial fat pad overlying the right atrium and pulmonary veins was recorded. Ganglia that contained various numbers of neurons, many with two or more nucleoli, were identified adjacent to the recording sites. Spontaneous activity was correlated with the cardiac cycle in 39% and with the respiratory cycle in 8% of the identified neurons. Neuronal activity occurred in specific phases of the cardiac cycle when arterial pressure was between approximately 70 and 175 mmHg. During increases in systolic pressure induced by positive inotropic agents or aortic occlusion, responses of neurons that displayed cardiovascular-related activity were enhanced. These responses persisted after acute decentralization. The activity of 14% of all identified neurons was altered when discrete regions of the heart, great thoracic vessels, or lungs were mechanically distorted by gentle touch. Trains of stimuli, but not single stimuli, delivered to the vagosympathetic complexes, stellate ganglia, or cardiopulmonary nerves activated ganglionic neurons in intact or acutely decentralized preparations. It is concluded that the activity of some cardiac ganglion neurons is related to cardiovascular or respiratory dynamics and that some of these neurons receive inputs from sympathetic and parasympathetic efferent axons as well as from cardiac mechanoreceptors.

Electrophysiologic properties and ventricular fibrillation in normal and myopathic hearts

1999 ◽  
Vol 77 (7) ◽  
pp. 510-519 ◽  
Author(s):  
Katherine M Kavanagh ◽  
Patricia A Guerrero ◽  
Bodh I Jugdutt ◽  
Francis X Witkowski ◽  
Jeffrey E Saffitz
Keyword(s):  
Ventricular Fibrillation ◽  
Myocardial Dysfunction ◽  
Myocardial Cell ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Control Group ◽  
Functional Abnormality ◽  
Ventricular Ejection Fraction ◽  
Anisotropic Properties

This study tests the hypothesis that moderate myocardial dysfunction is associated with altered myocardial anisotropic properties and structurally altered ventricular fibrillation (VF). Mongrel dogs were randomized to either a control group or a group that was rapidly paced at 250 beats/min until the left ventricular ejection fraction was [Formula: see text] 40%. Changes in anisotropic properties and the electrical characteristics of VF associated with the development of moderate myocardial dysfunction were assessed by microminiature epicardial mapping studies. In vivo conduction, refractory periods, and repolarization times were prolonged in both longitudinal and transverse directions in myopathic animals versus controls. VF was different in myopathic versus control animals. There were significantly more conducted deflections during VF in normal hearts compared with myopathic hearts. Propagated deflection-to-deflection intervals during VF were significantly longer in myopathic hearts compared with controls (125.5 ± 49.06 versus 103.4 ± 32.9 ms, p = 0.009). There were no abnormalities in cell size, cell shape, or the number of intercellular gap junctions and there was no detectable change in the expression of the gap junction proteins Cx43 and Cx45. Moderate myocardial dysfunction is associated with significant electrophysiological abnormalities in the absence of changes in myocardial cell morphology or intercellular connections, suggesting a functional abnormality in cell-to-cell communication.Key words: cardiomyopathy, anisotropy, fibrillation, defibrillation.

Abstract 165: The 18 kDa FGF-2 Prevents the Doxorubicin-induced Cardiac Damage and Amp-activated Kinase Activation, in vitro and in vivo

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Navid Koleini ◽  
Jon Jon Santiago ◽  
Barbara E Nickel ◽  
Robert Fandrich ◽  
Davinder S Jassal ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Cell Death ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Wild Type ◽  
Rat Cardiomyocytes ◽  
Ventricular Ejection Fraction ◽  
Compound C

Introduction: Protection of the heart from chemotherapeutic (Doxorubicin, DOX) drug-induced toxicity is a desirable goal, to limit side effects of cancer treatments. DOX toxicity has been linked to the activation (phosphorylation) of the AMP-activated kinase, AMPK. The 18 kDa low molecular weight isoform of fibroblast growth factor 2 (Lo-FGF-2) is a known cardioprotective and cytoprotective agent. In this study we have tested the ability of Lo-FGF-2 to protect from DOX-induced damage in rat cardiomyocytes in vitro, and in transgenic mouse models in vivo, in relation to AMPK activation. Methods: Rat neonatal cardiomyocytes in culture were exposed to DOX (0.5 μM) in the presence or absence of pre-treatment Lo-FGF-2 (10 ng/ml). Compound C was used to block phosphorylation (activity) of AMPK. Levels of cell viability/death (using Calcein-AM/Propidium iodide assay), phospho -and total AMPK, and apoptotic markers such as active caspase 3 were analyzed. In addition, transgenic mice expressing only Lo-FGF2, and wild type mice, expressing both high molecular weight (Hi-FGF2) as well as Lo-FGF2 were subjected to DOX injection (20 mg/kg, intraperitoneal); echocardiography was used to examine cardiac function at baseline and at 10 days post-DOX. Results: DOX-induced cell death of cardiomyocytes in culture was maximal at 24 hours post-DOX coinciding with significantly increased in activated (phosphorylated) AMPK. Compound C attenuated DOX-induced cardiomyocyte loss. Pre-incubation with Lo-FGF-2 decreased DOX induced cell death, and also attenuated the phosphorylation of AMPK post-DOX. Relative levels of phospho-AMPK were lower in the hearts of Lo-FGF2-expressing male mice compared to wild type. DOX-induced loss of contractile function (left ventricular ejection fraction and endocardial velocity) was negligible in Lo-FGF2-expressing mice but significant in wild type mice. Conclusion: Lo-FGF-2 protects the heart from DOX-induced damage in vitro and in vivo, by a mechanism likely involving an attenuation of AMPK activity.

scholarly journals P798 Right atrial phasic function and correlation with right ventricular function in patients with reduced left ventricular ejection fraction and no pulmonary hypertension:insights from 3D echocardiography

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
A E Vijiiac ◽  
D Muraru ◽  
F Jarjour ◽  
K Kupczynska ◽  
C Palermo ◽  
...  
Keyword(s):  
Left Ventricular Ejection Fraction ◽  
Ejection Fraction ◽  
Right Ventricular ◽  
Three Dimensional ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Pump Function ◽  
The Right ◽  
Conduit Function

Abstract Background The right atrium (RA) is a highly dynamic chamber with 3 mechanical functions (reservoir, conduit, booster pump) and prognostic implications in heart failure (HF) and pulmonary hypertension (PH). However, RA function and its interplay with the right ventricular (RV) performance in patients (pts) with reduced left ventricular ejection fraction (LVEF) and without PH remain to be clarified. Methods We used three-dimensional echocardiography to study 55 pts (61 ± 14 years, 43 men) with LVEF &lt; 40% no more than mild tricuspid regurgitation (TR), and maximum velocity of the TR jet &lt; 3 m/s. We measured the three-dimensional RA total, passive, active ejection volumes (EV) and the respective emptying fractions (EF). In addition, we compared RV volumes and ejection fraction (RVEF) between patients with normal and abnormal RA function. Results Mean LVEF was 30 ± 7%. Mean echo-derived pulmonary vascular resistance was 1.64 ± 0.54 Wood units. 28 pts (51%) had reduced RA reservoir function (total EF = 34 ± 9%), 34 pts (62%) had reduced RA conduit function (passive EF = 15 ± 4%), and 10 pts (18%) had reduced RA pump function (active EF = 11 ± 3%). Pts with reduced RA reservoir function showed larger RV end-systolic volume (RVESV 124 ± 48ml vs. 90 ± 32ml; p = 0.004) and lower RVEF (38 ± 8% vs. 46 ± 6%; p &lt; 0.001) than pts with normal RA function. Pts with reduced RA conduit function showed smaller RV stroke volume (RVSV 65 ± 19 ml vs. 80 ± 22ml; p = 0.009). Pts with impaired RA pump function showed larger RVESV (142 ± 45ml vs. 99 ± 41ml; p = 0.02) and lower RVEF (36 ± 6% vs. 43 ± 8%; p = 0.006). RVESV was positively correlated with total (r2 = 0.47, p &lt; 0.001), passive (r2 = 0.29, p = 0.03) and active (r2 = 0.39, p = 0.003) RAEV, while it was negatively correlated with total (r2=-0.41, p = 0.002), passive (r2=-0.34, p = 0.01) and active (r2=-0.31, p = 0.02) RAEF. RVSV showed a positive correlation with both total (r2 = 0.4, p = 0.002) and passive (r2 = 0.41, p = 0.002) RAEV. Finally, RVEF was positively correlated with total (r2 = 0.51, p &lt; 0.001), passive (r2 = 0.47, p &lt; 0.001), and active (r2 = 0.36, p = 0.007) RAEF. Conclusions RA dysfunction is not uncommon in pts with reduced LVEF, even in the absence of PH. In these pts, RA function is associated with significant changes in RV function. The RA acts as a dynamic modulator of RV pump function by redistributing RV filling and ejection force among reservoir, conduit and pump functions in the setting of altered hemodynamics. The clinical and prognostic significance of RA function in pts with reduced LVEF warrant further studies.

Unequal right and left ventricular ejection with ectopic beats

1962 ◽  
Vol 203 (6) ◽  
pp. 1141-1144 ◽  
Author(s):  
Jay M. Levy ◽  
Emmanuel Mesel ◽  
Abraham M. Rudolph
Keyword(s):  
Pulmonary Artery ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Pulmonary Flow ◽  
Anesthetized Dogs ◽  
Ectopic Beats ◽  
The Difference ◽  
The Right ◽  
Ventricular Depolarization

Simultaneous right and left ventricular stroke volumes were measured with electromagnetic flow probes in open-chest, anesthetized dogs. Atrial ectopic beats with normal ventricular depolarization produced differences between right and left ventricular stroke output, although the right and left ventricular pressures were proportionately reduced to an equal extent. This imbalance in volume ejected was a result of the differences in diastolic level, related to peak systolic pressure, in the aorta compared with pulmonary artery. With ventricular ectopic beats, the stimulated ventricle failed to develop the same percentage of control pressure as did the contralateral ventricle. The difference between aortic and pulmonary flow was thus less marked with right ventricular ectopic beats, and exaggerated with left ventricular ectopic beats.

Comprehensive transthoracic cardiac imaging in mice using ultrasound biomicroscopy with anatomical confirmation by magnetic resonance imaging

2004 ◽  
Vol 18 (2) ◽  
pp. 232-244 ◽  
Author(s):  
Yu-Qing Zhou ◽  
F. Stuart Foster ◽  
Brian J. Nieman ◽  
Lorinda Davidson ◽  
X. Josette Chen ◽  
...  
Keyword(s):  
Cardiac Imaging ◽  
Superior Vena ◽  
Main Pulmonary Artery ◽  
Vena Cava ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Ascending Aorta ◽  
High Frequency Ultrasound ◽  
The Right

High-frequency ultrasound biomicroscopy (UBM) has recently emerged as a high-resolution means of phenotyping genetically altered mice and has great potential to evaluate the cardiac morphology and hemodynamics of mouse mutants. However, there is no standard procedure of in vivo transthoracic cardiac imaging using UBM to comprehensively phenotype the adult mice. In this paper, the characteristic mouse thoracic anatomy is elucidated using magnetic resonance (MR) imaging on fixed mice. Besides the left parasternal and apical windows commonly used for transthoracic ultrasound cardiac imaging, a very useful right parasternal window is found. We present strategies for optimal visualization using UBM of key cardiac structures including: 1) the right atrial inflow channels such as the right superior vena cava; 2) the right ventricular inflow tract via the tricuspid orifice; 3) the right ventricular outflow tract to the main pulmonary artery; 4) the left atrial inflow channel, e.g., pulmonary vein; 5) the left ventricular inflow tract via the mitral orifice; 6) the left ventricular outflow tract to the ascending aorta; 7) the left coronary artery; and 8) the aortic arch and associated branches. Two-dimensional ultrasound images of these cardiac regions are correlated to similar sections in the three-dimensional MR data set to verify anatomical details of the in vivo UBM imaging. Dimensions of the left ventricle and ascending aorta are measured by M-mode. Flow velocities are recorded using Doppler at six representative intracardiac locations: right superior vena cava, tricuspid orifice, main pulmonary artery, pulmonary vein, mitral orifice, and ascending aorta. The methodologies and baseline measurements of inbred mice provide a useful guide for investigators applying the high-frequency ultrasound imaging to mouse cardiac phenotyping.

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