Epicardial Deformation Research Articles

Optical mapping of cardiac electromechanics in beating in vivo hearts

Optical mapping has been widely used in the study of cardiac electrophysiology in motion-arrested, ex vivo heart preparations. Recent developments in motion artifact mitigation techniques have made it possible to optically map beating ex vivo hearts, enabling the study of cardiac electromechanics using optical mapping. However, the ex vivo setting imposes limitations on optical mapping such as altered metabolic states, oversimplified mechanical loads, and the absence of neurohormonal regulation. In this study, we demonstrate optical electromechanical mapping in an in vivo heart preparation. Swine hearts were exposed via median sternotomy. Voltage-sensitive dye, either di-4-ANEQ(F)PTEA or di-5-ANEQ(F)PTEA, was injected into the left anterior descending artery. Fluorescence was excited by alternating green and amber light for excitation ratiometry. Cardiac motion during sinus and paced rhythm was tracked using a marker-based method. Motion tracking and excitation ratiometry successfully corrected most motion artifact in the membrane potential signal. Marker-based motion tracking also allowed simultaneous measurement of epicardial deformation. Reconstructed membrane potential and mechanical deformation measurements were validated using monophasic action potentials and sonomicrometry, respectively. Di-5-ANEQ(F)PTEA produced longer working time and higher signal/noise ratio than di-4-ANEQ(F)PTEA. In addition, we demonstrate potential applications of the new optical mapping system including electromechanical mapping during vagal nerve stimulation, fibrillation/defibrillation. and acute regional ischemia. In conclusion, although some technical limitations remain, optical mapping experiments that simultaneously image electrical and mechanical function can be conducted in beating, in vivo hearts.

A0524 Differentially Expressed Genes in Accumulated Epicardial Adipose Tissue Linked to Early Impaired Systolic Cardiac Deformation Ability in a Rat Model of Metabolic Syndrome

Objectives: This study aimed to detect early impairment of systolic cardiac function by two-dimensional spackle-tracking strain and strain rate analysis and it's link to epicardial adipose tissue (EAT) in a rat model of metabolic syndrome (MetS). Methods: Sixteen male six-week old SD rats were randomly divided into MetS and control groups. MetS model rats were injected with STZ (15 mg/kg) and fed with high-fat, high-salt diet and water containing 0.02% L-NAME and 10% glucose. All the rats were fed for six weeks. Plasma levels of glucose, insulin and lipids were measured. OGTT and blood pressure measurement were conducted. LVEF was calculated with M-mode echocardiography. Systolic strain and strain rate were analyzed with B-mode echocardiography. Differentially expressed genes in EAT was quantified by genome-wide expression profiling microarray. Results: MetS model rats had higher body weight, blood pressure, plasma glucose and lipids levels (P < 0.05). LVEF, endocardial systolic radial and circumferential strain and strain rate of left ventricle in MetS rats were not different from the controls (P > 0.05). Epicardial systolic radial strain and strain rate in MetS rats were also not different from the controls (P > 0.05). However, epicardial systolic circumferential strain and strain rate in MetS rats were less than the controls (P < 0.05). EAT mass related to impaired epicardial deformation ability negatively (P < 0.01). There were thirty-three differentially-expressed genes in hypertrophic cardiomyo pathway, cardiac muscle contraction pathway, adipo-cytokine signaling pathway or related to heart contraction and lipid storage in EAT in MetS rats. Conclusion: Early impairment of systolic cardiac deformation ability in MetS was possibly myocardial layer-specific. Differentially-expressed genes in EAT possibly played some effects on it.

Reduction of Visual Disruptions in Coronary Cine-Angiography for Better Diagnostic Viewing

Coronary angiography is an invasive medical imaging modality which is widely used as a preliminary diagnostic method in Interventional Cardiology for detection of luminal obstructions in Coronary Arteries (CA). Noise, non-uniform illumination, low contrast and epicardial motion are considered as the reported visual degradations which are automatically recorded in Coronary angiography. Further, those factors form certain unpredictable obstructions during the angiography based disease diagnosis. In this study, it has been proposed a frequency filtering based frame enhancement method for surmounting those problems and improving the visual quality of the angiograms. The proposed method is based on homomorphic butter worth high pass filter and empirically validated contrast stretching technique. Further, the optical flow based frame stabilization method has been applied in the later stages of the proposed method for correcting the epicardial deformations. The results of the study clearly emphasized the visual improvement obtained from this method. The enhanced angiography frames produced in this study can be recommended for reliable stenosis detection. Further, these enhanced frames can be further used for quantitative stenosis assessment.

Optical Mapping of Membrane Potential and Epicardial Deformation in Beating Hearts

Cardiac optical mapping uses potentiometric fluorescent dyes to image membrane potential (Vm). An important limitation of conventional optical mapping is that contraction is usually arrested pharmacologically to prevent motion artifacts from obscuring Vm signals. However, these agents may alter electrophysiology, and by abolishing contraction, also prevent optical mapping from being used to study coupling between electrical and mechanical function. Here, we present a method to simultaneously map Vm and epicardial contraction in the beating heart. Isolated perfused swine hearts were stained with di-4-ANEPPS and fiducial markers were glued to the epicardium for motion tracking. The heart was imaged at 750 Hz with a video camera. Fluorescence was excited with cyan or blue LEDs on alternating camera frames, thus providing a 375-Hz effective sampling rate. Marker tracking enabled the pixel(s) imaging any epicardial site within the marked region to be identified in each camera frame. Cyan- and blue-elicited fluorescence have different sensitivities to Vm, but other signal features, primarily motion artifacts, are common. Thus, taking the ratio of fluorescence emitted by a motion-tracked epicardial site in adjacent frames removes artifacts, leaving Vm (excitation ratiometry). Reconstructed Vm signals were validated by comparison to monophasic action potentials and to conventional optical mapping signals. Binocular imaging with additional video cameras enabled marker motion to be tracked in three dimensions. From these data, epicardial deformation during the cardiac cycle was quantified by computing finite strain fields. We show that the method can simultaneously map Vm and strain in a left-sided working heart preparation and can image changes in both electrical and mechanical function 5 min after the induction of regional ischemia. By allowing high-resolution optical mapping in the absence of electromechanical uncoupling agents, the method relieves a long-standing limitation of optical mapping and has potential to enhance new studies in coupled cardiac electromechanics.

Epicardial and Endocardial Deformations in Discrimination of Nonobstructive Hypertrophic Cardiomyopathy from Hypertensive Left Ventricular Hypertrophy

Epicardial and Endocardial Deformations in Discrimination of Nonobstructive Hypertrophic Cardiomyopathy from Hypertensive Left Ventricular Hypertrophy

Myocardial Deformation at Rest and Stress: The Reproducibility of Endocardial and Epicardial Deformation using VVI

Myocardial Deformation at Rest and Stress: The Reproducibility of Endocardial and Epicardial Deformation using VVI

The video technique developed for measuring epicardial strains on guinea pig's left ventricle

Single-plain video used for measurements of epicardial strains is a technique that yields minor interference with the studied mechanical properties of the ventricle. Due to its low temporal resolution, the existing technique is, however, not appropriate for small animals. We questioned whether the technique could be improved enough to cope with higher heart rates and miniaturization necessary for experiments on rats, mice and guinea pigs. Therefore, we developed a high-speed video system and used it for measuring epicardial strains in guinea pig hearts in situ with the open chest. The improvement was achieved in video hardware (camera: Dalsa D6-0256; framegraber: EPIX PIXCI D32) and software, the markers (glowing acrylate crystals; diameter ∼0.15 mm) and illumination (UVA light, OSRAM L). Three markers were attached onto the epicardium in the equatorial region of the left ventricular free wall, 1.5 mm apart, with fibrin glue. From their coordinates, we calculated two-dimensional finite strains with end diastole as the reference point. The accuracy of the displacement measurement of the technique and the error introduced by approximate-visual estimation of the left ventricle coordinate system were evaluated. The accuracy of the displacement measurement was ±1.6 μm and the temporal resolution was 2 ms. Error due to approximate coordinate system orientation was ±3% of the strain amplitude. The typical amplitude of strains was −0.06, −0.11 and 0.04 in circumferential, axial direction and in-plane shear, respectively. The improvements enable us to perform physiologically relevant measurements of epicardial deformations on guinea pig heart.

Estimation of epicardial strain using the motions of coronary bifurcations in biplane cinéangiography.

A quantitative method is described for estimating epicardial deformation from the motion of the superficial arteries. A structural model of the time-varying surface is constructed using tensor product basis functions which are bicubic Hermite in the spatial domain and sinusoidal in the temporal domain. The loci of the superficial coronary arteries are reconstructed interactively at diastasis and the bifurcations are tracked semiautomatically throughout a cardiac cycle. An initial surface is fitted to the vessels at diastasis and is subsequently deformed under the influence of the bifurcations. The Lagrange-Green strain tensor is used to obtain a complete description of surface strain over the entire region spanned by the model. The calculated deformation field varies smoothly over space and time and is not constrained by assumptions of isotropy or piecewise homogeneity. Results are presented for a single cycle of a human heart.

Mechanical effects of coronary perfusion in the passive canine left ventricle.

Mechanical effects of coronary perfusion on passive left ventricular filling were studied in seven isolated potassium-arrested dog hearts subjected to static pressure loading. With the use of a biplane video method, midanterior epicardial deformations were measured before, during, and after perfusion of the coronary circulation with a cardioplegic solution. During perfusion, there was a highly significant reduction (P less than 0.001) in ventricular compliance; the mean cavity volume change decreased by 50% at a filling pressure of 12 mmHg. The loss of compliance was reversible and increased with coronary artery pressure. The magnitudes of the principal epicardial extensions, determined by homogeneous strain analysis, also decreased significantly (P less than 0.001) by an average of 30-40% at ventricular pressures of 4-12 mmHg. But there was no change in the pattern of epicardial deformations. These findings, and similar significant falls in epicardial in-plane rotation (P less than 0.05) and angular translation (P less than 0.001), suggest that the main mechanical effect of the coronary circulation is homogeneous and uniform and is, therefore, probably associated with the microcirculation. We propose that this effect may be modeled by treating the myocardium as a porous elastic medium swollen with an incompressible fluid rather than by an increase in ventricular wall thickness due to filling of the coronary vessels.

Regional epicardial and endocardial two-dimensional finite deformations in canine left ventricle

We evaluated subepicardial and subendocardial two-dimensional finite deformations in the left ventricular (LV) anterior, lateral, and posterior regions in the closed-chest, conscious dog heart. Eight dogs underwent placement of 22 radiopaque markers in the LV myocardium. Sets of three markers were implanted in the anterior, lateral, and posterior subepicardium and subendocardium at the mid-ventricular level; reference markers were placed at apical and basal sites. Eight hours later, biplane videofluoroscopy was performed. Finite deformations for each subepicardial and subendocardial region were analyzed during three consecutive beats at end expiration. Circumferential shortening occurred in all layers and regions; similarly, longitudinal shortening occurred in all layers except that of the posterior endocardium. Values of principal strain were -0.19 +/- 0.08 (SD) and -0.10 +/- 0.03 for the anterior subendocardium and subepicardium, -0.20 +/- 0.07 and -0.10 +/- 0.02 for the lateral subendocardium and subepicardium, and -0.13 +/- 0.02 and -0.10 +/- 0.03 for the posterior subendocardium and subepicardium respectively (P less than 0.05 subendocardium vs. subepicardium). Second principal strain tended to be near zero or positive (from -0.01 +/- 0.05 to 0.04 +/- 0.05) in all regions. The end-systolic direction of principal strain was -29 +/- 32 degrees and -34 +/- 29 degrees in the anterior subepicardium and subendocardium, -47 +/- 10 degrees and -30 +/- 37 degrees in the lateral subepicardium and subendocardium, and -4 +/- 29 degrees and +7 +/- 23 degrees in the posterior subepicardium and subendocardium. Anterior and lateral directions of principal strain were similar in the subepicardial and subendocardial layers and oriented along the epicardial fiber axis, but the posterior direction tended to be circumferentially oriented.(ABSTRACT TRUNCATED AT 250 WORDS)

Passive Material Properties of Intact Ventricular Myocardium Determined From a Cylindrical Model

The equatorial region of the canine left ventricle was modeled as a thick-walled cylinder consisting of an incompressible hyperelastic material with homogeneous exponential properties. The anisotropic properties of the passive myocardium were assumed to be locally transversely isotropic with respect to a fiber axis whose orientation varied linearly across the wall. Simultaneous inflation, extension, and torsion were applied to the cylinder to produce epicardial strains that were measured previously in the potassium-arrested dog heart. Residual stress in the unloaded state was included by considering the stress-free configuration to be a warped cylindrical arc. In the special case of isotropic material properties, torsion and residual stress both significantly reduced the high circumferential stress peaks predicted at the endocardium by previous models. However, a resultant axial force and moment were necessary to cause the observed epicardial deformations. Therefore, the anisotropic material parameters were found that minimized these resultants and allowed the prescribed displacements to occur subject to the known ventricular pressure loads. The global minimum solution of this parameter optimization problem indicated that the stiffness of passive myocardium (defined for a 20 percent equibiaxial extension) would be 2.4 to 6.6 times greater in the fiber direction than in the transverse plane for a broad range of assumed fiber angle distributions and residual stresses. This agrees with the results of biaxial tissue testing. The predicted transmural distributions of fiber stress were relatively flat with slight peaks in the subepicardium, and the fiber strain profiles agreed closely with experimentally observed sarcomere length distributions. The results indicate that torsion, residual stress and material anisotropy associated with the fiber architecture all can act to reduce endocardial stress gradients in the passive left ventricle.

Discrepancies between myocardial blood flow and fiber shortening in the ischemic border zone as assessed with video mapping of epicardial deformation.

Myocardial function around the border of ischemia was investigated in eight open-chest dogs using video mapping of epicardial deformation. With this method, 40-60 white markers attached to the left ventricular epicardium were traced in time automatically. Before and 5-10 min after coronary artery occlusion, blood flow and epicardial deformation were determined in 30-40 regions with a spatial resolution of about 5 mm. Epicardial deformation was expressed as subepicardial fiber shortening and surface area decrease during the ejection phase. The latter indicates local contribution to stroke volume. The absolute values of these variables were normalized relative to the central ischemic (= 0%) and remote non-ischemic area (= 100%). The 50% contour line of a variable was defined as its border. The average distance between the borders of perfusion and function was not significantly different from zero, due to considerable variation in this distance both within one heart (+/- 5.7 mm) and between mean distances for different hearts (+/- 4.4 mm). The width of the transition zone (distance between the 20% and 80% contour lines) of surface area decrease and subepicardial fiber shortening was significantly larger (20.5 and 15.0 mm, respectively) than those of transmural and subepicardial blood flow (8.5 and 9.5 mm, respectively). The present results demonstrate that in a 20-mm zone around the border of ischemia, major discrepancies are present between perfusion and deformation.

Left ventricular epicardial deformation in isolated arrested dog heart.

We have developed a method for measuring epicardial deformation in the isolated arrested dog heart. A biplane video system was used to record the motion of discrete epicardial markers at midanterior sites (n = 4 hearts) and midposterior sites (n = 1) during quasi-static left ventricular (LV) filling. Experimental procedures, performed at room temperature, were completed within 20 min, and LV pressure-volume curves were repeatable and within the range of data presented by other authors. To obtain a complete description of local deformation, epicardial displacements derived from the video record were analyzed using homogeneous strain theory. Local epicardial strain was nonuniform; the mean ranges of midanterior major and minor extensions were 0-13.9 and 0-7.2%, respectively, for LV filling pressures of 0-20 mmHg. For the midanterior wall, the mean orientation of the major extension was 28-35 degrees below the LV circumference, compared with an orientation of approximately 62 degrees at the midposterior site. The results demonstrate the value of this preparation for studying passive ventricular mechanics and are not consistent with the predictions of mathematical models of ventricular stress and strain, in which it has been assumed that the material properties of the passive myocardium are isotropic.

Gradients in fiber shortening and metabolism across ischemic left ventricular wall.

Blood flow, metabolism, and fiber shortening in various layers of left ventricular wall were studied during the initial 5 min of ischemia. In open-chest dogs (n = 51) ischemia was induced by coronary arterial stenosis (median value of mean perfusion pressure distal to stenosis 3.3 kPa). Epicardial deformation measurements with an inductive technique allowed estimation of fiber shortening in inner (eendo,est) and outer layers (eepi) of left ventricular free wall during the ejection phase. The decrease of eendo,est occurred within a few seconds after onset of stenosis, whereas eepi started to decrease 30 s later. After 1 min, eendo,est diminished to zero concomitantly with a reduction of blood flow and creatine phosphate content in the inner layers by 68 and 46%, respectively. In contrast a 60% reduction of eepi was associated with a decrease in blood flow of only 32% and no significant decrease in creatine phosphate in the outer layers. H+ and inorganic phosphate were released simultaneously into the local venous blood starting within 1 min of ischemia. During the initial 5 min of ischemia the content of ATP and glycogen remained unchanged across the ischemic wall. Present results indicate that the decrease of fiber shortening in the inner layers is associated with severe metabolic dearrangements, as reflected by the depletion of creatine phosphate. They also indicate that, during coronary arterial stenosis, impaired fiber shortening in the outer layers may result from the impairment of mechanical function in the inner layers, rather than from metabolic disturbances in the outer layers themselves.

Mapping of epicardial deformation using a video processing technique

A method has been developed to measure deformation of the canine epicardium during the cardiac cycle simultaneously in a number (eight) of small regions (1 × 1 cm 2). Approximately 50 white markers (diameter 1.5 mm) are attached to the epicardium and their motion is recorded on tape by a video camera. Marker positions are detected by computer processing of the digitized images. In each region the three deformation parameters are calculated from the displacements of all markers in that region by means of a least-squares criterium. In the experimental situation in the center of the area of the epicardium analyzed the accuracy of measuring circumferential strain, base-to-apex strain and shear is ±0.005, ±0.005 and ±0.002 rad, respectively. The method has been applied in an experiment in which local ischemia of the left ventricular wall was induced by occluding the anterior descending branch of the left coronary artery. Healthy and ischemic regions could clearly be distinguished by the differences in deformation.

Estimation of Local Cardiac Wall Deformation and Regional Wall Stress from Biplane Coronary Cineangiograms

A new mathematical method was developed to estimate the local epicardial deformation, wall thickness, and the regional circumferential and longitudinal wall stress using biplane coronary cineangiograms. In this method, the motion images of the coronary artery bifurcation points were used as natural landmarks for the kinematic analysis of the ventricular deformation. In four dogs and a normal patient's coronary cineangiograms, the estimation results show the validity of the present analysis, compared to the experimental results based upon the implanted markers. Thus, the present method provides a new method of evaluating the regional wall deformation and wall stress together with the blood vessel conditions using the coronary cineangiography procedure.

Fiber shortening in the inner layers of the left ventricular wall as assessed from epicardial deformation during normoxia and ischemia

A mathematical model of left ventricular mechanics predicts that fiber shortening in the inner layers of the left ventricular wall can be estimated ( e endo, est ) from the magnitude of minimal ( e min, 0 ) and maximal shortening ( e max, 0 ) of the outer surface (=epicardium) of this wall. To evaluate this prediction. e endo, est and e min, 0 were compared with the shortening in the inner layers approximately along the fiber direction ( e endo ) as measured directly, before and during one minute of coronary artery occlusion. Deformation of the epicardium and the inner layers was determined by measuring mutual motion and angulation of three needles pierced into the myocardial wall, using an electromagnetic inductive technique. The proposed linear relations of e endo, est and e min, 0 with e endo were found to be significant. The needles hardly influenced wall deformation since similar values of epicardial deformation were found in separate, comparable, experiments ( n = 13) using a triplet of epicardial coils. So e endo, est and e min, 0 are useful estimates of fiber shortening in the inner layers during normoxia and ischemia, especially when the time course of events is followed in the same animal.

Prediction of fiber shortening in the inner layers of the left ventricular wall from epicardial deformation measurements during normoxia and ischemia: F.W. Prinzen, T. Arts, G.J. van der Vusse, R.S. Reneman. Departments of Physiology and Biophysics, University of Limburg, Maastricht, The Netherlands

Prediction of fiber shortening in the inner layers of the left ventricular wall from epicardial deformation measurements during normoxia and ischemia: F.W. Prinzen, T. Arts, G.J. van der Vusse, R.S. Reneman. Departments of Physiology and Biophysics, University of Limburg, Maastricht, The Netherlands

Epicardial deformation and left ventricular wall mechanisms during ejection in the dog.

Significant differences between epicardial and endocardial systolic stress in the wall of the left ventricle (LV) have been predicted by various models of LV mechanics. Yet a model incorporating transmural differences in fiber orientation and torsion, defined as a rotation of the apex with respect to the base around the long axis of the LV, predicts transmural equalization of stress and shortening along the fiber direction during the ejection phase. this equalization is due to an interplay between torsion and myocardial contraction. To assess the model hypothesis, predicted epicardial deformation during the ejection phase was compared with that measured experimentally. For this purpose 45 sets of measurements were performed in four open-chest dogs using a triangular array of inductive gauges for the assessment of epicardial circumferential strain (epsilon c), base-to-apex strain (epsilon z), and shear angle (gamma). Changes in shear angle are directly related to LV torsion. LV end-diastolic pressure was varied over a wide range (0-15 mmHg) by volume loading and bleeding. In the control state, the slope of the shear angle vs. volume strain curve (volume strain = 2 epsilon c + epsilon z), which is related to contraction, was found to be 0.74 +/- 0.10 (mean +/- SD). This compares reasonably wih the mathematical model prediction of a slope of 0.67. Due to an interplay between torsion and contraction, left ventricular fiber stress and fiber shortening might be uniformly distributed across the wall.

Measurement of deformation of canine epicardium in vivo during cardiac cycle.

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.