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Biomedical subjects

R Beyar

Publications and source records attributed to R Beyar.

At least 19 recordsLinked to original sources
PubMed1992

A conical model to describe the nonuniformity of the left ventricular twisting motion.

The systolic contraction and fiber shortening in the left ventricle (LV) produces torsional moments in the myocardium, resulting in a gradient of angular displacements about the long axis. This is manifested as a counterclockwise rotation of the apex relative to the base, when viewed from the apex. Recent studies with magnetic resonance imaging (MRI), using noninvasive magnetic tags, have revealed three important properties of the LV twist: (a) The angle of twist (i.e., the angular rotation of a slice relative to the basal slice) is consistently higher at the endocardium as compared to the epicardium; (b) The twist increases towards the apex; and (c) Straight MRI-tagged radial lines at end-diastole (ED) are slightly curved at end-systole (ES), implying a nonlinear transmural variation of the twist. The present study suggests that the geometry of the LV at ES can be represented by a thick-walled hollow cone, and that the transmural twist patterns from ED to ES can be described using the continuum mechanics approach and a small strain analysis of an isotropic cone subjected to external torque. The predicted results are compared with the noninvasive MRI measurements of transmural twist in eight human volunteers. Given the epicardial angles of twist of each slice, the predicted endocardial angles of twist are in good correlation with the experimental findings (r = 0.86, slope = 1.09, SEE = 4.1 degrees). In addition, the model reliably describes the changes in the twist magnitude from apex to base (no significant difference from experimental values, P = 0.2), and predicts the curvilinear pattern at ES of the originally straight ED radial lines. Thus, the conical model with uniform properties of the LV, reliably predicts the nonuniformity of the twist patterns, implying that the LV twist is strongly affected by LV geometry.

Adult↗
PubMed1992

Myocardial contrast echocardiography: influence of ischaemia and hyperaemia in an animal model.

To evaluate changes in myocardial contrast echocardiography during ischaemia and hyperaemia, contrast studies were performed in 16 open chest dogs. Time-intensity curves were generated using videodensitometry after contrast injections to demonstrate ischaemic and non-ischaemic areas of interest during a wide range of coronary blood flow levels. For each time-intensity curve, the peak contrast intensity (PCI), washout halftime (T1/2) and area under the curve (AUC) were calculated. PCI and AUC decreased significantly only with severe ischaemia (90% or more reduction in flow), and increased significantly with hyperaemia of more than 2.5 times baseline flow. Both ischaemia and hyperaemia were found to prolong the T1/2. There was only a moderate linear correlation between the magnitude of hyperaemia and myocardial contrast echocardiographic parameters. There was significantly less increase in myocardial contrast echocardiographic parameters during hyperaemia in segments supplied by a stenosed coronary artery.

Albumins↗
PubMed1991

Vital organ perfusion during assisted circulation by manipulation of intrathoracic pressure.

BACKGROUND: We have previously shown, in dogs with severe cardiac depression, that modest cyclic increases in intrathoracic pressure, starting synchronously with left ventricular isovolumic contraction, significantly increase aortic flow and pressure. However, little is known of changes in vital organ perfusion during this technique of assisted circulation. METHODS AND RESULTS: We studied regional organ flow using radioactive labeled microspheres in 13 20-25-kg mongrel dogs. In the control group, after chemical induction of cardiac depression with verapamil and propranolol, coronary flow fell from 129.1 +/- 14.4 to 51.6 +/- 11.3 ml/100 g/min (p less than 0.005) and continued to decline over a 14-minute time period (flow was 32.2 +/- 11.5 ml/100 g/min at 7 minutes and 20.7 +/- 9.5 ml/100 g/min at 14 minutes [n = 6]; all p less than 0.05). In the intervention group, regional blood flow was evaluated before and after the induction of cardiac depression and also during assisted circulation using 400-msec, 20-25-mm Hg intrathoracic pressure increases delivered by a circumthoracic pneumatic vest, starting synchronously with left ventricular isovolumic contraction. In the intervention group, coronary flow fell from 119 +/- 26.7 to 47.9 +/- 13.1 ml/100 g/min 1 minute after the induction of cardiac depression (p less than 0.005). With the initiation of assisted circulation, coronary flow increased to 55.8 +/- 19.2 ml/100 g/min at 7 minutes and fell to 23.1 +/- 15.9 ml/100 g/min on termination of assisted circulation at 14 minutes (p less than 0.05 and p = NS versus control group flows at 1 and 14 minutes, respectively). During assisted circulation, cerebral, renal, and small intestinal flows also increased (all p less than 0.05 versus flows during myocardial depression). No significant increase in hepatic flow was observed. CONCLUSIONS: In the canine model, manipulation of intrathoracic pressure appears to be an effective, short-term, noninvasive means of not only increasing aortic pressure but also increasing vital organ perfusion during cardiogenic shock. Further studies are needed to assess the usefulness of this technique of assisted circulation in humans.

Animals↗
PubMed1991

Regional three-dimensional geometry and function of left ventricles with fibrous aneurysms. A cine-computed tomography study.

BACKGROUND: To assess the extent and nature of the dysfunction surrounding aneurysms of the left ventricle (LV), we examined the parameters of local and global three-dimensional shape, size, and function of LVs of eight patients with histologically confirmed anterior fibrous aneurysms. METHODS AND RESULTS: Three-dimensional reconstructions of each LV were made from 10-12 short-axis fast cine-angiographic computed tomography (cine-CT) slices encompassing the entire heart at end diastole and end systole. Regional three-dimensional wall thickness, thickening, motion, curvature, and stress index were calculated for 84 elements encompassing the entire LV. The aneurysmal border was defined by a sharp decrease in end-diastolic wall thickness and separated the LV into an aneurysmal zone and a normal zone that was further divided into adjacent normal (AN) and remote normal (RN) zones. As expected, thickening was negligible in both the aneurysmal and the border zones. Although both the AN and the RN zones had normal wall thickness (1.05 +/- 0.20 and 1.09 +/- 0.20 cm, respectively), thickening was depressed in the AN (0.22 +/- 0.08 cm) but not the RN (0.44 +/- 0.19 cm) zones. The size of the dysfunction zone (defined as less than 2 mm thickening) was found to be considerably greater than the anatomic size of the aneurysm (60.9 +/- 13.7% versus 33.6 +/- 7.6% of the left ventricular endocardial area, respectively; p less than 0.001). In addition, the AN zone had a smaller curvature and a higher stress index than the RN zone. CONCLUSIONS: LVs with fibrous aneurysms are characterized by a relatively large region of nonfunction that encompasses the thin aneurysmal area and its transitional border zone, a normally functioning remote zone, and an intermediate region of normal wall thickness but with reduced function, which may be attributed to its low curvature and high stress index.

Algorithms↗
PubMed1991

Evaluation of contractile state by maximal ventricular power divided by the square of end-diastolic volume.

BACKGROUND: Maximal ventricular power (PWRmax) reflects contractile state and has the potential to be noninvasively determined. However, its sensitivities to preload, afterload resistance, and inotropic state are incompletely defined. The present study determines these dependencies and proposes a novel power-based contractile index that is little altered by load. METHODS AND RESULTS: Seven open-chest, autonomically blocked dogs were instrumented with a proximal aortic flow probe, central aortic and ventricular micromanometers, and a conductance catheter for ventricular chamber volume. Preload was transiently reduced by left atrial hemorrhage, and afterload was increased by intra-aortic balloon inflation. Inotropic state was pharmacologically altered by lidocaine, dobutamine, propranolol, or verapamil. PWRmax was highly preload sensitive, altering 1.7 +/- 0.1-fold a given percent change in end-diastolic volume (EDV). This preload dependence was reduced by dividing PWRmax by EDV but was virtually eliminated when PWRmax was divided by EDV2. This latter index also displayed little change in response to as much as 60% increases in afterload resistance. PWRmax/EDV2 varied directly with inotropic state, correlating to both the slope (Ees) of the end-systolic pressure-volume relation (PWRmax x 1,000/EDV2 = 0.31 x Ees - 0.04, r = 0.82, p less than 0.001) and the slope (A) of the dP/dtmax-EDV relation (PWRmax x 1,000/EDV2 = 0.025 x A + 0.02, r = 0.86, p less than 0.001). PWRmax values determined from the product of ventricular pressure and flow versus central aortic pressure and flow were nearly identical over a broad loading range, indicating that PWRmax may be noninvasively assessed (i.e., without requiring left ventricular chamber pressure). CONCLUSIONS: PWRmax divided by EDV2 provides a measure of contractile function that is little influenced by loading conditions and has potential for noninvasive clinical use.

Animals↗
PubMed1990

The slope of the end-systolic pressure-volume relationship compared with the global end-systolic pressure-volume ratio in humans.

The slope of the end-systolic pressure-volume relationship (Emax), which is generated clinically by load manipulation, as well as the "absolute" peak systolic pressure end-systolic volume ratio (denoted as pressure-volume ratio), have been suggested as indices defining left ventricular function. This study represents an attempt to determine the relationship between these two indices by studying 20 patients (16 with coronary artery disease and 4 with normal coronary arteries) undergoing cardiac catheterization. Left ventriculography was performed three times in each patient: (1) in the control baseline state, (2) after rapid intravenous infusion of 250-300 cc of saline, and (3) after sublingual administration of 5 mg isosorbide dinitrate. Emax was approximated by linear regression using the peak left ventricular pressure (replacing end-systolic pressure) and the smallest left ventricular (end-systolic) volume for these three different loads. Acute ischemia with typical chest pain and ECG changes developed in 4 patients during saline loading. The pressure-volume ratio showed no change with load manipulation in patients who did not demonstrate ischemia. In the 4 patients who developed acute ischemia, the pressure-volume ratio dropped from 4.4 +/- 1.3 to 2.9 +/- 0.9 mmHg/ml (p less than 0.001). In all of the patients, the pressure-volume ratio, but not the Emax, correlated with the ejection fraction (r = 0.6; p less than 0.05). In addition, the Emax line demonstrated a markedly nonphysiological Vo. There was no correlation between Emax and pressure-volume ratio.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Analysis and prediction of left ventricular performance under load changes during cardiac catheterization.

The applicability of a computer model, which relates the transmural mechanical distribution in the left ventricle (LV) to its global function at different loading conditions, was evaluated in patients with normal to near normal LV function undergoing cardiac catheterization. Left ventriculography and measurements of aortic and LV pressures were performed at baseline conditions and repeated following rapid volume expansion with intravenous infusion of 250 to 300 ml of physiologic saline and also after sublingual isosorbide-dinitrate (ISDN) administration. Twenty patients (18 men and 2 women, average age = 53 years) underwent coronary angiography and left ventriculography. Sixteen patients had coronary artery disease with one- to three-vessel involvement and 4 had normal coronary arteries. The measured input data into the model included the end-diastolic LV volume and wall thickness, aortic pressure, heart rate, and the peripheral resistance. The model parameters of myocardial contractility and arterial system capacitance for the control baseline conditions were estimated so that an accurate match was obtained between the predicted and the measured end-systolic (ES) volume and pressure. Using these parameters, model predictions for the two load perturbations were compared to the measurements. An excellent correlation was found between the predicted and measured LV ES volumes and peak-systolic pressures (PSP) (R2 greater than 0.994). In four patients, who developed ischemic symptoms during saline injection, the prediction of end-systole volumes were lower than the measured values, suggesting an actual reduction in contractility during acute ischemia. Therefore, the model is sensitive to contractility changes. The model predicts global LV performance, under different loading conditions, including stroke work, peak developed wall stress, velocity of fiber shortening, and myocardial oxygen consumption.

Cardiac Catheterization↗
PubMed1990

Force interval relationship (FIR) related to the global function of the left ventricle: a computer study.

A model which relates the left ventricular (LV) geometry, structure and sarcomere properties to its global function, recently proposed by the authors, is extended to account for contractility changes which are a function of the heart rate, prematurity of the beat and calcium transients within the cell. To characterise LV function and relate it to fibre function under varying rhythm conditions, a model of muscle force restitution, based on calcium kinetics, was used to calculate the maximum fibre stress at the optimum sarcomere length sigma o as the parameter which depends on the heart rate, the test pulse interval TPI, the action potential duration APD and the restitution time constant. The global LV force interval relationship FIR was then calculated, and by comparing the calculated FIR to the experimental measurement (in dogs) at the ventricular level, the constants of the restitution of force at the fibre level were derived. Based on these constants, the LV function under ejecting conditions at various rhythm disturbances was calculated and related to the local, distributed parameters. This approach provides a tool to describe ventricular function as well as transmural distribution of stress and sarcomere length at a wide variety of loading and rhythm conditions based on given 'muscle level' parameters.

Biomechanical Phenomena↗
PubMed1990

Mechanical pathophysiology of some heart diseases: a theoretical model study.

Sarcomere dynamics are related to the global left ventricular (LV) function in some representative pathological states, by using a theoretical model which combines sarcomere function, LV fibrous structure and geometry with the haemodynamic loading conditions. The analysis shows that pressure (concentric) hypertrophy due to hypertension or aortic stenosis is associated with an increase of the normal endocardial-to-epicardial gradient(s) of oxygen demand, which may be one of the causes for the development of endocardial fibrosis. The analysis also indicates that sarcomere shortening is relatively normal in compensated volume (eccentric) hypertrophy. Mitral stenosis demonstrates a case of decreased LV function, secondary to a chronic decrease in LV end diastolic volume, with sarcomeres that operate at their lowest length range. Conversely, the sarcomere function is depressed in cardiomyopathy; the heart's pumping function is maintained by appropriate adjustment mechanisms. However, the sarcomeres show minimal shortening and function at their highest length range with low (or zero) functional reserve. The study thus provides a quantitative tool that relates global LV function to local sarcomere dynamics in various pathological states.

Heart↗
PubMed1990

Effect of hyper- and hypovolaemia on regional myocardial oxygen consumption.

STUDY OBJECTIVE - The purpose of the investigation was to study the effect of preload on coronary blood flow and myocardial oxygen consumption in subendocardial and subepicardial regions of left ventricular free wall. DESIGN - Ventricular volume in anaesthetised open chest dogs was altered over a range of 20% to produce hypovolaemia (10-15% exsanguination) or hypervolaemia (colloid infusion), allowing measurements of regional blood flow and oxygen consumption with varying preloads. beta Adrenergic blockade was used to limit changes in inotropy, and heart rate was kept constant by pacing at 150 beats.min-1. SUBJECTS - 9 mongrel dogs of either sex weighing 24.9 (SEM 4.1) kg were studied. MEASUREMENTS and RESULTS - Left ventricular volume was calculated from ultrasonic measurements of long and short axis end diastolic diameters and wall thickness. Regional myocardial blood flow was estimated using radioactive microspheres, and oxygen consumption in each region was determined from microspectrophotometric measurements of oxygen saturations in small arteries and veins. Hypervolaemia increased subepicardial blood flow from 66.8(6.9) (normovolaemic) to 114.1(13.5) ml.min-1.100 g-1, and regional oxygen consumption from 4.08(0.57) to 6.44(1.08) ml.min-1.100 g-1. Values in the subendocardium were similar, except for oxygen consumption, which increased less than in the subepicardium. Left ventricular end diastolic volume, pressure, and output were each increased in hypervolaemia, but not dP/dt and systolic aortic pressure. Hypovolaemia reduced blood pressures without reducing end diastolic volume. CONCLUSIONS - Augmented flow work produced by increased preload (even in the absence of changes in pressure work) increases myocardial oxygen supply equally in the subepicardium and the subendocardium, while oxygen extraction and consumption are preferentially augmented in the subepicardium.

Animals↗
PubMed1990

Manipulation of external pressure as a method to assist the failing heart.

The development and state of the art in circulatory assistance using external pressure variations is reviewed. All of these techniques use the principle that by cyclic external pressure waves properly timed to the cardiac cycle, hemodynamic energy can be noninvasively transmitted to assist the circulation. Cyclic pressure waves to the lower body require that the high pressure phase occurs in diastole in order to augment cardiac output or coronary flow. In contrast, pressure waves to the chest would optimally augment cardiac output if they begin at the onset of ventricular systole. Manipulation of lung pressure by synchronized ventilation may be also utilized to augment cardiac output. The above methods are discussed in detail in the manuscript with special emphasis on the pathophysiology and mechanisms of cardiac assistance.

Animals↗
PubMed1990

Magnetic resonance imaging as a noninvasive standard for the quantitative evaluation of left ventricular mass, ischemia, and infarction.

Because magnetic resonance imaging (MRI) acquires data in a spatially unambiguous fashion and the three-dimensional interrelationships of one image plane to another are easily ascertained, there are far fewer technical restrictions imposed on this method than on other imaging techniques. Furthermore, the multiplanar nature of MRI image acquisition, in any plane desired, is a feature unique to this imaging technology. MRI is thus well suited to the highly accurate quantification of global and regional left ventricular (LV) size and function, and can be used as a standard for comparison to other techniques, once validated. Because the determination of LV mass by MRI requires no assumptions about ventricular shape, it should be well suited to the evaluation of both normal hearts and those distorted by infarction. We performed gated MRI on 15 dogs before and after myocardial infarction. LV mass was calculated with 5 short axis planes. The correlation was excellent between actual mass before infarction and after MI. Accuracy was similar for both end-diastole and end-systole. Thus, MRI accurately determines LV mass in both distorted and normal hearts. We have also developed a method for quantification and mapping of regional wall thickening throughout the LV as an index of regional ischemia by utilizing the 3D geometry to calculate the perpendicular wall thickness of a 3D volume element of tissue. This 3D volume element results in less variability of normal wall thickening and provides a better discriminator of ischemic from nonischemic zones in a canine model of acute ischemia, whereas there is considerably greater overlap between ischemic and normal zones with standard planar MRI techniques. The 3D method is more accurate than planar methods in avoiding biases resulting from the oblique course of an image plane through the LV wall, resulting in better distinction of ischemic from nonischemic tissue. Finally, the accurate assessment of regional LV function for the identification of ischemic or infarcted myocardium has been enhanced greatly by a new technique, myocardial tissue tagging, in which an electronic marker is applied to the myocardium which persists through ejection, enabling the accurate tracking of specific areas of the heart as they move and rotate through the cardiac cycle.

Cardiomegaly↗
PubMed1990

Three-dimensional mapping of acute ischemic regions using MRI: wall thickening versus motion analysis.

Three-dimensional (3D) endocardial wall motion and thickening were compared as quantitative methods for distinguishing ischemic from non-ischemic myocardium and for their potential to map regional left ventricular (LV) function. Data were obtained by gated magnetic resonance (MR) images in seven open-chest dogs with acute ischemia. The LVs were reconstructed in 3D at end diastole (ED) and end systole (ES) with a helical coordinate system that wraps the endocardium and epicardium. Thickness and percent wall thickening were calculated by a 3D volume element method. Wall motion was calculated by the 3D displacement of the endocardium perpendicular to the wall using both fixed and floating centroids. Monastral blue nonstaining identified the ischemic regions from five anatomical slices of the LV, which corresponded to the in vivo image planes. Thickening and motion were compared at the centers of the ischemic and the remote normal zones, in addition to comparing the functional maps of the entire LV to the postmortem anatomical maps. All methods distinguished between the center of the ischemic zone and the remote normal zone; however, thickening discriminated most strongly between zones. Comparison of the 3D in vivo maps with the 3D postmortem maps showed that the sensitivity, specificity, and overall accuracy of the thickening algorithm exceeded those obtained by the wall motion algorithms with fixed or floating centroids. Thus wall thickening utilizing the 3D volume element approach is superior to 3D wall motion algorithms in distinguishing ischemic from nonischemic zones and in mapping regional function in the entire LV.

Acute Disease↗
PubMed1990

Quantification and validation of left ventricular wall thickening by a three-dimensional volume element magnetic resonance imaging approach.

We have developed a method to quantify and map regional wall thickening throughout the left ventricle (LV) with magnetic resonance imaging. In contrast to methods that measure planar wall thickness and thickening, this method uses the three-dimensional (3D) geometry of the left ventricle to calculate the perpendicular thickness of the wall. We tested this method at three levels of increasing complexity using 1) phantom studies, 2) in vivo experiments in dogs with normal cardiac function, and 3) in vivo studies in dogs during acute ischemia. Experiments were conducted in 15 open-chest dogs imaged by a 0.38 T iron core magnet. Five short-axis images at end diastole and end systole were obtained with the spin echo technique by use of the QRS as a trigger for end diastole and the second heart sound, S2, to time end systole. After acquisition of preischemic images, acute ischemia was induced by either coronary artery ligation (n = 5) or intracoronary dental rubber injection (n = 5), which produced severe transmural ischemia. By use of computer-aided contouring of the endocardial and epicardial borders, each image was divided into 16 segments with radial lines originating from the midwall centroid. A 3D volume element was defined as that generated by connecting two matched planar segments in two adjacent image planes. This defined 64 volume elements comprising the entire left ventricle. Thickness and thickening before and during ischemia were then calculated by using the planar segments and the 3D volume elements. In phantom studies, the 3D method was accurate, independent of the angle of inclination of the image plane to the phantom wall, whereas the planar method showed considerable overestimation of thickness when the image plane was oblique to the phantom wall. In the dogs before induction of ischemia, the 3D method demonstrated the well-established normal taper in end-diastolic wall thickness from 1.10 +/- 0.02 cm at the base to 1.05 +/- 0.11 cm at the apex (p less than 0.01). By contrast, the planar method did not detect the decrease in thickness toward the apex (1.13 +/- 0.07 cm at the base vs. 1.16 +/- 0.14 cm at the apex, p = NS). During acute ischemia, thickening was calculated by both methods at the center of the ischemic zone defined by Monastral blue nonstaining and compared with the preischemic values.(ABSTRACT TRUNCATED AT 400 WORDS)

Acute Disease↗
PubMed1990

Noninvasive quantification of left ventricular rotational deformation in normal humans using magnetic resonance imaging myocardial tagging.

It has been postulated that rotation of the left ventricular apex with respect to the base is a component of normal systolic function in humans, but it has been difficult to measure it noninvasively. Tagging is a new magnetic resonance imaging technique that labels specific areas of myocardium by selective radio-frequency excitation of narrow planes orthogonal to the imaging plane before acquiring an image. Tags appear as black lines and persist in myocardium for 400-500 msec and, if applied at end diastole, will move with the myocardium through systole. Tagging was used to noninvasively quantify left ventricular torsion and circumferential-longitudinal shear (shearCL) in humans. Eight normal volunteers, aged 24-38 years, were imaged in a 0.38-T iron-core resistive magnet. Five short-axis left ventricular images, positioned to encompass the entire left ventricle (LV), were obtained separately at end systole. Four equiangular radial tags had been applied at end diastole, intersecting the myocardium at eight locations. We calculated the difference in angular displacement of each epicardial and endocardial tag point (a tag point being where the tag crossed the epicardium or endocardium) at end systole from the systolic position of the corresponding tag point on the basal plane. This value was called the torsion angle. From this, shearCL, the angle inscribed on the epicardial or endocardial surface between the systolic tag position, the corresponding basal tag position, and its projection onto the slice of interest could be calculated at 32 points in the left ventricular wall.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Aortic diameter and pressure-flow sequence identify mechanism of blood flow during external chest compression in dogs.

Aortic flow and pressure relations and aortic diameter were examined during sinus rhythm, internal cardiac massage, vest cardiopulmonary resuscitation, conventional manual cardiopulmonary resuscitation and high impulse manual cardiopulmonary resuscitation in 14 anesthetized large dogs. During sinus rhythm and during internal cardiac massage, ascending aortic flow and pressure increased simultaneously and the rise in ascending aorta pressure preceded the rise in descending aortic pressure by (mean +/- SEM) 28 +/- 4 and 30 +/- 1 ms, respectively. In contrast, during vest, conventional and high impulse cardiopulmonary resuscitation, ascending aortic flow lagged behind the initial rise in aortic pressure by 40 +/- 4 to 46 +/- 4 ms and ascending and descending aortic pressure increased simultaneously (p less than 0.001 for each external compression mode versus sinus rhythm and internal massage). The ratio of pulse pressure to stroke volume increased by an order of magnitude during all modes of external chest compression (p less than 0.001 versus sinus rhythm and internal massage) and aortic diameter decreased during vest and high impulse cardiopulmonary resuscitation (p less than 0.05 versus sinus rhythm and internal massage). The hemodynamics of external chest compression depart from the normal physiologic sequence of stroke volume-induced increase in aortic pressure and diameter. The rise in aortic pressure precedes flow into the aorta, stroke volume does not fully account for pulse pressure, and aortic diameter decreases during chest compression. These data support the hypothesis that blood flow is due to fluctuations in intrathoracic pressure for high impulse as well as vest and conventional cardiopulmonary resuscitation.

Animals↗