Open-chest Dogs Research Articles

Loss of apical suction assessed by noninvasive pressure differences and twist in acute heart failure: a novel method using vector flow mapping

Abstract Background Early diastolic intraventricular pressure difference (IVPD) reflects left ventricular (LV) apical suction, and IVPD is closely related to cardiac function, especially LV twist. Vector Flow Mapping (VFM) allows visualization of regional pressure distribution and noninvasive quantification of IVPD. The purpose of the present study was to investigate if and how IVPDs are related to LV twist in a model of acute heart failure (HF). Methods In 15 open-chest dogs, HF was induced by intracoronary injection of microspheres. The HF model was classified into two groups based on the LV end-diastolic pressure (LVEDP) (group1: LVEDP<18 mmHg (n=10), group2: LVEDP≥18 mmHg (n=8)). Color Doppler images from apical long-axis views were acquired at baseline and during HF. From these images, pressure differences (ΔP) were calculated along the LV inflow tract throughout the cardiac cycle. For the purpose of this study, the differences between apex and base during isovolumic relaxation time (ΔPIRT) and rapid early inflow period (ΔPE) were used for analyses. Furthermore, apical and basal short axis high frame rate 2D images were acquired, and peak rotation and peak twist were analyzed. Results LVEDP was 7±9, 14±2, 21±3 mmHg for baseline, group1 HF, and group2 HF, respectively. Pressure differences (both ΔPIRT and ΔPE) were visibly changed by the increase of LVEDP (Figure), and the magnitude of ΔPIRT, ΔPE and peak twist decreased significantly with the severity of heart failure. There were significant relationships between pressure differences (ΔPIRT and ΔPE) and dP/dtmin, tau, EF and peak twist (Table). In multivariate analyses, tau and peak twist were independent predictors for ΔPIRT and peak twist was independent predictor for ΔPE. Conclusion VFM analysis is feasible to noninvasively assess the IVPDs in acute heart failure. The IVPDs are closely related to the twisting motion of the LV, and reflect loss of apical suction during severe HF. Funding Acknowledgement Type of funding sources: None. VFM images of pressure differencesCorrelations of pressure differences

Regional heterogeneity of afterload sensitivity in myocardial strain.

The peak systolic strain decreases due to afterload augmentation. However, its deterioration (i.e., afterload sensitivity) may be different within the left ventricular (LV) segments. We investigated how afterload influences regional strain and whether there is regional heterogeneity of afterload sensitivity. Afterload was increased by aortic banding in 20 open-chest dogs. Short-axis images were acquired at baseline and during banding. Circumferential strain was analyzed in six segments, and the absolute decrease in the peak systolic strain during banding (Δε) was calculated for each segment. To assess the effect of the compensatory preload recruitment during banding, the endocardial lengths of the septum and free wall were measured at end-diastole, and the rate of increase due to banding was calculated. LV systolic pressure was significantly increased during banding (100 ± 14 vs. 143 ± 18mmHg, P < 0.001). The peak systolic strain in all segments was significantly decreased during banding. Δɛ in the anterior segment, which is a part of the free wall, was significantly lower than that in the inferoseptal segment (2.6 ± 4.7 vs. 6.5 ± 3.5%, P = 0.035). The rate of increase in endocardial length in the free wall was significantly larger than that in the septum (15.6 ± 10.4 vs. 8.1 ± 7.4%, P = 0.014). The decrease in septal strain during afterload augmentation was larger than that in free wall strain, indicating that there was regional heterogeneity of afterload sensitivity in circumferential strain. The larger compensatory preload recruitment in the free wall than in the septum is implicated as a cause of the heterogeneity.

Noninvasive assessment of intraventricular pressure difference in left ventricular dyssynchrony using vector flow mapping.

Diastolic intraventricular pressure difference (IVPD) reflects left ventricular (LV) diastolic function. The relative pressure imaging (RPI) enables the noninvasive quantification of IVPD based on vector flow mapping (VFM) and visualization of regional pressure distribution. LV dyssynchrony causes deterioration of cardiac performance. However, it remains unclear how IVPD is modulated by LV dyssynchrony. LV dyssynchrony was created in ten open-chest dogs by right ventricular (RV) pacing. The other ten dogs undergoing right atrial (RA) pacing set at the similar heart rate with RV pacing were used as controls. Echocardiographic images were acquired at baseline and during pacing simultaneously with LV pressure measurement by a micromanometer. Pressure difference (ΔP) was computed between the apex and the base of the LV inflow tract during a cardiac cycle by RPI and ΔP during isovolumic relaxation time (ΔPIRT), a parameter of diastolic suction, and that during early filling phase (ΔPE) were measured. During RV pacing, stroke volume (SV) and ΔPIRT decreased significantly, while ΔPE did not change compared to the baseline. During RA pacing, SV, ΔPIRT and ΔPE did not change significantly. ΔPIRT tended to correlate with -dP/dtmin and end-systolic volume, and significantly correlated with ejection fraction. IVPD during isovolumic relaxation time was decreased by LV dyssynchrony, while IVPD during early filling phase was not. A reduction of diastolic suction is observed in LV dyssynchrony and is significantly related to a decrease in SV.

Regional myocardial strain analysis via 2D speckle tracking echocardiography: validation with sonomicrometry and correlation with regional blood flow in the presence of graded coronary stenoses and dobutamine stress

BackgroundQuantitative regional strain analysis by speckle tracking echocardiography (STE) may be particularly useful in the assessment of myocardial ischemia and viability, although reliable measurement of regional strain remains challenging, especially in the circumferential and radial directions. We present an acute canine model that integrates a complex sonomicrometer array with microsphere blood flow measurements to evaluate regional myocardial strain and flow in the setting of graded coronary stenoses and dobutamine stress. We apply this unique model to rigorously evaluate a commercial 2D STE software package and explore fundamental regional myocardial flow-function relationships.MethodsSonomicrometers (16 crystals) were implanted in epicardial and endocardial pairs across the anterior myocardium of anesthetized open chest dogs (n = 7) to form three adjacent cubes representing the ischemic, border, and remote regions, as defined by their relative locations to a hydraulic occluder on the mid-left anterior descending coronary artery (LAD). Additional cardiac (n = 3) and extra-cardiac (n = 3) reference crystals were placed to define the cardiac axes and aid image registration. 2D short axis echocardiograms, sonometric data, and microsphere blood flow data were acquired at baseline and in the presence of mild and moderate LAD stenoses, both before and during low-dose dobutamine stress (5 μg/kg/min). Regional end-systolic 2D STE radial and circumferential strains were calculated with commercial software (EchoInsight) and compared to those determined by sonomicrometry and to microsphere blood flow measurements. Post-systolic indices (PSIs) were also calculated for radial and circumferential strains.ResultsLow-dose dobutamine augmented both strain and flow in the presence of mild and moderate stenoses. Regional 2D STE strains correlated moderately with strains assessed by sonomicrometry (Rradial = 0.56, p < 0.0001; Rcirc = 0.55, p < 0.0001) and with regional flow quantities (Rradial = 0.61, Rcirc = 0.63). Overall, correspondence between 2D STE and sonomicrometry was better in the circumferential direction (Bias ± 1.96 SD: − 1.0 ± 8.2% strain, p = 0.06) than the radial direction (5.7 ± 18.3%, p < 0.0001). Mean PSI values were greatest in low flow conditions and normalized with low-dose dobutamine.Conclusions2D STE identifies changes in regional end-systolic circumferential and radial strain produced by mild and moderate coronary stenoses and low-dose dobutamine stress. Regional 2D STE end-systolic strain measurements correlate modestly with regional sonomicrometer strain and microsphere flow measurements.

P2477Assessment of intraventricular flow dynamics in acute heart failure studied by Vector Flow Mapping

Abstract Background Although left ventricular (LV) flow dynamics should be closely related to LV morphology and function, little is known about how heart failure (HF) changes it. Pathline Analysis (PA), a recently developed software based on Vector Flow Mapping (VFM, Hitachi), enables us to trace the virtual blood particles entering to the LV in diastole and being ejected in systole. We investigated the change of flow dynamics in HF induced in dogs using PA. Methods In 15 open-chest dogs, HF was induced by intracoronary injection of microspheres. Color Doppler images of apical long-axis view were acquired using Prosound F75 (Hitachi) before and after HF and were analyzed by PA. We calculated the ratio of the numbers of entering particles in diastole and ejected particles in systole (ejection rate) and the distance reached by the particles in diastole corrected by the LV long-axis diameter (propagation distance). Apical and basal short axis images were acquired using GE Vivid E9 and were analyzed for peak rotation and peak twist. Results After inducing HF, LV end-diastolic pressure increased from 6±2 to 15±5 mmHg (p&lt;0.001) and ejection fraction (EF), apical peak rotation and peak twist decreased significantly (EF; 58±5 to 36±8%, apical peak rotation; 14±5 to 3±2 degree, peak twist; 19±5 to 6±3 degree, p&lt;0.05, respectively). PA showed most of the entering particles to the LV were ejected in the following systole at the control stage, but in HF, a significant part of the entering particles were not ejected and remained in the LV (Figure). Ejection rate decreased from 50±11 to 26±11% (p&lt;0.001) and the propagation distance decreased from 85±9 to 66±13% (p&lt;0.001) after inducing HF. There were significant relationships between indices obtained by PA and EF and peak twist (Table). Conclusion A significant part of inflow is not ejected directly to the outflow in the next systole and remains in the LV in HF, suggesting inefficient flow dynamics.

Detection of Regional Mechanical Activation of the Left Ventricular Myocardium Using High Frame Rate Ultrasound Imaging.

We have investigated the feasibility of noninvasive mapping of mechanical activation patterns in the left ventricular (LV) myocardium using high frame rate ultrasound imaging for the purpose of detecting conduction abnormalities. Five anesthetized, open-chest dogs with implanted combined sonomicrometry and electromyography (EMG) crystals were studied. The animals were paced from the specified locations of the heart, while crystal and ultrasound data were acquired. Isochrone maps of the mechanical activation patterns were generated from the ultrasound data using a novel signal processing method called clutter filter wave imaging (CFWI). The isochrone maps showed the same mechanical activation pattern as the sonomicrometry crystals in 90% of the cases. For electrical activation, the activation sequences from ultrasound were the same in 92% of the cases. The coefficient of determination between the activation delay measured with EMG and ultrasound was R 2 = 0.79 , indicating a strong correlation. These results indicate that high frame rate ultrasound imaging processed with CFWI has the potential to be a valuable tool for mechanical activation detection.

Immediate post renal transplant period and hypertension: concordance between clinic and ambulatory blood pressure

Background: Markedly increased pulse wave velocity (PWV) with aging has been reported in numerous studies. Arterial wave reflection (WR) timing based on of the Augmentation Index (AI) framework does not change appreciably, despite increased PWV. The cause for this apparent discordance has not been established. Although a distal shift of reflecting sites has been proposed, this proposition has been exclusively based on the timing of the inflection point, which is a very limited approach. We hypothesize that AI is not capable of detecting early-systolic effects of reflection, particularly when PWV is high, leading to an apparent reflection-free period in early ejection. Methods: Simultaneous aortic pressure and flow were measured in anesthetized, open-chest dogs (n1⁄45). Intravenous infusion of methoxamine (MTX) and nitroprusside (NTP) were used to increase and decrease WRs, respectively. A coupled left ventricle-arterial system model was used to alter reflection magnitude and timing. Effects of reflection in early-systole were assessed with a systolic pressure-flow ratio (SPFR). Results: SPFR in the case of NTP remained close to aortic characteristic impedance (Zc) [horizontal dashed line] up until peak flow (Fig.1A). In control and MTX, SPFR grew increasingly divergent from Zc before peak flow (Fig.1B-C). Even when an inflection point is observed on the pressure waveform (Fig.1D, inset), SPFR diverges from Zc before the inflection, indicative of early-systole WRs. Modeling studies confirmed the dog experiments in a noise-free environment; only when wave reflections are substantially delayed and/or minimal does SPFR equal Zc in earlysystole. Divergence from this relation is due to WRs. Conclusion:WRs can alter pressure-flow relations in early-systole, prior to time of peak flow and the inflection point on the pressure waveform. Since AI is blind to early-systolic WRs, it should not be used to assess WR timing, especially when PWV is high. This is a particularly important limitation of AI to recognize when studying older subjects as well as those with hypertension in which PWV is elevated. When an appropriate method is used to gauge WR magnitude and timing in earlysystole, elevated PWV is indeed associated with earlier effects of reflections.

Fractal regional myocardial blood flows pattern according to metabolism, not vascular anatomy

Regional myocardial blood flows are markedly heterogeneous. Fractal analysis shows strong near-neighbor correlation. In experiments to distinguish control by vascular anatomy vs. local vasomotion, coronary flows were increased in open-chest dogs by stimulating myocardial metabolism (catecholamines + atropine) with and without adenosine. During control states mean left ventricular (LV) myocardial blood flows (microspheres) were 0.5-1 ml·g(-1)·min(-1) and increased to 2-3 ml·g(-1)·min(-1) with catecholamine infusion and to ∼4 ml·g(-1)·min(-1) with adenosine (Ado). Flow heterogeneity was similar in all states: relative dispersion (RD = SD/mean) was ∼25%, using LV pieces 0.1-0.2% of total. During catecholamine infusion local flows increased in proportion to the mean flows in 45% of the LV, "tracking" closely (increased proportionately to mean flow), while ∼40% trended toward the mean. Near-neighbor regional flows remained strongly spatially correlated, with fractal dimension D near 1.2 (Hurst coefficient 0.8). The spatial patterns remain similar at varied levels of metabolic stimulation inferring metabolic dominance. In contrast, adenosine vasodilation increased flows eightfold times control while destroying correlation with the control state. The Ado-induced spatial patterns differed from control but were self-consistent, inferring that with full vasodilation the relaxed arterial anatomy dominates the distribution. We conclude that vascular anatomy governs flow distributions during adenosine vasodilation but that metabolic vasoregulation dominates in normal physiological states.

Abstract 13917: Post-systolic Shortening in the Ischemic Myocardium is Attenuated in Multivessel Disease

Background: Post-systolic shortening (PSS) is myocardial shortening that occurs after end-systole and is considered as a sensitive marker of myocardial ischemia. Empirically, PSS in patients with multivessel disease is smaller than that in those with single vessel disease. Although this seems to be due to a decrease of difference in contraction between the ischemic and the surrounding myocardium, no study has elucidated it. We investigated the relationship between PSS and the difference of contraction between the ischemic and surrounding myocardium in an animal model which underwent left anterior descending coronary artery (LAD) occlusion (single vessel disease model) followed by left circumflex coronary artery (LCx) occlusion (multivessel disease model). Methods: In 7 open-chest dogs, left ventricular short-axis images (GE Vivid E9) and hemodynamic data were acquired at 3 conditions: (1) at baseline, (2) during LAD occlusion, and (3) during both LAD and LCx occlusion. Circumferential strains were analyzed in 6 segments by speckle tracking software. The amplitude of PSS (ε PSS ) and end-systolic strain (ε ES ) were measured and the difference of ε ES between a segment perfused by the LAD and the average of the other 5 segments was calculated (Δε ES ). Results: In the LAD segment, dyskinetic motion and PSS occurred during LAD occlusion but they were paradoxically attenuated during both LAD and LCx occlusion. ε PSS significantly correlated with Δε ES (r=0.95, p&lt;0.05). Although ε PSS significantly decreased during both occlusion compared to LAD occlusion, ε PSS corrected by Δε ES (ε PSS /Δε ES ) did not decrease (figure). Conclusions: PSS in the ischemic myocardium was attenuated when the surrounding myocardium also became ischemic. The difference of contraction between the ischemic and the surrounding myocardium at end-systole seems to be a determinant of the amplitude of PSS. A parameter ε PSS /Δε ES may be useful for assessing ischemia in patients with multivessel disease.

Abstract 12842: Regional Relaxation Abnormality Does Not Precede Regional Contraction Abnormality in the Ischemic Myocardium Immediately After Coronary Occlusion

Background: Although it has been reported that diastolic dysfunction precedes systolic dysfunction in the whole ventricle in the ischemic cascade, it is unclear whether the relaxation abnormality precedes the contraction abnormality in the region of ischemic insult. We investigated the beat-by-beat change of contraction and relaxation parameters after coronary occlusion. Methods: In 13 open-chest dogs, left ventricular short-axis images were continuously acquired with high frame rate speckle tracking echocardiography (109.3 fps, GE Vivid E9) along with hemodynamic data before and after left circumflex coronary artery occlusion (20 consecutive heartbeats after occlusion). Circumferential strain and strain rate were analyzed in the ischemic and non-ischemic regions. Peak systolic strain (ε s ), end-systolic strain (ε es ), and contraction duration as regional contraction parameters and the first positive peak of the strain rate (SR first positive peak ) as a regional relaxation parameter were measured. Results: Negative dP/dt began to decrease and tau began to prolong after the 15th beat of occlusion. In the ischemic region, ε es and contraction duration significantly decreased after the 15th beat, and ε s significantly decreased at the 20th beat. However, SR first positive peak did not decrease during 20 consecutive heartbeats but rather significantly increased after the 15th beat (0.51 ± 0.10 vs. 1.34 ± 0.15 /s, p&lt;0.05). Because the contraction duration was prolonged in the non-ischemic region after the 15th beat, dyssynchrony during the isovolumic relaxation period became remarkable (figure, arrowheads). Conclusions: In the ischemic myocardium immediately after coronary occlusion, the regional relaxation parameter did not become abnormal before the contraction parameter became abnormal. The deterioration of diastolic parameters for the whole ventricle (negative dP/dt and tau) seemed to be due to dyssynchrony during the isovolumic relaxation period.

Sympathetic denervation of heart and kidney induces similar effects on ventricular electrophysiological properties.

We aimed to investigate whether sympathetic denervation of the heart and kidney had similar effects on ventricular effective refractory period (ERP) and action potential duration (APD) restitution properties in a canine model. Twenty-four anaesthetised open-chest dogs (17-20 kg) were assigned to a sham operation group (n=8), a cardiac sympathetic denervation group (CSD, n=8) or a renal sympathetic denervation group (RSD, n=8). CSD was performed by ablating the caudal half of the LSG and T2-T4 thoracic sympathetic ganglia, while RSD was performed by ablating four sites on the adventitial surface of each renal artery. The ventricular electrophysiological properties were determined at four time points: baseline, 0 min, 30 min, and 60 min after interventions. The results showed that, when compared to the control group at the time point of 60 min after interventions, both CSD and RSD significantly reduced heart rate, prolonged the QT interval and ventricular ERP and APD, decreased the ERP dispersion and the slopes of APD restitution curves, and suppressed the APD alternans without affecting blood pressure and corrected QT interval. However, there were no significant differences in these parameters between CSD and RSD groups at the same time point. This study showed that sympathetic denervation of the heart and kidney induced similar electrophysiological effects in ventricles.

Vector flow mapping for assessing Beagle dogs′ left ventricular vortex in selective bi-polar single site cardiac pacing

Objective To investigate the changes of left ventricular(LV) vortex strength(VS) and distribution during selective cardiac pacing in a phases of cardiac cycle using vector flow mapping techniques, and associate with LV mechanical performance, so as to provide basic experimental database for optimizing the sites of the artificial cardiac pacing in clinic conditions. Methods Eight heathy open-chest Beagle dog models were employed for selective right ventricular apical(RVAP), left ventricular apical(LVAP) and lateral wall pacing(LVLP). The standard two-dimensional apical three views with color Doppler flow and dynamic two-dimensional images were acquired consecutively in three cardiac cycles for further off-line analysis, conventional parameters were measured at same time. Results Compared with baseline, LVSV, LVEF, LVCO and dp/dtmax were both reduced, and the parameters obtained leftside cardiac pacing were lower than that of right ventricular pacing (P<0.05), there′s no significant difference in E/Vp. The vortex pattern, distribution and vorticity at six typical phases induced by selective cardiac pacing were totally different from those at baseline with sinus rhythm, and leftside pacing were worsen than RVAP, the LVAP were most obvious. On multivariable regression analysis, the VS during ES(VSES) at baseline was independently related to late-diastolic VS and longitudinal strain (R2=0.63, P<0.001 and P=0.003, respectively). Conclusions The selective cardiac pacing could induce intracardiac vortex changes and differ from that at baseline, and the persistence of vortex from late diastole into ES is a haemodynamic measure of coupling between diastole and systole. Key words: Echocardiography; Ventricular function, left; Cardiac pacing, artificial; Vortex; Vector flow mapping

Vagus nerve stimulation reverses ventricular electrophysiological changes induced by hypersympathetic nerve activity.

What is the central question of this study? Previous studies have shown that hypersympathetic nerve activity results in ventricular electrophysiological changes and facilitates the occurrence of ventricular arrhythmias. Vagus nerve stimulation has shown therapeutic potential for myocardial infarction-induced ventricular arrhythmias. However, the actions of vagus nerve stimulation on hypersympathetic nerve activity-induced ventricular electrophysiological changes are still unknown. What is the main finding and its importance? We show that vagus nerve stimulation is able to reverse hypersympathetic nerve activity-induced ventricular electrophysiological changes and suppress the occurrence of ventricular fibrillation. These findings further suggest that vagus nerve stimulation may be an effective treatment option for ventricular arrhythmias, especially in patients with myocardial infarction or heart failure. Vagus nerve stimulation (VNS) has shown therapeutic potential for myocardial infarction-induced ventricular arrhythmias. This study aimed to investigate the effects of VNS on ventricular electrophysiological changes induced by hypersympathetic nerve activity. Seventeen open-chest dogs were subjected to left stellate ganglion stimulation (LSGS) for 4h to simulate hypersympathetic tone. All animals were randomly assigned to the VNS group (n=9) or the control group (n=8). In the VNS group, VNS was performed at the voltage causing a 10% decrease in heart rate for hours3-4 during 4h of LSGS. During the first 2h of LSGS, the ventricular effective refractory period (ERP) and action potential duration (APD) were both progressively and significantly decreased; the spatial dispersion of ERP, maximal slope of the restitution curve and pacing cycle length of APD alternans were all increased. With LSGS+VNS during the next 2h, there was a significant return of all the altered electrophysiological parameters towards baseline levels. In the eight control dogs that received 4h of LSGS without VNS, all the parameters changed progressively, but without any reversals. The ventricular fibrillation threshold was higher in the VNS group than in the control group (17.3±3.4 versus 11.3±3.8V, P<0.05). The present study demonstrated that VNS was able to reverse LSGS-induced ventricular electrophysiological changes and suppress the occurrence of ventricular fibrillation.

Abstract 13030: Post-systolic Shortening and Early Systolic Lengthening in the Ischemic Segment are Affected by the Contractility in its Adjacent Segment

Background: Post-systolic shortening (PSS) and early systolic lengthening (ESL) are sensitive markers of acute myocardial ischemia and the magnitude of these deformation is considered proportional to the severity of ischemia. Theoretical and mathematical models have suggested these deformation is caused by the difference of contractility between the ischemic and its adjacent normal segments. However, it has not been fully confirmed in an in vivo model yet. The aim of the study was to investigate whether PSS and ESL are affected by the contractility of its adjacent segment in an animal model which underwent left anterior descending coronary artery (LAD) occlusion (ischemic segment) followed by left circumflex coronary artery (LCx) occlusion (adjacent segment). Methods: In 6 open-chest dogs, left ventricular short-axis images with frame rate of over 90 fps (GE Vivid E9) and hemodynamics data were acquired at 3 conditions: (1) at baseline, (2) during LAD occlusion, and (3) during both LAD and LCx occlusion. Circumferential strain was analyzed in the LAD and LCx segments by speckle tracking software. End-systolic strain (ε ES ) and the amplitude of PSS and ESL (ε PSS and ε ESL ) were measured. Results: During LAD occlusion, ε PSS and ε ESL in the LAD segment significantly increased compared with baseline (ε PSS , 1.2 ± 1.1% vs. 9.5 ± 2.7%, p&lt;0.05; ε ESL , 1.3 ± 1.0% vs. 8.5 ± 4.2%, p&lt;0.05). During both LAD and LCx occlusion, ε ES in the LCx segment decreased, and both ε PSS and ε ESL in the LAD segment significantly decreased compared with during LAD occlusion (ε PSS , 9.5 ± 2.7% vs. 2.8 ± 1.3%, p&lt;0.05; ε ESL , 8.5 ± 4.2% vs. 2.3 ± 1.9%, p&lt;0.05) (figure). Conclusions: PSS and ESL diminished with the decrease of contractility in its adjacent segment. This suggests PSS and ESL occur based on the interplay of contraction between ischemic and adjacent segments and do not always reflect the severity of ischemia.

Abstract 13873: Quantitative Characteristics of Left Ventricular Vortex Flow in the Short and Long Axis Views by High Frame Rate Echocardiographic Particle Image Velocimetry

Background: Vortex flow in the left ventricle (LV) has three-dimensional structure and plays an important role in avoiding excessive dissipation of energy. However, quantitative characteristics of long and short axis (LAX and SAX) vortex flow have not been elucidated. Echocardiographic particle image velocimetry (Echo-PIV) is an emerging technique to evaluate instantaneous vortical flow inside the LV. However, it has a limitation of underestimation of high velocities due to limited frame rate. Moreover, previous investigations have mainly focused on vortex from LAX view. Therefore, we used high frame rate Echo-PIV to quantitate vortex flow in SAX as well as in LAX views to understand characteristics of vortex three-dimensionally. Methods: Echocardiographic contrast images of the LV SAX and LAX were acquired from 8 open-chest healthy dogs. The acquisition frame rate was 135 frames per second and the contrast bubbles density was optimized for blood flow analysis. Echo-PIV analysis was performed off-line by using commercially available software and vorticity data were calculated in the region of interest (ROI) throughout the cardiac cycle. ROI was manually placed on the vortex. Vortex strength was defined as the averaged vorticity within the ROI. Results: In SAX, counterclockwise vortex was seen near the anterior wall, and in LAX clockwise vortex was seen in the anterior mid-ventricle. Both in SAX and LAX views, vortex strength showed significant phasic variations being largest in isovolumic contraction (vortex strength, SAX 9.2±2.3/s, p&lt;0.001; LAX -12.0±2.4/s, p&lt;0.001), and smallest in isovolumic relaxation (SAX -0.8±0.8/s, p&lt;0.001; LAX -1.9±1.9/s, p&lt;0.001). Conclusion: High frame rate Echo-PIV successfully demonstrated a complicated pattern of intracardiac vortex with phasic variation of its strength throughout a cardiac cycle in both SAX and LAX. This method may be a useful tool to assess physiological role of vortex in the flow dynamics.

Carotid baroreceptor stimulation prevents arrhythmias induced by acute myocardial infarction through autonomic modulation.

: Electrical carotid baroreceptor stimulation (CBS) has shown therapeutic potential for resistant hypertension and heart failure by resetting autonomic nervous system, but the impacts on arrhythmias remains unclear. This study evaluated the effects of CBS on ventricular electrophysiological properties in normal dog heart and arrhythmias after acute myocardial infarction (AMI). In the acute protocol, anesthetized open chest dogs were exposed to 1 hour left anterior descending coronary occlusion as AMI model. Dogs were received either sham treatment (Control group, n = 8) or CBS (CBS group, n = 8), started 1 hour before AMI. CBS resulted in pronounced prolongation of ventricular effective refractory period and reduction of the maximum action potential duration restitution slope (from 0.85 ± 0.15 in the baseline state to 0.67 ± 0.09 at the end of 1 hour, P < 0.05) before AMI. Number of premature ventricular contractions (277 ± 168 in the Control group vs. 103 ± 84 in the CBS group, P < 0.05) and episodes of ventricular tachycardia/ventricular fibrillation (7 ± 3 in the Control group vs. 3 ± 2 in the CBS group, P < 0.05) was decreased compared with the control group during AMI. CBS buffered low-frequency/high-frequency ratio raise during AMI. Ischemic size was not affected by CBS. CBS may have a beneficial impact on ventricular arrhythmias induced by AMI through modulation of autonomic tone.

The morphology of unipolar potentials predicts the depth of activation foci

BackgroundThe depth of an arrhythmic focus is a major determinant of ablation procedural outcome. This study examined the relationship between the morphology of unipolar potentials and the depth and horizontal distance to activation foci. MethodsUnipolar left ventricular epicardial mapping was performed in 7 open-chest dogs, using silicon sheets with 12 unipolar electrodes 1mm apart, during bipolar pacing from an octopolar plunge electrode with 1-mm interelectrode spacing. The morphology of the unipolar electrograms was classified as QS, rS, qrS, qRS, rsr’S, or rsR’S. ResultsA QS complex was recorded immediately above a subepicardial or mid-myocardial pacing site. An rS complex was recorded away from a subepicardial pacing site. A positive wave originating from a down sloping deflection (R-in-QR) such as r wave in qrS, R wave in qRS, r′ wave in rsr’S or R′ wave in rsR’S complexes was observed when the recording was above a deep myocardial pacing site or away from a mid-myocardial pacing site. The amplitude of negative wave immediately before R-in-QR (Q-in-QR) was inversely correlated with the horizontal (R=−0.40; P<0.0001) and linear (R=−0.22; P=0.0006) distance to the pacing site, and the amplitude of R-in-QR was positively correlated with the horizontal (R=0.25; P=0.0001) and linear (R=0.29; P<0.0001) distance to the pacing site. The amplitude of the initial r wave was not correlated with the depth or horizontal and linear distance to the pacing site. ConclusionThe morphology of unipolar electrograms predicted the horizontal distance and the depth of nearby foci of activation.

Influence of Cardiac Decentralization on Cardioprotection

The role of cardiac nerves on development of myocardial tissue injury after acute coronary occlusion remains controversial. We investigated whether acute cardiac decentralization (surgical) modulates coronary flow reserve and myocardial protection in preconditioned dogs subject to ischemia-reperfusion. Experiments were conducted on four groups of anesthetised, open-chest dogs (n = 32): 1- controls (CTR, intact cardiac nerves), 2- ischemic preconditioning (PC; 4 cycles of 5-min IR), 3- cardiac decentralization (CD) and 4- CD+PC; all dogs underwent 60-min coronary occlusion and 180-min reperfusion. Coronary blood flow and reactive hyperemic responses were assessed using a blood volume flow probe. Infarct size (tetrazolium staining) was related to anatomic area at risk and coronary collateral blood flow (microspheres) in the anatomic area at risk. Post-ischemic reactive hyperemia and repayment-to-debt ratio responses were significantly reduced for all experimental groups; however, arterial perfusion pressure was not affected. Infarct size was reduced in CD dogs (18.6±4.3; p = 0.001, data are mean±1SD) compared to 25.2±5.5% in CTR dogs and was less in PC dogs as expected (13.5±3.2 vs. 25.2±5.5%; p = 0.001); after acute CD, PC protection was conserved (11.6±3.4 vs. 18.6±4.3%; p = 0.02). In conclusion, our findings provide strong evidence that myocardial protection against ischemic injury can be preserved independent of extrinsic cardiac nerve inputs.

Partitioning pulmonary vascular resistance using the reservoir-wave model

The conventional determination of pulmonary vascular resistance does not indicate which vascular segments contribute to the total resistance of the pulmonary circulation. Using measurements of pressure and flow, the reservoir-wave model can be used to partition total pulmonary vascular resistance into arterial, microcirculation, and venous components. Changes to these resistance components are investigated during hypoxia and inhaled nitric oxide, volume loading, and positive end-expiratory pressure. The reservoir-wave model defines the pressure of a volume-related reservoir and the asymptotic pressure. The mean values of arterial and venous reservoir pressures and arterial and venous asymptotic pressures define a series of resistances between the main pulmonary artery and the pulmonary veins: the resistance of large and small arteries, the microcirculation, and veins. In 11 anaesthetized, open-chest dogs, pressure and flow were measured in the main pulmonary artery and a single pulmonary vein. Volume loading reduced each vascular resistance component, whereas positive end-expiratory pressure only increased microcirculation resistance. Hypoxia increased the resistance of small arteries and veins, whereas nitric oxide only decreased small-artery resistance significantly. The reservoir-wave model provides a novel method to deconstruct total pulmonary vascular resistance. The results are consistent with the expected physiological responses of the pulmonary circulation and provide additional information regarding which segments of the pulmonary circulation react to hypoxia and nitric oxide.

A two-for-one bargain: using cilnidipine to treat hypertension and its comorbidities.

A two-for-one bargain: using cilnidipine to treat hypertension and its comorbidities.