Wall Thickening Fraction Research Articles

Relationship between Augmentation Index and Wall Thickening Fraction during Hypotension in an Animal Model of Myocardial Ischemia-Reperfusion and Heart Failure.

Non-invasive indices to evaluate left ventricular changes during ischemic heart failure are needed to quantify the myocardial impairment and the effectiveness of therapeutic manoeuvres. The aims of this work were to calculate the Wall Thickening Fraction (WTF) and the Augmentation Index (AIx) and to assess the relationship between WTF and AIx using data obtained from an animal model with heart failure followed by a myocardial ischemia stage and a reperfusion stage. Nine Corriedale sheep that had been monitored for 10 minutes during a basal stage underwent 5-minute myocardial ischemia, followed by 60-minute reperfusion. Seven of them were subjected to an induced heart failure through an overdose of halothane, two of which were treated with intra-aortic counterpulsation during the reperfusion stage. The remaining two animals were monitored during their ischemia-reperfusion stage. Data obtained in the 5 animals suffering from heart failure followed by myocardial ischemia showed that: a) heart failure induction determined decrease in cardiac output, cardiac index and systolic and diastolic aortic pressure (AoP) with respect to their basal values (p<0.05), b) myocardial ischemia decreased the WTF compared with basal and induced heart failure values (p<0.05), c) during the reperfusion stage accompanied by induced heart failure, WTF increased with respect to values observed during the ischemia induction stage (p<0.05); nevertheless, basal values were not recovered after reperfusion (p<0.05). During this 60-minute stage, systolic and diastolic AoP values were lower (p<0.05) than those at the basal stage. AIx and WTF values calculated from synchronically recorded values of aortic pressure and left ventricular wall thickness during the reperfusion stage in all animals (n = 9) showed a negative correlation (p<0.05). Analysed data provided evidence of a negative relationship between a left ventricular index of myocardial function and an arterial index obtained from AoP waves.

VIEWING ONLY POSTERS1323Evaluation of right ventricular transverse strain and strain rate in patients with acute ST-segment elevation myocardial infarction: a cardiac magnetic resonance feature tracking study1333Cardiac resynchronization in ischemic heart failure patients: a comparison between therapy guided by cardiac magnetic resonance imaging and 2D-speckle tracking echocardiography1338Cardiac magnetic resonance versus bisphosphonate scintigraphy for diagnosis of cardiac amyloidosis1341Strain relaxation index, a novel

VIEWING ONLY POSTERS1323Evaluation of right ventricular transverse strain and strain rate in patients with acute ST-segment elevation myocardial infarction: a cardiac magnetic resonance feature tracking study1333Cardiac resynchronization in ischemic heart failure patients: a comparison between therapy guided by cardiac magnetic resonance imaging and 2D-speckle tracking echocardiography1338Cardiac magnetic resonance versus bisphosphonate scintigraphy for diagnosis of cardiac amyloidosis1341Strain relaxation index, a novel

Abstract 15656: Global Intracoronary Infusion of Allogeneic Cardiosphere-Derived Cells (CDCs) Immediately After Reperfusion Stimulates Myocyte Regeneration in Remote Viable Myocardium in Swine With Acute Myocardial Infarction

Introduction: Previous studies evaluating regenerative strategies have focused on administering stem cells to the infarct related artery. Unfortunately, this does not stimulate cardiac regeneration nor prevent myocyte loss in viable remote myocardium that becomes dysfunctional due to LV remodeling. Hypothesis: We hypothesized that administrating allogeneic CDCs to the entire heart (global CDC infusion) at the time of reperfusion could improve function, stimulate myocyte regeneration and prevent myocyte loss throughout the LV. Methods: Yorkshire swine (n=12) underwent a one hour LAD occlusion. Ejection fraction (EF) decreased from 63 ± 2% at baseline to 44 ± 2% after infarction (p&lt;0.05 vs. baseline). Immediately after reperfusion animals were randomized to allogeneic intracoronary CDCs or vehicle in a blinded fashion (n=6 each). Allogeneic CDCs (20 x 10^6 CDCs, cyclosporine 100 mg/day) were infused into the 3 major coronary distributions without interrupting flow. Four weeks later we assessed myocardial function (echo), myocyte proliferation (Ki67), infarct size (TTC), myocyte nuclear density and cell size in comparison to vehicle. Results: After 4 weeks, global CDC infusion increased wall thickening and ejection fraction despite the fact that infarct volume was not different (Table). CDCs stimulated myocyte proliferation (Ki67) in border and remote regions by 3-fold. As a result, myocyte number (nuclear density) increased by 34 % and cell size decreased by 7% in viable infarct border and remote regions. Conclusion: Global infusion of allogeneic CDCs immediately after reperfusion 1.) stimulates myocyte regeneration in viable myocardium remote from the infarct and 2.) improves regional and global LV function without altering infarct size. Thus, treating viable remote myocardium as well as the infarct related artery with allogeneic CDCs may afford a widely available approach to reverse LV dysfunction in patients with acute myocardial infarction.

Diagnostic usefulness of quantitative tissue velocity imaging and anatomic M-mode echocardiography for coronary artery diseases: A pilot study.

To explore the potential clinical usefulness and determine optimal diagnostic criteria of quantitative tissue velocity imaging and anatomic M-mode echocardiography in patients with coronary artery disease (CAD). We used quantitative tissue velocity imaging for the measurement of systolic myocardial velocity, and anatomic M-mode echocardiography for the measurement of ventricular wall-thickening fraction in 44 subjects with suspected CAD. Subjects were classified as patients if coronary angiography demonstrated a stenosis ≥ 50%, and as controls if it was strictly normal. The diagnostic criteria, sensitivity, and specificity were assessed by receiver-operator curves. Controls had greater mean systolic myocardial velocity and ventricular wall-thickening fraction in the basal (6.59 ± 1.25 cm/s and 0.44 ± 0.05) and mid segment (5.23 ± 0.93 cm/s and 0.43 ± 0.04) than patients (5.02 ± 1.17 cm/s and 0.29 ± 0.04, 3.27 ± 1.29 cm/s and 0.29 ± 0.04, respectively, p < 0.001). Mid-segment ventricular wall-thickening fraction offered 95% sensitivity (95% CI 88.7% to 98.4%), and 98.3% specificity (95% CI 90.9% to 1.0) with an optimal cut-off point of 0.349, yielding better results than systolic myocardial velocity, which provided 83% sensitivity (95% CI 74.2% to 89.8%), 90% specificity (95% CI 79.5% to 96.2%), and optimal cut-off point 4.47. The combination of systolic myocardial velocity and ventricular wall-thickening fraction offered 97% sensitivity (95% CI 91.5% to 99.4%) Mid-segment ventricular wall-thickening fraction might be suitable for the evaluation of patients with CAD.

Automated detection of myocardial ischaemia by epicardial miniature ultrasound transducers — a novel tool for patient monitoring during cardiac surgery☆

Early detection of myocardial ischaemia in cardiac surgery is important. We have developed an ultrasonic system for continuous myocardial monitoring by use of miniature transducers. The aim of this study was to investigate the system's ability to detect ischaemia in patients undergoing off-pump coronary artery bypass grafting (CABG), and whether automated signal analysis could detect ischaemia. In 10 patients scheduled for CABG, ultrasound transducers were fixed to the epicardium in the area supplied by left anterior descending artery (LAD), and in a remote area for control. M-mode images with measurements of wall-thickening velocities were presented in real time and systolic (S') and post-systolic velocities (PSVs) were recorded. An automated algorithm for ischaemia detection was developed, using end-systolic wall thickening as a fraction of total wall thickening. Registrations were made at baseline and during LAD occlusion. Echocardiographic strain was used as reference. Nine of 10 patients developed ischaemia during LAD occlusion, with resulting decrease in systolic and increase in post-systolic wall-thickening velocities (P<0.001). In these nine patients, Vdiff shifted below zero with no overlap between baseline and LAD occlusion (P<0.001). The automated wall-thickening fraction was reduced from 0.93±0.05 to 0.57±0.15 (P=0.001). A cut-off value of 0.85 could completely separate normal from ischaemic myocardium in all patients. The ultrasonic system detected regional ischaemia during LAD occlusion. An automated analysis algorithm demonstrated excellent ability to detect ischaemia. This technology can develop into a useful tool to detect ischaemia in cardiac surgery.

??-Opioid Receptor Antagonism Improves Recovery from Myocardial Stunning in Chronically Instrumented Dogs

We tested the hypothesis that the selective kappa-opioid receptor antagonist nor-binaltorphimine (nor-BNI) improves recovery from myocardial stunning. Ten dogs were chronically instrumented for measurement of heart rate, left atrial, aortic and left ventricular pressure (LVP), and the maximum rate of LVP increase (LV dP/dt(max)) and decrease (LV dP/dt(max)), coronary blood flow velocity and myocardial wall-thickening fraction. Regional myocardial blood flow was determined with fluorescent microspheres. Catecholamine plasma levels were measured by high-performance liquid chromatography, and beta-endorphin and dynorphin plasma levels by radioimmunoassay. An occluder around the left anterior descending artery (LAD) allowed induction of a reversible LAD-ischemia. Animals underwent two experiments in a randomized crossover fashion on separate days: (a) 10 min LAD-occlusion (control experiment), (b) second ischemic episode 24 h after nor-BNI (2.5 mg/kg IV) (intervention). Dogs receiving nor-BNI showed an increase in wall-thickening fraction, LV dP/dt(max) and LV dP/dt(min) before ischemia and during the whole reperfusion (P < 0.05 versus control experiment). After nor-BNI pretreatment, dynorphin levels increased after induction of ischemia to a peak level of 15.1 +/- 3.6 pg/mL (P < 0.05 versus control experiment). The increase in plasma beta-endorphin during ischemia and early reperfusion was attenuated after nor-BNI. Compared with the control experiment, nor-BNI left global hemodynamics, regional myocardial blood flow, and catecholamine levels unchanged. In conclusion, nor-BNI improves recovery from myocardial stunning after regional myocardial ischemia in chronically instrumented dogs.

A five-dimensional mathematical model for regional and global changes in cardiac uptake and motion

The objective of this work was to simultaneously introduce known regional changes in contraction pattern and perfusion to the existing gated Mathematical Cardiac Torso (MCAT) phantom heart model. We derived a simple integral to calculate the fraction of the ellipsoidal volume that makes up the left ventricle (LV), taking into account the stationary apex and the moving base. After calculating the LV myocardium volume of the existing beating heart model, we employed the property of conservation of mass to manipulate the LV ejection fraction to values ranging between 13.5% and 68.9%. Multiple dynamic heart models that differ in degree of LV wall thickening, base-to-apex motion, and ejection fraction, are thus available for use with the existing MCAT methodology. To introduce more complex regional LV contraction and perfusion patterns, we used composites of dynamic heart models to create a central region with little or no motion or perfusion, surrounded by a region in which the motion and perfusion gradually reverts to normal. To illustrate this methodology, the following gated cardiac acquisitions for different clinical situations were simulated analytically: 1) reduced regional motion and perfusion; 2) same perfusion as in (1) without motion intervention; and 3) washout from the normal and diseased myocardial regions. Both motion and perfusion can change dynamically during a single rotation or multiple rotations of a simulated single-photon emission computed tomography acquisition system.

Comparison of myocardial gated single photon emission computerised tomography, planar radionuclide ventriculography and echocardiography in evaluating left ventricular ejection fraction, wall thickening and wall motion

Left ventricular ejection fraction (LVEF) and wall thickening are fundamental aspects of cardiac function. Recently, gated single photon emission computerised tomography (GSPECT) and anatomical M-mode echocardiography are new techniques, which have been introduced for the evaluation of left ventricular wall thickening and ejection fraction. These, however, have not been evaluated against established techniques, including equilibrium radionuclide ventriculography (ERNV), which remains the current gold standard for the evaluation of LVEF. We examined the concordance between LVEF, wall motion and wall thickening scores derived from GSPECT, echocardiography and ERNV, in a group of 16 patients with suspected ischaemic heart disease. Estimated ejection fraction correlated better between ERNV and gated SPECT (R2 = 0.93) than between echocardiography and either gated SPECT (R2 = 0.62) or ERNV (R2 = 0.71). There was poor correlation between gated SPECT and anatomical M-mode echocardiography in the assessment of wall thickening (83/150, 56%; kappa= 0.31, p < 0.05) and similar correlation (100/150, 66%; kappa = 0.29, p < 0.01) for wall motion analysis. In conclusion, estimations of ejection fraction by all the three studied modalities agreed to a degree sufficient for routine clinical practice. However, estimates of wall thickening from echocardiography cannot be used interchangeably with those derived from gated myocardial perfusion SPECT.

Xenon improves recovery from myocardial stunning in chronically instrumented dogs.

In this study we tested the hypothesis that inhalational administration of xenon improves recovery from myocardial stunning. Ten dogs were chronically instrumented for measurement of heart rate; left atrial, aortic, and left ventricular pressure; coronary blood-flow velocity; and myocardial wall-thickening fraction. Regional myocardial blood flow was determined with fluorescent microspheres. Catecholamine plasma levels were measured by high-performance liquid chromatography. An occluder around the left anterior descending artery (LAD) allowed the induction of a reversible LAD ischemia. Animals underwent 2 experimental conditions in a randomized crossover fashion on separate days: (a) 10 min of LAD occlusion under fentanyl (25 microg. kg(-1). h(-1)) and midazolam (0.6 mg. kg(-1). h(-1)) (control) and (b) a second ischemic episode under the same basal anesthesia with concomitant inhalational administration of 75 +/- 1 vol% xenon (intervention). Anesthesia was induced 35 min before LAD occlusion and was discontinued after 20 min of reperfusion. Dogs receiving xenon showed a significantly better recovery of wall-thickening fraction up to 12 h after ischemia. The increase in plasma epinephrine during emergence from anesthesia and in the early reperfusion period was significantly attenuated in the xenon group. There were no differences between groups concerning global hemodynamics, blood-flow velocity, or regional myocardial blood flow. In conclusion, inhalational administration of 75 vol% xenon improves recovery from myocardial stunning in chronically instrumented dogs under fentanyl/midazolam anesthesia.

Short-term administration of ethanol does not affect functional recovery from myocardial stunning in awake dogs.

Chronic ingestion of small doses of ethanol protects the myocardium from ischemic damage. It was demonstrated that short-term administration of ethanol (SAE) enhances the recovery of stunned myocardium in acutely instrumented, anesthetized dogs. It is unclear whether this beneficial effect of SAE also occurs in awake dogs. Therefore, we investigated the effects of SAE on regional myocardial stunning in awake dogs. Thirty-six dogs were chronically instrumented for measurement of heart rate, left atrial, aortic, and left ventricular pressure, left systolic ventricular contactility (dP/dt(max)) and diastolic ventricular function (dP/dt(min)), and regional myocardial wall-thickening fraction (WTF). Occluders around the left anterior descending (LAD) artery allowed the induction of reversible ischemia in the LAD-perfused myocardium. The dogs were assigned to one of three groups that differed in the dose of ethanol administered in the ethanol experiment (I, 0.125 g/kg [n = 12]; II, 0.25 g/kg [n = 12]; III, 0.5 g/kg [n = 12]). In each group, the dogs underwent two ischemic episodes (randomized crossover fashion; separate days): 10 min of LAD occlusion after the application of ethanol IV over 30 min (ethanol group) and without ethanol (control). WTF and hemodynamic variables were measured at baseline and at predetermined time points until complete recovery of myocardial stunning occurred. LAD-ischemia led to a significant decrease of LAD-WTF in all groups. There was no difference in WTF and hemodynamic variables with or without SAE during reperfusion. We conclude that SAE (0.125 g/kg, 0.25 g/kg, and 0.5 g/kg) does not significantly affect myocardial stunning in conscious dogs. In contrast to previous experiments in anesthetized dogs, short-term administration of ethanol does not alter myocardial stunning in conscious dogs.

Naloxone prevents increased atrial natriuretic peptide release during regional myocardial ischaemia and stunning in awake dogs

Atrial natriuretic peptide (ANP) release is increased in patients with ischaemic left ventricular dysfunction. A beneficial effect of naloxone on recovery from myocardial stunning was shown previously. The aim of this study was to investigate the effects of naloxone on ANP release during regional myocardial ischaemia and stunning in awake dogs. Ten dogs were chronically instrumented for measurement of heart rate, left atrial, aortic, and left ventricular pressure (LVP), LV dP x dtmax/min(-1), and myocardial wall-thickening fraction. An occluder around the left anterior descending artery (LAD) allowed induction of reversible ischaemia in the LAD-perfused myocardium. Each dog underwent two ischaemic episodes (randomized crossover fashion; separate days): 10 min of LAD occlusion (1) after application of naloxone (63 microg kg(-1)), and (2) without naloxone. ANP levels were measured at baseline (BL) and at predetermined time points until complete recovery of myocardial stunning occurred. LAD ischaemia-induced release of ANP (peak level: 182 (30) vs 27 (7) pg ml(-1) BL) only in the control group without naloxone. Between 1 and 180 min of reperfusion, ANP levels were significantly higher only in the control group (P<0.05). Pre-ischaemic application of naloxone prevents this ischaemia-induced ANP-release in conscious dogs.

Hemin, inducer of heme-oxygenase 1, improves functional recovery from myocardial stunning in conscious dogs

Objective: To examine the effects of pretreatment with hemin, an inducer of the potential antioxidative enzyme heme-oxygenase 1 (HO-1) or heat-shock protein 32, on myocardial stunning. Design: Randomized animal study. Setting: Animal laboratory of a university hospital. Participants: Chronically instrumented mongrel dogs (n = 44). Interventions: Dogs underwent chronic instrumentation for measurement of hemodynamics and myocardial wall thickening fraction (WTF). Experiments with 12 dogs were performed on separate days in a crossover fashion: (1) 10 minutes of left anterior descending (LAD) coronary artery occlusion after application of hemin (9 mg/kg/d) for 1 week and (2) 10 minutes of LAD coronary artery occlusion without hemin pretreatment. In control experiments (n = 32), the reversible induction of HO-1, using gel electrophoresis and Western blotting, was determined. Measurements and Main Results: WTF was measured as a baseline value before hemin administration and at predetermined time points until complete recovery from stunning. LAD artery occlusion caused a significant reduction in the WTF in the LAD-perfused area with and without hemin, without significant hemodynamic changes. At all time points, after 1 minute of reperfusion, the WTF as percentage of baseline values was significantly higher after hemin pretreatment (p < 0.05). Baseline WTF values were reached after 24 hours with and after >48 hours without hemin pretreatment (p < 0.05). Conclusion: Hemin pretreatment attenuates myocardial stunning in conscious dogs. Copyright © 2001 by W.B. Saunders Company

Naloxone improves functional recovery of myocardial stunning in conscious dogs through its action on the central nervous system

This study tests the hypothesis that naloxone, but not its quarternary salt, naloxone methiodide (which does not enter the central nervous system), improves recovery from myocardial stunning in conscious dogs. Twenty dogs were chronically instrumented for measurement of heart rate, left atrial, aortic and left ventricular pressure (LVP), LV dP x dtmax(-1) and myocardial wall thickening fraction (WTF). Regional myocardial blood flow was determined with coloured microspheres. Occluder around the left anterior descending artery (LAD) allowed induction of reversible LAD ischaemia. Each of the 20 dogs underwent two LAD ischaemic challenges. Experiments (performed on separate days, in crossover fashion) were: (i) 10 min of LAD occlusion after application of naloxone 63 microg kg(-1) or naloxone methiodide 63 microg kg(-1) and (ii) occlusion without naloxone or naloxone methiodide. WTF was measured at baseline and until complete recovery occurred. LAD ischaemia significantly reduced LAD WTF with (mean (SD) 54 (15)% lower than baseline) and without naloxone (55 (16)% lower than baseline), without significant haemodynamic differences. Between I to 30 min of reperfusion, WTF was significantly higher with naloxone (P < 0.05). There was no difference in WTF with or without naloxone methiodide. We conclude that naloxone improved recovery from myocardial stunning in conscious dogs, and that this was centrally mediated.

Effect of transmyocardial laser revascularization on chronic ischemic hearts in sheep.

We investigated the effect of transmyocardial laser revascularization (TMR) on myocardial function and regional blood flow in an animal model of ischemic heart disease. Chronic ischemia was induced in 11 sheep by the application of coronary stenosis on the left anterior descending (LAD) and circumflex coronary artery (LCX). Ten weeks later, in six of them, transmyocardial channels were created in the anterior free wall and in the posterior wall of the left ventricle. Five animals served as controls. The myocardial function was assessed by echocardiography taken at baseline and every 2 weeks after coronary stenosis and after TMR. Myocardial perfusion was measured by colored microspheres, injected at baseline, immediately after coronary stenosis, before and after TMR, and at 20 weeks after coronary stenosis. The hearts were retrieved at 20 weeks for light microscopic examination. The left ventricular end-diastolic and end-systolic cavity area was elevated 20 weeks after coronary stenosis in the control and TMR groups. There was no difference between groups (analysis of variance; ANOVA, non-significant). The wall thickening fraction (WTF) decreased progressively and significantly after coronary stenosis in both groups. The WTF was further acutely reduced by TMR, and recovered gradually to the pre-TMR level. No significant difference in WTF was observed between the TMR and control groups. The resting myocardial blood flow was significantly increased by TMR at 20 weeks (P=0.03). Light microscopic examination revealed channel patency in 49% of the laser scars at 10 weeks post-TMR. A dense capillary network was observed at the edges of the surrounding scar. In an experimental model of ischemic heart disease, TMR developed angiogenesis in the lased channels, but, however, failed to improve myocardial function.

Intravenous pretreatment with magnolol protects myocardium against stunning.

Magnolol, an antioxidant, has been reported to possess various protective effects on the cardiovascular system. However, its effect on myocardial stunning has not been elucidated. The purpose of this study was to investigate the antistunning effect of magnolol by evaluating the recovery of regional myocardial function after 10-minute coronary artery occlusion in anesthetized, open-chest rabbits. There was no significant hemodynamic change after intravenous infusion of magnolol. Systolic wall thickening fraction (WThF) measured with an epicardial Doppler sensor in animals pretreated with normal saline and vehicle solution remained significantly depressed (60 +/- 7% and 77 +/- 4% of baseline WThF, respectively) 3 hours after coronary artery reperfusion (CAR). Pretreatment with magnolol (10(-7) and 10(-6) g/kg, intravenous infusion) significantly enhanced the recovery of systolic wall thickening fraction (98 +/- 1 and 99 +/- 1% of baseline WThF, respectively) 60 minutes after CAR. This study demonstrated that intravenous pretreatment with magnolol protected myocardium against stunning.

Chronic Heart Failure Model Induced by Coronary Embolization in Sheep

To create a model of chronic heart failure in a large animal. Heart failure was induced in sheep by single intracoronary injection of polymer macrobeads, which were administered into left main coronary artery (n=3) or selectively into left anterior descending (n=4) or left circumflex (n=5) coronary artery. The animals were followed by echocardigraphy for 20 weeks. Measurements comprised fractional area change (FAC), and diastolic ventricular area (EDVA) and regional wall-thickening fraction (WT%). EDVA increased from 14.2+/-2.1 cm2 prior to embolization to 16.9+/-3.1 cm2 on day 1 (p<0.05), and remained significantly increased until completion of the follow-up period. FAC dropped from 47.9+/-4.6% at baseline to 29.3+/-4.4% on day 1 (p<0.001) and remained significantly depressed until 20 weeks later. In 9 selectively embolized animals WT% of the embolized area decreased from 33.8+/-8.0% at baseline to 5.3+/-2.6% on day 1 and remained significantly decreased. A simple model of chronic heart failure was developed. It shows relatively high stability over time and may prove beneficial in experimental work on ventricular assist devices.

Thoracic epidural anesthesia does not affect functional recovery from myocardial stunning in sevoflurane-anesthetized dogs

Objective: A beneficial effect of thoracic epidural anesthesia (TEA) on recovery from myocardial stunning was previously shown in awake dogs. The aim of this study was to investigate the effects of TEA on recovery from myocardial stunning in sevoflurane-anesthetized dogs. Design: Randomized animal study. Setting: Animal laboratory of a university hospital. Participants: Chronically instrumented mongrel dogs. Interventions: Six dogs were chronically instrumented for measurement of hemodynamics and myocardial wall thickening fraction (WTF). The following experiments were performed on separate days in a crossover fashion: (1) 10 minutes of ischemia of the left anterior descending (LAD) coronary artery during sevoflurane anesthesia without TEA and (2) 10 minutes of ischemia during sevoflurane anesthesia with TEA. Measurements and Main Results: WTF was measured awake (baseline) and at predetermined time points until complete recovery of myocardial function occurred. Induction of anesthesia led to a decrease of WTF compared with baseline. Induction of ischemia led to a further decrease of WTF to negative values, which returned to positive values within the first minute of reperfusion. There were no differences between the two experimental conditions at any of the time points measured. In awake dogs, TEA improved the recovery from myocardial stunning compared with the control experiment. There was no difference between conscious dogs with TEA or sevoflurane-anesthetized dogs with or without TEA. Conclusion: TEA has no additional protective effect on the recovery of WTF during sevoflurane anesthesia.

Clonidine Improves Recovery from Myocardial Stunning in Conscious Chronically Instrumented Dogs

Clonidine, an alpha2-adrenergic agonist, has been widely used in anesthesia because of its sedative, analgesic, sympatholytic, and specific hemodynamic effects. The use of clonidine in myocardial ischemia is controversial because of its bradycardic and hypotensive effects. In the present study, we tested the hypothesis that clonidine improves recovery from myocardial stunning in conscious dogs. Seven dogs were chronically instrumented to allow measurement of left atrial pressure (LAP), aortic blood pressure (ABP), left ventricular pressure (LVP), maximal rate of increase of LVP (LVdP/dtmax), and myocardial wall thickening fraction (WTF). The myocardial blood flow was measured using colored microspheres. To compensate for any potential interaction between the two ischemic episodes, experiments were performed on separate days in a cross-over fashion (four animals underwent Condition 1, and three underwent Condition 2 as their first experiment). The ischemic episodes involved 1) 10 min of ischemia of the left anterior descending (LAD) coronary artery without any intervention, and 2) 10 min of LAD ischemia 30 min after 10 microg/kg iv clonidine. WTF was measured before the induction of ischemia or the application of clonidine (baseline) and at predetermined time points until complete recovery of myocardial function. WTF recovered faster during the first 2 h of reperfusion when clonidine was administered. The increase in plasma epinephrine was attenuated by clonidine during ischemia, but there was no change during reperfusion. The increase of plasma norepinephrine levels was attenuated during ischemia and reperfusion. The hemodynamic effects of clonidine did not depress myocardial perfusion or impair myocardial function. In this study, we investigated the effects of IV clonidine on myocardial stunning in chronically instrumented dogs. Clonidine improved the recovery from myocardial stunning and attenuated increases in catecholamine plasma levels.

Thoracic Epidural Anesthesia and the Patient with Heart Disease

Thoracic Epidural Anesthesia and the Patient with Heart Disease

Interaction of nimodipine and propofol in dogs. Hemodynamics and cardiodynamics

Nimodipine is frequently used for treatment of cerebral vasospasm in patients undergoing intracerebral vascular surgery and during intensive care therapy of patients with subarachnoid haemorrhage. Propofol is being increasingly used as a hypnotic drug in neuroanaesthesia and for sedation in critically ill patients. There is evidence of a propofol effect on voltage-dependent calcium channels; hence, the administration of propofol may interact with the haemodynamic effects of nimodipine. We investigated the haemodynamic interactions of both compounds in chronically instrumented dogs. Five mongrel dogs were chronically instrumented for measurement of heart rate (HR), left atrial (LAP), aortic (ABP), and left ventricular pressure (LVP), LV dP/dt, cardiac output (CO), systemic vascular resistance (SVR), coronary blood flow velocity (CBFV), and myocardial wall-thickening fraction (WTF). After complete recovery from surgery and assessment of normal resting blood gas values and temperature, all animals received on separate days either propofol 30 mg/kg.h (P), nimodipine in two maintenance doses in the awake state (N), or the combination of nimodipine and propofol (N+P). The maintenance doses of nimodipine in N and N+P were 1 and 2 micrograms/kg.min for 40 min each after a bolus of either 10 or 20 micrograms/kg min over 2 min. Measurements were performed as controls, in the middle (20 min), and at the end (40 min) of each maintenance infusion of nimodipine or at equivalent points in time in group P (Fig. 1). Animals receiving propofol were mechanically ventilated after endotracheal intubation. Blood gas values were kept within the normal range. All data were analysed with repeated measures of ANOVA followed by student's t-test with Bonferroni correction. There was no statistically significant difference for any of the measured parameters between N and N+P or between the two maintenance doses of nimodipine (Table 1). HR was significantly higher with both doses of nimodipine in the awake state compared to the control values (123 +/- 7.1 and 146 +/- 6.4 vs 78 +/- 2.4/min). The administration of nimodipine with and without propofol led to a significant increase in CBFV (Fig. 2). However, there was no difference in CBFV between nimodipine in the awake state and in combination with propofol (Fig. 2). We conclude that administration of propofol does not alter the systemic haemodynamic and regional myocardial effects of a nimodipine infusion in a dose of 1 or 2 micrograms/kg.min in chronically instrumented dogs.