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Right ventricular failure is a leading cause of death in patients who require the left ventricular assist device. Previous reports suggested right ventricular functional deterioration during left ventricular assist but lacked a method by which right ventricular function could be quantified adequately. This study examined the effects of left ventricular volume unloading on right ventricular systolic function by means of the stroke work/end-diastolic volume relationship, a load-insensitive index of myocardial performance. In 12 anesthetized open-chested dogs, right ventricular and left ventricular pressures were measured with micromanometers while ultrasonic dimension transducers measured left and right ventricular orthogonal diameters. Left ventricular unloading was accomplished with left atrial-to-femoral artery bypass with a centrifugal pump. Data were recorded during transient vena caval occlusion in the control state and with maximal left ventricular unloading by full support by the left ventricular assist device. Modified ellipsoidal geometry was used to calculate simultaneous biventricular volumes, and linear regression analysis of right ventricular stroke work versus end-diastolic volume was used to quantify right ventricular systolic function. Average slope and x intercept of this relationship under control conditions were 2.2 +/- 0.3 X 10(4) erg/ml and 10.7 +/- 5.0 ml, respectively. During full support by the left ventricular assist device (mean flow rate, 2.4 +/- 0.3 L/min), left ventricular end-diastolic volume decreased by 31% (p less than 0.01), left ventricular septal-free wall diameter decreased by 7% (p less than 0.001), and rate of rise of right ventricular peak positive pressure declined by 13% (p less than 0.05). The corresponding slope and x intercept of the right ventricular stroke work/end-diastolic volume relationship during full unloading of left ventricular assist device were 2.3 +/- 0.3 X 0.3 X 10(4) erg/ml and 14.3 +/- 4.8 ml, respectively; these values were not significantly different from control values (p greater than 0.5). Additionally, analysis of right ventricular end-diastolic pressure-volume relationships suggested improved right ventricular chamber compliance, although the effects were small and did not reach statistical significance (p = 0.10). These data imply that marked alterations in biventricular geometry accompanying left ventricular volume unloading by the left ventricular assist device in a normal heart do not significantly alter right ventricular performance characteristics.
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PMID:Effects of the left ventricular assist device on right ventricular function. 232 18

To evaluate the acute changes in left ventricular (LV) performance before and immediately after percutaneous aortic valvuloplasty, 25 patients underwent first-pass radionuclide angiocardiography for construction of pressure-volume loops. Simultaneously, high-fidelity micromanometric aortic and LV pressures were recorded. Echocardiographic wall thickness was used to define wall stress. After valvuloplasty, no acute changes were observed in the heart rate, aortic systolic pressure, cardiac output or degree of aortic insufficiency. Valvuloplasty decreased the peak aortic valve gradient from 73 to 40 mm Hg (p less than 0.001) and the mean gradient from 61 to 30 mm Hg (p less than 0.001); aortic valve area increased from 0.55 to 0.80 cm2 (p less than 0.001). Meridional end-systolic wall stress decreased from 83 to 55 X 10(3) dynes/cm2 (p less than 0.01). LV ejection fraction increased from 0.41 to 0.48 (p less than 0.01). LV end-diastolic volume decreased from 186 to 160 ml (p less than 0.001), end-systolic volume decreased from 115 to 87 ml (p less than 0.001) and end-diastolic pressure decreased from 22 to 17 mm Hg (p less than 0.01). LV stroke work decreased from 16.0 to 14.0 X 10(6) erg (p less than 0.001). No change was observed in peak positive LV dP/dt or the end-systolic pressure-volume ratio. This study documents variable and complex changes in the measures of cardiac function after aortic valvuloplasty. A decrease in the amount of LV outflow obstruction with maintenance of the cardiac output at a decreased level of LV filling occurs.
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PMID:Changes in left ventricular systolic performance immediately after percutaneous aortic balloon valvuloplasty. 233 30

Development of an index of myocardial contractility that is both load independent and easily quantified in vivo has been a difficult task. Recently, three measures of contractile state have been advocated that appear to fulfill these requirements: the end-systolic pressure-length relationship (ESPLR), the ESPLR area, and regional preload recruitable stroke work (PRSW). Because the effects of halothane and isoflurane on these indices of contractility have yet to be studied, the purpose of this investigation was to compare the effects of these volatile anesthetics on contractile function as evaluated via these techniques in chronically instrumented dogs. Because autonomic nervous system tone substantially influences systemic hemodynamics in vivo, experiments were performed in the presence of pharmacologic blockade of the autonomic nervous system. Four groups comprised the 36 experiments that were performed with nine dogs. Following inhalational induction, the dogs were maintained on 1.5 MAC and 2 MAC of halothane or isoflurane. Pressure-length loops were generated after 1 h of equilibration using preload reduction via partial inferior vena caval occlusion or afterload augmentation by a phenylephrine infusion. The PRSW and ESPLR were then calculated, respectively. Slope and length intercept variables obtained from the ESPLR failed to significantly change from control with increasing levels of anesthetic depth despite substantial decreases in other indices of contractility. However, combination of slope and length intercept parameters into the ESPLR area model proved to be a sensitive and easily calculable measure of depressed myocardial function. Similarly, regional PRSW slope precisely reflected changes in contractile state when halothane (62 +/- 10 for control to 30 +/- 6 erg.cm-2.10(-3).mm-1 at 2 MAC) or isoflurane (83 +/- 14 for control to 55 +/- 8 erg.cm-2.10(-3).mm-1 at 2 MAC) were administered. The PRSW slope also demonstrated a significant difference in depressed contractility when equianesthetic concentrations of halothane and isoflurane were compared (63 +/- 7% of control with halothane versus 86 +/- 4% of control with isoflurane at 1.5 MAC; 50 +/- 5% of control with halothane versus 70 +/- 6% of control with isoflurane at 2 MAC). The ESPLR area also accurately demonstrated the differential depression in contractile function suggested by recent in vitro studies when equianesthetic doses of halothane and isoflurane were compared in vivo. Therefore, while ESPLR slope and length intercept variables fail as indices of myocardial contractility, ESPLR area and regional PRSW slope were shown to be useful indicators of contractile state in the conscious and anesthetized dog.
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PMID:Comparison of end-systolic pressure-length relations and preload recruitable stroke work as indices of myocardial contractility in the conscious and anesthetized, chronically instrumented dog. 201 75

Activated leukocytes release oxygen free radicals and cause microvascular occlusion. This experiment tests the hypothesis that reperfusion with leukocyte-depleted blood reduces injury after extended ischemic preservation. An in vitro model consisting of an isolated, working neonatal piglet heart and an adolescent support pig was used. Hearts were arrested with a cold crystalloid cardioplegic solution, excised, and stored in 4 degrees C saline for 12 hours. Two groups were compared. In group 1 piglets (n = 8), reperfused with whole blood, the maximum stroke work index was 0.91 +/- 0.29 x 10(3) erg/gm (mean +/- standard error of the mean). Group 2 piglets (n = 6), reperfused with blood depleted of leukocytes by a polyester filter, had a maximum stroke work index of 11.6 +/- 1.0 x 10(3) erg/gm. This difference was highly significant (p less than 0.0001). Group 1 exhibited severe injury with myofibrillar necrosis, mitochondrial disruption, nuclear chromatin clumping, and moderate interstitial edema. Group 2 had normal ultrastructure on electron microscopic examination. We conclude that reperfusion with leukocyte-depleted blood prevents reperfusion injury and results in excellent myocardial function after long-term heart preservation.
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PMID:Prevention of reperfusion injury in the neonatal heart with leukocyte-depleted blood. 270 58

In seven conscious, chronically instrumented dogs, left ventricular volume was calculated with an ellipsoidal model from the anteroposterior, septal-free wall, and base-to-apex left ventricular dimensions, measured by implanted ultrasonic transducers. Matched micromanometers measured left and right ventricular transmural and transseptal pressures. Ventricular pressures and volumes were varied by inflation of implanted vena caval and pulmonary arterial occluders. When compared with vena caval occlusion at matched left ventricular end-diastolic volumes, graded pulmonary arterial occlusions were associated with higher right ventricular systolic pressures, reduced left-to-right transseptal systolic pressure gradients, and leftward systolic septal displacement, with increased septal-free wall segment shortening (all p less than 0.05). Graded pulmonary arterial occlusions, like vena caval occlusions, reduced left ventricular end-diastolic volume, but left ventricular stroke work at a given end-diastolic volume was greater during pulmonary arterial occlusions (2,674 +/- 380 10(-3) erg) than during vena caval occlusion (1,886 +/- 450 10(-3) erg, p less than 0.05). These data indicate that, while transient pulmonary arterial occlusion reduces left ventricular preload, the concomitant increase in right ventricular systolic pressure, which is the pressure external to the interventricular septal segment of the left ventricle, augments septal shortening and assists left ventricular pump function at a given preload through direct systolic ventricular interaction.
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PMID:Effect of acutely increased right ventricular afterload on work output from the left ventricle in conscious dogs. Systolic ventricular interaction. 273 31

The optimal conditions for preservation of the neonatal heart for transplantation remain uncertain. An isolated, working neonatal piglet heart model was used to compare a standard extracellular-like cardioplegic solution followed by storage at 4 degrees C in normal saline for 12 hr (n = 8) to cardioplegia and storage at 4 degrees C for 24 hr in an intracellular-like solution (n = 7). Seven of eight hearts in the 12-hr Extracellular Group failed to regain function, with a maximum stroke work index (SWI), developed at a left ventricular end-diastolic pressure (LVEDP) of 9 mm Hg of 0.91 +/- 0.30 x 10(3) erg/g (mean +/- standard error of the mean), 7.1% of nonpreserved control hearts. In contrast, all hearts arrested and stored for 24 hr in the intracellular solution regained function with a maximum SWI, again at a LVEDP of 9 mm Hg of 9.51 +/- 1.98 X 10(3) erg/g, 73.7% of control (P less than 0.05). Ultrastructural changes seen by electron microscopy paralleled the functional results. We conclude that an intracellular arrest and storage solution may be superior to conventional solutions for extended preservation of the neonatal heart.
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PMID:Improved neonatal heart preservation with an intracellular cardioplegia and storage solution. 277 Feb 77

The deleterious effect of hyperkalemic cardioplegic solutions on coronary endothelium has been documented and has also been demonstrated with University of Wisconsin solution. We evaluated a new extracellular University of Wisconsin formulation for efficacy in heart preservation. Six neonatal piglet hearts were arrested with and stored in the standard intracellular University of Wisconsin solution (group 1: K+ 125 mEq/L, Na+ 29 mEq/L). Six piglet hearts were preserved for 24 hours with an extracellular University of Wisconsin solution that differed only in the concentrations of potassium and sodium (group 2: K+ 25 mEq/L, Na+ 129 mEq/L). Hearts underwent modified reperfusion with leukocyte-depleted aspartate-glutamate enriched blood cardioplegic solution followed by conversion to a left-sided working mode on a Langendorff circuit with perfusion from a support pig. Stroke work index was calculated at left ventricular end-diastolic pressures of 3, 6, 9, and 12 mm Hg. Sixty minutes after reperfusion, there was no significant difference in stroke work index between group 1 (16.4 +/- 1.9 x 1000 erg/gm) and group 2 (15.3 +/- 2.7 x 1000 erg/gm). There was also no significant difference in high-energy phosphate stores or myocardial water content between the two groups. Extracellular University of Wisconsin solution provides myocardial preservation equivalent to standard University of Wisconsin solution while preventing exposure of coronary endothelium to high levels of potassium, which justifies its use in clinical heart transplantation.
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PMID:Extracellular and standard University of Wisconsin solutions provide equivalent preservation of myocardial function. 756 41

Cardiopulmonary bypass results in a "euthyroid sick" state. Recently, interest has focused on the relationship between low serum triiodothyronine levels and postoperative cardiovascular hemodynamics. The present study was undertaken to more clearly define the acute effects of triiodothyronine on myocardial mechanics and energetics after hypothermic global ischemia using an ex-vivo canine heart preparation to model the clinical condition. Experiments were performed on isolated hearts subjected to hyperkalemic arrest with 90 minutes of hypothermic (10 degrees C) ischemia. Isolated hearts were cross-perfused by euthyroid support dogs in which triiodothyronine levels spontaneously decreased by 65% to 75% (p < 0.01) after the initiation of cross-perfusion. In nine heart preparations, triiodothyronine (Triostat) was given as a bolus dose (0.2 micrograms/kg) after 1 hour of baseline data collection with a subsequent measurable rise in serum triiodothyronine levels (p < 0.01). In six postischemic hearts, reverse triiodothyronine was given as a 0.2 micrograms/kg bolus. Triiodothyronine was also administered to a group of eight nonischemic, continuously perfused isolated hearts. Intrinsic myocardial contractility was assessed by analysis of the preload recruitable stroke work area, energetic efficiency from the myocardial oxygen consumption-pressure-volume area relationship, and coronary vascular resistance from analysis of coronary flow and perfusion pressure. Acute administration of triiodothyronine to postischemic hearts improved the preload recruitable stroke work area from 9.5 +/- 1.42 to 14.9 +/- 2.03 x 10(7) erg/ml, a 56% increase from baseline (p < 0.001), but had no effect on the preload recruitable stroke work area of the nonischemic hearts. The inotropic response resulting from triiodothyronine treatment did not alter the myocardial oxygen consumption-pressure-volume area relationship. Triiodothyronine treatment was associated with significantly decreased coronary resistance and increased coronary flow through a range of diastolic loading conditions in the postischemic hearts. The biologically inactive thyroid hormone metabolite reverse triiodothyronine was without effect on any of the measured parameters. On the basis of these results, we conclude that the low triiodothyronine state of cardiopulmonary bypass can be reproduced in this isolated heart model and that acute triiodothyronine treatment results in a unique inotropic action manifest only in the postischemic reperfused myocardium and is accomplished without oxygen wasting effects.
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PMID:Triiodothyronine improves left ventricular function without oxygen wasting effects after global hypothermic ischemia. 787 6

The effects of different cardioplegia temperatures on myocardial protection with continuous aerobic blood cardioplegia were studied in a canine model of acute regional injury after left anterior descending coronary artery occlusion and subsequent revascularization. Twenty-five animals underwent 90 minutes of occlusion followed by revascularization during 60 minutes of electromechanical arrest with continuous retrograde blood cardioplegia delivered at one of three temperatures: 18 degrees C (n = 8), 28 degrees C (n = 8), and 37 degrees C (n = 9). Left ventricular protection was assessed in a right heart bypass model in terms of the left ventricular pressure-volume relationships, myocardial oxygen consumption, regional myocardial blood flow, adenosine trisphosphate concentration, and water content. The preload recruitable stroke work relationship at 90 minutes after reperfusion was better in the 18 degrees C and 28 degrees C groups than that in the 37 degrees C group (18 degrees C, 85 +/- 14 erg x 10(3)/mL; 28 degrees C, 77 +/- 17 erg x 10(3)/mL; 37 degrees C, 58 +/- 13 erg x 10(3)/mL; p < 0.05). The maximum elastance and stress-strain relationships showed there were no significant differences between the groups at 90 minutes. The myocardial oxygen consumption was greatest in the 37 degrees C group during the first hour after reperfusion (18 degrees C, 5.4 +/- 1.4 mL O2.min-1.100 g-1; 28 degrees C, 4.7 +/- 1.1 mL O2.min-1.100 g-1; 37 degrees C, 6.3 +/- 1.6 mL O2.min-1.100 g-1; p < 0.05). The regional myocardial blood flow, adenosine triphosphate concentration, and myocardial water content were similar in the three groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Aerobic blood cardioplegia for revascularization of acute infarct: effects of delivery temperature. 794 16

The physiological effects of intravenous ouabain on left ventricular (LV) systolic function and metabolic-to-mechanical energy transfer were examined in eight conscious dogs. LV pressure and volume were measured using micromanometers and ultrasonic dimension transducers during transient vena caval occlusions under control conditions and after increasing doses of ouabain. Doppler coronary flow and coronary sinus O2 saturations were used to determine arterial-to-coronary sinus O2 content difference and thereby to calculate LV O2 consumption; total mechanical energy was computed as the sum of LV stroke work and the product of end-diastolic volume and LV mean ejection pressure, neglecting LV unstressed cavitary volume. The slope (10(4) erg/ml) of the stroke work vs. end-diastolic volume relationship increased progressively with rising doses of ouabain from 7.0 +/- 1.6 at control to 9.6 +/- 1.7 after ouabain 0.75 mg (P = 0.0002). Regression analysis of LV O2 consumption (mW/cm3) vs. total mechanical energy (mW/cm3) yielded a linear relationship that did not change with 0.75 mg of ouabain (P > 0.4). These data indicate that ouabain possesses a significant positive inotropic effect on the intact left ventricle without a change in energy transfer efficiency or O2 wasting.
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PMID:Effects of cardiac glycosides on myocardial function and energetics in conscious dogs. 797 36


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