Residual stress produced by ventricular volume reduction surgery has little effect on ventricular function and mechanics: a finite element model study.

OBJECTIVES: Residual stress is the stress (force per unit area) that remains when all external loads (eg, left ventricular chamber and pericardial pressures) are removed. It has been suggested that ventricular volume reduction surgery can reconstitute the residual stress-strain state of the left ventricle. To determine the extent to which residual stress is involved, we used a mathematical (finite element) model to simulate the effect of volume reduction operations on left ventricular stroke volume/end-diastolic pressure (Starling) relationships, as well as on regional distributions of stress in the local muscle fiber direction (fiber stress). METHODS: The nonlinear stress-strain relationship for the diastolic myocardium was anisotropic with respect to the local muscle fiber direction. An elastance model for active fiber stress was incorporated in an axisymmetric geometric model of the dilated, poorly contractile left ventricular wall. RESULTS: When residual stress is implemented in the model simulation of volume reduction operations, the additional decrease in stroke volume at fixed left ventricular end-diastolic pressure is small (10% volume reduction: 2.0% at 1 mm Hg and 2.0% at 20 mm Hg; 20% volume reduction: 2.2% at 1 mm Hg and 3.1% at 20 mm Hg). Furthermore, there is little change in the mean fiber stress throughout the left ventricular wall (10% volume reduction: +1.0% at end-diastole and -0.3% at end-systole; 20% volume reduction: +2.1% at end-diastole and -1.0% at end-systole). CONCLUSIONS: These results suggest that residual stress produced by volume reduction operations has little effect on left ventricular function and the mean fiber stresses at end-diastole and end-systole.

Mechanism underlying mechanical dysfunction in the border zone of left ventricular aneurysm: a finite element model study.

BACKGROUND: The global left ventricular dysfunction characteristic of left ventricular aneurysm is associated with muscle fiber stretching in the adjacent noninfarcted (border zone) region during isovolumic systole. The mechanism of this regional dysfunction is poorly understood. METHODS: An anteroapical transmural myocardial infarct was created by coronary arterial ligation in an adult Dorset sheep and was allowed to mature into left ventricular aneurysm for 10 weeks. The animal was imaged subsequently using magnetic resonance imaging with simultaneous recording of intraventricular pressures. A realistic mathematical model of the three-dimensional ovine left ventricle with an anteroapical aneurysm was constructed from multiple short-axis and long-axis magnetic resonance imaging slices at the beginning of diastolic filling. RESULTS: Three model simulations are presented: (1) normal border zone contractility and normal aneurysmal material properties; (2) greatly reduced border zone contractility (by 50%) and normal aneurysmal material properties; and (3) greatly reduced border zone contractility (by 50%) and stiffened aneurysmal material properties (by 1000%). Only the latter two simulations were able to reproduce experimentally observed stretching of border zone fibers during isovolumic systole. CONCLUSIONS: The mechanism underlying mechanical dysfunction in the border zone region of left ventricular aneurysm is primarily the result of myocardial contractile dysfunction rather than increased wall stress in this region.

Effect of induction and reperfusion with warm substrate-enriched cardioplegia on ventricular function.

BACKGROUND: This study tested the hypothesis that induction and reperfusion with warm substrate-enriched (IRWSE) blood cardioplegia improves postoperative left ventricular (LV) function in patients undergoing elective coronary bypass surgery (CABG). METHODS: After giving informed consent, 67 patients scheduled for CABG surgery were randomized to either IRWSE + cold blood (CB) or CB alone. IRWSE cardioplegia consisted of 37 degrees C substrate-enriched (glutamate, aspartate, hyperkalemic) anterograde and retrograde blood cardioplegic solution followed by non-substrate-enriched cardioplegic solution given at 4 degrees C to 8 degrees C. LV function was measured with ventriculograms, volume conductance catheters, echocardiography, and multiple gated (image) acquisition. RESULTS: The end-systolic pressure-volume relationship was improved postbypass in the IRWSE + CB group (CB, 1.5 +/- 0.74 mm Hg/mL vs IRWSE + CB, 2.1 +/- 1.2 mm Hg/mL; p = 0.042). The postoperative ejection fraction (EF%) was better preserved in the CB group (CB, 65 +/- 11.53% vs IRWSE + CB, 58.62 +/- 11.75%; p < 0.04). CONCLUSIONS: Our results demonstrate a transient improvement in LV systolic function in the immediate postbypass period in CABG patients in the IRWSE + CB group. The intraoperative benefits of the IRWSE + CB technique did not persist in the postoperative period.

Collection of process data after cardiac surgery: initial implementation with a Java-based intranet applet.

BACKGROUND: Using a Java-based intranet program (applet), we collected postoperative process data after coronary artery bypass grafting. METHODS: A Java-based applet was developed and deployed on a hospital intranet. Briefly, the nurse entered patient process data using a point and click interface. The applet generated a nursing note, and process data were saved in a Microsoft Access database. In 10 patients, this method was validated by comparison with a retrospective chart review. In 45 consecutive patients, weekly control charts were generated from the data. When aberrations from the pathway occurred, feedback was initiated to restore the goals of the critical pathway. RESULTS: The intranet process data collection method was verified by a manual chart review with 98% sensitivity. The control charts for time to extubation, intensive care unit stay, and hospital stay showed a deviation from critical pathway goals after the first 20 patients. Feedback modulation was associated with a return to critical pathway goals. CONCLUSIONS: Java-based applets are inexpensive and can collect accurate postoperative process data, identify critical pathway deviations, and allow timely feedback of process data.

Radio frequency heating of chronic ovine infarct leads to sustained infarct area and ventricular volume reduction.

OBJECTIVE: Myocardial infarct expansion and subsequent left ventricular remodeling are associated with increased incidence of congestive failure and mortality. Collagen is known to denature and contract when heated above 65 degrees C. We therefore tested the hypothesis that radio frequency heating of myocardial infarct tissue with application of a restraining patch causes a sustained reduction in myocardial infarct area and left ventricular volume. METHODS: Thirteen male Dorset sheep underwent surgical coronary artery ligation. At least 14 weeks later, animals were randomized to either radio frequency infarct heating (95 degrees C) with application of a restraining patch or a sham operation. Before treatment, after treatment, and 10 weeks later, left ventricular volume was measured with transdiaphragmatic echocardiography and myocardial infarct area was measured with an array of sonomicrometry crystals. RESULTS: Radio frequency infarct heating causes an acute decrease of 34% (-215 +/- 82 mm(2); P =.0002) in infarct area at end-diastole that is maintained at 10 weeks (-144 +/- 79 mm(2); P =.0002). Radio frequency infarct heating causes a downward trend in end-diastolic left ventricular volume measured by echocardiography of 20% (-15.7 +/- 6.3 mL; P = no significant difference) and end-systolic left ventricular volume of 32% (-17.1 +/- 9.8 mL; P =.09), which are significantly decreased at 10 weeks (-13.6 +/- 22.3 mL; P =.007 and -15.3 +/- 21.9 mL; P =.008, respectively). Radio frequency infarct heating causes an acute improvement in systolic function (P <.001), a sustained increase in left ventricular ejection fraction (+0.11%; P =.06), and preserved stroke volume. CONCLUSION: Radio frequency heating of chronic left ventricular myocardial infarct causes a sustained reduction in infarct area and left ventricular volume. This technique may beneficially reverse infarct expansion and left ventricular remodeling after myocardial infarction.

The effect of diastolic stiffness on ventricular function after partial ventriculectomy: a finite element simulation.

Partial ventriculectomy (PV) has been proposed by Batista and colleagues to improve cardiac function in patients with dilated cardiomyopathy (DCM); however, results have been mixed. We tested the hypothesis that preoperative diastolic function affects the stroke volume/end-diastolic pressure (Starling) relationship after PV. A previously described finite element simulation of DCM and PV was used. Diastole and end systole were represented by separate elastic finite element models with different unloaded shapes and nonlinear material properties. Left ventricular (LV) end-systolic elastance (E(ES)), diastolic compliance (DC), and Starling relationships were calculated. DC was varied by changing Ogden material property alpha(i) from 12 (compliant) to 20 (stiff). PV was simulated at 20% LV mass reduction. The slope of the Starling relationship increased from 1.82 to 1.21 as alpha(i) increased from 12 to 20. Partial ventriculectomy increased the Starling relationship in each case from 1.34 to 1.01 respectively. However, the net result in each case is a decrement in the Starling relationship with resection, and the smallest decrement was associated with the highest diastolic stiffness (alpha(i) = 20). Partial ventriculectomy depressed the Starling relationship for all values of diastolic compliance. It is expected that patients with a higher diastolic stiffness should do better.

Ventricular volume, chamber stiffness, and function after anteroapical aneurysm plication in the sheep.

OBJECTIVE: The success of left ventricular aneurysm plication depends on how the procedure affects both end-systolic elastance and diastolic compliance and how those changes affect ventricular function (stroke work/end-diastolic volume [PRSW] and stroke volume/end-diastolic pressure [Starling] relationships). METHODS: Five male Dorsett sheep were surgically instrumented with coronary artery snares, an inferior vena caval occluder, and an ascending aortic ultrasonic flow probe. One week later an anteroapical myocardial infarction was produced by tightening the coronary snares. Ten weeks after myocardial infarction, the left ventricular aneurysm was plicated. Absolute left ventricular volume was measured by long-axis transdiaphragmatic echocardiography, and relative changes in left ventricular volume were measured with a conductance catheter. End-systolic elastance, diastolic compliance, PRSW, and Starling relationships were measured immediately before myocardial infarction, 10 weeks after myocardial infarction (immediately before plication), and immediately after and 6 weeks after aneurysm plication. RESULTS: After plication, end-diastolic and end-systolic left ventricular volumes return to preinfarction values. The slopes of end-systolic elastance, diastolic compliance, and PRSW decrease 10 weeks after myocardial infarction, increase with aneurysm plication, and then decrease 6 weeks after aneurysm plication. The Starling relationship undergoes a downward parallel shift with aneurysm plication. CONCLUSION: Aneurysm plication abruptly decreases left ventricular volume and diastolic compliance, increases end-systolic elastance and PRSW, but decreases the Starling relationship. The net effect on left ventricular function is mixed. Furthermore, left ventricular remodeling 6 weeks after aneurysm plication causes left ventricular volume, end-systolic elastance, diastolic compliance, PRSW, and the Starling relationship to return to preplication values.

L-arginine infusion dilates coronary vasculature in patients undergoing coronary bypass surgery.

BACKGROUND: Nitric oxide-dependent factors (serotonin, activated platelets, acetylcholine) cause vasodilation in normal coronary arteries but vasoconstrict atherosclerotic vessels. This experiment tested the hypothesis that intravenous systemic infusions of L-arginine, a precursor for nitric oxide production, dilate the coronary vascular bed of patients undergoing coronary artery bypass graft surgery. METHODS: Twenty patients scheduled for coronary artery bypass graft surgery surgery were studied in a prospective, blinded, randomized clinical trial. Saphenous vein graft blood flow was measured with a transit time flow probe, and coronary vascular resistance was calculated. After weaning from bypass, patients were given a venous infusion (placebo or 10% arginine hydrochloride [30 g]) over 15 min. Arterial blood samples for the determination of L-arginine and L-citrulline levels were drawn before, 10 min after starting infusion, and 10 min after end of infusion. RESULTS: The placebo group experienced an increase in mean arterial pressure and coronary vascular resistance and a decrease in graft blood flow. Patients in the L-arginine group maintained their baseline values. Mean arterial pressure (L-arginine, 88+/-17 to 92+/-13 mmHg vs. placebo, 80+/-12 to 92+/-9 mmHg, P = 0.021), coronary vascular resistance (L-arginine, 97,000+/-60,000 to 99,600+/-51,000 dynes x s x cm(-5) vs. placebo, 81,000+/-69,000 to 117,000+/-64,000 dynes x s x cm(-5), P = 0.05), and graft blood flow (L-arginine, 55+/-25 to 50+/-19 ml/min vs. placebo, 60+/-34 to 46+/-18, P = 0.05) remained more stable in the L-arginine-treated patients. CONCLUSIONS: Systemic L-arginine infusion reduced postbypass coronary vasoconstriction. There were no adverse events associated with the drug infusion.

The effect of ventricular volume reduction surgery in the dilated, poorly contractile left ventricle: a simple finite element analysis.

OBJECTIVES: Ventricular volume reduction surgery has been proposed by Batista to improve cardiac function in patients with dilated cardiomyopathy. However, limited clinical data exist to determine the efficacy of this operation. A finite element simulation is therefore used to determine the effect of volume reduction surgery on left ventricular end-systolic elastance, diastolic compliance, stroke work/end-diastolic volume (preload recruitable stroke work), and stroke work/end-diastolic pressure (Starling) relationships. METHODS: End-diastole and end-systole were represented by elastic finite element models with different unloaded shapes and nonlinear material properties. End-systolic elastance, diastolic compliance, preload recruitable stroke work, and Starling relationships, as well as energy expenditure per gram of unresected myocardium, were calculated. Two different types of volume reduction surgery (apical and lateral) were simulated at 10% and 20% left ventricular mass reduction. RESULTS: Ventricular volume reduction surgery causes diastolic compliance to shift further to the left on the pressure-volume diagram than end-systolic elastance. Volume reduction surgery increases the slope of the preload recruitable stroke work relationship (dilated cardiomyopathy 0.006 J/mL; 20% lateral volume reduction surgery 0.009 J/mL) but decreases the slope of the Starling relationship (dilated cardiomyopathy 0.028 J/mm Hg; 20% lateral volume reduction 0.023 J/mm Hg). For a given amount of resection, lateral volume reduction has a greater effect than apical volume reduction. Ten-percent and 20% lateral volume reduction reduces energy expenditure by 7% and 17%, respectively. CONCLUSION: Ventricular volume reduction surgery shifts end-systolic elastance and diastolic compliance to the left on the pressure-volume diagram. The net effect on ventricular function is mixed. Volume reduction surgery increases the slope of preload recruitable stroke work, but increased diastolic compliance causes a small decrease in the Starling relationship (3 mm Hg difference between dilated cardiomyopathy and volume reduction surgery at stroke work = 0.5 J).

Dynamic three-dimensional imaging of the mitral valve and left ventricle by rapid sonomicrometry array localization.

OBJECTIVES: The first objective was to develop a quantitative method for tracking the three-dimensional geometry of the mitral valve. The second was to determine the complex interrelationships of various components of the mitral valve in vivo. METHODS AND RESULTS: Sixteen sonomicrometry transducers were placed around the mitral vale anulus, at the tips and bases of both papillary muscles, at the ventricular apex, across the ventricular epicardial short axis, and on the anterior chest wall before and during cardiopulmonary bypass in eight anesthetized sheep. Animals were studied later on 17 occasions. Reproducibility of derived chord lengths and three-dimensional coordinates from sonomicrometry array localization, longevity of transducer signals, and the dynamics of the mitral valve and left ventricle were studied. Reproducibility of distance measurements averages 1.6%; Procrustes analysis of three-dimensional arrays of coordinate locations predicts an average error of 2.2 mm. Duration of serial sonomicrometry array localization signals ranges between 60 and 151 days (mean 114 days). Sonomicrometry array localization demonstrates the saddle-shaped mitral anulus, its minimal orifice area immediately before end-diastole, and uneven, apical descent during systole. Papillary muscles shorten only 3.0 to 3.5 mm. Sonomicrometry array localization demonstrates nonuniform torsion of papillary muscle transducers around a longitudinal axis and shows rotation of papillary muscular bases toward each other during systole. CONCLUSION: Tagging of ventricular structures in experimental animals by sonomicrometry array localization images is highly reproducible and suitable for serial observations. In sheep the method provides unique, quantitative information regarding the interrelationship of mitral valvular and left ventricular structures throughout the cardiac cycle.

Use of sonomicrometry and multidimensional scaling to determine the three-dimensional coordinates of multiple cardiac locations: feasibility and initial implementation.

We describe a new method which uses sonomicrometry and the statistical technique of multidimensional scaling (MDS) to measure the three-dimensional (3-D) coordinates of multiple cardiac locations. We refer to this new method as sonomicrometry array localization (SAL). The new method differs from standard sonomicrometry in that each piezoelectric transducer element is used as both transmitter and receiver and the set of intertransducer element distances is measured. MDS calculates the 3-D coordinates of each sonomicrometry transducer element from the set of intertransducer element distances. The feasibility of this new method was tested with mathematical simulations which demonstrated the ability of MDS to compensate for signal error and missing intertransducer element distances. We describe the design elements of a modified digitally controlled sonomicrometer in which a single transducer element can sequentially broadcast to as many as eight receiver elements. That design is used to validate SAL in a water bath and in ex vivo and living hearts. Correlation with caliper measurement in the water bath (y int. = 3.91 +/- 3.36 mm, slope = 1.04 +/- 0.05, r2 = 0.969 +/- 0.027) and with radiography in ex vivo (y int. = -0.87 +/- 0.92 mm, slope = 0.97 +/- 0.02, r2 = 0.960 +/- 0.023) and in vivo hearts (y int. = 2.98 +/- 2.59 mm, slope = 1.01 +/- 0.06, r2 = 0.953 +/- 0.031) was excellent. Sonomicrometry array localization is able to accurately measure the 3-D coordinates of multiple cardiac locations. It can potentially measure myocardial deformation and remodeling after ischemic or valvular injury.

Pathogenesis of acute ischemic mitral regurgitation in three dimensions.

Changes in the geometric and intravalvular relationships between subunits of the ovine mitral valve were measured before and after acute posterior wall myocardial infarction in three dimensions by means of sonomicrometry array localization. In 13 sheep, nine sonomicrometer transducers were attached around the mitral anulus and to the tip and base of each papillary muscle. Five additional transducers were placed on the epicardium. Snares were placed around three branches of the circumflex coronary artery. One to 2 weeks later, echocardiograms, dimension measurements, and left ventricular pressures were obtained before and after the coronary arteries were occluded. Data were obtained from seven sheep. Coronary occlusion infarcted 32% of the posterior left ventricle and produced 2 to 3+ mitral regurgitation by Doppler color flow mapping. Multidimensional scaling of dimension measurements obtained from sonomicrometry transducers produced three-dimensional spatial coordinates of each transducer location throughout the cardiac cycle before and after infarction and onset of mitral regurgitation. After posterior infarction, the mitral anulus enlarges asymmetrically along the posterior anulus, and the tip of the posterior papillary muscle moves 1.5 +/- 0.3 mm closer to the posterior commissure at end-systole. The posterior papillary muscle also elongates 1.9 +/- 0.3 mm at end-systole. The left ventricle enlarges asymmetrically and ventricular torsion along the long axis changes. The development of postinfarction mitral regurgitation appears to be the consequence of multiple small changes in ventricular shape and contractile deformation and in the spatial relationship of mitral valvular subunits.

Changes in passive mechanical stiffness of myocardial tissue with aneurysm formation.

BACKGROUND: Myocardium undergoes complex cellular and histochemical alterations after acute myocardial infarction. These structural changes directly affect the mechanical stiffness of infarcted and remote myocardia. Previous investigations of infarct stiffness have been limited to uniaxial testing, which does not provide a unique description of the tissue's three-dimensional material properties. This study describes the first serial measurements of biaxial mechanical properties of sheep myocardium after anteroapical infarction. METHODS AND RESULTS: Anteroapical infarctions of 23.7 +/- 2.5% of the left ventricular mass were produced by coronary arterial ligation in sheep. Biaxial force-extension measurements were made on freshly excised squares (6.45 cm2) of remote, noninfarcted, and infarcted myocardia before and 4 hours, 1 week, 2 weeks, and 6 weeks after ligation. Adjacent myocardial samples were assayed for hydroxyproline content. Force-extension data and a derived constitutive equation were used to describe stresses and strains and material properties of each sample. In sheep, anteroapical infarctions evolve into thin left ventricular aneurysms that consist of predominantly fibrous tissue with disrupted groups of muscle cells encased in scar. In the infarct, Cauchy stresses at 15% extensions (control stresses: circumferential, sigma C, 19.4 +/- 3.3 g/cm2; longitudinal, sigma L, 54.8 +/- 34.8 g/cm2) increase within 4 hours, peak at 1 to 2 weeks (sigma C, 338.5 +/- 143.6 g/cm2; sigma L, 310.7 +/- 45.9 g/cm2), and then decrease 6 weeks after infarction (sigma C, 115 +/- 47.2 g/cm2; sigma L, 53.2 +/-28.9 g/cm2). Stresses in the remote myocardium follow a similar time course but to a lesser extent than the infarcted region. Hydroxyproline content, a measure of collagen content, does not correlate with infarct stiffness but progressively increases to 69.7 +/- 7.6 micrograms/mg after 6 weeks. Stress-extension curves demonstrate directional anisotropy of both infarcted and remote myocardia. CONCLUSIONS: The findings indicate that infarcted myocardium becomes more stiff during the first 1 to 2 weeks after anteroapical infarction and then more compliant. The infarct also exhibits directional anisotropy. These observations underscore the importance of ventricular material properties during the remodeling process after acute myocardial infarction and may partially explain the progressive left ventricular dilatation and functional deterioration that occur in some patients after anteroapical infarction.

Left ventricular assist without thoracotomy: clinical experience with the Dennis method.

A method to provide left ventricular circulatory assistance without thoracotomy was developed and implemented in 2 patients. The left atrium is cannulated from the neck by passing a catheter across the interatrial septum (Dennis technique) using fluoroscopic and echocardiographic imaging. To facilitate ambulation, the arterial catheter is connected to the right axillary artery. Left atrial to axillary arterial flow is produced by a centrifugal pump. Two patients were perfused at 2.7 to 3.5 L/min for 5 and 6.5 days. One patient had successful coronary angioplasty during perfusion and remains alive 1 year later. The other patient died of sepsis and anuria that preceded implementation of circulatory assistance. The Dennis method of continuous left ventricular circulatory assistance avoids thoracotomy, requires a minimal operation, is portable and inexpensive, uses widely available equipment, and is particularly suitable for patients in cardiogenic shock after acute myocardial infarction. The method is safe and cost-effective, and merits wider application in selected patients.

Large animal model of ischemic mitral regurgitation.

A large animal model of ischemic mitral regurgitation (MR) that resembles the multiple presentations of the human disease was developed in sheep. In 76 sheep hearts, the anatomy of the coronary arterial circulation was determined by observation and polymer casts. Two variations, types A and B, which differed by the vessel that supplied the left ventricular apex, were found. In all hearts, the circumflex coronary artery has three marginal branches and terminates in the posterior descending coronary artery. The amount and location of left ventricular (LV) mass supplied by each marginal circumflex branch was determined by dye injection and planimetry. In type A hearts, ligation of the first and second marginal branches infarcts 23% +/- 3.0% of the LV mass, does not infarct either papillary muscle, significantly (p < 0.001) increases LV cavity size 48% at the high papillary muscle level by 8 weeks, and does not cause MR. Ligation of the second and third marginal branches infarcts 21.4% +/- 4.0% of the LV mass, includes the posterior papillary muscle, significantly increases (p < 0.001) LV cavity size 75%, and causes severe MR by 8 weeks. Ligation of the second and third marginal branches and the posterior descending coronary artery infarcts 35% to 40% of the LV mass, increases LV cavity size 39% within 1 hour, and causes massive MR. After moderate (21% to 23%) LV infarction, development of ischemic MR requires both LV dilatation and posterior papillary muscle infarction; neither condition alone produces MR. Large posterior wall infarctions (35% to 40%) that include the posterior papillary muscle produce immediate, severe MR.(ABSTRACT TRUNCATED AT 250 WORDS)

Repair of left ventricular aneurysm. Changes in ventricular mechanics, hemodynamics, and oxygen consumption.

Anteroapical left ventricular aneurysms were produced in 23 sheep by coronary arterial ligation. Plication of the aneurysm does not change stroke volume or cardiac output and does not significantly change left ventricular oxygen consumption from the preoperative value of 5.1 +/- 2.6 ml/100 gm per minute. Plication, however, does increase left ventricular end-systolic elastance from 3.2 +/- 0.9 to 4.4 +/- 1.5 mm Hg/mm (p = 0.005). In nine of these sheep the midsagittal plane of the left ventricle was imaged by means of an array of sonomicrometry crystals before and after plication of the aneurysm. Regional wall stresses at end-systole and end-diastole and changes in diastolic function were calculated for anterior and posterior ventricular walls in the border zone adjacent to the aneurysm and in more basilar myocardium remote from the infarct. Plication significantly reduced end-systolic wall stresses and systolic stress integrals in the posterior border zone and remote myocardium, but it did not significantly change anterior wall systolic stresses or stress integrals. Plication also decreased diastolic stretching of border zone myocardium. Plication of anteroapical left ventricular aneurysm produced a shorter, more spherical ventricle and removed the dyskinetic segments but altered deformation (strain) in both circumferential and longitudinal directions. The changes in ventricular wall geometry and deformation provide an explanation for the increased ventricular end-systolic elastance and unchanged stroke volume observed after aneurysm plication.

Left ventricular mechanics of ejecting, postischemic hearts during left ventricular circulatory assistance.

We measured the effects of left ventricular circulatory assistance on ventricular mechanics of ejecting sheep hearts before and after global ischemia. Flows from left atrium to femoral artery ranged between 20 and 100 ml/kg/min during circulatory assistance. In preischemic, ejecting hearts increasing flow through the left ventricular assist device progressively decreased stroke volume, end-diastolic volume, and circumferential systolic wall stress, but only slightly decreased end-systolic volume. In postischemic, ejecting hearts left ventricular assistance progressively and substantially decreased both end-diastolic volume and end-systolic volume; at high flows, end-systolic volume returned to the normal range of preischemic hearts. High flows through the assist device also shifted end-systolic points of pressure-volume loops leftward and increased the stroke work/end-diastolic volume ratio in ejecting postischemic hearts; these observations raise the possibility that left ventricular circulatory assistance acutely improves myocardial contractility of postischemic hearts.

Myocardial oxygen utilization after reversible global ischemia.

We tested in 20 sheep the hypothesis that oxygen consumption increases after reversible, global myocardial ischemia. Left ventricular oxygen consumption before and after 25 minutes of warm (37 degrees C) global ischemia was linearly related to a function (integral) of left ventricular circumferential systolic wall stress, altered by changing afterload. The relation is expressed in the two regression equations: LVO2 (preischemic) = 1.06.SSI + 16.8 (n = 129; r = 0.79); LVO2 (postischemic) = 4.35.SSI + 5.6 (n = 89; r = 0.65). The fourfold increase in slope (4.35 versus 1.06) indicates (p = 0.0001) a massive increase of oxygen consumption in postischemic, globally "stunned" myocardium. The inferences are that globally stunned myocardium causes severe impairment of oxygen utilization efficiency, and increased vulnerability to further ischemia if coronary vessels are diseased.

Large animal model of left ventricular aneurysm.

In 28 Dorsett sheep, ligation of the distal homonymous (equivalent to human left anterior descending) and second diagonal coronary arteries produced a constant transmural infarct of 22.9% +/- 2.5% (mean +/- standard deviation) of the left ventricular mass. Serial left ventriculograms showed that within four hours the infarct segment expands, wall thickness decreases, and aneurysmal dilatation occurs and progresses over the next 60 days in all sheep. Epicardial ventricular point references indicated that adjacent noninfarcted myocardium participates in the formation of the aneurysm. Anatomy of the coronary vasculature was studied in 22 excised sheep hearts. In sheep, coronary arterial anatomy is remarkably constant. The left coronary artery provides all of the blood supply to the left ventricle and septum and only a small rim of both the anterior and posterior right ventricles. Cardiac veins from the left ventricle drain into the coronary sinus, which also receives the left azygos vein. Right ventricular veins drain separately. The essentially separate coronary circulations to the two ventricles, the paucity of coronary collateral circulation, and the consistent evolution of left ventricular infarcts into aneurysms are important advantages of the ovine model for both metabolic and ventricular mechanical studies of acute myocardial infarction and left ventricular aneurysm.

Measurement of end-systolic pressure-volume relations by intra-aortic balloon occlusion.

A new situ technique has been developed for measuring peak end-systolic elastance, Emax, that does not alter intrinsic or reflex-stimulated cardiac contractility. Afterload is varied by the inflation of an intra-aortic balloon catheter positioned in the ascending aorta. Balloon inflation is timed to interrupt ventricular ejection transiently at different times during the ejection phase, therefore, producing contraction at different ventricular volumes. Simultaneous measurement of left ventricular pressure and aortic flow during the occlusion sequence allows pressure versus ejected volume loops to be generated, from which the end-systolic pressure-volume relation is determined. End-systolic pressure-volume relation (ESPVR) was measured in six anesthetized Dorsett sheep with normal and enhanced contractile states. ESPVR was analyzed using both linear and nonlinear techniques. Although nonlinear components were seen in ESPVR, for the pressure-volume data range produced by the transient occlusions, linear approximations of ESPVR fit the end-systolic data points well. In the normal state, Emax, the slope of the linear ESPVR, was 1.01-5.08 mm Hg/ml in animals with body weights of 23-32 kg. After epinephrine infusion, Emax increased from 3.07 +/- 1.49 to 5.79 +/- 1.97 mm Hg/ml, which is consistent with previous investigations. Linear and nonlinear volume intercepts had a small increase with positive inotropic stimulation. Furthermore, serial measurements of Emax tracked cardiac function in depressed hearts with rapidly changing contractility.