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Biomedical subjects

Benjamin M Jackson

Publications and source records attributed to Benjamin M Jackson.

At least 19 recordsLinked to original sources
PubMed2006

Effects of hemodynamic alterations on anterior mitral leaflet curvature during systole.

OBJECTIVES: The application of repair techniques to treat mitral valve incompetence has increased progressively during the past 20 years. Unfortunately, recent reports have demonstrated the longevity of these repairs to be less than previously believed. Most repair failures are stress related. Computational models to optimize valve repair are in development, but to be brought to fruition, a better understanding of dynamic leaflet geometry is necessary. In this study, sonomicrometry was used in an ovine model to compute systolic leaflet curvature at varying afterloads and states of contractility. METHODS: The anterior leaflet of 12 sheep was instrumented with 5 piezoelectric transducers in a cruciate array. Systolic blood pressure ranged from 90 to 200 mm Hg with increasing phenylephrine hydrochloride infusion. Epinephrine was used to vary contractile state. Leaflet curvature was calculated continuously (200 Hz) during systole. RESULTS: Anterior leaflet curvature in the septolateral direction was double that in the intercommisural direction. There were also significant changes in leaflet curvature during systole. Curvature in neither direction was affected by afterload. Epinephrine augmented intercommisural curvature in a dose-independent fashion, whereas it had no effect on curvature in the septolateral direction. CONCLUSIONS: Dynamic mitral anterior leaflet geometry was found to be amazingly constant over a wide range of hemodynamic conditions. These data provide information about leaflet geometry that will aid in the construction of realistic computational models. Such models may facilitate the design of annuloplasty rings and surgical techniques that minimize leaflet stress and increase mitral valve repair longevity.

Animals↗
PubMed2006

Role of acetaminophen in acute myocardial infarction.

Acetaminophen, the active ingredient in Tylenol, is a widely used drug that is well known for its analgesic and antipyretic properties. Acetaminophen is a commonly used alternative to nonsteroidal anti-inflammatory drugs, which have recently been demonstrated to increase mortality after acute myocardial infarction (AMI). The safety and potential cardioprotective properties of acetaminophen in the setting of AMI have recently been investigated; however, the results from these studies have been inconclusive. Using both large (ovine) and small (rabbit) collateral-deficient animal models, we studied the effects of acetaminophen in the setting of reperfused AMI. In both species we studied the effects of acetaminophen on myocardial salvage and ventricular function. Additionally, we studied the effects of acetaminophen on myocardial perfusion in sheep and on myocyte apoptosis in rabbits. Sixteen sheep and twenty-two rabbits were divided into two groups and administered acetaminophen or a vehicle before undergoing ischemia and reperfusion. The ischemic period was 60 min in sheep and 30 min in rabbits. All animals were reperfused for 3 h. There were no significant differences observed in myocardial perfusion, myocyte apoptosis, or infarct size in acetaminophen-treated animals. Acetaminophen increased cardiac output and mean arterial pressure before ischemia in sheep but had no effect on any other hemodynamic parameter. In rabbits, no effect on cardiac output or blood pressure was detected. These results support the role of acetaminophen as a safe drug in the postmyocardial infarction setting; however, no significant cardioprotective effect of the drug could be demonstrated.

Acetaminophen↗
PubMed2006

Repeat operative sentinel lymph node biopsy.

Because sentinel lymph node (SLN) biopsy continues to be used for staging in patients with breast cancer, physicians treating these patients will be faced with in-breast recurrences and new primary breast cancers in the treated breast. Repeat operative SLN biopsy might be feasible in this clinical scenario. This report describes the case of a patient with an ipsilateral different-site, recurrent, infiltrating ductal carcinoma 14 months after lumpectomy; negative SLN biopsy result; and radiation therapy, now with a positive SLN biopsy result.

Breast Neoplasms↗
PubMed2005

Early ventricular restraint after myocardial infarction: extent of the wrap determines the outcome of remodeling.

BACKGROUND: Early infarct expansion initiates adverse remodeling, leads to left ventricular dilatation and portends a poor long-term outcome. Early mechanical prevention of infarct expansion has been proposed as a method to improve remodeling, but the extent of ventricular restraint necessary to optimize the salutary effect is not known. We tested the hypothesis that left ventricular restraint (wrap) is superior to infarct stiffening (patch). METHODS: Infarction of 20% to 25% of the left ventricle was induced by coronary ligation in 69 sheep. Infarcts were either anteroapical (n = 33) or posterobasal (n = 36). Animals with each infarct received either no treatment (anteroapical, n = 26; posterobasal, n = 17), infarct stiffening with a localized Marlex mesh patch (posterobasal, n = 9) or left ventricular wrapping with Merseline mesh (anteroapical, n = 7; posterobasal, n = 10). End-systolic volume, end-diastolic volume, end-systolic muscle to cavity area ratio, left ventricular sphericity, ejection fraction, and degree of mitral regurgitation as determined by quantitative echocardiography were assessed before infarction and at 2, 5, and 8 weeks after infarction to evaluate the extent of left ventricular remodeling. RESULTS: Control animals in both groups experienced adverse remodeling. Anteroapical infarct animals developed large left ventricular aneurysms and the posterobasal infarct animals developed severe mitral regurgitation. Early infarct stiffening did not significantly improve any aspect of remodeling due to the posterobasal infarct. Early left ventricular wrapping significantly improved remodeling after both types of infarctions. CONCLUSIONS: Early left ventricular wrapping attenuates infarct expansion and has a salutary effect on remodeling. Simple infarct stiffening alone is not effective.

Animals↗
PubMed2005

Early postinfarction ventricular restraint improves borderzone wall thickening dynamics during remodeling.

BACKGROUND: Early infarct expansion impairs function of normally perfused borderzone myocardium (BZM), initiates adverse remodeling, and portends a poor long-term outcome. Early ventricular restraint has been demonstrated to improve global remodeling but its effect on BZM function has not been assessed. Using an ovine model of infarct induced remodeling and MRI, we tested the hypothesis that ventricular restraint early after MI preserves BZM function and reduces remodeling. METHODS: Six sheep had a large anterior infarction after ligation of all diagonal branches. One week after infarction 3 sheep had placement of a cardiac support device (CSD) to restrain infarct expansion. Global remodeling and borderzone wall thickening strain were assessed using tagged MRI before and 8 weeks after infarction. RESULTS: Global remodeling was greatly reduced in the CSD group compared with control. The BZM systolic wall thickening was similar in both groups at baseline (13.5% +/- 2.0%, control; 12.8% +/- 2.0%, CSD, p = 0.8). After 8 weeks of infarction-induced remodeling, systolic wall thickening strain decreased significantly to 4.9% +/- 0.7% in the control group (p = 0.03). In contrast, systolic wall thickening was preserved in the CSD group at 8 weeks (11.0% +/- 1.6%, p = 0.3). In the control group all thickening occurred during isovolemic contraction, plateauing during ejection. The CSD improved late systolic borderzone wall thickening, although dynamics remained perturbed. CONCLUSIONS: Ventricular restraint early after MI improves both contractile function of the BZM and global ventricular remodeling. The dynamics of BZM wall thickening are impaired during remodeling. The CSD significantly improves but does not completely maintain baseline BZM wall thickening dynamics.

Animals↗
PubMed2005

Borderzone geometry after acute myocardial infarction: a three-dimensional contrast enhanced echocardiographic study.

BACKGROUND: Regional myocardial geometry, function, and perfusion status are critical variables for understanding infarction-induced left ventricle (LV) remodeling. Three-dimensional contrast echocardiography (3DCE) is uniquely suited to measure these parameters. We evaluate the ability of 3DCE to assess geometric changes in the normally perfused but hypocontractile borderzone myocardium (BZM) immediately after a myocardial infarction (MI) in an ovine model, and we compare 3DCE with two-dimensional contrast echocardiography (2DCE) in the long and short axis. METHODS: Four sheep were studied with 3DCE and 4 were studied using 2DCE, before and 30 minutes after an anteroapical MI. Each 3DCE data set was acquired over 18 consecutive cardiac cycles. The LV geometry was reconstructed and perfusion data spatially correlated, thereby constituting a 3D model of ventricular geometry and perfusion. The borderzone was defined as the contrast-perfused myocardium adjacent to the infarct. RESULTS: The 2DCE short-axis analysis demonstrated decreased curvature and decreased wall thickness in the borderzone after MI. These findings are consistent with increased BZM wall stress. However, the long-axis 2DCE analysis demonstrated increased BZM wall thickness and a surprising change in BZM concavity acutely after infarction. The 3DCE analysis confirmed these findings and added additional information regarding regional variability in BZM geometry that was not evident in the two orthogonal 2D views. CONCLUSIONS: This study provides evidence that regional changes in BZM geometry are more complex than previously believed and are not necessarily indicative of increased regional stress. The superiority of 3DCE over 2DCE for assessing these changes is strongly supported.

Animals↗
PubMed2005

Surgical treatment of ischemic mitral regurgitation might not influence ventricular remodeling.

OBJECTIVES: Surgical treatment for ischemic mitral regurgitation has become more aggressive. However, no clinical study has demonstrated that surgical correction of chronic ischemic mitral regurgitation improves survival. We used 4 well-developed ovine models of postinfarction left ventricular remodeling to test the hypothesis that ischemic mitral regurgitation does not significantly contribute to postinfarction left ventricular remodeling. METHODS: Infarction of 21% to 24% of the left ventricular mass was induced by means of coronary ligation in 77 sheep. Infarctions varied only by anatomic location in the left ventricle: anteroapical, n = 26; anterobasal, n = 16; laterobasal, n = 9; and posterobasal, n = 20. Six additional sheep had ring annuloplasty before posterobasal infarction. End-systolic and end-diastolic left ventricular volume, end-systolic muscle-to-cavity area ratio, left ventricular sphericity, ejection fraction, and degree of ischemic mitral regurgitation, as determined by means of quantitative echocardiography, were assessed before infarction and at 2, 5, and 8 weeks after infarction. RESULTS: All infarcts resulted in significant postinfarction remodeling and decreased ejection fraction. Anteroapical infarcts lead to left ventricular aneurysms. Only posterobasal infarcts caused severe and progressive ischemic mitral regurgitation. Remodeling because of posterobasal infarcts was not more severe than that caused by infarcts at other locations. Furthermore, prophylactic annuloplasty prevented the development of mitral regurgitation after posterobasal infarction but had no effect on remodeling. CONCLUSION: The extent of postinfarction remodeling is determined on the basis of infarct size and location. The development of ischemic mitral regurgitation might not contribute significantly to adverse remodeling. Ischemic mitral regurgitation is likely a manifestation rather than an important impetus for postinfarction remodeling.

Animals↗
PubMed2004

Prevention of ischemic mitral regurgitation does not influence the outcome of remodeling after posterolateral myocardial infarction.

OBJECTIVES: This study was designed to test the hypothesis that ischemic mitral regurgitation (IMR) results from, but does not influence, the progression of left ventricular (LV) remodeling after posterolateral infarction. BACKGROUND: Surgical correction of chronic IMR is being increasingly recommended. METHODS: Three groups of sheep had coronary snares placed around the second and third obtuse marginal coronary arteries. Occlusion of these vessels in the control group resulted in progressive IMR over eight weeks. In a second group, Merseline mesh was fitted to cover the exposed LV before infarction. In a third group, a ring annuloplasty was placed before infarction to prevent IMR. Remodeling and degree of IMR were assessed with echocardiography at baseline and at 30 min and two, five, and eight weeks after infarction. RESULTS: Eight weeks after infarction, mean IMR grade was significantly higher in control animals than mesh and annuloplasty animals. At eight weeks, LV end-systolic volume and end-systolic muscle-to-cavity-area ratio (ESMCAR) were significantly better in mesh-treated sheep than in control sheep; also, at eight weeks, ESMCAR and akinetic segment length were significantly better in mesh-treated sheep than in annuloplasty sheep. Ejection fraction was significantly higher in the mesh than the annuloplasty group. There was no significant difference in any measure of remodeling between the annuloplasty and control groups. CONCLUSIONS: Prophylactic ventricular restraint reduces infarct expansion, attenuates adverse remodeling, and reduces IMR severity. Prevention of IMR by prophylactic ring annuloplasty does not influence remodeling. Ischemic mitral regurgitation is a consequence, not a cause, of postinfarction remodeling; infarct expansion is the more important therapeutic target.

Animals↗
PubMed2004

Influence of inotropy and chronotropy on the mitral valve sphincter mechanism.

BACKGROUND: This study was designed to isolate and quantify the effects of ventricular inotropic and chronotropic state on the normal mitral valve annular sphincter mechanism. METHODS: Sonomicrometry tansducers were placed around the mitral annulus in six sheep; atrial pacing wires were also placed. One week later, esmolol was titrated to produce a baseline hemodynamic state with a heart rate of 90 bpm; hemodynamic and sonomicrometry data were recorded. Then animals were paced at 120 bpm and 150 bpm; data were recorded at each heart rate. Isoproterenol infusion was titrated to achieve a heart rate, without pacing, of 120 and 150 bpm; again, data were recorded. Annular area was calculated at end diastole (ED) and end systole (ES) for all experiments using sonomicrometry array localization. Analysis of variance was used to assess the independent effects of heart rate and inotropic state on annular area. RESULTS: Atrial pacing at 120 bpm produced ES and ED annular areas of 777 +/- 150 mm(2) and 748.8 +/- 140.1 mm(2), respectively. At the same heart rate, isoproterenol-treatment resulted in significantly smaller ES and ED areas: 699 +/- 160 mm(2) and 641.9 +/- 156.5 mm(2), respectively. Atrial pacing at 150 bpm produced ES and ED annular areas of 745.2 +/- 131.3 mm(2) and 723.7 +/- 141.3 mm(2), respectively. At the same heart rate, isoproterenol-treatment resulted in significantly smaller ES and ED areas: 652.8 +/- 146.4 mm(2) and 569.7 +/- 155.9 mm(2), respectively. CONCLUSIONS: The inotropic state of the left ventricle directly affects the mitral valve annular orifice area, independent of heart rate. This inotropic effect on valve size is more pronounced at ED than at ES in the sheep.

Adrenergic beta-Agonists↗
PubMed2004

The dynamic anterior mitral annulus.

BACKGROUND: The anterior mitral annulus is considered a fixed structure. Recent data suggest otherwise. This study tested the hypothesis that the size of the anterior annulus varies with hemodynamic loading and ventricular contractility. METHODS: Sonomicrometry array localization measured annular area, total annular circumference, anterior circumference, and posterior circumference in 6 sheep before and after neosynephrine increased systolic blood pressure by at least 150% during atrial pacing at 120 beats/min. In 6 additional animals the same dimensions were measured during atrial pacing (at 120 and 150 beats/min) and during isoproteronol infusions to increase heart rate to 120 and 150 beats/min. RESULTS: Neosynephrine increased systolic total annular circumference from 99.7 +/- 5.5 mm to 106.9 +/- 9.6 mm. Anterior circumference increased from 40.8 +/- 4.0 mm to 45.3 +/- 5.7 mm whereas posterior circumference only increased from 59.0 +/- 5.5 mm to 61.6 +/- 7.0 mm. Low isoproteronol infusion decreased systolic total annular circumference from 107.5 +/- 8.3 mm to 101.9 +/- 10.6 mm. Most of this change occurred in the posterior circumference. Higher infusions of isoproteronol decreased total annular circumference from 106.8 +/- 8.3 mm to 98.3 +/- 9.7 mm. At this higher inotropic state the decrease in annular size was similar in the anterior and posterior annulus. CONCLUSIONS: In sheep, the anterior annulus is a dynamic structure that varies in size in response to changes in hemodynamic loading and ventricular contractility.

Adrenergic beta-Agonists↗
PubMed2004

The effect of regional ischemia on mitral valve annular saddle shape.

BACKGROUND: The mitral valve annulus has a distinctive saddle shape. Recent finite element analysis indicates this shape may contribute to normal valve function by increasing leaflet curvature and reducing leaflet stress. This study tests the hypothesis that acute ischemic mitral regurgitation (AIMR) is associated with loss of annular saddle shape. METHODS: Sonomicrometry array localization (SAL) measured the three-dimensional geometry of the mitral annulus in 6 sheep before and after 30 min of posterior ischemia that produced severe AIMR. Using this SAL data the annular height to commissural width ratio (AHCWR), a measure of annular saddle shape, was calculated throughout the cardiac cycle and reported as a percentage. RESULTS: The normal mitral annulus accentuated its saddle shape rapidly during isovolemic contraction: AHCWR increased from 11.6% +/- 1.1%-13.9% +/- 1.6% (p < 0.001). During ejection AHCWR remained relatively constant ranging from a minimum of 14.1% +/- 1.5% to a maximum of 14.9% +/- 1.3%. During ischemia AHCWR was found to be significantly smaller (p < 0.05) during isovolemic contraction, ejection, and isovolemic relaxation, but not during diastolic filling. Whereas ischemia did not affect AHCWR at end diastole (11.6% +/- 2.8%), the isovolemic accentuation of the saddle shape was lost. CONCLUSIONS: The normal mitral annulus accentuates its saddle shape during systole. This accentuation is eliminated during ischemia that causes AIMR. These data suggest an association between annular saddle shape and valve competency.

Animals↗
PubMed2004

The potential role of ventricular compressive therapy.

Early infarct expansion is associated with progressive ventricular dilatation and contractile dysfunction, and heralds a poor long-term prognosis. The pathophysiology of ventricular remodeling leading to CHF is hypothesized to begin with infarct expansion, which causes increased stress in the myocardium adjacent to the infarct. Increased stress in normally perfused border zone myocardium results in the production of cytokines and ROS, which in turn stimulate myocyte apoptosis, disruption of the ECM, and fibrosis. The value of ventricular compressive therapy in established CHF with the Acorn CSD is unclear. Early clinical and laboratory studies indicate that the device can be placed safely using standard surgical techniques, and that constrictive physiology is surprisingly rare. In the few patients who have received the device, however, the clinical benefit has not been dramatic. A final assessment awaits a well-designed clinical trial comparing isolated CSD placement with optimal medical management, the primary end points being death or the need for organ replacement. In contrast, the value of early ventricular compressive therapy (ie, the prophylactic prevention of infarct expansion) has been demonstrated experimentally: early ventricular restraint dramatically ameliorates remodeling. This strategy probably represents the best application of ventricular compressive therapy. Future work must ascertain the best timing for such an intervention.

Animals↗
PubMed2003

Emergency mitral valve replacement in the octogenarian.

Acute mitral regurgitation secondary to a ruptured papillary muscle or primary chord, in the setting of profound cardiogenic shock, is one of the more challenging cases in adult cardiac surgery. Some would consider such a clinical situation in an octogenarian futile and, in the current era of health care cost containment, a potential waste of resources. We present two such cases with successful outcomes.

Acute Disease↗
PubMed2003

Annuloplasty ring selection for chronic ischemic mitral regurgitation: lessons from the ovine model.

BACKGROUND: Chronic ischemic mitral regurgitation (CIMR) is poorly understood and repair operations are often unsatisfactory. This study elucidates the mechanism of CIMR in an ovine model. METHODS: Sonomicrometry array localization measured the three-dimensional geometry of the mitral annulus and subvalvular apparatus in five sheep before and 8 weeks after a posterior infarction of the left ventricle that produced progressive severe CIMR. RESULTS: End systolic annular area increased from 647 +/- 44 mm(2) to 1,094 +/- 173 mm(2) (p = 0.01). Annular dilatation occurred equally along the anterior (47.0 +/- 5.6 mm to 60.2 +/- 4.9 mm, p = 0.001) and posterior (53.8 +/- 3.1 mm to 68.5 +/- 8.4 mm, p = 0.005) portions of the annulus. The tip of the anterior papillary muscle moved away from both the anterior and posterior commissures by 5.2 +/- 3.2 mm (p = 0.021) and 7.3 +/- 2.2 mm (p = 0.002), respectively. The distance from the tip of the posterior papillary muscle to the anterior commissure increased by 11.0 +/- 5.7 mm (p = 0.032) while the distance from the tip of the posterior papillary muscle to the posterior commissure remained constant. CONCLUSIONS: Progressive dilatation of both the anterior and posterior mitral annuli, increased annular area, and asymmetric ventricular dilatation combine to cause CIMR by distortion of mitral valve geometry and tethering of leaflet coaptation. Therefore complete ring annuloplasty may be superior to partial annuloplasty in the treatment of CIMR.

Animals↗
PubMed2002

Border zone geometry increases wall stress after myocardial infarction: contrast echocardiographic assessment.

After myocardial infarction (MI), the border zone expands chronically, causing ventricular dilatation and congestive heart failure (CHF). In an ovine model (n = 4) of anteroapical MI that results in CHF, contrast echocardiography was used to image short-axis left ventricular (LV) cross sections and identify border zone myocardium before and after coronary artery ligation. In the border zone at end systole, the LV endocardial curvature (K) decreased from 0.86 +/- 0.33 cm(-1) at baseline to 0.35 +/- 0.19 cm(-1) at 1 h (P < 0.05), corresponding to a mean decrease of 55%. Also in the border zone, the wall thickness (h) decreased from 1.14 +/- 0.26 cm at baseline to 1.01 +/- 0.25 cm at 1 h (P < 0.05), corresponding to a mean decrease of 11%. By Laplace's law, wall stress is inversely proportional to the product K. h. Therefore, a 55% decrease in K results in a 122% increase in circumferential stress; a 11% decrease in h results in a 12% increase in circumferential stress. These findings indicate that after MI, geometric changes cause increased dynamic wall stress, which likely contributes to border zone expansion and remodeling.

Animals↗
PubMed2002

Extension of borderzone myocardium in postinfarction dilated cardiomyopathy.

This study tests the hypothesis that hypocontractile, borderzone myocardium adjacent to an expanding infarct becomes progressively larger and more hypocontractile as remodeling continues. Early infarct expansion following anteroapical myocardial infarction (MI) is associated with progressive ventricular dilation and heart failure. The contribution of perfused, hypocontractile, borderzone myocardium to this process is unknown. Using a sheep model of anteroapical infarction, sonomicrometry array localization and serial microsphere injections were used to track changes in regional myocardial contractility, geometry, and perfusion. Eight sheep were studied before and after infarction and two, five, and eight weeks later. Thirty intertransducer chord lengths were analyzed to measure regional contractility and serial changes in regional geometry at end systole. Beginning as a narrow band of fully perfused hypocontractile myocardium adjacent to the infarction, borderzone myocardium extends to involve additional contiguous myocardium that progressively loses contractile function as the heart remodels. Three distinct myocardial zones develop as a result of transmural MI: infarct, borderzone (perfused but hypocontractile), and remote (perfused and normally functioning).This study demonstrates that hypocontractile, fully perfused borderzone myocardium extends to involve contiguous normal myocardium during postinfarction remodeling. This borderzone myocardium is a unique type of perfused, hypocontractile myocardium, which is distinct from hibernating or stunned myocardium. Preventing extension of borderzone myocardium by medical or surgical means offers the prospect of preventing late-onset heart failure following transmural expanding MIs.

Animals↗
PubMed2002

Effect of annular shape on leaflet curvature in reducing mitral leaflet stress.

BACKGROUND: Leaflet curvature is known to reduce mechanical stress. There are 2 major components that contribute to this curvature. Leaflet billowing introduces the most obvious form of leaflet curvature. The saddle shape of the mitral annulus imparts a more subtle form of leaflet curvature. This study explores the relative contributions of leaflet billowing and annular shape on leaflet curvature and stress distribution. METHODS AND RESULTS: Both numerical simulation and experimental data were used. The simulation consisted of an array of numerically generated mitral annular phantoms encompassing flat to markedly saddle-shaped annular heights. Highest peak leaflet stresses occurred for the flat annulus. As saddle height increased, peak stresses decreased. The minimum peak leaflet stress occurred at an annular height to commissural width ratio of 15% to 25%. The second phase involved data acquisition for the annulus from 3 humans by 3D echocardiography, 3 sheep by sonomicrometry array localization, 2 sheep by 3D echocardiography, and 2 baboons by 3D echocardiography. All 3 species imaged had annuli of a similar shape, with an annular height to commissural width ratio of 10% to 15%. CONCLUSION: The saddle shape of the mitral annulus confers a mechanical advantage to the leaflets by adding curvature. This may be valuable when leaflet curvature becomes reduced due to diminished leaflet billowing caused by annular dilatation. The fact that the saddle shape is conserved across mammalian species provides indirect evidence of the advantages it confers. This analysis of mitral annular contour may prove applicable in developing the next generation of mitral annular prostheses.

Animals↗