Benjamin M. Jackson

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.

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.

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.

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.

Infarct size and location determine development of mitral regurgitation in the sheep model.

OBJECTIVE This study tests the hypothesis that neither small nor large myocardial infarctions that include the anterior papillary muscle produce mitral regurgitation in sheep. METHODS Coronary arterial anatomy to the anterior left ventricle and papillary muscle was determined by dye injection in 41 sheep hearts and by triphenyl tetrazolium chloride in 13. Development of acute or chronic mitral regurgitation and changes in left ventricular dimensions were studied by use of transdiaphragmatic echocardiography in 21 sheep after infarction of 24% and 33% of the anterior left ventricular mass. These data were compared with previous data from large and small posterior left ventricular infarctions. RESULTS Ligation of two diagonal arteries infarcts 24% of the left ventricular mass and 82% of the anterior papillary muscle. Ligation of both diagonals and the first circumflex branch infarcts 33% of the left ventricle and all of the anterior papillary muscle. Neither infarction causes mitral regurgitation, although left ventricular cavity dimensions increase significantly at end systole. After the smaller infarction, the left ventricular cavity enlarges 150% over 8 weeks without mitral regurgitation. CONCLUSIONS In sheep small and large infarctions of the anterior wall that include the anterior papillary muscle do not produce either acute or chronic mitral regurgitation despite left ventricular dilatation. In contrast large posterior infarctions produce immediate mitral regurgitation owing to asymmetric annular dilatation and discoordination of papillary muscle relationships to the valve. After small posterior infarctions that include the posterior papillary muscle, mitral regurgitation develops because of annular and ventricular dilatation during remodeling.

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.

Distortions of the Mitral Valve in Acute Ischemic Mitral Regurgitation

BACKGROUND In the absence of papillary muscle rupture, the precise deformations that cause acute postinfarction mitral valve regurgitation are not understood and impair reparative efforts. METHODS In 6 Dorsett hybrid sheep, sonomicrometry transducers were placed around the mitral annulus (n = 6) and at the tips and bases of both papillary muscles (n = 4). Later, specific circumflex coronary arteries were occluded to infarct approximately 32% of the posterior left ventricle and produce acute 2 to 3+ mitral regurgitation. Before and after infarction, distance measurements between sonomicrometry transducers produced three-dimensional coordinates of each transducer every 5 ms. RESULTS After infarction, the annulus dilated asymmetrically orthogonal to the line of leaflet coaptation, but the annular area increased only 9.2% +/- 6.3% (p = 0.02). At end-systole, posterior papillary muscle length increased 2.3 +/- 0.9 mm (p = 0.005); the posterior papillary muscle tip moved closer to the annular plane and centroid, and the anterior papillary muscle tip moved away. CONCLUSIONS Small deformations in mitral valvular spatial geometry after large posterior infarctions are sufficient to produce moderate to severe mitral regurgitation. The most important changes are asymmetric annular dilatation, prolapse of leaflet tissue tethered by the posterior papillary muscle, and restriction of leaflet tissue attached to the anterior papillary muscle.

Risk factors, outcomes, and clinical manifestations of spinal cord ischemia following thoracic endovascular aortic repair

OBJECTIVE The purpose of this study was to assess the incidence, risk factors, and clinical manifestations of spinal cord ischemia (SCI) after thoracic endovascular aortic repair (TEVAR). METHODS A retrospective review of a prospectively collected database was performed for all patients undergoing TEVAR at a single academic institution between July 2002 and June 2010. Preoperative demographics, procedure-related variables, and clinical details related to SCI were examined. Logistic regression analysis was performed to identify risk factors for the development of SCI. RESULTS Of the 424 patients who underwent TEVAR during the study period, 12 patients (2.8%) developed SCI. Mean age of this cohort with SCI was 69.6 years (range, 44-84 years), and 7 were women. One-half of these patients had prior open or endovascular aortic repair. Indication for surgery was either degenerative aneurysm (n = 8) or dissection (n = 4). Six TEVARs were performed electively, with the remaining done either urgently or emergently due to contained rupture (n = 2), dissection with malperfusion (n = 2), or severe back pain (n = 2). All 12 patients underwent extent C endovascular coverage. Multivariate regression analysis demonstrated chronic renal insufficiency to be independently associated with SCI (odds ratio [OR], 4.39; 95% confidence interval [CI], 1.2-16.6; P = .029). Onset of SCI occurred at a median of 10.6 hours (range, 0-229 hours) postprocedure and was delayed in 83% (n = 10) of patients. Clinical manifestations of SCI included lower extremity paraparesis in 9 patients and paraplegia in 3 patients. At SCI onset, average mean arterial pressure (MAP) and lumbar cerebrospinal fluid (CSF) pressure was 77 mm Hg and 10 mm Hg, respectively. Therapeutic interventions increased blood pressure to a significantly higher average MAP of 99 mm Hg (P = .001) and decreased lumbar CSF pressure to a mean of 7 mm Hg (P = .30) at the time of neurologic recovery. Thirty-day mortality was 8% (1 of 12 patients). The single patient who expired, never recovered any lower extremity neurologic function. All patients surviving to discharge experienced either complete (n = 9) or incomplete (n = 2) neurologic recovery. At mean follow-up of 49 months, 7 of 9 patients currently alive continued to exhibit complete, sustained neurologic recovery. CONCLUSION Spinal cord ischemia after TEVAR is an uncommon, but important complication. Preoperative renal insufficiency was identified as a risk factor for the development of SCI. Early detection and treatment of SCI with blood pressure augmentation alone or in combination with CSF drainage was effective in most patients, with the majority achieving complete, long-term neurologic recovery.

Presentation, complications, and natural history of penetrating atherosclerotic ulcer disease

OBJECTIVES Increased utilization of computed tomography angiography (CTA) has increased the radiologic diagnosis of penetrating atherosclerotic ulcers (PAUs), which are defined as the ulceration of atherosclerotic plaque through the internal elastic lamina into the aortic media. However, the presentation, treatment indications, and natural history of this disease process remain unclear. METHODS The radiology database at a single university hospital was searched retrospectively for the CTA diagnosis of PAU from January 2003 to June 2009. All scans were interpreted by a cardiovascular radiologist. Information on PAU characteristics and need for surgical repair due to PAU disease was collected. PAU stability or progression was assessed by follow-up CTA, if available. Only PAUs in the aortic arch, descending thoracic aorta, and abdominal aorta were included. RESULTS Three hundred eighty-eight PAUs were diagnosed by CTA interpretation. PAU location was in the aortic arch in 27 (6.8%) cases, the descending thoracic aorta in 243 (61.2%) cases, and the abdominal aorta in 118 (29.7%) cases. Two hundred twenty-four (57.7%) PAUs were isolated (without saccular aneurysm or intramural hematoma); 108 (27.8%) PAUs had associated saccular aneurysms; and 56 (14.4%) PAUs had associated intramural hematoma. Rupture was present in 16 (4.1%) cases. Fifty (12.9%) PAUs underwent repair with thoracic endovascular aortic repair (TEVAR) (n = 30), endovascular aneurysm repair (EVAR) (n = 10), or open surgery (n = 10); primary indications for repair were saccular aneurysm (n = 26), rupture (n = 16), and persistent or recurrent symptoms (n = 8). Even if initially treated conservatively with resolution of pain, symptomatic PAU disease was more likely to require repair than asymptomatic PAU disease (36.2% vs 7.8%, P < .001). Follow-up CTA was available for 87 PAUs, 20 (23.0%) of which demonstrated radiographic disease progression at a mean follow-up of 8.4 ± 10.3 months. Symptomatic PAU disease was more likely to progress than asymptomatic disease (42.9% vs 16.7%, P = .029). CONCLUSIONS For PAUs diagnosed on CTA at a single institution, 4.1% were ruptured and 12.9% underwent repair. Close follow-up imaging appears to be indicated for PAUs, particularly in the case of symptomatic disease, which is more likely to require repair and to undergo radiographic progression.

Limb Ischemia During Femoral Cannulation for Cardiopulmonary Support

OBJECTIVES Extracorporeal membrane oxygenation and extracorporeal cardiopulmonary support (ECMO/CPS) are potentially life-saving techniques for patients with cardiopulmonary collapse. Complications include lower extremity ischemia from femoral artery cannulation. We examined the outcomes of patients placed on ECMO/CPS, including the rate of limb ischemia. METHODS All instances of ECMO/CPS over a 3-year period (2006-2009) at a single university hospital were examined retrospectively for cannulation strategy, perfusion strategy, mortality, and limb ischemia. Potential predictors of limb ischemia with femoral artery cannulation were age, gender, body surface area (BSA), body mass index (BMI), and arterial cannula size. RESULTS Fifty-eight patients were placed on ECMO/CPS. Of these, 43 patients (74%) had femoral arterial cannulation. In 10 patients, the superficial femoral artery (SFA) was cannulated prophylactically (without antecedent limb ischemia) and perfused in the antegrade direction from a branch of the ECMO/CPS circuit. In 7 of the remaining 33 patients (21%), limb ischemia developed requiring decannulation with fasciotomy (n = 4) or additional cannulation of the SFA with branching of the ECMO/CPS circuit (n = 3). One patient with ipsilateral leg ischemia required eventual amputation. Patients with limb ischemia were significantly younger than those who did not develop limb ischemia (P = .001). BSA, BMI, and cannula size did not predict limb ischemia. Overall 30-day mortality following the initiation of ECMO/CPS was 79%. There was no correlation between limb ischemia and mortality. CONCLUSIONS Younger patients may be at increased risk for lower extremity arterial insufficiency with femoral cannulation for ECMO/CPS. Prophylactic or expectant SFA cannulation are reasonable approaches.