Duplex ultrasound imaging to detect limb stenosis or kinking of endovascular device.

OBJECTIVE: We attempted to correlate duplex ultrasound (DU) findings with the clinical outcome of graft limb stenosis or kinking after endovascular aneurysm repair (EVAR). METHODS: Between 1998 and 2010, 248 patients underwent EVAR and postoperative DU surveillance of 496 graft limbs in our accredited noninvasive vascular laboratory by one of three experienced technologists. Routine DU surveillance was performed 1 week, 6 months, and annually after EVAR. Peak systolic velocities (PSVs) were measured in the body and midportion and distal attachment site of both limbs of the graft, and adjacent PSV ratios were calculated. RESULTS: None of 479 graft limbs with a PSV of <300 cm/s occluded during long-term follow-up (mean, 22.3 months; range, 1-123 months). Of 17 graft limbs with a PSV >300 cm/s, seven occluded (0 of 479 vs 7 of 17, P < .01; sensitivity, 100%; specificity, 98%), five underwent prophylactic intervention (mean adjacent PSV ratio, 7.3), and five (30%) remained patent without intervention (mean PSV ratio, 3.2). CONCLUSIONS: This large series of DU surveillance for failing EVARs grafts suggests that graft limbs with PSVs <300 cm/s can be safely monitored. However, limbs with more elevated PSVs may benefit from prophylactic intervention or more frequent surveillance to prevent limb occlusion.

Deformation analysis of 3D tagged cardiac images using an optical flow method.

BACKGROUND: This study proposes and validates a method of measuring 3D strain in myocardium using a 3D Cardiovascular Magnetic Resonance (CMR) tissue-tagging sequence and a 3D optical flow method (OFM). METHODS: Initially, a 3D tag MR sequence was developed and the parameters of the sequence and 3D OFM were optimized using phantom images with simulated deformation. This method then was validated in-vivo and utilized to quantify normal sheep left ventricular functions. RESULTS: Optimizing imaging and OFM parameters in the phantom study produced sub-pixel root-mean square error (RMS) between the estimated and known displacements in the x (RMSx = 0.62 pixels (0.43 mm)), y (RMSy = 0.64 pixels (0.45 mm)) and z (RMSz = 0.68 pixels (1 mm)) direction, respectively. In-vivo validation demonstrated excellent correlation between the displacement measured by manually tracking tag intersections and that generated by 3D OFM (R >or= 0.98). Technique performance was maintained even with 20% Gaussian noise added to the phantom images. Furthermore, 3D tracking of 3D cardiac motions resulted in a 51% decrease in in-plane tracking error as compared to 2D tracking. The in-vivo function studies showed that maximum wall thickening was greatest in the lateral wall, and increased from both apex and base towards the mid-ventricular region. Regional deformation patterns are in agreement with previous studies on LV function. CONCLUSION: A novel method was developed to measure 3D LV wall deformation rapidly with high in-plane and through-plane resolution from one 3D cine acquisition.

Ventricular restraint prevents infarct expansion and improves borderzone function after myocardial infarction: a study using magnetic resonance imaging, three-dimensional surface modeling, and myocardial tagging.

BACKGROUND: Infarct expansion is associated with impaired borderzone function, adverse remodeling, and poor long-term prognosis. We hypothesized that left ventricular restraint early after myocardial infarction limits infarct expansion, preserves borderzone function, and reduces remodeling. METHODS: We used an ovine model as well as high spatial and temporal resolution cardiac magnetic resonance imaging to quantify total and infarcted left ventricular epicardial surface area at baseline and 1 week and 12 weeks after anterior wall infarction in 10 animals. Five animals were randomly assigned to treatment with left ventricular restraint (Acorn cardiac support device) 1 week after infarction. Five animals were untreated controls. Total left ventricular surface area was measured by importing the end-diastolic magnetic resonance imaging-derived epicardial contours into custom software, which creates a three-dimensional surface from the two-dimensional magnetic resonance imaging contours. Infarct area was calculated from magnetic resonance imaging-detectable titanium markers placed at the infarct border. Borderzone radial and circumferential strains during systole were also assessed using myocardial tagging techniques as a measure of contractile function. RESULTS: The infarct area 1 week after infarction was 1,177 +/- 386 mm(2) in the control group and 1,124 +/- 427 mm(2) in the cardiac support device group. After 12 weeks, infarct area was 3,666 +/- 1,013 mm(2) in the control group and 1,227 +/- 301 mm(2) in the cardiac support device group. Borderzone systolic radial strain decreased from 12.6% +/- 0.77% to 3.6% +/- 0.3% after infarction in the control group and 13.7% +/- 0.87% to 4.7% +/- 0.3% in the cardiac support device group. At 12 weeks after infarction, radial strain was 3.4% +/- 0.5% in the control group and 6.7% +/- 0.4% in the cardiac support device group. CONCLUSIONS: Early postinfarction left ventricular restraint limits infarct expansion and improves borderzone contractile function.

The surgical treatment of end-stage heart failure.

Cardiac failure remains the leading cause of death in the Western World today. After myocardial insult, as the heart remodels and dilates, an increase in wall tension occurs secondary to increased radius of curvature, leading to increased myocardial oxygen consumption, decreased subendocardial blood flow, impaired energetics, and increased arrhythmias. Poor prognosis directly correlates with the degree of remodeling. Despite improvements in left ventricular function and long-term outcomes seen with pharmacologic therapy, the results remain far from perfect and the mortality continues to be high. The surgical armamentarium for treating end-stage heart failure is broad and new types of surgical treatments continue to emerge as alternatives to cardiac transplantation for the treatment of end-stage heart failure. Furthermore, surgical therapies that were once contraindicated for use in the failing heart are now being used to halt or reverse ventricular remodeling and improve cardiac function. Therefore, an aggressive approach to surgical revascularization, correction of mitral insufficiency, surgical reversal of left ventricular remodeling, and long-term use of mechanical ventricular assistance should be considered in any heart failure patient who has exhausted pharmacologic therapy.

Infarct size reduction and attenuation of global left ventricular remodeling with the CorCap cardiac support device following acute myocardial infarction in sheep.

BACKGROUND: Whether mechanical restraint of the left ventricle (LV) can influence remodeling following myocardial infarction (MI) remains poorly understood. The following discussion details three studies examining the effects of surgically placing a cardiac support device (CSD) over the entire epicardial surface, on infarct expansion, global cardiac function and myocyte geometry and function post-MI. METHODS: The effects of passive constraint on infarct expansion and global cardiac function/myocardial energetics were investigated in 10 sheep (5 MI only; 5 MI + CSD) using pressure-volume analysis and magnetic resonance imaging (MRI). Additionally, 11 sheep (5 MI only; 6 MI + CSD) were used to study the effects of passive restraint on myocyte geometry and function post-MI, with 10 additional uninstrumented sheep serving as controls. Baseline data was collected followed by the creation of an anterior infarct. 1 week post-infarct the animals underwent a second set of data collection studies followed by placement of the CSD in the experimental groups. Additional data was collected at 2 and 3 months post-MI. The animals in the myocyte function group underwent additional studies immediately following the 3 month time point. RESULTS: Infarct expansion was diminished as a result of the CSD. At 1 week post-MI the akinetic area was similar in both groups. At the terminal time-point, the akinetic area in the control group was similar to the 1-week time-point whereas, in the CSD group, the area of akinesis decreased (P = 0.001). A comparison of the two groups at the terminal time-point demonstrates a significantly diminished area of akinesis in the CSD group (P = 0.004). The relative area of akinesis followed a similar pattern. The CSD group also exhibited a decrease in end-diastolic volume (control 110.3 +/- 19.8 mL vs. CSD 67.6 +/- 4.7 mL, P = .006) and an improved ejection fraction (control 15.5% +/- 5.7% vs. CSD 29.46% +/- 4.42%, P = .008) relative to the control group. Myocardial energetics were also enhanced in the CSD group as evidenced by significant improvements in potential energy (control 2,015 +/- 503 mL x mm Hg/beat vs. CSD 885 +/- 220 mL x Hg/beat, P = .006), efficiency (control 39.4% +/- 13.6% vs. CSD 59.8% +/- 8.5%, P = .044), and oxygen consumption (control 0.072 +/- 0.013 mL O(2)/beat vs. CSD 0.052 +/- 0.007 mL O(2)/beat, P = .034). Isolated LV myocyte shortening velocity was reduced by 35% from control values (P < 0.05) in both MI groups. LV myocyte beta-adrenergic response was reduced with MI, but normalized in the MI + CSD group. Relative collagen content was increased and matrix metalloproteinase-9 was decreased within the MI border region of the CSD group. CONCLUSIONS: The CorCap cardiac support device retarded infarct expansion, improved global and regional cardiac function and beneficially modified LV and myocyte remodeling post-MI. These findings provide evidence that non-pharmacological strategies can interrupt adverse LV remodeling post-MI.

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.

Cardiac support device modifies left ventricular geometry and myocardial structure after myocardial infarction.

BACKGROUND: Whether mechanical restraint of the left ventricle (LV) can influence remodeling after myocardial infarction (MI) remains poorly understood. This study surgically placed a cardiac support device (CSD) over the entire LV and examined LV and myocyte geometry and function after MI. METHODS AND RESULTS: Post-MI sheep (35 to 45 kg; MI size, 23+/-2%) were randomized to placement of the CorCap CSD (Acorn Cardiovascular, Inc) (MI+CSD; n=6) or remained untreated (MI only; n=5). Uninstrumented sheep (n=10) served as controls. At 3 months after MI, LV end-diastolic volume (by MRI) was increased in the MI only group compared with controls (98+/-8 versus 43+/-4 mL; P<0.05). In the MI+CSD group, LV end-diastolic volume was lower than MI only values (56+/-7 mL; P<0.05) but remained higher than controls (P<0.05). Isolated LV myocyte shortening velocity was reduced by 35% from control values (P<0.05) in both MI groups. LV myocyte beta-adrenergic response was reduced with MI but normalized in the MI+CSD group. LV myocyte length increased in the MI group and was reduced in the MI+CSD group. Relative collagen content was increased and matrix metalloproteinase-9 was decreased within the MI border region of the CSD group. CONCLUSIONS: A CSD beneficially modified LV and myocyte remodeling after MI through both cellular and extracellular mechanisms. These findings provide evidence that nonpharmacological strategies can interrupt adverse LV remodeling after MI.

Passive ventricular constraint to improve left ventricular function and mechanics in an ovine model of heart failure secondary to acute myocardial infarction.

OBJECTIVE: This study investigated the effects on global cardiac function and myocardial energetics of limiting progressive dilatation after infarction by means of a woven polyester jacket cardiac support device. We hypothesized that placement of the cardiac support device results in a decrease in myocardial wall stress and improvement in cardiac function and myocardial energetics. METHODS: To investigate the effect of passive constraint on left ventricular function and mechanics, a total of 10 sheep were studied with pressure-volume analysis and magnetic resonance imaging. A baseline study was followed by the creation of an anterior infarct. After 1 week, the animals underwent a second study. The cardiac support device was then placed over the epicardium in 5 sheep; the remaining animals served as controls. A terminal study was performed at 2 months after the infarct. RESULTS: The cardiac support device group at the terminal study exhibited a decrease in end-diastolic volume (control 110.3 +/- 19.8 mL vs cardiac support device 67.6 +/- 4.7 mL, P =.006) and an improved ejection fraction (control 15.5% +/- 5.7% vs cardiac support device 29.46% +/- 4.42%, P =.008) relative to the control group. Myocardial energetics were also enhanced in the cardiac support device group, as evidenced by the significant improvements in potential energy (control 2015 +/- 503 mL. mm Hg/beat vs cardiac support device 885 +/- 220 mL. mm Hg/beat, P =.006), efficiency (control 39.4% +/- 13.6% vs cardiac support device 59.8% +/- 8.5%, P =.044), and oxygen consumption (control 0.072 +/- 0.013 mL O(2)/beat vs cardiac support device 0.052 +/- 0.007 mL O(2)/beat, P =.034). CONCLUSION: Passive constraint with the cardiac support device after infarct prevents further remodeling and may stimulate reverse remodeling in heart failure secondary to acute myocardial infarction. These results suggest that in human beings placement of the cardiac support device after a large anterior myocardial infarction may be effective in halting the remodeling process that often leads to end-stage heart failure. If proved effective, placement of a cardiac support device after large heart attacks has the potential to decrease the incidence of heart failure that results after large myocardial infarctions.

Ventricular constraint using the acorn cardiac support device reduces myocardial akinetic area in an ovine model of acute infarction.

BACKGROUND: Left ventricular remodeling secondary to acute myocardial infarction (AMI) is characterized by ventricular dilatation and regional akinesis. In this study, we investigated the effect of passive constraint on akinetic area development. METHODS AND RESULTS: The effect of passive constraint on akinetic area was investigated in 10 sheep using tissue-tagging magnetic resonance imaging (MRI). A baseline MRI study was followed by the creation of an anterior infarct. After 1 week, the animals received a second MRI study. A cardiac support device (CSD) was then placed over the epicardium in 5 sheep whereas the remaining animals served as controls. A terminal study was performed at the 2-month postinfarct in both groups. The akinetic area at 1-week postinfarct was similar in both groups. At the terminal time-point, the akinetic area in the control group was similar to the 1-week time-point whereas in the CSD group, the area of akinesis decreased (P=0.001). A comparison of the 2 groups at the terminal time-point demonstrates a significantly diminished area of akinesis in the CSD group (P=0.004). The relative area of akinesis followed a similar pattern. End-systolic and end-diastolic wall thickness was significantly greater in the CSD group at terminal (P=0.001). In addition, the minimum wall thickness was greater in the CSD group compared with the controls (P=0.04). CONCLUSIONS: Passive constraint reduced akinetic area development secondary to AMI. The attenuation of regional wall stress may prevent the incorporation of the border zone into the infarct, decreasing infarct size and providing a promising new therapy for patients after an AMI.