[Experimental study of the radial deformability of stents].
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Biomedical subjects
Publications and source records attributed to R Beyar.
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We report the acute and 30-day results with a new serpentine-design, tubular, stainless steel, balloon-expandable stent (beStent) in the first 100 patients. One hundred forty-eight stents were used to treat 103 narrowings in the left anterior descending (n = 46), left circumflex (n = 20), and right coronary (n = 37) arteries. There were 85 de novo and 18 restenotic lesions (lesion length: < 10 mm [31], 10 to 20 mm [43] > 20 mm [29]; lesion type: A [10] B1 [29], B2 [20], C [44]; total occlusions, 23. More than 1 stent was used in 31 patients for treatment of long lesions that could not be covered by 1 stent. The stents used were 15-mm (n = 106), 25-mm (n = 38), or 35-mm (n = 4) long. Stent implantation strategy involved predilatation, deployment, and high-pressure dilatation, using the same balloon if possible. Clinical in-hospital success was 97% (2 patients had stent thrombosis that was recanalyzed, with myocardial infarction developing in 1, and 1 patient died on day 14 from retroperitoneal bleeding treated with surgery and complicated by sepsis). One-month event-free survival was 96%, with 1 death on day 21 due to hypertensive crisis. There were no other major adverse cardiac events in this first complex cohort of patients. In conclusion, the initial experience with this stent demonstrates its safety and efficiency for treating simple and complex coronary disease, with a relatively low rate of complications. Long-term clinical follow-up awaits further investigation.
BACKGROUND: Apex rotation has been shown to provide a reliable index of the dynamics of left ventricular (LV) twist. In this study, we aimed to characterize twist at baseline and during acute ischemia in 20 patients undergoing percutaneous transluminal coronary angioplasty to the left anterior descending (LAD) artery and to test whether an old myocardial infarction or collateral flow affected twist dynamics. METHODS AND RESULTS: Among patients with no previous infarction, five had no collaterals (group A) and six had angiographically visible collaterals (group B). Previous anterior infarction was present in nine patients (group C). Data were acquired with the LAD angioplasty wire passed beyond the apex using a view aligned with the LV long axis. Frame-by-frame dynamics of apex rotation were measured from the angular movement of the portion of the wire that traversed the apex. Aortic pressure recordings allowed precise temporal definition of the cardiac cycle. Dynamics of apex rotation were measured at fixed intervals until 60 seconds of occlusion and up to 60 seconds of reperfusion. In group A, counterclockwise apex rotation (twist) during ejection of -22.0+/-1.7 degrees (mean+/-SEE) was followed by rapid clockwise rotation (untwist) during isovolumic relaxation. During 60 seconds of ischemia, maximum apex rotation decreased to -8.2+/-2.0 degrees (P<.001 versus baseline). In group B, baseline apex rotation was similar (-26.2+/-6.9 degrees) to that in group A, but ischemia had less effect, with apex rotation values of -17.7+/-3.4 degrees (P<.05 versus group A values). Group C was characterized by reduced baseline apex rotation values (-9.7+/-3.1 degrees, P<.05 versus group A values), with little change observed during ischemia (-8.1+/-2.6 degrees). CONCLUSIONS: Apex rotation, an index of ventricular twist, is sensitive to acute ischemia in patients without previous myocardial infarction. Visible collaterals to the ischemic region attenuate the acute ischemic response at 60 seconds. Previous myocardial infarction causes abnormalities in the baseline twist pattern with no further deterioration at 60 seconds of ischemia.
Phasic coronary flow is determined by the dynamic interaction between central hemodynamics and myocardial and ventricular mechanics. Various models, including the waterfall, intramyocardial pump and myocardial structural models, have been proposed for the coronary circulation. Concepts such as intramyocardial pressure, local elastance and others have been proposed to help explain the coronary compression by the myocardium. Yet some questions remain unresolved, and a new model has recently been proposed, linking a muscle collagen fibrous model to a physiologically based coronary model, and accounting for transport of fluids across the capillaries and lymphatic flow between the interstitial space and the venous system. One of the unique features of this model is that the intramyocardial pressure (IMP) in the interstitial space is calculated from the balance of forces and fluid transport in the system, and is therefore dependent on the coronary pressure conditions, the myocardial function and the transport properties of the system. The model predicts a wide range of experimentally observed phenomena associated with coronary compression.
The cardiac system, denoted as the Cardionome, represents one of the most exciting challenges to human ingenuity. Critical to our survival, it consists of a tantalizing array of interacting phenomena, from ionic transport, membrane channels and receptors through cellular metabolism, energy production, fiber mechanics, microcirculation, and electrical activation to the clinically observed global functions. These are measured by pressure, volume, shape, coronary flow, heart rate, and other changes. It is a complex interactive system requiring the intense efforts of capable scientists in the life sciences, including medicine, exact sciences, engineering and biomedical technology devoted to address these multivariable, multidisciplinary challenges, so as understand and control the pathologies involved. Here we present some of our past interactive studies and highlight two new models, one demonstrating micro to macro integration, and one involving tissue-organ interaction of various parameters. These models yield new insights into cardiac performance.
We mapped the three dimensional (3D) regional right ventricular (RV) motion using Cine-CT in 9 normal subjects and compared it to data from 10 patients with left ventricular (LV) aneurysm. The endocardial borders were traced and the RV's reconstructed in 3D. Regional perpendicular RV systolic motion was evaluated by our 3D stroke-volume-element approach, and the circumferential and longitudinal variations determined. The normal RV is characterized by higher endocardial motion in the posterior relative to the anterior regions (p < 0.0001), and no longitudinal (apex-to-base) gradient. In hearts with LV aneurysms, similar circumferential variations in wall motion are accompanied with a longitudinal increase in systolic motion, from apex to the base (p < 0.0001). Therefore, a 3D method for measurement of RV regional motion was developed and applied to normal and LV aneurysm patients, showing that LV aneurysm causes RV motion abnormality at the apex, compensated by an increased basal motion.
BACKGROUND: The acute angiographic results with the self-expanding nitinol stent have not been reported. We aim to provide angiographic data of the effect of self expansion and balloon assistance on the results. This is analyzed with respect to stent gain, arterial- and stent-recoil. METHODS AND RESULTS: The self-expanding nitinol coil stent is inherently different than balloon-expandable stents in its mechanism of deployment and the way that radial arterial expansion is achieved. Between January 1995 and June 1996, 86 stents were deployed in 64 patients undergoing elective angioplasty at the Rambam Medical Center, Haifa, Israel. The stent deployment procedure involved stent release assisted by high pressure balloon dilatation. The baseline, post-balloon, post-stenting and post-stent-dilatation characteristics were recorded with similar views, digitized to a PC and analyzed by image processing software. Using computerized analysis, arterial- and stent-recoil and stent gain were calculated for the average stented segment lesion (0.48 +/- 0.42, 0.22 +/- 0.37, 0.28 +/- 0.37, respectively). Balloon angioplasty increased the minimal luminal diameter from 1.07 +/- 0.73 mm at baseline, to 2.24 +/- 0.57 mm; stent deployment further increased the diameter to 2.63 +/- 0.48 mm, and within-stent balloon dilatation to 2.96 +/- 0.62 mm. CONCLUSIONS: The self-expanding nitinol stent exerts its effect on both the MLD and the average stented diameter through its intrinsic radial force aided by post-deployment within-stent balloon dilatation. A significant correlation was found between stent gain and arterial recoil (slope = 0.59, r = 0.68, p < 0.001) but not with stent-artery recoil. Therefore, with the negligible effect of stent recoil, the acute benefit of the nitinol stent is directly proportional to arterial recoil, a feature which is also common to balloon-expandable stents.
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BACKGROUND: There is a paucity of experimental data regarding self-expanding stents. This study evaluated the acute and chronic effects of CardioCoil, a self-expanding nitinol coil stent, in porcine coronary arteries. METHODS: Twenty-three self-expanding nitinol stents were implanted without associated balloon angioplasty in normal coronary arteries of 12 pigs, which were serially sacrificed up to 6 months. Angiographic and histologic analyses were performed to evaluate the deployment characteristics, patency rates, neointimal response, and unique features of the self-expanding nature of the CardioCoil stent. RESULTS: All stents were successfully deployed and remained patent acutely. Three undersized stents migrated proximally and there was one episode of subacute thrombosis in an oversized stent. The remaining stents were patent throughout the survival period and neointimal responses were favorable for up to 6 months (all mean neointima < 200 microns up to 6 months). There was evidence of continuing stent expansion over time (stent diameter 2.85 +/- 0.78 mm immediately after deployment and 3.24 +/- 0.97 mm at follow-up) and the majority of stent struts were in the adventitia by 6 months. Re-endothelization occurred starting one week after implantation and was complete by 8 weeks. CONCLUSIONS: This study shows that the CardioCoil self-expanding nitinol coil stent, is associated with favorable deployment characteristics and patency rates, although appropriate sizing is more crucial than with balloon-expandable stents. More importantly, there appears to be a "dissociation' between the deep vessel wall injury by the chronic strut expansion process and the neointimal reaction, unlike balloon-expandable stents.
BACKGROUND: The Cardiocoil (InStent) is a self-expanding nitinol coil that is restrained on a delivery catheter in a compressed state and deployed by a wire based release mechanism. We provide the initial data on the acute results of the use of this stent in a multi-center study in Europe. We also briefly review the other non-coronary applications of this stent. METHODS: One-hundred two stents were implanted in 76 patients for suboptimal results or dissections. There were 39 LAD lesions, 28 RCA lesions and 9 Circumflex lesions. There were eight total occlusions. Lesions were short in 41% (< 10 mm), tubular (between 10 and 20 mm) in 37%, and diffuse (> 20%) in 22%. Stent deployment included predilatation to the reference arterial side and post dilatation after stent deployment. RESULTS: Stent deployment was successful in all cases in which lesions could be crossed. In cases where the stent did not cross the lesion (n=3) it was removed uneventfully. There were no stent losses. Complications included subacute thrombosis in 4/76 (5.3%) patients (1- a long total RCA lesion, 2- diffuse proximal LAD diseases). There were no late acute events after stenting and no stent related mortality. Angiographic quantitative analysis showed that the stent expands by both its intrinsic self-expanding properties and by post deployment balloon assistance. CONCLUSIONS: The self-expanding coil stent for cardiovascular interventions is safe and effective in treating a variety of complex lesions. It provides adequate support to the arterial wall, preventing acute recoil and tacking dissections to the arterial wall. The long-term efficiency of this stent awaits further clinical testing.
We aim to present here the experience with newer stents for coronary and peripheral interventions. Specifically, the design and technical considerations of the self-expanding nitinol coil stents for coronary and vascular indications, as well as the design and clinical experience with the tubular stainless steel balloon-expandable serpentine stents for coronary and peripheral interventions are discussed. The animal and clinical experience with both types of stent have shown that the mechanisms of deployment and expansion are different for these inherently different stents. The self-expanding coil stent, providing adequate scaffolding in various types of coronary lesions is deployed by self expansion, aided to a significant extent by balloon expansion. Long-term outside pressure on the wall may lead to further stent expansion as has been shown with this stent, which may be an important parameter in the restenosis process. The tubular balloon-expandable serpentine stent does not have the feature of long-term expansion, however, is characterized by superior scaffolding properties and unique features that allow its safe use in the most complex coronary diseases. Long-term clinical results are pending for these two families of stents.
Our earlier description of the intracellular control (IC) of contraction of a single cell, based on coupling calcium kinetics with cross-bridge cycling, is extended here to study the performance of a multicellular inhomogeneous tissue common in pathophysiological situations. Inhomogeneity in calcium affinity or in cross-bridge kinetics is first simulated by analyzing two fiber segments connected as parallel or serial duplexes. The calculated characteristics of the parallel duplex are tested against our experimental data with two parallel nonuniform rat papillary fibers. The predicted serial duplex behavior is compared with reported experimental data of the effects of segmental hypoxia along a papillary fiber. Fiber inhomogeneity leads to polyphasic contraction of the fiber segments, reduces muscle length shortening, and affects the control of relaxation. We next investigated the force generated by a nonuniform tissue containing small areas of necrosis, evident in subendocardial infarction. Theoretical analysis suggests that the IC mechanism decreases the extension of cell necrosis by lowering the energy consumption of the viable cells in the ischemic zone. The study emphasizes the importance of IC in determining the global and local function of the inhomogeneous myocardium.
PURPOSE: To evaluate a new self-expanding nitinol coil stent in stenotic or occluded peripheral arteries. METHODS: Seventy-three symptomatic patients (58 men; mean age 67 years) were treated with nitinol stents for lesions in the iliac artery (9 stenoses); superficial femoral artery (SFA) (39 stenoses, 6 occlusions); popliteal artery and tibioperoneal trunk (9 stenoses, 7 occlusions); and 3 bypass grafts. Mean diameter stenosis was 84.4% +/- 9.9% (range 75% to 100%), and mean lesion length was 45 +/- 23 mm (range 20 to 120 mm). RESULTS: Eighty-eight 40-mm-long stents with diameters between 5 and 8 mm were implanted percutaneously for suboptimal dilation (n = 45); dissection (n = 21); and restenosis (n = 7). All stents but one were implanted successfully; the malpositioned stent was removed, and another stent was successfully deployed. There were 3 (4.1%) failures due to thrombosis at 24 hours. During the mean 16-month follow-up (range to 44 months), 4 restenoses (3 femoral, 1 popliteal) have occurred; 2 were treated with repeat dilation and 2 underwent bypass. Primary and secondary patency rates at 18 months were 87% and 90%, respectively, for all lesions (iliac: 100% for both; femoral: 85% and 88%; popliteal: 87% and 100%). CONCLUSIONS: This new nitinol stent seems to be safe and effective with favorable long-term results, even in distal SFA lesions and popliteal arteries. Its flexibility and resistance to external compression allow its placement in tortuous arteries and near joints.
Interventional cardiology emerged with the development of balloon angioplasty some 20 years ago, and has undergone tremendous changes since then. The coronary balloon was brought to a mature development stage, being the major "workhorse" of interventional cardiology. Various atherectomy techniques, aimed at removing plaque material, have been developed and showed immediate beneficial effects on the angioplasty results. Laser angioplasty is still looking for an appropriate place in interventional cardiology, with most of the results to date being disappointing. Stents are emerging as a breakthrough technology which has been proven to prevent restenosis and provide an important adjunctive device for suboptimal results following balloon angioplasty. Medically coated stents may have an important impact on the future of interventional cardiology. Novel imaging and flow measurement technologies are being further developed and optimized to assist clinical decisions and treatment strategies in interventional cardiology. In summary, interventional cardiologists today are provided with a set of tools from which they can select the appropriate ones for each lesion subset. Together with the appropriate adjunctive pharmaceutical therapy, prevention of restenosis is on the horizon.
BACKGROUND: Left ventricular (LV) twist has been defined as the counterclockwise rotation of the ventricular apex with respect to the base during systole. We recently showed that, since base rotation is minimal, measurement of apex rotation reflects the dynamics of LV twist. Since ischemia is known to affect endocardial and epicardial fiber force and shortening and therefore the transmural balance of torsional moments, we hypothesized that ischemia has a significant effect on apex-rotation amplitude and on untwisting during the isovolumic relaxation (IVR) period. METHODS AND RESULTS: With an optical device coupled to the LV apex, apex rotation was recorded simultaneously with LV pressure, ECG, LV segment length, and minor-axis diameters in 16 open-chest dogs. Ischemia was caused by a 1- to 2-minute snare occlusion of either the left anterior descending (LAD) or circumflex (LCx) arteries. LAD ischemia had a pronounced effect on apex rotation: an increase in apex-rotation amplitude attributed to subendocardial dysfunction at 10 seconds of ischemia; maximum apex rotation occurring later (during the IVR period) throughout the ischemia; a paradoxical relaxation pattern of initial untwisting followed by twisting and untwisting during the IVR period with ischemia; and a decrease in the amplitude of apex rotation with ischemia, possibly due to transmural dysfunction. LCx occlusion had similar effects on apex rotation, except that apex-rotation amplitude was not increased at 10 seconds of occlusion and the amplitude of apex rotation did not decrease with severe ischemia. Under control preischemic conditions, a linear relationship between apex rotation and segment length was observed during ejection and a different, steeper relationship during IVR. With regionally ischemic segments, this relationship became nonlinear for both ejection and IVR. CONCLUSIONS: Both LAD and LCx ischemia had profound effects on the dynamics of apex rotation. A paradoxical relaxation pattern occurred with ischemia. We suggest that these observations are due to changes in the dynamic transmural balance of torsional moments that determine LV twist.
BACKGROUND: Left ventricular twist or torsion has been defined as the counterclockwise rotation of the ventricular apex with respect to the base during systole. We have recently shown that since base rotation is minimal, measurement of apex rotation reflects the dynamics of left ventricular (LV) twist. Since the mechanisms by which load and contractility affect twist are controversial, we aimed to determine the relation between apex rotation and volume, contractility, and heart rate under conditions in which dimensions and pressures were accurately measured. METHODS AND RESULTS: Using our optical device coupled to the LV apex, apex rotation was recorded simultaneously with LV pressure, ECG, LV segment length, and minor-axis diameters (sonomicrometry) in 12 open-chest dogs. Using vena caval occlusion and volume loading, a linear end-diastolic (ED) relation between apex rotation and LV area index was obtained (slope, 0.61 +/- 0.06 degrees/percent change; intercept, -60.1 +/- 6.2 degrees; n = 10) that differed from the end-systolic (ES) relation (slope, 1.36 +/- 0.27 degree/percent change; intercept, -132.5 +/- 24.9 degrees; P < .005). With changes in contractility, afterload, or heart rate, for both ED and ES the apex rotation-volume points fell within the range of the relations established by changing preload, suggesting that volume is the major determinant of twist. Vena caval occlusion (preload and afterload decrease) caused an increase in amplitude of apex rotation, with maximal apex rotation occurring earlier in ejection. In contrast, acute volume loading (predominant preload increase) caused a small decrease in the amplitude of apex rotation, and twist relaxation was delayed into the isovolumic relaxation period. Likewise, with single-beat aortic occlusion (increased afterload), there was a slight decrease in the amplitude of apex rotation, and maximal apex rotation was delayed into the isovolumic relaxation period. Paired pacing (increased contractility) increased the total amplitude of apex rotation by 42% and caused a delay in untwisting until the end of the isovolumic relaxation period. An increase in heart rate over 150 beats per minute resulted in a significant decrease in the amplitude of apex rotation with a similar delay of twist relaxation into the isovolumic relaxation period. CONCLUSIONS: The effects of load, contractility, and heart rate manipulations on LV twist as measured throughout the cardiac cycle by the optical apex rotation method are manifested by changes in both the amplitude and dynamics of torsion. LV twist at ED and ES is primarily a function of volume; this relation appears to be unaltered by heart rate, afterload, and contractility. Whereas decreased load caused early untwisting, increases in preload, afterload, heart rate, and contractility caused a consistent pattern of delay in twist relaxation.
BACKGROUND: Distortion of the left ventricular (LV) cavity in patients with right ventricular pressure overload (RVPO) is well known. However, no direct measurements of regional myocardial function in terms of myocardial shortening and wall thickening are available; therefore, exactly how RVPO disturbs LV regional performance remains unclear. By using three-dimensional (3D) tagged magnetic resonance imaging, we were able to measure regional systolic function directly. Our objective was to study the relation between the distortion of the LV circular shape and regional LV function. METHODS AND RESULTS: In nine patients with RVPO and six healthy volunteers, four parallel short-axis images (with 12 radial tags) and two mutually orthogonal long-axis images (with four parallel tags) were generated, and endocardial and epicardial borders were manually traced. By integration of the short- and long-axis images, 3D reconstruction of the LV tracking points from end diastole to end systole was obtained. Data from the midventricular two short-axis image slices were analyzed. These were then divided into anterior, lateral, posterior, and septal regions. Circumferential and longitudinal shortening were then calculated from the endocardial and epicardial tag intersection points. Wall thickness and thickening were calculated by the 3D volume-element approach. An eccentricity index (EI), the ratio of septum-to-free-wall to anteroposterior diameters, was used to describe the shape of the LV cavity. The regional curvature was also measured. The RVPO group was characterized by flattening of the septum and LV lateral wall, decreased EI reflecting the distorted LV shape, altered distribution of endocardial circumferential shortening, and preserved ejection fraction. Changes in EI closely correlated with the septal curvature. The EI was smaller at end systole, reflecting further shape distortion relative to end diastole. Reduced myocardial performance, as measured by wall thickening and circumferential and longitudinal shortening fractions, was observed for the septum. A reduction in endocardial circumferential shortening of the septal and lateral walls was directly related to the end-systolic EI. In addition, whereas for healthy subjects a linear relation between area ejection fraction and endocardial circumferential shortening was observed, in RVPO patients a curvilinear (quadratic) relation was observed. CONCLUSIONS: In patients with RVPO, compared with healthy subjects, the septal function was reduced, as evidenced by reduced thickening and shortening fractions. The distortion in LV cavity at end systole due to the flattening of the septum contributes to preserved systolic ventricular function and nonuniform distribution in endocardial circumferential shortening.