Integrated microscopy techniques for comprehensive pathology evaluation of an implantable left atrial pressure sensor.

The safety and efficacy of an implantable left atrial pressure (LAP) monitoring system is being evaluated in a clinical trial setting. Because the number of available specimens from the clinical trial for histopathology analysis is limited, it is beneficial to maximize the usage of each available specimen by relying on integrated microscopy techniques. The aim of this study is to demonstrate how a comprehensive pathology analysis of a single specimen may be reliably achieved using integrated microscopy techniques. Integrated microscopy techniques consisting of high-resolution gross digital photography followed by micro-computed tomography (micro-CT) scanning, low-vacuum scanning electron microscopy (LVSEM), and microground histology with special stains were applied to the same specimen. Integrated microscopy techniques were applied to eight human specimens. Micro-CT evaluation was beneficial for pinpointing the location and position of the device within the tissue, and for identifying any areas of interest or structural flaws that required additional examination. Usage of LVSEM was reliable in analyzing surface topography and cell type without destroying the integrity of the specimen. Following LVSEM, the specimen remained suitable for embedding in plastic and sectioning for light microscopy, using the positional data gathered from the micro-CT to intersect areas of interest in the slide. Finally, hematoxylin and eosin (H&E) and methylene blue staining was deployed on the slides with high-resolution results. The integration of multiple techniques on a single specimen maximized the usage of the limited number of available specimens from the clinical trial setting. Additionally, this integrated microscopic evaluation approach was found to have the added benefit of providing greater assurance of the derived conclusions because it was possible to cross-validate the results from multiple tests on the same specimen.

Effects of beta(-)-emitting (188)Re balloon in stented porcine coronary arteries: an angiographic, intravascular ultrasound, and histomorphometric study.

BACKGROUND: Restenosis within stents may be prevented by ionizing radiation from an intravascular source. METHODS AND RESULTS: A liquid beta(-) radiation ((188)Re) balloon was evaluated in a randomized and blinded porcine coronary model of stent restenosis. Group A pigs (n=17) received 0,16, 22, or 29 Gy at 0.5-mm depth, followed by stenting. Restenosis was quantified by angiography, ultrasound, and histomorphometry at 30 days. Group B (n=7) was stented first and then treated with 0 or 29 Gy with follow-up at 60 days. There was a measurable effect at 16 Gy, which improved with increasing doses. At 29 Gy, the histological stenotic area was reduced by 67% (22% versus 66% in controls, P<0.001). Radiation after stenting was equally effective; the stenotic area was reduced (21% versus 65%, P<0.001). At 16 Gy, the vessel just distal to the stent was significantly smaller than control vessels because of intimal thickening (P=0.003). Radiated vessels had distinctive histology consisting of neointimal fibrin and reduced smooth muscle cells and matrix (P<0.0001). CONCLUSIONS: (188)Re balloon brachytherapy in porcine coronary arteries results in dose-dependent and injury-independent inhibition of stent restenosis for up to 60 days. Restenosis at the borders of the irradiated zone is a potential limitation and may be related to underdosing. Brachytherapy with the (188)Re balloon appears to be safe and feasible for clinical studies.

In vitro and in vivo studies of PEO-grafted blood-contacting cardiovascular prostheses.

The initial step of thrombus formation on blood-contacting biomaterials is known to be adsorption of blood proteins followed by platelet adhesion. Poly(ethylene oxide) (PEO) has been frequently used to modify biomaterial surfaces to minimize or prevent protein adsorption and cell adhesion. PEO was grafted onto a number of biomaterials in our laboratory. Nitinol stents and glass tubes were grafted with PEO by priming the metal surface with trichlorovinylsilane (TCVS) followed by adsorption of Pluronic and y-irradiation. Nitinol stents were also coated with Carbothane for PEO grafting. Chemically inert polymeric biomaterials, such as Carbothane, polyethylene, silicone rubber, and expanded polytetrafluoroethylene (e-PTFE), were first adsorbed with PEO-polybutadiene-PEO (PEO-PB-PEO) triblock copolymers and then exposed to gamma-irradiation for covalent grafting. For PEO grafting to Dacron (polyethylene terephthalate), the surface was sequentially treated with PEO-PB-PEO and Pluronics followed by gamma-irradiation. In vitro studies showed substantial reduction in fibrinogen adsorption and platelet adhesion to the PEO-grafted surfaces compared with control surfaces. Fibrinogen adsorption was reduced by 70-95% by PEO grafting on all surfaces, except for e-PTFE. The platelet adhesion corresponded to the fibrinogen adsorption. When the PEO-grafted surfaces were tested ex vivo/in vivo, however, the expected beneficial effect of PEO grafting was inconsistent. The beneficial effect of the PEO grafting was most pronounced on the PEO-grafted nitinol stents. Thrombus formation was reduced by more than 85% by PEO grafting on metallic stents. Only moderate improvement (i.e. 35% decrease in platelet deposition) was observed with PEO-grafted tubes of polyethylene, silicone rubber, and glass. For PEO-grafted heart valves made of Dacron, however, no effect of PEO grafting was observed at all. It appears that the extent of thrombus formation on PEO-grafted biomaterials was directly related to the extent of tissue damage during implantation surgery. Platelets can be activated and form aggregates in the bulk blood, and the formed platelet aggregates may be able to deposit on the PEO monolayer overcoming its repulsive property. Our studies indicate that the testing of in vitro platelet adhesion should include adhesion of large platelet aggregates, in addition to adhesion of individual platelets. Furthermore, the surface modification methods should be improved over the current monolayer grafting concept so that the repulsive force by the grafted PEO layers is large enough to prevent adhesion of platelet aggregates formed in the bulk blood before arriving at the biomaterial surface.

Effects of clopidogrel, aspirin and combined therapy in a porcine ex vivo model of high-shear induced stent thrombosis.

AIMS: Use of ticlopidine in coronary stenting is limited by delayed onset of action. We studied the effects of clopidogrel, a rapidly acting analog of ticlopidine alone, and in combination with aspirin, in inhibiting stent thrombosis. METHODS: Unpolished nitinol stents were deployed in a porcine ex vivo arteriovenous shunt and exposed to flowing arterial blood at a shear rate of approximately 1500. s-1. Stent thrombus, platelet aggregation and bleeding times were measured at baseline and after treatment. RESULTS: Intravenous clopidogrel produced a rapid (within 30 min) and dose-dependent inhibition of stent thrombosis, with 87% reduction at a dose of 10 mg.kg-1 (P < 0.001). Aspirin alone (10 mg.kg-1) was minimally effective (20% inhibition P > 0.05) in inhibiting stent thrombosis. Combined treatment with clopidogrel and aspirin produced 95-98% inhibition of stent thrombosis, even at low doses of clopidogrel (2.5-5.0 mg.kg-1) (P < 0.0001). At effective doses both clopidogrel and combined therapy produced significant prolongation of bleeding time (P < 0.05) and inhibition of platelet aggregation (P < 0.05). CONCLUSION: Clopidogrel, either alone or combined with aspirin, may have a potential role in preventing stent thrombosis in high-risk clinical situations.

Characterization of a positron emitting V48 nitinol stent for intracoronary brachytherapy.

Percutaneous transluminal coronary angioplasty (PTCA) is currently one of the most common treatments for obstructive coronary artery disease. The long term success of the treatment, however, is severely limited by restenosis. Recently, different investigators have begun to study the possibility of radiation therapy in restenosis prevention and have shown promising results. However, an optimal radiation delivery device for delivering a highly localized radiation dose to the arterial medial layer while preserving the viability of the artery has yet to be established. In this article, we discuss the development of a unique mixed gamma/beta brachytherapy source capable of delivering high radiation dose to a 0.5 mm thick vessel wall by proton-beam activating an existing nickel titanium stent to produce vanadium-48. The dose distribution of the activated stent is determined by computer simulation using MCNP Monte Carlo code and is verified by radiochromic film measurement.

Highly localized arterial remodeling in patients with coronary atherosclerosis: an intravascular ultrasound study.

BACKGROUND: Preservation of luminal area and symmetry in the presence of irregular plaques necessitates local expansion of the artery wall. METHODS AND RESULTS: Cross-sectional dimensions of coronary arteries in 65 patients were measured with the use of intravascular ultrasound. A total of 104 arterial segments were studied, of which 88 had atherosclerosis; 16 served as nonatherosclerotic control segments. Three features of atherosclerotic arterial segments were classified: (1) plaque formation, (2) lumen shape, and (3) shape of arterial external elastic lamina. With our intravascular ultrasound-based three-level classification system, we identified three patterns that accounted for 89% of all atherosclerotic arterial segments: (1) concentric plaque with a circular lumen and a circular external elastic lamina (n= 17), (2) eccentric plaque with a circular lumen and an oval external elastic lamina (n=35), and (3) eccentric plaque with an oval lumen and a circular external elastic lamina (n=26). A circular lumen was preserved in 66% of all atherosclerotic arterial segments. Arterial segments with a circular lumen in the presence of an eccentric plaque had a significantly larger lumen area than the other two main groups (P<.05). CONCLUSIONS: With our intravascular ultrasound-based classification, we provided information regarding the local remodeling response in the coronary artery wall. In a majority of cases, a circular lumen is maintained. Failure of this highly localized response to be operative may contribute to the development of stenotic lesions at a specific site in the artery.

Effects of GP IIb/IIIa receptor monoclonal antibody (7E3), heparin, and aspirin in an ex vivo canine arteriovenous shunt model of stent thrombosis.

BACKGROUND: Thrombosis is an important limitation of metallic coronary stents, especially in smaller vessels in which shear rates are high. Monoclonal antibody to platelet glycoprotein IIb/IIIa receptor (7E3) has been shown to inhibit shear-induced platelet aggregation. In this study, we compared the effects of 7E3, heparin, and aspirin on stent thrombosis in an ex vivo arteriovenous shunt model of high-shear blood flow. METHODS AND RESULTS: An ex vivo arteriovenous shunt was created in 10 anesthetized dogs. Control rough-surface slotted-tube nitinol stents (n = 72) expanded to 2 mm in diameter in a tubular perfusion chamber were interposed in the shunt and exposed to flowing arterial blood at a shear rate of 2100s-1 for 20 minutes. The animals were treated with intravenous murine 7E3 (Fab')2 (0.2, 0.4, and 0.8 mg/kg), heparin (100 U/kg), or aspirin (10 mg/kg). Effects of the test agents on thrombus weight, platelet aggregation, platelet P-selectin expression, bleeding time, and activated clotting time (ACT) were quantified. 7E3 reduced stent thrombosis by 95% (20 +/- 1 to 1 +/- 1 mg, P < .001) and platelet aggregation by 94% (14 +/- 2 to 1 +/- 1 omega, P < .001) at the highest dose (0.8 mg/kg). 7E3 significantly prolonged bleeding time but had no effect on ACT and platelet P-selectin expression. Heparin prolonged ACT but had no significant effect on stent thrombosis or platelet aggregation. Aspirin, although it inhibited platelet aggregation by 65%, had no effect on stent thrombosis (19 +/- 2 versus 20 +/- 1 mg in controls). CONCLUSIONS: 7E3 produced a dose-dependent inhibition of acute stent thrombosis under high-shear flow conditions. Stent thrombosis was resistant to heparin and aspirin. Thus, 7E3 may be an effective agent for preventing stent thrombosis.

Preserved vasodilatory response to nitroglycerin in saphenous vein bypass grafts.

BACKGROUND: Uncertainty exists regarding the effects of nitroglycerin on atherosclerotic segments of coronary arteries, and information on vasoreactivity of saphenous vein bypass grafts is sparse. Intravascular ultrasound enables identification of atherosclerosis in angiographically normal segments and allows continuous determination of alterations in cross-sectional lumen areas. METHODS AND RESULTS: Patients with documented coronary atherosclerosis were studied. Vessel morphology and lumen area at baseline and after 100 to 200 micrograms nitroglycerin were assessed at 10-second intervals for 60 seconds in vessel segments without angiographically apparent lesions. Coronary artery saphenous vein bypass grafts from 11 patients were compared with native coronary arteries in 16 different patients. Atherosclerosis was present in all vessel segments studied. There was a rapid increase in lumen area compared with baseline after intravascular nitroglycerin in both native coronary arteries and saphenous vein bypass grafts. Maximum lumen area dilatation was 19.6 +/- 12.2% in saphenous vein bypass grafts and 19.7 +/- 13.1% in native coronary arteries. An earlier peak response in saphenous vein bypass grafts (34.5 +/- 6.9 seconds) compared with native coronary arteries (44.7 +/- 8.5 seconds; P = .003) was found. Vessel wall area remained constant during vasodilation, but there was a significant reduction in measured wall thickness (P = .034). CONCLUSIONS: In patients with documented coronary artery disease, intravascular ultrasound reveals substantial atherosclerosis in angiographically normal vessel segments. In these vessel segments, both native coronary arteries and saphenous vein bypass grafts exhibit prompt vasodilation with the intravascular administration of nitroglycerin. The vasodilatory capacity in response to nitroglycerin seems to be preserved in transposed, denervated, and devascularized saphenous veins.

Coronary artery restenosis after balloon angioplasty in humans is associated with circumferential coronary constriction.

Therapies that inhibit intimal hyperplasia do not prevent restenosis after coronary artery balloon angioplasty, suggesting that additional mechanisms may be responsible for restenosis in humans. Using an intravascular ultrasound (Hewlett-Packard Sonos Intravascular Imaging System). 3.5F, 30-MHz (Boston Scientific) monorail imaging catheter, we studied 17 patients with clinical and angiographic restenosis at an average (mean +/- SD) of 7 +/- 6 months after balloon angioplasty (13 men age, 71 +/- 10 years; 12 left anterior descending coronary arteries, 4 right coronary arteries, and 1 left circumflex coronary artery) The lumen area (L.A), vessel wall area (VWA), and total cross-sectional area (CSA) within the external elastic lamina were measured at the restenosis site and at proximal and distal reference sites, which were defined as adjacent segments with the least amount of plaque. Consistent with coronary angiography findings, decreased LA at the restenotic site was detected in all 17 patients. The unique finding was that total CSA at the restenotic site was significantly decreased compared with both proximal and distal reference sites (10.1 +/- 2.4 versus 14.8 +/- 3.2 mm2 and 10.1 +/- 2.4 versus 13.8 +/- 3.1 mm2, respectively, P < .001), whereas VWA (intima plus media) was slightly increased at the angioplasty site compared with both proximal and distal reference sites (8.0 +/- 2.3 versus 7.6 +/- 2.3 mm2 and 8.0 +/- 2.3 versus 6.7 +/- 2.3 mm2, respectively, P = NS). Eighty-three percent of the loss in LA at the restenotic site was due to constriction of the total CSA, while the increase in VWA at the restenotic site accounted for only a 17% loss in LA. We then compared these results with the morphology of coronary artery segments in 14 patients without restenosis. These coronary artery segments had been previously treated with balloon angioplasty (7 +/- 5 months). Unlike that in restenotic lesions, the total CSA within the external elastic lamina at the sites of previous angioplasty was similar to that in distal and proximal reference sites (P = NS). Significant and consistent reduction in arterial CSA, with a minor increase in VWA, characterizes human coronary lesions that cause angiographic restenosis. These data suggest that in humans, "recoil" and/or vascular contraction with healing in response to balloon injury is a major contributor to restenosis after balloon angioplasty.

Inhibition of acute stent thrombosis under high-shear flow conditions by a nitric oxide donor, DMHD/NO. An ex vivo porcine arteriovenous shunt study.

BACKGROUND: Coronary stenting is limited by subacute thrombosis, especially in smaller-diameter vessels, in which shear rates are high. The objective of the present study was to determine whether local delivery of a new type of NO donor, the NO adduct of N,N'-dimethylhexanediamine (DMHD/NO), inhibits acute stent thrombosis (ST) at high-shear flow. METHODS AND RESULTS: Effects of local infusion of DMHD/NO; intravenous aspirin, and heparin on ST were evaluated in an ex vivo porcine AV shunt model. Nitinol stents (2 mum in diameter, n = 120) were placed in a tubular chamber and perfused with blood from pigs (n = 13) at a shear rate of 2100s-1 for 20 minutes. ST was quantified by measurement of dry thrombus weight(TW). Effects on platelet aggregation (PA), blood pressure, bleeding time, and activated clotting time (ACT) were also examined. There was a dose-dependent inhibition of ST and PA by DMHD/NO. TW was reduced by 95% (1 +/- 2 versus 16 +/- 4 mg control, mean +/- SD, P < .001), and PA was reduced by 75% (4 +/- 3 versus 14 +/- 9 omega/min control, P < .05) at the highest dose of 10 mumol/L. DMHD/NO had no effects on bleeding time, ACT, or blood pressure. In contrast, aspirin (10 mg/kg), despite inhibiting PA, had no effects on TW (12 +/- 5 versus 16 +/- 8 mg control, P = .3). Heparin (200 U/kg) reduced TW by 33% (14 +/- 4 versus 21 +/- 3 mg control, P < .05) and prolonged ACT. CONCLUSIONS: Local delivery of DMHD/NO produced a 15-fold inhibition of acute ST at high-shear flow without producing adverse systemic hemostatic or hemodynamic effects. Thus, treatment with DMHD/NO may be an effective strategy for prevention of stent thrombosis.

Contribution of inadequate compensatory enlargement to development of human coronary artery stenosis: an in vivo intravascular ultrasound study.

OBJECTIVES: This intravascular ultrasound study sought to examine to what extent native coronary artery stenosis is accompanied by vessel wall thickening or inadequate compensatory enlargement (relative vessel constriction), or both. BACKGROUND: In human femoral arteries, inadequate compensatory enlargement is reported to be a paradoxic mechanism for the development of severe arterial lumen narrowing. However, it is unclear in human coronary arteries whether inadequate compensatory enlargement contributes to the development of critical arterial stenosis. METHODS: Thirty-five primary coronary artery lesions from 30 patients (19 men, 11 women; mean [+/- SD] age 65 +/- 13 years) were imaged by intravascular ultrasound. The vessel cross-sectional area and lumen area were measured, and the wall area (vessel cross-sectional area minus lumen area) was calculated at the lesion site and at the proximal and distal reference sites. We defined compensatory enlargement to be present when the vessel cross-sectional area at the lesion site was larger than that at the proximal reference site, inadequate compensatory enlargement when the vessel cross-sectional area at the lesion site was smaller than that at the distal reference site and intermediate remodeling when the vessel cross-sectional area at the lesion site was intermediate between the two reference sites. RESULTS: Compensatory enlargement was observed in 19 (54%) of 35 lesions, inadequate compensatory enlargement in 9 (26%) of 35 and intermediate remodeling in 7 (20%) of 35. In the inadequate compensatory enlargement group, reduction of the vessel cross-sectional area contributed to 39% of lumen reduction. CONCLUSIONS: Compensatory enlargement commonly (54%) occurs at stenotic coronary lesions. However inadequate compensatory enlargement results in a substantial amount (39%) of the lumen area reduction in 26% of primary coronary artery lesions.

Absence of focal compensatory enlargement or constriction in diseased human coronary saphenous vein bypass grafts. An intravascular ultrasound study.

BACKGROUND: No in vivo data are available on the occurrence of compensatory enlargement or vessel constriction in diseased human coronary saphenous vein bypass grafts (SVBGs). The aim of this intravascular ultrasound (IVUS) study was to examine to what extent lumen reduction is accompanied by (1) vessel wall thickening and (2) arterial wall constriction in SVBGs. METHODS AND RESULTS: We used IVUS to examine 43 SVBGs from 42 patients (32 men, 10 women; mean age, 72 +/- 5 years) 8 to 23 (11 +/- 4) years after SVBG. IVUS images were obtained with a 3.5F monorail ultrasound catheter with a 30-MHz frequency and were analyzed at the lesion site, the reference site, and an intermediate site. The lumen area was significantly (P < .01) decreased; the vessel wall area (SVBG cross-sectional area minus lumen area) and the plaque area (area within the external elastic lamina minus lumen area) were significantly (P < .01) increased from the reference site through the lesion site. However, SVBG cross-sectional area was the same at these three sites (24.0 +/- 8.1 versus 24.4 +/- 8.6 versus 24.5 +/- 8.6 mm2, P = NS), and the external elastic lamina area was also quite constant in each vessel (17.8 +/- 6.0 versus 17.7 +/- 6.4 versus 17.6 +/- 6.2 mm2, P = NS). CONCLUSIONS: These in vivo IVUS data from human coronary SVBGs demonstrate that (1) no focal compensatory enlargement or vessel constriction occurred in stenotic segments compared with the reference segments and that (2) the absence of focal compensatory enlargement appears to be a potentially important factor in the progression of stenoses in coronary SVBGs.

Usefulness of a prototype directional catheter for excimer laser coronary angioplasty in narrowings unfavorable for conventional excimer or balloon angioplasty.

We report clinical and angiographic results in 53 patients with 57 significant coronary or saphenous vein graft narrowings treated with directional excimer laser angioplasty. The target vessels were the left main (1%), anterior descending (32%), circumflex (19%), right coronary artery (39%), and vein grafts (9%). Lesions were morphologic class B1 (18%), B2 (79%), or C (3%), with 40 de novo and 17 restenotic lesions. Adjunctive balloon angioplasty was used in 53 lesions (93%). Mean pre- and postprocedural minimal lumen diameters were 0.6 +/- 0.3 and 1.9 +/- 0.7 mm (p < 0.001), corresponding to a mean diameter stenosis of 72 +/- 20% and 27 +/- 16%. Procedural success rate was 91%. Cumulative risk of death, Q-wave myocardial infarction, or emergency bypass operation was 9% (5 patients). Of patients who had a successful laser procedure, 28 (60%) with 30 lesions underwent angiographic follow-up at 6 +/- 3 months after the procedure. Restenosis rates (> 50% diameter restenosis or acute gain loss) were 37% and 23%, respectively. Four patients underwent bypass, 3 angioplasty, and 1 patient died from cancer. This study demonstrates the feasibility of directional application of laser energy to selected unfavorable narrowings for conventional excimer laser or balloon angioplasty. Further evaluation of this device using the now standard saline infusion technique is necessary to establish its ultimate role as a primary interventional device.

Effects of inhibition of nitric oxide formation on the regulation of coronary blood flow in anesthetized dogs.

In 11 open-chest dogs with a flowmeter on the left circumflex artery, L-NMMA, a selective inhibitor of nitric oxide-formation, was subselectively infused into the left circumflex artery at a rate of 2.5 mg/ml (ml/min) to avoid systemic hemodynamic effects. The coronary blood flow at normal arterial blood pressure was similar prior to and during L-NMMA infusion. However, when the arterial blood pressure was raised by inflating a balloon in the descending aorta, the nitric oxide suppression induced a dramatic increase in coronary vascular resistance by almost 40% compared to control conditions without L-NMMA infusion at identically elevated arterial blood pressure. L-NMMA induced a significant downward shift and flattening of the pressure-flow relation over a pressure range from 60-150 mmHg. Peak hyperemic coronary flow after 20-s transient coronary occlusion was similar prior to and during L-NMMA infusion, but the duration of the hyperemic flow response was significantly shortened during L-NMMA infusion indicating exaggerated constriction after hyperemic stimulus. The EDRF/nitric oxide-system plays an important role for the regulation of coronary blood flow by counteracting autoregulatory constrictor responses to increased driving pressure and shear stress in the intact canine circulation.

Digital angiographic impulse response analysis of myocardial perfusion: influence of heart rate and blood pressure changes on microcirculatory transit time measurement in the normal canine coronary circulation.

The study describes the effect of acute changes in aortic blood pressure and heart rate in the intact normal canine coronary circulation on digital angiographic measurements of the mean transit time of the microcirculation compartment and on direct flow meter measurement of resting and maximal hyperemic coronary blood flow. The mean transit time of the radiographic contrast material through the normal coronary circulation was calculated in 20 dogs by the impulse response analysis from serial digital coronary angiograms under systematically changed blood pressure and heart rate conditions. The mean aortic blood pressure (MAP) was controlled by the inflation of a balloon in the descending aorta (70-150 mmHg). The heart rate was altered by atrial pacing (90, 120, and 150/min). The mean transit times (T mu) of contrast material across the myocardial microcirculation which had been recently shown to correlate with coronary flow reserve (CFR) in stenosed arteries in the canine model were calculated under resting and hyperemic flow conditions from 428 selective coronary angiograms after a hand-injected contrast bolus, T mu was found to be heart rate independent. T mu-1 was linearly correlated with MAP (r = 0.7). There was no difference in T mu under resting and hyperemic flow conditions at comparable MAP. The corresponding distribution volume (V mu) of the microcirculation was calculated as the product of the mean transit time T mu and the measured coronary blood flow. Under resting flow conditions, V mu decreased with rising MAP. Furthermore, V mu increased with rising heart rate, V mu was constant during blood pressure or heart rate changes under hyperemic flow conditions. The data suggest that CFR whether by direct measurements of flow or by radiographic assessment of contrast material kinetics should be standardized with respect to hemodynamic conditions of heart rate and MAP.

Influence of expanded balloon diameter on Palmaz-Schatz stent recoil.

After successful stent implantation, the residual luminal diameter of the stented vessel is usually smaller than the maximal stent-expanded balloon diameter. The goal of this study was to determine whether immediate vessel diameter recoil after Palmaz-Schatz stenting is affected by the final expanding balloon diameter used during stent deployment. Single Palmaz-Schatz balloon expandable stents were successfully placed in 108 stenotic lesions. There were 68 patients with 75 saphenous vein graft (SVG) and 30 patients with 33 native coronary artery lesions, including 26 restenotic and 82 de novo occlusive (> 50% diameter stenosis) lesions. Quantitative coronary angiography was used for the assessment of stent recoil, defined as the difference between the minimal diameter of the fully expanded balloon and the postprocedure minimal lumen diameter divided by minimal diameter of the fully expanded balloon. A strong correlation (r = 0.94) was found between the minimal diameter of the fully expanded balloon and poststenting minimal lumen diameter. Immediate recoil was 11.3 +/- 7.5%, responsible on an average for 0.4 +/- 0.2-mm acute lumen loss. Recoil was less in SVG than in coronary arteries (9.7 +/- 6.6% vs. 14.0 +/- 7.8%; P = 0.004, and 0.3 +/- 0.2 vs. 0.4 +/- 0.2 mm; p = 0.01). Lesions were divided into four subgroups, based on the final stent expanding balloon diameter: (1) < or = 3.0 mm (n = 33); (2) > 3 < or = 3.5 mm (n = 43); (3) > 3.5 < or = 4 mm (n = 23); and (4) > 4 mm (n = 9).(ABSTRACT TRUNCATED AT 250 WORDS)

Stent implantation of saphenous vein graft aorto-ostial lesions in patients with unstable ischemic syndromes: immediate angiographic results and long-term clinical outcome.

OBJECTIVES: This study examined the immediate angiographic and long-term clinical results of stenting saphenous vein graft aorto-ostial stenosis at a single center. BACKGROUND: Data on the feasibility, safety and short- and long-term clinical results of stent implantation in aorto-ostial lesions in patients with unstable angina are limited. METHODS: Palmaz or Palmaz-Schatz stents were deployed in 29 patients (mean [+/- SD] age 70 +/- 10 years) with complex (B2 or C) vein graft aorto-ostial lesion morphology. All patients had angina at rest; 23 (79%) had a previous myocardial infarction; and 13 (45%) had two previous bypass operations (mean graft age 9 +/- 5 years). Mean left ventricular ejection fraction was 42 +/- 13%. RESULTS: Thirty-two stents were deployed in 25 new and 4 restenotic aorto-ostial lesions. Ten additional stents were implanted in five patients for eight lesions other than at ostial locations. Stent implantation was successful in all patients. There was no death, Q wave myocardial infarction, bypass surgery or stent thrombosis in the first 30 days. Stenting improved minimal lumen diameter from 0.7 +/- 0.5 mm (95% confidence interval [CI] 0.5 to 0.8) to 3.3 +/- 0.5 mm (CI 3.2 to 3.5) and percent diameter stenosis from 80 +/- 13% (CI 75% to 85%) to 1 +/- 12% (CI -3% to 6%) (p < 0.001 for both variables). Immediate loss from recoil was 0.2 +/- 0.2 mm (CI 0.2 to 0.3), corresponding to a percent recoil of 7 +/- 5% (CI 5% to 9%). Clinical follow-up in all patients at a mean of 11 +/- 8 months revealed that 27 patients (94%) were free of death or myocardial infarction. Bypass surgery and balloon angioplasty were required in one (3%) and two (6%) patients, respectively. In 21 (88%) of the remaining 24 patients, symptoms were lessened by two or more symptom classes. CONCLUSIONS: Palmaz or Palmaz-Schatz stent implantation for saphenous vein graft aorto-ostial stenosis has a high likelihood of immediate success and is associated with a large immediate gain in lumen diameter. Thirty-day and long-term adverse event rates are low. These data suggest that stenting saphenous vein graft aorto-ostial lesions is an acceptable therapeutic option in selected elderly patients with unstable angina and large-diameter vessels.

Increased coronary perforation in the new device era. Incidence, classification, management, and outcome.

BACKGROUND: The incidence of coronary perforation using new percutaneous revascularization techniques may be increased compared with PTCA. Still, perforation is uncommonly reported, and the optimal management and expected outcome remain unknown. The objectives of the study were to determine the incidence of coronary perforation using balloon angioplasty (percutaneous transluminal coronary angioplasty, PTCA) and new revascularization techniques and to develop optimal strategies for its management based on classification and outcome. METHODS AND RESULTS: Eleven sites with frequent use of new revascularization devices and prospective coding of consecutive procedures for coronary perforation during 1990 to 1991 contributed to a perforation registry. Patients with perforation were matched by device with an equal-sized cohort without perforation. Data were collected centrally, and all procedural cineangiograms were reviewed at a core angiographic laboratory. A classification scheme based on angiographic appearance of the perforation (I, extraluminal crater without extravasation; II, pericardial or myocardial blushing; III, perforation > or = 1-mm diameter with contrast streaming; and cavity spilling) was evaluated as a predictor of outcome and as a basis for management. Perforation was observed in 62 of 12,900 procedures reported (0.5%; 95% confidence interval, 0.4% to 0.6%), more commonly with devices intended to remove or ablate tissue (atherectomy, laser) than with PTCA (1.3%, 0.9% to 1.6% versus 0.1%, 0.1% to 0.1%; P < .001). The perforation population was notable for its advanced age (67 +/- 10 years) and high incidence of female sex (46%) (both P < .001 compared with patients without perforation). Perforation could be treated expectantly or with PTCA but without cardiac surgery in 85%, 90%, and 44% of class I, II, and III perforations, respectively. Class I perforations (n = 13, 21%) were associated with death in none, myocardial infarction in none, and tamponade in 8%. The incidences of these adverse events were 0%, 14%, and 13% in class II perforations (n = 31, 50%) and 19%, 50%, and 63% in non-cavity spilling class III perforations, respectively (n = 16, 26%). Two of the 15 instances of cardiac tamponade (13%) were delayed, occurring within 24 hours after dismissal from the catheterization laboratory. CONCLUSION: The incidence of perforation, while low, is increased with new devices. Women and the elderly are at highest risk. The clinical risk after perforation can be classified angiographically, but even low-risk perforations occasionally have poor clinical outcome. Patients should be observed for delayed cardiac tamponade for at least 24 hours.