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Biomedical subjects

M K Hong

Publications and source records attributed to M K Hong.

At least 109 records · Page 6Linked to original sources

Comparison of six-month results of coronary stenting versus balloon angioplasty alone in patients with acute myocardial infarction.

The purpose of this study was to compare results of delayed elective stent implantation on the infarct-related artery with conventional balloon angioplasty in 97 patients with acute myocardial infarction at 7 to 10 days after symptom onset (stenting in 45 patients, balloon angioplasty in 52 patients). In selected patients, intracoronary stent implantation on the infarct-related artery at 7 to 10 days after symptom onset of acute myocardial infarction is safe, feasible, and may reduce the the frequency of late restenosis compared with balloon angioplasty (the angiographic restenosis rate: 13% in patients with stents vs 52% in patients with balloon angioplasty, p <0.05).

Catheterization↗

Coronary stenting (Cordis) without anticoagulation.

We evaluated the effect of antithrombotic regimens on subacute thrombosis and short-term clinical courses after successful implantation of the Cordis coronary stent, which is a flexible, balloon expandable, radiopaque tantalum stent. Two hundred seventy-five consecutive patients with 290 lesions were treated with 356 Cordis stent implantations. According to poststent antithrombotic regimen, patients were divided into 3 groups; 165 patients with 175 lesions received aspirin 200 mg/day, ticlopidine 500 mg/day, and warfarin for 1 month (group 1), 66 patients with 69 lesions received aspirin and ticlopidine (group 2), and 44 patients with 46 lesions received aspirin alone (group 3) after successful Cordis stenting. The overall procedural success rates were 97.7% in group 1, 98.6% in group 2, and 100% in group 3. More than 65% of the patients were eligible for elective stenting. The overall rate of stent thrombosis was 1.8%: 1.2% in patients assigned to the treatment with aspirin, ticlopidine, and warfarin; 0% in patients with aspirin and ticlopidine; and 6.8% in patients assigned to the treatment with aspirin alone. In conclusion, the Cordis coronary stent is an effective endovascular stent in various clinical indications including unstable angina and acute myocardial infarction. Antiplatelet therapy using aspirin and ticlopidine after successful Cordis coronary stenting is a promising alternative to anticoagulation therapy to overcome the drawbacks of stenting. However, poststent antithrombotic therapy with aspirin alone is associated with a significant rate of stent thrombosis.

Anticoagulants↗

Increased restenosis in diabetes mellitus after coronary interventions is due to exaggerated intimal hyperplasia. A serial intravascular ultrasound study.

BACKGROUND: The increased risk of restenosis after catheter-based coronary interventions in diabetic patients has not been determined. Intravascular ultrasound (IVUS) has shown that the decrease in arterial area is responsible for most of the late lumen loss in nonstented lesions and that intimal hyperplasia is responsible for all of the late lumen loss in stented lesions. METHODS AND RESULTS: Serial (postintervention and follow-up at 5.6 +/- 3.3 months) IVUS was used to study 251 native coronary lesions in 241 patients; 63 patients had treated diabetes mellitus (oral hypoglycemic drugs or insulin). Interventional procedures included percutaneous transluminal coronary angioplasty, directional or rotational atherectomy, excimer laser angioplasty, or Palmaz-Schatz stents. The external elastic membrane (EEM), stent, and lumen areas were measured. The plaque+media (P+M) area in nonstented lesions was calculated as EEM minus lumen area, and the intimal hyperplasia (IH) area in stented lesions was calculated as stent minus lumen area. The anatomic slice selected for serial analysis had an axial location within the target lesion at the smallest follow-up lumen area. Nonstented lesions in diabetics and nondiabetics had a similar decrease in EEM cross-sectional area (CSA; 1.9 +/- 2.8 versus 1.8 +/- 4.2 mm2; P = .6350). However, nonstented lesions in diabetics had a greater increase in P+M CSA (1.3 +/- 2.8 versus 0.6 +/- 2.5 mm2, P = .0720), and the increase in P+M CSA contributed a greater percentage to the decrease in lumen CSA. In stented lesions, the decrease in lumen CSA (5.2 +/- 2.5 versus 2.0 +/- 2.3 mm2) and the increase in IH CSA (5.0 +/- 2.8 versus 1.8 +/- 2.0 mm2) were greater in diabetics than nondiabetics (P = .0009 and P = .0007, respectively). These findings were even more striking in (nonstented and stented) restenotic lesions. CONCLUSIONS: Serial IVUS analysis showed that the main reason for increased restenosis in diabetes mellitus was exaggerated intimal hyperplasia in both stented and nonstented lesions.

Aged↗

Influence of guiding catheter selection on the measurement of coronary flow reserve.

The impact of guiding catheter selection on the measurement of coronary flow reserve was assessed by injecting increasing doses of adenosine through 3 different catheters often used during coronary interventions. When guiding catheters with side holes were used, an approximate doubling of the adenosine dose was required to produce a coronary flow reserve response similar to a 12-micrograms dose of adenosine injected through guiding catheters without side holes.

Adenosine↗

Continuous subcutaneous angiopeptin treatment significantly reduces neointimal hyperplasia in a porcine coronary in-stent restenosis model.

BACKGROUND: In-stent restenosis results primarily from neointimal hyperplasia. This study evaluated the efficacy and the optimal mode of administration of angiopeptin, a somatostatin analogue with antiproliferative activity, in a porcine coronary in-stent restenosis model. METHODS AND RESULTS: Forty pigs were randomly assigned to one of four groups (n = 10 per group): (1) controls receiving saline infusion at the site of stent implantation via a local delivery catheter, (2) local treatment group receiving one-time treatment (200 (micrograms angiopeptin) at the site of stent placement, (3) systemic treatment group receiving continuous angiopeptin over a 1-week period via a subcutaneous osmotic pump (200 micrograms/kg total dose) and (4) combined local and systemic treatment group. Then, one oversized Palmaz-Schatz stent (mean ratio of stent to artery diameters, 1.3:1) was implanted in the left anterior descending coronary artery. The degree of neointimal reaction was evaluated 4 weeks later by angiography (maximal percent diameter stenosis), intravascular ultrasound (total in-stent neointimal volume), and histology (maximal area stenosis). Systemic treatment produced the least neointimal hyperplasia and significantly reduced in-stent restenosis compared with the control group by all end points, despite similar degrees of injury. Angiography showed 25 +/- 17% versus 50 +/- 17% diameter stenosis in the systemic angiopeptin group versus the control group (P < .0001), intravascular ultrasound revealed 23 +/- 10 versus 58 +/- 27 mm3 neointimal volume in the systemic angiopeptin versus control group (P = .0002), and histology showed 41 +/- 16% versus 69 +/- 18% area stenosis (P = .0016) in the systemic angiopeptin versus control group. Plasma angiopeptin levels revealed rapid clearance (within 6 hours) after local therapy, whereas the levels persisted for up to 2 weeks in the systemic group. CONCLUSIONS: This study shows that continuous subcutaneous treatment with angiopeptin after stent implantation significantly reduces in-stent restenosis by inhibiting neointimal hyperplasia.

Animals↗

Feasibility and efficacy of locally delivered enoxaparin via the Channeled Balloon catheter on smooth muscle cell proliferation following balloon injury in rabbits.

To determine the potential utility of local treatment of enoxaparin on restenosis, four groups of rabbits underwent balloon injury of bilateral iliac arteries with the Channeled Balloon (balloon/artery = 1.1), followed by assigned treatment (5 controls received local saline, 7 local-treatment rabbits received a one-time local delivery of 10 mg/kg of enoxaparin, 5 systemic-treatment rabbits received 10 mg/kg of enoxaparin subcutaneously once daily for 1 wk, and 5 combined-treatment rabbits received both local and systemic enoxaparin). The percentage of nuclei positive for proliferating cell nuclear antigen/microns2 of media 1 wk later was 1.97 +/- 2.01 for the control group, 2.68 +/- 2.52 for the local group, 0.22 +/- 0.32 for the systemic group, and 0.07 +/- 0.09 for the combined group (P < 0.0001 by Kruskal-Wallis test, with P < 0.05 for combined treatment group vs. controls or local treatment group and systemic vs. local groups). Feasibility study with 3H-enoxaparin showed intramural retention of 0.1-0.2% of locally delivered amount for 24 h. We conclude that one-time local delivery of enoxaparin following angioplasty is ineffective in inhibiting medial smooth muscle cell proliferation, most likely due to low efficiency. Only sustained treatment resulted in significant reduction.

Angioplasty, Balloon↗

In vitro and in vivo properties of murine monoclonal antibody for a novel immature thymocyte-differentiated antigen, JL1.

JL1 is a novel thymocyte-differentiated antigen strictly confined to stage II immature cortical thymocytes. It is expressed in several types of leukemias and lymphomas. Murine anti-JL1 monoclonal antibody labeled with 131I and 99mTc showed 60-70% of immunoreactivity and 1.4-1.9 x 10(9) L/mol of affinity constant. The incubation of the radiolabeled antibody with Molt-4 cells showed no evidence of modulation or shedding. Localization indices increased from day 3 to day 5 in SCID mice bearing Molt-4 cells.

Animals↗

Successful treatment of coronary artery perforation during angioplasty using autologous vein graft-coated stent.

We report a case of successful treatment of coronary artery perforation and cardiac tamponade with an autologous vein graft-coated stent, which were developed during percutaneous transluminal coronary angioplasty. The method reported here may be an effective alternative to emergency surgery and should be considered when coronary artery perforation does not respond to conventional prolonged inflation with perfusion catheter.

Aged↗

Acute and chronic effects of self-expanding nitinol stents in porcine coronary arteries.

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.

Alloys↗

Single-dose intramuscular administration of sustained-release Angiopeptin reduces neointimal hyperplasia in a porcine coronary in-stent restenosis model.

BACKGROUND: In-stent restenosis results primarily from neointimal hyperplasia. In a previous study we showed that continuous subcutaneous Angiopeptin infusion for 1 week significantly reduces neointimal hyperplasia in a porcine coronary overstretch in-stent restenosis model. The present study evaluated the relative efficacy of immediate-release and sustained-release Angiopeptin in the same model. METHODS: Thirty pigs (n = 10 in each group) were randomly assigned to three groups: controls receiving no Angiopeptin (Group 1); a sustained-release treatment group receiving one time intramuscular administration of 20 mg of Angiopeptin (Group 2); and a systemic treatment group receiving continuous Angiopeptin over a 1-week period via a subcutaneous osmotic pump (200 micrograms/kg total dose) (Group 3). One oversized Palmaz-Schatz stent (mean stent/artery = 1.25) was subsequently implanted in the left anterior descending coronary artery. The degree of neointimal reaction was evaluated 4 weeks later by angiography (maximal per cent diameter stenosis) and histology (maximal neointimal area corrected for injury score). RESULTS: A trend towards a reduction in diameter stenosis was observed by angiography, despite a similar degree of injury (25 +/- 17% in Group 1, 13 +/- 8% in Group 2, and 14 +/- 9% in Group 3; P = 0.072 by ANOVA). Histology demonstrated that both Angiopeptin treatment strategies significantly reduced in-stent neointimal area compared with the control group (1.65 +/- 0.97 mm2 in Group 1 versus 0.93 +/- 0.41 mm2 in Group 2 versus 0.85 +/- 0.28 mm2 in Group 3; P = 0.016 by ANOVA). Measurement of plasma Angiopeptin levels revealed comparable levels in both treatment groups, which persisted for up to 2 weeks. CONCLUSIONS: This study shows that single-dose intramuscular administration of sustained-release Angiopeptin reduces in-stent restenosis as effectively as the prolonged systemic treatment requiring a subcutaneous pump. Thus, a practical, effective, pharmacologic therapy for preventing in-stent restenosis may be available and should be evaluated in patients.

Animals↗

A randomized animal study evaluating the efficacies of locally delivered heparin and urokinase for reducing in-stent restenosis.

BACKGROUND: In-stent restenosis is primarily due to neointimal hyperplasia. Results from recent nonrandomized studies suggest that local delivery of heparin or urokinase to the site of angioplasty or stenting results in a lower rate of restenosis. OBJECTIVE: To determine whether local delivery of heparin or urokinase reduces in-stent restenosis. METHODS AND RESULTS: Thirty-three pigs were assigned randomly to one of three groups: controls (n = 9) administered local saline infusion, the heparin group (n = 15) administered local heparin (6000 u/10 min), and the urokinase group (n = 9) administered local urokinase (250000 u/10 min), via a local delivery catheter (Dispatch) at the site of subsequent stent implantation. Prior to local delivery, all of the animals were subjected to balloon injury (balloon:artery diameter ratio approximately or = 1.3) to facilitate intramural drug impregnation. After local therapy, one Palmaz-Schatz stent (mean stent: artery diameter ratio approximately or = 1.25) was implanted within the left anterior descending coronary artery. The degree of neointimal hyperplasia was evaluated 4 weeks later by angiography (as the maximal percentage diameter stenosis) and histology (as the maximal neointimal area stenosis). We found no difference in percentage diameter stenosis (46 +/- 18% control, 42 +/- 27% heparin group, and 37 +/- 20% urokinase group, P = 0.7) and corrected neointimal area (1.06 +/- 0.42 mm2 control, 0.94 +/- 0.29 mm2 heparin, and 0.88 +/- 0.26 mm2 urokinase group, P = 0.7) among groups at follow-up. The activated clotting time rose slightly for heparin-treated animals, suggesting that systemic delivery had occurred, whereas fibrinogen levels did not change in urokinase-treated animals. CONCLUSIONS: Local deliveries of heparin and urokinase via the Dispatch catheter, at the chosen dosages, do not reduce in-stent neointimal hyperplasia in this porcine model.

Animals↗

Altered compliance and residual strain precede angiographically detectable early atherosclerosis in low-density lipoprotein receptor deficiency.

BACKGROUND: This study was performed to detect changes in vascular biomechanical properties early in atherogenesis. METHODS AND RESULTS: Age- and weight-matched LDL-receptor deficient Watanabe hypercholesterolemic male rabbits (Group I: n = 11) and normal rabbits (Group II: n = 11) were studied. Fasting plasma lipoprotein concentrations, aortic angiography and intravascular ultrasound, in vivo aortic compliance evaluation, ex vivo aortic residual strain measurements, aortic lipid content and histopathology were determined. Plasma cholesterol was increased 9.8 fold and aortic cholesterol content was increased from 20 to 43 fold in Group I compared to Group II, respectively (P < .00005). Angiography revealed no stenoses in either group, whereas intravascular ultrasound and histological studies of Group I showed small circumferential plaques with < 10% cross-sectional area involvement. The residual strain in Group I was significantly increased in the ascending thoracic aorta (22.1 +/- 6.9% versus 10.4 +/- 3.2% in Group II, P < .0001), descending thoracic aorta (15.7 +/- 7.2% versus 4.8 +/- 1.3% in Group II, P < .0001), and abdominal aorta (18.0 +/- 4.8% versus 8.3 +/- 6.3% in Group II, P < .005). Changes in residual strain were inversely correlated with the aortic cholesterol content in the ascending thoracic aorta (r = -.72; P = -.001), descending thoracic aorta (r = -.95; P < .001), and abdominal aorta (r = -.51; P = .019). CONCLUSIONS: Early atherosclerosis in LDL-receptor deficient rabbits, undetectable by angiography yet observed by intravascular ultrasound imaging and histology, is associated with marked changes in ex vivo residual strain. Alterations in vascular biomechanical properties, associated with changes in cholesterol content, may have physiologic consequences and may be useful in detecting and quantitating early atherosclerosis.

Animals↗

Intravascular ultrasound to discern device-specific effects and mechanisms of restenosis.

Restenosis continues to be the "Achilles heel" of transcatheter interventions. While attempts to reduce restenosis by inhibiting cellular proliferation through pharmacologic or mechanical means have been unsuccessful, stents, which inhibit acute recoil and chronic remodeling, have been shown convincingly to reduce restenosis in 2 randomized clinical trials. Intravascular ultrasound (IVUS) allows transmural, tomographic imaging of coronary arteries in humans in vivo to subdivide restenosis into the two basic underlying components: tissue proliferation and arterial remodeling. In studies performed at the Washington Hospital Center, in nonstented lesions 73% of late lumen loss was due to arterial remodeling (a decrease in arterial, or external elastic membrane cross-sectional area) and 27% was due to tissue growth (an increase in plaque plus media cross-sectional area). These findings were confirmed by 2 other studies: the Optimal Atherectomy Restenosis Study (OARS) and the Serial Ultrasound analysis of REstenosis (SURE) Trial. IVUS was also used to study the mechanisms by which stents reduce restenosis. Stents created a larger final lumen cross-sectional area and, for all practical purposes, abolished arterial remodeling to offset a stent-related increase in neointimal tissue accumulation. Neointimal hyperplasia is solely responsible for in-stent restenosis and therefore appears to be a pure model for studying strategies to limit tissue proliferation.

Angioplasty, Balloon, Coronary↗

Increased basal tone and hyperresponsiveness to acetylcholine and ergonovine in spasm-related coronary arteries in patients with variant angina.

We compared the basal coronary artery tone and the constrictive responses to acetylcholine (Ach) and ergonovine (Erg) among three groups of patients: 31 patients (group 1) with variant angina in whom spasm was provoked by low doses of acetylcholine (intracoronary 20 micrograms) or ergonovine (intravenous 50 micrograms); 35 patients (group 2) in whom spasm was provoked by higher doses of acetylcholine (intracoronary 100 micrograms) or ergonovine (intravenous cumulative dose of 350 micrograms); and 26 control subjects. Patients with variant angina in whom spasm was provoked by low doses of acetylcholine or ergonovine, had a higher incidence of coexisting angiographic evidence of coronary artery disease, multi-vessel spasm and more frequent episodes of angina. The basal coronary artery tone at the spastic and non-spastic sites of the spasm-related artery was significantly elevated in group 1 compared to group 2 (44 +/- 17 vs. 14 +/- 11% and 26 +/- 14 vs. 16 +/- 10%, respectively, P < 0.05), but not in the non-spasm related artery. The magnitude of vasoconstrictive responses to acetylcholine and ergonovine at the non-spastic sites was also greater in group 1 than in group 2 and the control groups (acetylcholine: 40 +/- 20 vs. 26 +/- 11, 27 +/- 12%; ergonovine: 37 +/- 18 vs. 12 +/- 8, 13 +/- 10%, respectively, P < 0.05). However, the basal coronary artery tone was not elevated at the spastic and non-spastic sites in group 2 compared to that in the control subjects. These findings suggest that the basal coronary artery tone is increased in patients with variant angina, with increased frequency of angina suggestive of higher disease activity at the spastic and non-spastic sites of the spasm-related artery, and this may be related to pathogenesis of coronary artery spasm.

Acetylcholine↗