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C Bauters

Publications and source records attributed to C Bauters.

At least 109 records · Page 6Linked to original sources
PubMed1995

Site-specific therapeutic angiogenesis after systemic administration of vascular endothelial growth factor.

PURPOSE: Recent experimental studies have established the feasibility of therapeutic angiogenesis; in all cases, this has been achieved with local administration of angiogenic growth factors. This study was designed to investigate the hypothesis that systemic administration of an angiogenic growth factor specifically mitogenic for endothelial cells--vascular endothelial growth factor (VEGF)--could augment collateral vessel development in a rabbit ischemic hindlimb model. METHODS: Ten days after the ligation of the external iliac artery and excision of the common and superficial femoral arteries in one limb of New Zealand white rabbits, heparin (800 IU, n = 13), VEGF (1 mg, n = 3; 5 mg, n = 5), heparin (800 IU) + VEGF (1 mg, n = 5; 5 mg, n = 7), or saline solution (n = 8) was injected as a single bolus in a marginal ear vein. Collateral vessel formation and limb perfusion were assessed 10 and 30 days after treatment. RESULTS: Animals in both VEGF-treated groups had a significantly higher (p < 0.01) increase in calf blood pressure ratio at day 10 (control, 0.44 +/- 0.02; heparin, 0.47 +/- 0.02; VEGF, 0.60 +/- 0.01; heparin+VEGF, 0.61 +/- 0.02) and day 30 (control, 0.49 +/- 0.05; heparin, 0.48 +/- 0.02; VEGF, 0.70 +/- 0.03; heparin+VEGF, 0.73 +/- 0.03). Both VEGF-treated groups had a significantly higher (p < 0.05) angiographic score at day 30 (control, 0.28 +/- 0.01; heparin, 0.28 +/- 0.01; VEGF, 0.37 +/- 0.01; heparin+VEGF, 0.38 +/- 0.02). Maximum flow reserve at day 30 in the ischemic limb was higher (p < 0.05) in VEGF-treated rabbits (control, 1.87 +/- 0.07; heparin, 1.92 +/- 0.08; VEGF, 2.42 +/- 0.16; heparin+VEGF, 2.33 +/- 0.12). Capillary density was higher (p < 0.01) in the ischemic muscles of VEGF-treated rabbits (control, 156 +/- 10/mm2; heparin, 178 +/- 8/mm2; VEGF, 230 +/- 10/mm2; heparin+VEGF, 233 +/- 8/mm2). CONCLUSIONS: This series of in vivo experiments demonstrates that intravenous administration of VEGF, with or without heparin, results in both anatomic and physiologic evidence of enhanced collateral vessel formation in the rabbit ischemic hindlimb. Single-bolus systemic administration of VEGF may be a feasible therapeutic strategy in patients with lower-extremity ischemia.

Animals↗
PubMed1995

Restenosis after coronary angioplasty.

The major disadvantage of using percutaneous transluminal coronary angioplasty to treat patients with atherosclerotic coronary disease is the frequent occurrence of restenosis after an initially successful procedure. Studies in animals and histological observations in man have demonstrated that restenosis is characterized by neointimal hyperplasia due to smooth muscle cell proliferation and to the synthesis of extracellular matrix. Improvements in technology or pharmacological interventions have had no significant impact on the rate of restenosis. In spite of our increased understanding of the molecular mechanisms of restenosis. no effective treatment is available at the present time. Gene therapy, which has produced encouraging initial results in experimental models, may provide a solution in the medium term.

Angioplasty, Balloon, Coronary↗
PubMed1995

Two-pronged antiplatelet therapy with aspirin and ticlopidine without systemic anticoagulation: an alternative therapeutic strategy after bailout stent implantation.

BACKGROUND: Intracoronary stent implantation for failed angioplasty is associated with a relatively high incidence of coronary and peripheral complications. On the basis of previous clinical and experimental data, we investigated a protocol of intensive antiplatelet therapy, with aspirin (200 mg) and ticlopidine (500 mg), without oral anticoagulation, and with only periprocedural heparin, after stent implantation. METHODS: Between November 1993 and May 1994, 650 patients underwent balloon angioplasty in our institution. Stent implantation was attempted in 45 patients because of acute (58%) or threatened acute (22%) closure, or because the result of the primary angioplasty was inadequate (9%). RESULTS: Stents were successfully implanted in 42 (93%) patients. Two patients were not enrolled in the protocol (referring physician preference in one, metallic heart valve prosthesis in the other). In the remaining 40 patients, two sustained Q-wave infarctions and three sustained non Q-wave infarctions, which were already established at the time of stent implantation. No further clinical events occurred during hospitalization. During follow-up (mean 3.2 months) none of the patients died and none developed unstable angina or myocardial infarction. Ticlopidine-related rash occurred in two patients who were consequently put on warfarin therapy instead. CONCLUSIONS: Antiplatelet therapy with ticlopidine and aspirin, without systemic anticoagulation, appears to be a promising alternative to the classical approach with heparin and warfarin therapy, which requires intensive biological monitoring. This approach considerably simplifies patient management, and it could reduce the need for prolonged hospitalization.

Aged↗
PubMed1995

Time course of increased cellular proliferation in collateral arteries after administration of vascular endothelial growth factor in a rabbit model of lower limb vascular insufficiency.

Proliferation of vascular cells has been previously shown to contribute to spontaneous development of coronary collaterals. Recent studies from several laboratories have established that collateral artery growth in both the heart and limb can be enhanced by administration of angiogenic growth factors, or therapeutic angiogenesis. In this study, we sought (1) to define the extent and time course of endothelial cell (EC) and smooth muscle cell (SMC) proliferation accompanying spontaneous collateral development during limb ischemia and (2) to determine the extent to which proliferative activity of ECs and SMCs is augmented during therapeutic angiogenesis with vascular endothelial growth factor (VEGF), a heparin-binding EC-specific mitogen. Ten days after induction of limb ischemia by surgically excising the femoral artery of rabbits, either VEGF (500 to 1000 micrograms) or saline was administered as a bolus into the iliac artery of the ischemic limb. Cellular proliferation was evaluated by bromodeoxyuridine labeling for 24 hours at day 0 (immediately before VEGF administration) and at days 3, 5, and 7 after VEGF, EC proliferation in the midzone collaterals of VEGF-treated animals increased 2.8-fold at day 5 (P < 0.05 versus control), and returned to baseline levels by day 7. SMC proliferation in midzone collaterals also increased 2.7-fold in response to VEGF (P < 0.05). No significant increase in EC or SMC proliferation was observed in either the stem or re-entry collaterals of VEGF-treated animals compared with untreated ischemic control animals. Reduction of hemodynamic deficit in the ischemic limb measured by lower limb blood pressure was documented at day 7 after VEGF (P < 0.01 versus untreated, ischemic control). These data thus (1) establish the contribution of cellular proliferation to collateral vessel development in limb ischemia and (2) support the concept that augmented cellular proliferation contributes to the enhanced formation of collateral vessels after therapeutic angiogenesis with VEGF.

Animals↗
PubMed1995

Angiotensin converting enzyme inhibition prevents proto-oncogene expression in the vascular wall after injury.

OBJECTIVES: Angiotensin converting enzyme (ACE) inhibitors reduce neointimal hyperplasia after balloon denudation, but the mechanisms are not completely understood. It has been demonstrated that nuclear oncogenes are induced in the vascular wall in the hours immediately after injury, and that the same genes are induced by angiotensin II in vascular smooth muscle cells. It has therefore been suggested that the effects of ACE inhibitors on the response of the vessel wall could be mediated by an inhibition of proto-oncogene expression. METHODS AND RESULTS: Sixteen New Zealand White rabbits were randomly assigned for histologic analysis to receive placebo (n = 9) or 1 mg/kg per day perindopril (n = 7). After treatment for 7 days balloon aortic injury was performed. The treatment was continued and the rabbits were killed 28 days after injury. In the perindopril group the neointimal cross-sectional area was significantly smaller than in the control group. Six untreated rabbits were used to assess the time course of proto-oncogene expression in the aortic wall after injury in the present model. After extraction, total aortic RNA was hybridized with myc, fos and jun probes. Based on the results, the effects of ACE inhibition on proto-oncogene expression were tested 1 h after balloon denudation. Accordingly, 24 rabbits were randomly assigned to pretreatment for 7 days with placebo or with 1 or 10 mg/kg per day perindopril (n = 8, for each group) and were killed 1 h after injury. Expression of c-myc was not altered by pretreatment. However, 1 mg/kg per day perindopril induced significant reductions of 50% in c-jun and 45% in c-fos expression compared with control. No additional effect was obtained with the higher dose. CONCLUSION: The effect of ACE inhibition on intimal hyperplasia is associated with a reduction in early cellular events such as c-fos and c-jun expression. These results suggest that potent ACE inhibition at the time of vascular injury may be required to limit the hyperplastic response of the vessel wall.

Animals↗
PubMed1995

Neointimal thickening after balloon denudation is enhanced by aldosterone and inhibited by spironolactone, and aldosterone antagonist.

OBJECTIVE: The aim was to examine the effects of aldosterone and of an aldosterone antagonist, spironolactone, on neointimal thickening in a rabbit model of balloon injury. METHODS: Eighteen rabbits underwent aortic and iliac balloon injury and were randomised to subcutaneous infusion of aldosterone (70 micrograms.kg-1.d-1) or vehicle solution for 28 d. Eighteen other rabbits were randomised to receive daily subcutaneous injections of spironolactone (50 mg.kg-1.d-1) or of vehicle for 7 d before injury and for 28 d after the procedure. All animals were then killed just after measurement of plasma renin activity and of arterial pressure. Vessels were fixed and five cross sections were analysed per rabbit (three aortic; two from iliac artery). Mean values of neointimal area and of the neointimal area/medial area ratio were calculated. RESULTS: Aldosterone treatment was associated with a decrease in renin activity and a non-significant increase in mean arterial pressure. Aldosterone significantly augmented the neointimal thickening in the iliac artery [0.42(SEM 0.07) v 0.24(0.03) mm2, P < 0.05] but not in the aorta [0.63(0.08) v 0.59(0.12) mm2, NS]. Spironolactone significantly inhibited intimal thickening, both in the iliac artery [0.09(0.02) v 0.29(0.01) mm2, P < 0.001] and in the aorta [0.31(0.03) v 0.59(0.06) mm2, P < 0.001]. Spironolactone administration was associated with an increase in renin activity and a decrease in mean arterial blood pressure. CONCLUSIONS: Aldosterone administration enhances neointimal thickening after injury and spironolactone, an aldosterone antagonist, is a potent inhibitor of neointimal thickening in the same model. This suggests a role for aldosterone in the pathophysiology of neointimal proliferation after balloon injury and for aldosterone antagonists in its prevention.

Aldosterone↗
PubMed1994

Effect of balloon inflation in angiographically normal coronary segments during coronary angioscopy: a quantitative angiographic study.

Visualization of coronary stenoses by coronary angioscopy is facilitated by inflating an occlusive cuff located near the distal end of the device to temporarily interrupt blood flow. In animal models, this procedure induces substantial endothelial denudation. Experimental studies show that endothelial denudation may lead to neointimal hyperplasia at the denuded site. This study was designed to determine whether angioscopy was associated with significant changes in lumen diameter at the site of cuff inflation. We studied 52 consecutive patients undergoing coronary angioscopy. We measured with use of quantitative edge-detection angiography [computer-assisted evaluation of stenosis and restenosis (CAESAR) system] the mean and minimal lumen diameters at the site of cuff inflation localized by filming the inflated cuff during angioscopy and at control non-instrumented segments on angiograms performed before angioscopy, after angioscopy, and at 6 months follow-up. Follow-up angiograms were performed in 80% of eligible patients. At follow-up, the mean (3.22 +/- 0.54 mm) and minimal (2.76 +/- 0.58 mm) diameters of the segment exposed to the inflated cuff were not significantly different from the equivalent values (3.22 +/- 0.58 and 2.75 +/- 0.61 mm) before angioscopy. No significant changes occurred in the mean or minimal diameters of the control segments over the same period. The late change (follow-up minus pre-angioscopy) in mean lumen diameter at the cuff inflation site (-0.005 +/- 0.18 mm) was not significantly different from that at the control site (0.004 +/- 0.20 mm).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

[Silent ischemia].

Silent myocardial ischaemia is a very common phenomenon in patients with coronary artery disease. It may occur in patients with clinical manifestations of angina, be detected during the post-myocardial infarction period or in patients totally asymptomatic. Whatsoever, it is well demonstrated that silent myocardial ischaemia has a very potent prognostic value. Therapeutic implications are similar to those in symptomatic ischaemia. Indications for myocardial revascularization by mean of angioplasty or bypass grafting may be discussed and depend on ventricular function and extension of coronary lesions.

Angina Pectoris↗
PubMed1994

Physiological assessment of augmented vascularity induced by VEGF in ischemic rabbit hindlimb.

This study was designed to assess the physiological consequences of augmented vascularity induced by administration of vascular endothelial growth factor (VEGF), an endothelial cell-specific mitogen, in a rabbit model of hindlimb ischemia. Ten days after excision of the common and superficial femoral arteries from one hindlimb of 24 New Zealand White rabbits, VEGF (n = 15) or saline (control; n = 9) was selectively injected into the ipsilateral internal iliac artery. Limb perfusion was evaluated immediately pre-VEGF (baseline) and again at days 10 and 30. A Doppler guide wire was advanced to the internal iliac artery to record flow velocity at rest and at maximum flow velocity provoked by intra-arterial injection of papaverine. At baseline and at day 10, no differences in flow parameters were observed between the control and the VEGF-treated animals. By day 30, however, flow at rest (P < 0.05), maximum flow velocity (P < 0.001), and maximum blood flow (P < 0.001) were all significantly higher in the VEGF-treated group. These physiological findings complement previous-anatomic studies by providing evidence that a single intra-arterial bolus of VEGF augments flow, particularly maximum flow, in the rabbit ischemic hindlimb. These data thus support the notion that VEGF administration represents a potential treatment strategy for certain patients with lower extremity ischemia.

Animals↗
PubMed1994

Angiopeptin inhibits oncogene induction in rabbit aorta after balloon denudation.

BACKGROUND: Angiopeptin, a synthetic cyclic octapeptide analogue of somatostatin, reduces neointimal hyperplasia after balloon denudation of rabbit aorta if administered before injury. The aim of this study was to analyze the effect of angiopeptin pretreatment on the level of expression of the c-fos and c-jun protooncogenes, early markers of smooth muscle cell proliferation, after balloon denudation of rabbit aorta. METHODS AND RESULTS: For histological analysis of the effect of angiopeptin on neointimal thickening after aortic balloon denudation, rabbits were randomized into three groups: group 1 (controls), twice-daily injections of saline begun 24 hours before balloon denudation (n = 9); group 2, twice-daily injections of angiopeptin 10 micrograms/kg begun 24 hours before balloon denudation (n = 9); and group 3, twice-daily injections of angiopeptin 10 micrograms/kg begun 1 hour after balloon denudation (n = 7). The degree of neointimal thickening 28 days after balloon denudation was significantly less in group 2 than in group 1 (neointimal area: group 1, 0.59 +/- 0.11 mm2; group 2, 0.22 +/- 0.05 mm2; P < .05. Neointima/media: group 1, 0.85 +/- 0.17; group 2, 0.23 +/- 0.05; P < .05). When angiopeptin was started 1 hour after denudation (group 3), however, the neointimal area (0.52 +/- 0.09 mm2) and the neointima/media ratio (0.76 +/- 0.10) were not statistically different from the control group. For analysis of protooncogene induction, rabbits received twice-daily subcutaneous injections of saline (n = 7), angiopeptin 10 micrograms/kg (n = 8), or angiopeptin 100 micrograms/kg (n = 4) begun 24 hours before balloon denudation. The animals were killed 30 minutes after balloon denudation, and total aortic RNA was hybridized with fos and jun probes. Expression of c-fos and c-jun was detected 30 minutes after injury; angiopeptin pretreatment at 20 micrograms.kg-1.d-1 induced a 41% reduction in c-fos expression and a 42% reduction in c-jun expression compared with control animals. The inhibitory effect at the higher dose of angiopeptin was similar. CONCLUSIONS: Our results show that the inhibitory effect of angiopeptin on neointimal thickening is related to events that occur very early after injury and suggest that the inhibition of smooth muscle cell activation may be responsible, at least in part, for this effect.

Animals↗
PubMed1994

Exercise-induced ST-segment depression in patients without restenosis after coronary angioplasty. Relation to preprocedural impaired left ventricular function.

BACKGROUND: ST-segment depression during exercise testing is frequently observed in the absence of restenosis after coronary angioplasty. METHODS AND RESULTS: We studied the determinants of this phenomenon in 70 consecutive patients with unstable angina related to a single left anterior descending coronary artery lesion who had successful angioplasty without restenosis (< 50% stenosis by quantitative angiography). We compared preangioplasty clinical, angiographic, and hemodynamic variables in the group with positive (ExT Pos, n = 35; ST depression, 2.3 +/- 0.9 mm) and negative (ExT Neg, n = 35; ST depression, 0.3 +/- 0.5 mm) results on exercise testing at follow-up angiography. At this time, minimal lumen diameter (1.7 +/- 0.4 mm) and mean residual stenosis (34 +/- 11%) in the ExT Pos group were not significantly different from the values (1.9 +/- 0.5 mm, 38 +/- 10%) in the ExT Neg group. Before angioplasty, the ExT Pos group had a lower ejection fraction (63 +/- 8% versus 68 +/- 9%, P < .05), more marked anterior hypokinesis estimated by the extent of anterior wall contraction on quantitative ventriculography (P < .05), and a greater end-systolic volume (30 +/- 11 versus 25 +/- 9 mL/m2, P < .05) than the ExT Neg group. At follow-up angiography, regional anterior wall motion was normal in 68 patients (97%). Anterior hypokinesis before angioplasty was strongly associated (P < .01) with a positive exercise test at control (71% compared with 31% in patients with normal wall motion before angioplasty). CONCLUSIONS: In the absence of significant epicardial stenosis after angioplasty, ST-segment depression is strongly associated with the presence of preprocedural regional ventricular dysfunction that has recovered at follow-up angiography.

Aged↗
PubMed1994

Long-term oral administration of L-arginine reduces intimal thickening and enhances neoendothelium-dependent acetylcholine-induced relaxation after arterial injury.

BACKGROUND: Nitric oxide (NO), in addition to its potent vasorelaxant properties, may participate in growth regulation of cultured smooth muscle cells. It was recently demonstrated that in vivo endothelial injury induces the production of NO from L-arginine in the arterial wall. METHODS AND RESULTS: We studied the effects of long-term administration of L-arginine, the precursor of NO, on neointimal thickening and on neoendothelium-dependent vasorelaxation 4 weeks after balloon denudation of normocholesterolemic rabbit iliac arteries. Rabbits were fed with either a standard diet or a diet supplemented with L-arginine (2.25%) in their drinking water 3 days before and during 4 weeks after balloon denudation. The effectiveness of L-arginine supplementation was confirmed by measurement of plasma arginine levels. L-Arginine had no effect on hemodynamic parameters. All animals were killed 4 weeks after balloon denudation, and a digital histomorphometric analysis of three serial nonconsecutive histological cross sections per iliac artery was performed. Intimal thickening was reduced (P < .05) from 0.43 +/- 0.08 (SE) mm2 in controls (n = 8) to 0.24 +/- 0.02 mm2 in treated animals (n = 8). Ten animals (n = 5 in each group) were used for in vitro vasoreactivity assessment 4 weeks after balloon denudation. Neoendothelium-dependent acetylcholine-induced relaxation (10(-8) mol/L to 3.10(-5) mol/L) in treated animals (Emax = -24.1 +/- 5.5%) was significantly greater than in controls (Emax = -8.9 +/- 2.2%). Endothelium-independent relaxation did not differ between groups (Emax = -58.1 +/- 6.5% in L-arginine-supplemented animals versus -52.9 +/- 6.8% in controls). CONCLUSIONS: Our results demonstrate that L-arginine, a precursor of NO, reduces neointimal thickening after balloon denudation and improves neoendothelial-dependent acetylcholine-induced relaxation.

Acetylcholine↗
PubMed1994

Evidence for time-dependent activation of monocytes in the systemic circulation in unstable angina but not in acute myocardial infarction or in stable angina.

BACKGROUND: Platelet activation plays a pivotal role in the pathogenesis of acute coronary disease. Monocytes are involved in the progression of atherosclerosis and are potent activators of blood coagulation through their ability to synthesize tissue factor (TF). The aim of this study was to compare markers of monocyte and coagulation activation in the systemic blood of patients with unstable angina, acute myocardial infarction, or stable angina. METHODS AND RESULTS: We studied 26 patients with unstable angina (10 +/- 5 hours after the onset of the last episode of pain), 18 patients with acute myocardial infarction (5 +/- 4 hours after the onset of pain), and 34 patients with stable angina. We measured levels of TF expression in peripheral blood mononuclear cells (isolated by gradient centrifugation and incubated for 16 hours, with or without endotoxin stimulation), levels of plasma prothrombin fragment 1 + 2 (F1 + 2), and levels of fibrinogen in peripheral blood. In patients with unstable angina, both stimulated and unstimulated cells exhibited higher levels of TF expression than in patients with stable angina (P = .0001). In patients with acute myocardial infarction, monocyte TF activity did not differ from that in patients with stable angina. Mean levels of F1 + 2 and of fibrinogen did not differ significantly between groups. Only in the unstable angina group, a modest correlation was found between fibrinogen (r = .72, P = .005) and F1 + 2 levels (r = .54, P = .001) levels and the degree of monocyte TF expression. In patients with unstable angina, monocyte TF expression (both stimulated and unstimulated, assessed by biological activity and by antigen techniques) and fibrinogen levels were correlated with the time elapsed from the beginning of the most recent episode of pain (.61 < r < .72, .02 < P < .0001). By contrast, there was no correlation between these variables and the time from onset of pain in patients with acute myocardial infarction. CONCLUSIONS: A time-dependent activation of systemic monocytes and a time-dependent increase in fibrinogen levels occurs in unstable angina but not in myocardial infarction. These findings provide further evidence that a specific inflammatory process occurs in unstable angina. Further studies are required to determine whether monocyte activation is a cause or a consequence of plaque instability in patients with unstable angina and to clarify the interrelations between platelet and monocyte activation in these circumstances.

Adult↗
PubMed1994

[Predictive factors of primary success after coronary angioplasty. Qualitative and quantitative angiography of 3679 coronary stenosis before and after dilatation].

This study summarises the authors' experience of the prediction of primary success of coronary balloon angioplasty. A qualitative and quantitative angiographic study of 3679 coronary stenoses was undertaken before and after dilatation. Total occlusions before angioplasty and dilatations of saphenous vein bypass grafts were excluded. Two parameters were noteworthy: the occurrence of acute occlusion of the lesion during or immediately after angioplasty and the degree of residual stenosis as assessed by quantitative angiography. After multivariate analysis, 3 factors seemed strongly predictive of the risk of acute occlusion: the percentage stenosis before angioplasty, a left coronary artery stenosis and stenosis situated at the point of angulation of an artery. Quantitative angiographic studies identified 4 factors predictive of significant residual stenosis: the percentage stenosis before angioplasty, the irregularity of the contours of the lesion stenosis situated at the point of angulation of an artery and the presence of calcification. This study therefore shows at least two important discordances with the ACC/AHA morphological classification of coronary stenosis: firstly, excentricity would not seem to be a risk factor for primary failure of angioplasty and, secondly, excluding total occlusions, the percentage coronary stenosis before angioplasty as assessed by quantitative coronary angiography would seem to be the main predictive factor of both the risk of occlusion and the degree of residual stenosis.

Aged↗
PubMed1993

Discordant results of visual and quantitative estimates of stenosis severity before and after coronary angioplasty.

The ability to accurately estimate the severity of epicardial coronary stenoses is critical in the assessment of the immediate and long-term results of percutaneous transluminal coronary angioplasty (PTCA). We prospectively compared visual estimates, performed by experienced interventional cardiologists, with computerized quantitative angiographic measurements of stenosis severity in a group of patients (n = 305) before, immediately after and 6 months after PTCA. Before PTCA the visual estimate of the mean (+/- SD) percentage stenosis severity, 80.6 (+/- 9.7)%, was significantly (P < 0.001) higher than the equivalent value, 73.4 (+/- 11.1)%, obtained with use of quantitative angiography. Immediately after PTCA the visual estimate of the mean residual stenosis, 18.8 (+/- 12.3)%, was significantly (P < 0.0001) lower than the equivalent quantitative estimate, 37.4 (+/- 14)%. Additionally, the residual stenosis was more frequently (18% vs. 3%) classified as significant (> 50%) by quantitative angiography. At follow-up, quantitative measurements of stenosis severity showed a Gaussian distribution with a mean of 54.8 (+/- 21)%, whereas visual estimates had a bimodal distribution with populations greater than 70% and less than 50%. Visual estimates provide an inaccurate assessment of the immediate and medium term results of PTCA. Quantitative measurements suggest that the immediate results of PTCA are frequently misclassified as successful by the operator. Conversely, restenosis rates are underestimated by the operators suggesting that a more objective method must be used in trials to assess the impact of new therapies on the rate of restenosis.

Angioplasty, Balloon, Coronary↗