YUKIO OZAKI

Objective - To examine the vasoconstrictor response to ergonovine and the vasodilator response to isosorbide dinitrate in spastic and non-spastic coronary segments from 31 patients undergoing serial angiographic follow up of variant angina. Methods - Coronary angiograms and ergonovine provocation tests were repeated at an interval of 45 (SD 15) months apart. While all 31 patients showed a positive response to ergonovine initially, vasospastic responsiveness persisted in only 16 patients at follow up (group 1) and not in the other 15 patients in whom symptoms of variant angina had resolved (group 2). Mean luminal diameter of 170 normal or near normal entire coronary segments (American Heart Association classification) were measured (a) at baseline, (b) after the administration of ergonovine, and (c) after the administration of isosorbide dinitrate, during both the initial and follow up angiograms using a computer based quantitative angiography analysis system (CAAS II). Results - In vasospastic patients (initial and follow up angiograms in group 1, and initial angiogram in group 2), basal tone was significantly higher in spastic segments compared to adjacent segments or segments in non-spastic vessels. The diagnostic sensitivity and specificity at 20% increase in basal coronary tone for the prediction of vasospasm were 77% and 73%, respectively. Conclusions - Coronary artery tone may change in proportion to the activity of variant angina over several years. Contrary to some previous reports, the estimation of basal coronary tone may be useful in the assessment of vasospastic activity in patients with variant angina.

Background Automated stenosis analysis is a common feature of commercially available quantitative coronary angiography (QCA) systems, allowing automatic detection of the boundaries of the stenosis, interpolation of the expected dimensions of the coronary vessel at the point of obstruction, and angiogaphically derived estimation of atheromatous plaque size. However, the ultimate meaning of this type of analysis in terms of the degree of underlying atherosclerotic disease remains unclear. We investigated the relationship between stenosis analysis performed with QCA and the underlying degree of atherosclerotic disease judged by intracoronary ultrasound (ICUS) imaging. Methods and Results In 40 coronary stenoses, automated identification of the sites of maximal luminal obstruction and the start of the stenosis was performed with QCA by use of curvature analysis of the obtained diameter function. Plaque size at these locations also was estimated with ICUS, with an additional ICUS measurement immediately proximal to the start of the stenosis. Crescentlike distribution of plaque, indicating an atheroma-free are of the arterial wall, was recorded. At th site of the obstruction, total vessel area measured with ICUS was 16.65+/-4.04 mm(2), whereas an equivalent measurement obtained from QCA-interpolated reference dimensions was 7.48+/-3.30 mm(2) (P=.0001). Plaque area derived from QCA data was significantly less than that calculated from ICUS (6.32+/-3.21 and 13.29+/-4.22 mm(2), respectively; mean difference, 6.92+/-4.43 mm(2); P=.0001). At the start of the stenosis identified by automated analysis, ICUS plaque area was 9.38+/-3.17 mm(2), and total vessel area was 18.77+/-5.19 mm(2) (50+/-11% total vessel area stenosis). The arterial wall presented a disease-free segment in 28 proximal locations (70%) but in only 5 sites (12%) corresponding to the start of the stenosis and none at the obstruction (P=.0001). At the site of obstruction, all vessels showed a complete absence of a disease-free segment, and the atheroma presented a cufflike or all-around distribution with a variable degree of eccentricity. Conclusions At the site of maximal obstruction, QCA underestimated plaque size as measured with ICUS. Atherosclerotic disease was consistently present at the start of the stenosis and was used as a reference site by automated stenosis analysis. At the start of the stenosis, ICUS demonstrated a mean 50+/-11% total vessel area stenosis; with a characteristic loss of disease-free arcs of arterial wall present in proximal locations. Thus, the site identified by automated stenosis analysis as the start of the stenosis does not represent a disease-free site but rather the place where compensatory vessel enlargement fails to preserve luminal dimensions, a phenomenon that seems related to the observed loss of a remnant are of normal arterial wall.

The use of 2-dimensional intravascular ultrasound (2-D IVUS) to improve the outcome of coronary stenting has gained clinical acceptance, and recently 3-D IVUS has been introduced to clinical practice. However, there have been no comprehensive studies comparing the measurements of the coronary dimensions after stenting obtained by the different approaches of IVUS and quantitative coronary angiography. We examined the minimal luminal cross-sectional area of 38 stents using 2-D IVUS, 3-D IVUS, and 2 standard methods of quantitative coronary angiography, edge detection (ED) and videodensitometry (VD). Correlations between 2-D IVUS and ED (r = 0.72; p < 0.0001), VD (r = 0.87; p < 0.0001), and 3-D IVUS (r = 0.81; p < 0.0001) were higher than the correlations seen between 3-D IVUS and ED (r 0.58; p < 0.0005) and VD (r = 0.70; p < 0.0001). The measurements by 2-D and 3-D IVUS (8.32 +/- 2.50 mm(2) and 8.05 +/- 2.66 mm(2)) were larger than the values obtained by the quantitative angiographic techniques ED and VD (7.55 +/- 2.22 mm(2) and 7.27 +/- 2.21 mm(2)). Thus, concordance was seen among all of the 4 techniques, confirming the validity of using IVUS for determination of the minimal luminal cross-sectional area after coronary stenting. A particularly good correlation was found between VD and IVUS, perhaps because measurement of the luminal area is the basic quantification approach of both techniques, whereas the lower correlations of ED with IVUS and VD may be explained by the dependence of ED on the angiographic projections used, which is especially important in eccentric stent configurations.

Background The new, less shortening, self-expanding Wallstent is characterized by longitudinal flexibility, a protective membrane, a low profile, and a customized range of diameters (3.5 to 6.0 mm). The recent modification of the braiding angle of the Wallstent has resulted in a new device with less shortening on expansion and a concomitant reduction in radial force. We hypothesized that the enforced mechanical remodeling produced by the selection of an oversized Wallstent might result in improved accommodation of subsequent reactive intimal hyperplasia and prevention of chronic recoil of the vessel. Methods and Results To prove this hypothesis, we recently implanted 44 new, less shortening Wallstents in 35 native coronary arteries in 35 patients with acute or threatened closure after balloon angioplasty, according to a strategy of oversizing of Wallstent diameter and complete coverage of the lesion length. The initial and B-month follow-up angiograms were analyzed with a computer-based quantitative coronary angiography (QCA) system. Acute gain (minimal luminal diameter [MLD] post minus MLD pre) and late loss (MLD post minus MLD at follow-up) were examined. Stent deployment was successful in 44 of 44 attempts (100%). Nominal stent diameter used was 1.40 mm larger than the maximal vessel diameter. One patient (3%) with a dilated but unstented lesion proximal to the stented segment sustained a subacute occlusion on day 1 associated with myocardial infarction. Event-free survival at 30 days after stent implantation was 97% (34 of 35 patients). Of the 34 patients eligible for 6-month angiographic follow-up, 3 who were asymptomatic declined repeat angiography. MLD (and percent diameter stenosis [% DS]) changed from 0.83+/-0.50 mm (72%) pre through 3.06+/-0.48 mm (15%) post to 2.27+/-0.74 mm (28%) at follow-up. Acute gain was 2.23+/-0.63 mm, and late loss was 0.78+/-0.61 mm. Angiographic restenosis (>50% DS) was observed in 5 of 31 patients (16%) at 6 months, all of whom underwent repeat angioplasty. Thus, the overall event-free survival at 6-month follow-up was 83% (29 of 35 patients). Conclusions The oversized Wallstent implantation with complete coverage of the lesion length conveyed a favorable B-month clinical and angiographic outcome. The large acute gain obtained by the Wallstent afforded greater accommodation of the subsequent late loss. The enforced mechanical remodeling by oversized new Wallstents may result in prevention of acute and chronic recoil of the vessel wall and subsequently a lower restenosis rate at follow-up.

Coronary stents were developed to overcome the two main limitations of balloon angioplasty, acute occlusion and long-term restenosis. Coronary stents can tack back intimal flaps and seal the dissected vessel wall, thereby treating acute or threatened vessel closure after unsuccessful balloon angioplasty. After successful balloon angioplasty, stents can prevent late vessel remodeling (chronic vessel recoil) by mechanically enforcing the vessel wall and resetting the vessel size, resulting in a low incidence of restenosis. All currently available stents are composed of metal, and the long-term effects of their implantation in the coronary arteries are still not clear. Because of the metallic surface, they are also thrombogenic; therefore, rigorous antiplatelet or anticoagulant therapy is theoretically required. Furthermore, they have an imperfect compromise between scaffolding properties and flexibility, resulting in an unfavorable interaction between stents and unstable or thrombus-laden plaque. Finally, they still induce substantial intimal hyperplasia that may result in restenosis. Future stents can be made less thrombogenic by modifying the metallic surface or coating it with an antithrombotic agent or a membrane eluting an antithrombotic drug. The unfavorable interaction with the unstable plaque and the thrombus burden can be overcome by covering the stent with a biological conduit, such as a vein, or a biodegradable material that can be endogenous, such as fibrin, or exogenous, such as a polymer. Finally, the problem of persisting induction of intimal hyperplasia may be overcome with the use of either a radioactive stent or a stent eluting an antiproliferative drug.

Objective - To examine the vasoconstrictor response to ergonovine and the vasodilator response to isosorbide dinitrate in spastic and non-spastic coronary segments from 31 patients undergoing serial angiographic follow up of variant angina. Methods - Coronary angiograms and ergonovine provocation tests were repeated at an interval of 45 (SD 15) months apart. While all 31 showed a positive response to ergonovine initially, vasospastic responsiveness persisted in only 16 patients at follow up (group 1) and not in the other 15 patients in whom symptoms of variant angina had resolved (group 2). Mean luminal diameter of 170 normal or near normal entire coronary segments (American Heart Association classification) were measured (a) at baseline, (b) after the administration of ergonovine, and (c) after the administration of isosorbide dinitrate, during both the initial and follow up angiograms using a computer based quantitative angiography analysis system (CAAS II). Results - In vasospastic patients (initial and follow up angiograms in group 1, and initial angiogram in group 2), basal tone was significantly higher in spastic segments compared to adjacent segments or segments in non-spastic vessels. The diagnostic sensitivity and specificity at 20% increase in basal coronary tone for the prediction of vasospasm were 77% and 73%, respectively. Conclusions - Coronary artery tone may change in proportion to the activity of variant angina over several years. Contrary to some previous reports, the estimation of basal coronary tone may be useful in the assessment of vasospastic activity in patients with variant angina.

Limited information is provided by angiography on on plague morphology and composition before balloon angioplasty: Identification of plaques associated with reduced lumen gain or a high complication rate may provide the rationale for using alternative revascularization devices. We studied 60 patients with quantitative angiography and intracoronary ultrasound (ICUS) before and after balloon dilation. Angiography was used to measure transient wall stretch and elastic recoil. ICUS was used to investigate the mechanisms of lumen enlargement among different plaque compositions and in the presence of a disease-free wall (minimal thickness less than or equal to 0.6 mm). Compared with ultrasound, angiography underestimated the presence of vessel calcification (13% vs 78%), lumen eccentricity (35% vs 62%), and wall dissection (32% vs 57%). ICUS measurements showed that balloon angioplasty increased lumen area from 1.82 +/- 0.51 to 4.81 +/- 1.43 mm(2). Lumen enlargement was the result of the combined effect of an increase in the total cross-sectional area of the vessel (wall stretching, 43%) and of a reduction in the area occupied by the plaque (plaque compression or redistribution, 57%). Vessels with a disease-free wall had smaller lumen gain than other types of vessels (2.13 +/- 1.26 vs 3.59 +/- 1.51 mm(2), respectively, p <0.01). Wall stretching was the most important mechanism of lumen enlargement in vessels with a disease-free wall (79% vs 37% in the other vessels). Angiography revealed a direct correlation between temporary stretch and elastic recoil that was responsible for 26% of the loss of the potential lumen gain. Thus, lumen enlargement after balloon angioplasty is the combined result of wall stretch and plaque compression or redistribution. ICUS indicates that vessels with a remnant are of disease-free wall are dilated mainly by wall stretching compared with other types of vessels and are associated with a smaller lumen gain.

Objectives. This study was designed to examine whether oversized implantation of the new, less shortening Wallstent provides a more favorable long-term clinical and angiographic outcome in chronic total occlusions than does conventional coronary balloon angioplasty. Background. Restenosis and reocclusion remain major limitations of balloon angioplasty for chronic total occlusions. Enforced mechanical remodeling by implantation of the oversized Wallstent may prevent elastic recoil and improve accommodation of intimal hyperplasia. Methods. Lumen dimension was measured by a computer- based quantitative coronary angiography system (CAAS II). These measurements (before and after intervention and at 6-month follow-up) were compared between the groups with Wallstent implantation (20 lesions, 20 patients) and conventional balloon angioplasty (266 lesions, 249 patients) for treatment of chronic total occlusion. Acute gain (minimal lumen diameter after intervention minus that before intervention), late loss (minimal lumen diameter after intervention minus that at follow-up) and net gain (acute gain minus late loss) were examined. Results. Wallstent deployment was successful in all patients. High pressure intra-Wallstent balloon inflation (mean ± SD 14 ± 3 atm) was performed in all lesions. Although vessel size did not differ between the Wallstent and balloon angioplasty groups, acute gain was significantly greater in the Wallstent group (2.96 ± 0.55 vs. 1.61 ± 0.34 mm, p < 0.0001). Although late loss was also significantly larger in the Wallstent group (0.81 ± 0.95 vs. 0.43 ± 0.68 mm, p < 0.05), net gain was still significantly greater in this group (2.27 ± 1.00 vs. 1.18 ± 0.69 mm, p < 0.0001). Angiographic restenosis (≤50% diameter stenosis) occurred at 6 months in 29% of lesions in the Wallstent group and in 45% of those in the balloon angioplasty group (p = 0.5150). Conclusions. Implantation of the oversized Wallstent, with full coverage of the lesion length, ensures resetting of the vessel size to its original caliber before disease and allows greater accommodation of intimal hyperplasia and chronic vessel recoil. Wallstent implantation provides a more favorable short- and long- term clinical and angiographic outcome than does conventional balloon angioplasty for chronic total occlusions.

We examined the influence of vessel size using an intention-to-treat approach in 259 patients who underwent stent implantation and in 257 patients who underwent balloon angioplasty alone in the BENESTENT trial. In the stented population, smaller vessel size was associated with a higher stent:vessel ratio, a greater relative gain and a greater subsequent loss index, and a higher risk of adverse cardiac events. In the balloon angioplasty population small vessel size conveyed an increased requirement for revascularization but did not increase the risk of procedural failure or myocardial infarction during follow-up. Logistic regression indicated that decreasing vessel size (as a continous variable) was associated with an increasing risk of a cardiac event for both the stent and balloon angioplasty populations.

To determine the reliability of geometric (edge-detection) quantitative coronary angiographic analysis (QCA) of restenosis within a new Cordis tantalum stent, QCA and intracoronary ultrasound (ICUS) measurements were compared in both an experimental restenosis model and in the clinical follow-up of patients. In the experimental series, PlexiglasTM phantom vessels with concentric stenosis channels ranging from 0.75 to 3.0 mm in diameter and with a reference diameter of 3.0 mm were imaged both before and after their insertion in tantalum stents. In the clinical series, the agreement of QCA and ICUS measurements were studied in 23 patients who had undergone coronary implantation of the new tantalum stent and in 23 patients who had undergone balloon angioplasty 6 months previously. The reliability of QCA declined in the presence of the radiopaque stent (accuracy of QCA decreased from -0.07 to -0.12 mm), whereas the reliability of lumen measurements by ICUS was independent of the presence of the radiopaque stent (-0.12 and -0.13 mm). Without the stent, the average minimal luminal diameter (MLD) obtained by QCA of the 1.00 mm Plexiglas vessel was 1.00 ± 0.01 mm, and the 3.00 mm reference vessel diameter was 2.81 ± 0.05 mm, providing a 64 ± 1% diameter stenosis. After introduction of the stent, the average MLD and reference vessel diameter were 0.99 ± 0.06 and 3.36 ± 0.17 mm, respectively, providing a diameter stenosis of 71 ± 2%. ICUS measurements (2.77 mm) of the reference vessel diameter (3.00 mm) were unaffected by the presence of the stent. Agreement of ICUS and QCA measurements (ICUS - QCA) was poorer in patients who had undergone balloon angioplasty (0.68 ± 0.42 mm) than in patients who had stent implantation (-0.05 ± 0.42 mm). In the 6-month follow-up of patients who had undergone implantation of a highly radiopaque Cordis tantalum stent, assessment of restenosis was reliably quantified by QCA with the use of the MLD rather than the percent diameter stenosis. Although ICUS measurements are unaffected by the radiopaque stent, the mechanical problem of ICUS catheter wedging in stenoses of < 1.00 mm and the substantial cost of ICUS catheters will restrict the widespread application of ICUS for the assessment of intrastent restenosis. © 1995.

Background Whether focal vasospasticity plays a pathogenic role in the progression or regression of corollary atherosclerosis is unknown. To determine whether evidence for such a role exists, we studied long-term changes in coronary luminal measurements in patients with vasospastic angina. Methods and Results Quantitative coronary angiography and repeated ergonovine provocation tests were performed 45+/-16 months apart in 30 patients. All patients had vasospastic anginal symptoms and coronary spasm on the initial provocation test. Of the 30 patients, 16 had persistent symptoms of vasospastic angina and showed coronary spasm at the same site on the follow-up angiogram (group 1), while the remaining 14 whose vasospastic anginal symptoms disappeared at follow-up demonstrated a negative response to ergonovine on the followup tests (group. 2). There was no significant difference in patients' baseline characteristics between the two groups. Long-term changes in minimal (MLD) and mean (MEAN) luminal diameter were measured (in millimeters) after administration of isosorbide dinitrate in 19 spastic and 93 nonspastic segments in group 1 and in 17 previously spastic and 81 nonspastic segments in group 2. Both MLD and MEAN were measured in 210 coronary segments of the 30 patients at baseline and after administration of ergonovine and isosorbide dinitrate by use of a computer-based quantitative coronary angiography system. Stenosis progression and regression of individual lesions were defined as a change in MLD of greater than or equal to 0.40 mm. In group 1, both the MLD and MEAN of 19 spastic segments were significantly smaller (progression) at follow-up compared with the initial angiogram (MLD, 2.21+/-0.54 initially versus 1.95+/-0.65 at follow-up, P<.01; MEAN, 2.80+/-0.56 initially versus 2.56+/-0.58 at follow-up, P<.01), whereas the MLD and MEAN of 93 nonspastic segments in group 1 were not significantly different between the initial and follow-up angiograms (MLD, 2.47+/-0.67 initially Versus 2.44+/-0.69 at follow-up, P=NS; MEAN, 2.96+/-0.69 initially versus 2.91+/-0.68 at followup, P=NS). In group 2 the MLD of the 17 previously spastic segments significantly improved (regression) at follow-up (MLD, 1.99+/-0.68 initially versus 2.24+/-0.54 at follow-up, P<.05); the MLD and, MEAN of the 81 nonspastic segments were not significantly different (MLD, 2.36+/-0.59 initially versus 2.39+/-0.60 at follow-up, P=NS; MEAN, 2.81+/-0.58 initially versus 2.81+/-0.61 at follow-up, P=NS). In group 1, significant stenosis progression of individual lesions was observed more frequently at spastic than nonspastic segments (6 of 19 versus 10 of 93, P<.05), whereas stenosis regression was observed in no spastic and 3 nonspastic segments (P=NS). In group 2, stenosis progression was observed at I previously spastic segment and 4 nonspastic segments (P=NS), while significant stenosis regression of individual lesions was seen more commonly in previously spastic than nonspastic segments (6 of 17 versus 7 of 81, P<.01). Conclusions These results have demonstrated in patients an association between persistent vasospastic activity and progression of atherosclerosis and an association between cessation of vasospastic activity and regression of atherosclerosis.

The reliability of quantitative coronary angiography (QCA) measurements is of fundamental importance for the study and practice of interventional cardiology, In vivo validation results have consistently reported a tendency for QCA systems to overestimate small luminal diameters, Such a systematic error may result in the underestimation of luminal gain during intracoronary procedures and in the underestimation of progression of coronary artery disease during longitudinal studies. We report the in vivo validation results of an experimental adaptive edge-detection algorithm that was developed to reduce overestimation of small luminal diameters by incorporating a dynamic function of variable kernel size of the derivative operator and variable weighting of the first and second derivatives of the brightness profile, The results of the experimental algorithm were compared to those of the conventional parent edge detection algorithm with fixed parameters. Dynamic adjustment of the edge-detection algorithm parameters was found to improve measurements of small (<0.8-mm) luminal diameters as evidenced by an intercept of +.07 mm for the algorithm with variable weighting compared to +0.21 mm for the parent algorithm with fixed weighting, A slope of <1 was found for both the parent and experimental algorithms with subsequent underestimation of large luminal diameters. Systematic errors in a QCA system can be identified and corrected by the execution of objective in vivo validation studies and the consequent refinement of edge-detection algorithms, The overestimation of small luminal diameters may be overcome by the incorporation of a dynamic edge-detection algorithm, Further refinements in edge-detection algorithms will be required to address the issue of underestimation of large luminal diameters before the absolute values derived from QCA measurements can be considered accurate over the full range of clinically encountered luminal diameters. (C) 1995 Wiley-Liss, Inc.

Background Postmortem-derived findings support the common beliefs that lipid-rich coronary plaques with a thin, fibrous cap are prone to rupture and that rupture and superimposed thrombosis are the primary mechanisms causing acute coronary syndromes. In vivo imaging with intracoronary techniques may disclose differences in the characterization of atherosclerotic plaques in patients with stable or unstable angina and thus may provide clues to which plaques may rupture and whether rupture and thrombosis are active. Methods and Results We assessed the characteristics of the ischemia-related lesions with coronary angiography and intracoronary angioscopy and determined their compositions with intracoronary ultrasound in 44 patients with unstable and 23 patients with stable angina. The angiographic images were classified as noncomplex (smooth borders) or complex (irregular borders, multiple lesions, thrombus). Angioscopic images were classified as either stable (smooth surface) or thrombotic (red thrombus). The ultrasound characteristics of the lesion were classified as poorly echo-reflective, highly echo-reflective with shadowing, or highly echo-reflective without shadowing. There was a poor correlation between clinical status and angiographic findings. An angiographic complex lesion (n=33) was concordant with unstable angina in 55% (24 of 44); a noncomplex lesion (n=34) was concordant with stable angina in 61% (14 of 23). There was a good correlation between clinical status and angioscopic findings. An angioscopic thrombotic lesion (n=34) was concordant with unstable angina in 68% (30 of 44); a stable lesion (n=33) was concordant with stable angina in 83% (19 of 23). The ultrasound-obtained composition of the plaque was similar in patients with unstable and stable angina. Conclusions Angiography discriminates poorly between lesions in stable and unstable angina. angioscopy demonstrated that plaque rupture and thrombosis were present in 17% of stable angina and 68% of unstable angina patients. Currently available ultrasound technology does not discriminate stable from unstable plaques.

To determine the feasibility and safety of deployment of this new stent, we deployed 28 AVE Micro stents in 23 native coronary artery lesions in 20 patients who developed acute or threatened closure after balloon angioplasty (BA). Ten stents were deployed in the left anterior descending artery, 10 in the circumflex, and 8 in the right coronary artery, Luminal dimensions were measured using a computer-based quantitative coronary angiographic analysis system (CAAS II). Stent deployment was successful in 27 of 28 attempts (96%). In 1 patient with a threatened closure of the left anterior descending artery associated with proximal vessel tortuosity, attempted stent deployment was unsuccessful. The clinical course of the other 19 patients in whom stent deployment was successful was free of coronary reintervention, bypass surgery, and death. A myocardial infarction was observed in 2 patients (10%), in 1 of whom the stent was implanted within 24 hours after the onset of acute myocardial infarction, and in the other acute vessel occlusion was present for 58 minutes before stent implantation. No subacute occlusion was observed. Event-free survival at 30 days after stent implantation was 85% (17 of 20 patients). Minimal luminal diameter was 0.85 +/- 0.57 mm before and 1.19 +/- 0.66 mm after BA, 2.61 +/- 0.39 mm during balloon inflation, 3.26 +/- 0.46 mm during and 2.74 +/- 0.51 mm after stenting, 3.43 +/- 0.52 mm during balloon inflation after stenting (Swiss Kiss), and 2.85 +/- 0.48 mm after Swiss Kiss. Average percent diameter stenosis was reduced from 69% before through 56% after BA to 17% after stenting. During the initial stent implantation, stent recoil was 0.52 +/- 0.30 mm (16 +/- 9% of minimal luminal diameter during stent inflation), A Swiss Kiss was performed in 14 stents with an average pressure of 14 +/- 4 atm, and residual stenosis was reduced from 2.55 mm (21% diameter stenosis) to 2.85 mm (15% diameter stenosis) in these lesions, Angiographic success (<30% residual diameter stenosis) was achieved in all stented lesions. The results of this early experience would indicate that the new AVE Micro stent may be deployed with a high procedural success rate and a minimal learning curve. Implantation of the stent for the bailout management of failed BA can be achieved with a low incidence of adverse cardiac events and a high angiographic success rate.

Background Computerized quantitative coronary angiography (QCA) has fundamentally altered our approach to the assessment of coronary interventional techniques and strategies aimed at the prevention of recurrence and progression of stenosis. It is essential, therefore, that the performance of QCA systems, upon which much of our scientific understanding has become integrally dependent, is evaluated in an objective and uniform manner. Methods and Results We validated 10 QCA systems at core laboratories in North America and Europe. Cine films were made of phantom stenoses of known diameter (0.5 to 1.9 mm) under four experimental conditions: in vivo (coronary arteries of pigs) calibrated at the isocenter or by use of the catheter as a scaling device and in vitro with 50% contrast and 100% contrast. The cine films were analyzed by each automated QCA system without observer interaction. Accuracy and precision were taken as the mean and SD of the signed differences between the phantom stenoses, and the measured minimal luminal diameters and the correlation coefficient (r), the SEE, the y intercept, and the slope were derived by their linear regression. Performance of the 10 QCA systems ranged widely: accuracy, +0.07 to +0.31 mm; precision, +/-0.14 to +/-0.24 mm; correlation (r), .96 to .89; SEE, +/-0.11 to +/-0.16 mm; intercept, +0.08 to +0.31 mm; and slope, 0.86 to 0.64. Conclusions There is a marked variability in performance between systems when assessed over the range of 0.5 to 1.9 mm. The range of accuracy, intercept, and slope values of this report indicates that absolute measurements of luminal diameter from different multicenter angiographic trials may not be directly comparable and additionally suggests that such absolute measurements may not be directly applicable to clinical practice using an on-line QCA system with a different edge detection algorithm. Power calculations and study design of angiographic trials should be adjusted for the precision of the QCA system used to avoid the risk of failing to detect small differences in patient populations. This study may guide the fine-tuning of algorithms incorporated within each system and facilitate the maintenance of high standards of QCA for scientific studies.

The mechanisms of immediate and late changes after percutaneous transluminal coronary angioplasty (PTCA) and directional coronary atherectomy (DCA) were assessed by serial ultrasound imaging in 18 patients treated with PTCA and 16 treated with DCA before, immediately after, and 6 months after coronary interventions, A reduction in plaque area was the main operative mechanism of DCA, explaining 66% of lumen enlargement, In the PTCA group the increase in lumen area was the result of a more balanced combination of plaque reduction (52% of lumen increase) and increase in total lumen area (48%); p < 0.05 versus DCA. In the PTCA group, this last mechanism was prevalent (p < 0.05) in the lesions showing wall fracture or dissection after treatment and in the lesions with a mixed or calcific composition, In the PTCA group, concentric lesions showed a greater plaque compression than eccentric lesions (p < 0.02). plaque increase was responsible for 92% and 32% of the late lumen loss after DCA and after PTCA, respectively (p < 0.05). In PTCA patients, a chronic reduction in total vessel area was the main operative mechanism of lumen reduction (67%) and was prevalent in lesions with a mixed or calcific composition (p < 0.05).

Objectives.: This study sought to determine whether the location of coronary spastic activity may change over time in patients with persistent variant angina. Background.: Although electrocardiographic studies have provided indirect evidence to indicate that the location of ischemia may change in patients with variant angina, it has not been tested by quantitative angiography whether the location of vasospastic activity may change over time. Methods.: Paired ergonovine provocation tests and coronary angiography were performed at a mean (±SD) interval of 43 ± 13 months apart in patients with persistent symptoms of vasospastic angina in the absence of significant atherosclerosis. A total of 87 spastic and nonspastic segments of 87 major vessels in 29 patients were analyzed by quantitative angiography at baseline, after the administration of ergonovine and after isosorbide dinitrate at the initial and follow-up tests. Results.: In 13 patients (group 1), coronary spasm was observed in the same 16 coronary segments at both the initial and follow-up ergonovine provocation tests. In 16 patients (group 2), the following angiographic changes occurred between the initial and follow-up tests in 48 major vessels: Of the 23 segments that developed spasm at the initial test, 10 did not have spasm at the follow-up test; of the 25 vessels that did not demonstrate spasm on the initial test, 12 demonstrated spasm on the follow-up test (a new site of spasm). Thus, in 22 (46%) of 48 vessels, fluctuation of spastic location was observed at follow-up. Conclusions.: Quantitative coronary angiography and repeated ergonovine tests revealed that some patients with persistent vasospastic angina demonstrate fluctuation of vasospastic location, whereas others exhibit a fixed location of vasospasm. Vasospastic angina may not only be a transient disease restricted in location, but may also be a persistent and variable condition involving multiple vessels over many years. © 1995 American College of Cardiology.

The recent progress of quantitative coronary angiography (QCA) has paralleled our advances in interventional cardiology and has contributed significantly to our current understanding of coronary artery disease. QCA offers a scientific medium for the study of acute procedural results and serial changes over long term follow up. Changes in the absolute minimal luminal diameter (MLD) have been utilized for the study of acute luminal gain and subsequent restenosis following coronary interventional procedures and changes in both the minimal and the mean luminal diameter (MEAN) have been utilized for the study of progression/regression of coronary artery disease. While there has been a growth in the deployment of videotape as a recording medium ml account of the recent development of digital acquisition systems, the suitability of video recordings for QCA has not been established. To estimate the reliability of angiographic images recorded on videotape, experimental and clinical angiograms were recorded simultaneously on both 35 mm cinefilm and videotape with normal images and with edge enhancement on a digital angiographic system. In the experimental phantom study, cinefilm gave the closest values to true phantom diameter as compared with videotape with normal recording and edge enhancement. In the clinical study, edge enhancement on cinefilm improved accuracy, precision and correlation more than on videotape with normal images. It is concluded that cinefilm is still the most reliable recording medium for quantitative angiographic analysis in scientific studies, while edge enhancement in a digital angiographic system may improve accuracy and precision of luminal quantification in video recording. With the advent of complementary or competitive imaging modalities for coronary luminal quantification, defence by cinefilm based QCA of its title 'the gold standard' for scientific research and subsequent growth of its role in clinical practice will become critically dependent upon the demonstration of superior reliability of QCA measurements obtained by cinefilm.

In 62 patients with angina pectoris Canadian Class III and IV the luminal dimensions of 25 pre-PTCA and 56 post-PTCA lesions without occlusion were examined with a 4.3 F30 MHz mechanical ultrasound imaging catheter, and analysed off-line using ultrasound cross-sectional area (U-CSA) measurements from s-VHS video images (n = 81). In addition, 42 angiographically normal coronary segments were examined At the site of the examination, the U-CSA was integrated centrally to the leading edge echo of the inner contour of the vessel wall and the corresponding angiographic cinefilm images were analysed by edge detection using the Cardiovascular Angiography Analysis System. The obstruction diameter (at the lesion) and the mean vessel diameter (at normal sites) were (sed to calculate the angiographic cross-sectional area (A-CSA) assuming a circular model. U-CSA values were compared with the corresponding A-CSA values using t-test and linear regression analysis. The study showed that larger CSA are measured with ultrasound than,vith angiography. (P < 0.0001). An acceptable correlation was found between U-CSA and A-CSA values in normal coronary segments (correlation coefficient. r = 0.73, mean diff = 1.44 +/- 1.22 mm(2)). However, the correlation was poor at the site of pre-PTCA lesions (r = 0.62, mean diff = 1.81 +/- 1.14 mn(2)) and deteriorating following PTCA (r = 0.47, mean diff:= 1.28 +/- 2.20 mm(2)). No correlation was found between the degree of lumen eccentricity measured with intracoronary ultrasound (ICUS) and the individual differences between U-CSA and A-CSA values. It ions concluded that U-CSA at coronary lesions shows poor correlation with A-CSA. Basic methodological differences between the techniques may explain the overestimation of cross-sectional areas by ICUS.

Although use of videotape for the recording of coronary angiograms continues to grow, the validity of quantitative coronary angiographic analysis of video images remains unknown. To estimate the realibility of angiographic images recorded on videotapes, experimental and clinical angiograms were recorded simultaneously on both 35 mm cinefilm and super-VHS videotape with normal images and with spatial filtering of the images (edge enhancement) on a digital cardiac imaging system. The experimental angiographic studies were performed with plexiglass blocks and stenosdis phantom of 0.5 to 3.0 mm in diameter. The clinical angiograms were recorded in 20 patients undergoing percutaneous transluminal coronary angioplasty (31 frames before and 20 frames after percutaneous transluminal coronary angioplasty). The cinefilm and corresponding videotapes were analyzed off-line with the new version of the coronrary angiography analysis system. For the experimental study, measurements of minimal luminal diameter obtained from cinefilm, normal-image videotape, and edge-enhanced videotape were compared with the true phanton diameter. In the clinical study the agrrement between measurements obtained from cinefilm and measurements from normal-image videotape and edge-enhanced videotape was examined. In the phantom series the accuracy and precision of quantitative coronary angiography measurement for cinefilm were -0.10 ± 0.08 mm, for normal-image videotape -0.11 ± 0.18 mm, and for edge-enhanced videotape - 0.10 ± 0.11 mm (mean ± SD). In the clinical series, the differences between measurements from cinefilm and normal-image videotape were 0.14 ± 0.20 mm and from cinefilm and edge-enhanced videotape 0.04 ± 0.13 mm. In the experimental phantom study, the use of cinefilm resulted in the most precise measurements. In the clinical study, edge-enhanced videotape provided the highest agreement with measurements obtained from cinefilm. These findings suggest that cinefilm is moore reliable than video as a recording medium for quantitative coronary analysis in scientific studies; however, for routine practice, videotape and edge-enhanced images may provide an acceptable alternative. © 1995.

While the Wallstent was the first stent ever implanted in a human coronary artery in March 1986, the prototype of the stent had a high incidence of acute thrombotic occlusions shortly after implantation. To overcome this limitation the design of the Wallstent was modified to reduce the degree of shortening and metallic burden and to lessen thrombogenicity. We report the results of the first group of patients to undergo implantation of the new Wallstent. Thirty-six Wallstents were electively deployed in coronary artery bypass grafts (CABG) in 30 patients. Initial angiographic success (< 50% residual diameter stenosis as determined by quantitative coronary angiography) was achieved in all patients. During the in-hospital phase, no major adverse cardiac event was observed (reintervention, re-CABG, myocardial infarction or death). Following hospital discharge, one patient had a subacute stent occlusion with chest pain and elevation of cardiac enzymes at 11 days and another patient had a small non-Q wave myocardial infarction with a patent Wallstent (MLD; 2.66 mm) at 22 days. During 6 month follow-up, five patients required balloon angioplasty (four for restenosis and one for stent occlusion). The results of this preliminary study indicate that the new Wallstent may reduce the risk of acute thrombotic occlusion in comparison with its prototype and may convey a favourable outcome in patients with angina after CABG.

Quantitative coronary angiography (QCA) is a validated and widely accepted method to investigate changes in arterial dimension over time. Calibration of measurements is enabled by the use of the coronary catheter as a scaling device. The dimensions and laminar composition of coronary catheters, however, have changed significantly over recent years and the suitability of the current generation of coronary catheters for calibration purposes has not been validated. We therefore recorded 57 coronary guiding catheters on cinefilm, and compared their automated quantitative measurements (Cardiovascular Angiography Analysis System, CAAS) with their true values (precision micrometer). We found an overall underestimation of quantitatively derived dimensions, ranging from −8.9 to +4% for water‐filled catheters and from −15.5 to −3.9% for contrast‐filled catheters. In conclusion, while the current generation of coronary guiding catheters shows a wide variety in radiological quality, it can be clearly detected by the CAAS system, and is suitable for calibration of QCA measurements (with the exception of the DVI atherectomy catheter), provided that calibration is done on contrast‐empty catheters. © Wiley‐Liss, Inc. Copyright © 1994 John Wiley & Sons, Ltd.

Long-term changes in vasocontractility were examined in 23 coronary segments from 20 patients with variant angina using computer-based quantitative coronary angiography and ergonovine provocation tests repeated at an interval of 42 ± 14 months. Measurements of vasospasticity at the sites of fixed stenoses were compared with values predicted by an elementary geometric theory based on the assumption that the cross-sectional area of a vessel wall is constant regardless of its state of vasoconstriction. While all patients were symptomatic initially, only 11 remained symptomatic at follow-up. At the initial provocation test, the response was correctly predicted in four segments, was lower than expected in one, and was stronger in 18. At follow-up, only one of the four segments in which the response had been initially predicted correctly again showed the predicted response and the remaining three showed a response weaker than expected; the one segment which was initially hypocontractile remained hypocontractile at follow-up; and of the 18 segments which were initially hypercontractile, 12 exhibited hypercontractility again, four had the predicted value and the remaining two showed hypocontractility. In one one of 23 segments did the geometric theory predict the behaviour of vasospasticity at the site of fixed stenosis on both tests. Vasospastic responsiveness is a dynamic process demonstrating temporal variability and is not directly predicted by geometric theory. © 1994 The European Society of Cardiology.

Computer‐assisted contour detection and videodensitometric cross sectional area assessment of coronary artery obstructions on the CAAS II system were validated in vitro and in vivo by angiographic cinefilm recording and automated measurement of stenosis phantoms (luminal diameter 0.5, 0.7, 1.0, 1.4, 1.9 mm) which were first inserted in a plexiglass model and then serially implanted in swine coronary arteries. “Obstruction diameter” (OD) and “obstruction area” (OA) values obtained from 10 in vitro and 19 in vivo images at the site of the artificial stenoses were compared with the true phantom dimensions. The in vitro assessment of OD yielded an accuracy of 0.00±0.11 mm (correlation coefficient: r = 0.98, y = 0.18 + 0.82x, standard error of estimate: SEE = 0.08), whereas the in vivo measurement of OD gave an accuracy of −0.01 ± 0.18 mm (r = 0.94, y = 0.22 + 0.82x, SEE = 0.15). The assessment of OA gave an accuracy of −0.08 ± 0.21 mm2 in vitro (r = 0.97, y = 0.08 + 0.99x, SEE = 0.22) and −0.22 ± 0.32 mm2 in vivo (r = 0.95, y = 0.21 + 1.01x, SEE = 0.33). The mean reproducibility was ±0.09 mm for geometric measurements and ±0.21 mm2 for videodensitometric assessments, respectively. Thus, due to inherent limitations of the imaging chain, the reliability of geometric coronary measurements is still far superior to videodensitometric assessments of vessel cross sectional areas. © 1993 Wiiey‐Liss, Inc. Copyright © 1993 John Wiley & Sons, Ltd.

Chronologic changes of coronary spasm were examined by repeated ergonovine provocation tests during angiography. A total of 322 patients who had variant angina without severe atherosclerosis demonstrated a positive response to the first test. Ninety of these patients had recurrent variant anginal symptoms after an angina-free period of 38 ± 12 months (mean ± SD). Of these 90 patients, 76 (84%) had symptoms or electrocardiographic (ECG) findings similar to those of the first test. The initial 9 of these 76 patients underwent a second provocation test and showed coronary responses analogous to those on the first test. Of the 90 patients, 14 (16%) had different symptoms or ECG findings from those elicited at the first episode. All 14 patients again had a positive response to a second ergonovine test and the following angiographic changes were observed in the three major vessels between the two tests. Of the 21 vessels that had spasm on the first test, eight vessels (19%) did not have spasm on the second test. Of the 21 vessels that did not demonstrate spasm on the first test, 10 (24%) demonstrated spasm on the second test. In the present study it is concluded that the majority of patients with recurrent angina seemed to have consistency in the location of coronary spasm, while in some patients the fluctuation of coronary spasm was confirmed by two ergonovine provocation tests. © 1992.

To re-evaluate the concept of “high lateral” myocardial infarction, angiographic findings were analysed in 29 patients with remote infarction and abnormal Q waves in lead I or aVL but no abnormal Q waves in other leads and no prominent R wave in lead V1. All patients except one showed asynergy in the anterior segment on right anterior oblique left ventriculogram. Asynergies in other segments were, if present, mild or small. Critical narrowing was present in the diagonal branches or in their “parent” arteries (that is, the left anterior descending artery or left main trunk) in 28 patients but in the circumflex artery in only 3 patients. Thus, the traditional concept that a “high lateral” infarction is myocardial necrosis of the basal aspect of the left ventricle, receiving its blood supply from the circumflex artery, needs correction. “High lateral infarction” corresponds to necrosis of the area between the obtuse margin and the inter-ventricular groove ordinarily supplied by the diagonal branches of the left anterior descending artery. Such infarctions are expressed by asynergy of the anterior segment rather than the posterior segment. © 1988, The Japanese Circulation Society. All rights reserved.