Coronary dissection: a predictor of restenosis?

To determine if arterial dissection resulting from transluminal coronary angioplasty (TCA) leads to a greater incidence of restenosis, 273 consecutive patients who had undergone TCA with at least 1 year of follow-up were examined. Success was graded as a greater than or equal to 20% increase in intraluminal diameter. Dissection was defined as a prominent intimal defect at the site of angioplasty. Restenosis was defined as a 50% loss of the initial angiographic gain. Of 216 patients in whom TCA was successful, 64 (30%) had dissections at the site of angioplasty and 152 (70%) had no dissection. During follow-up, 135 patients were asymptomatic with normal results of exercise tolerance tests, recurrent symptoms developed in 81 patients, and 64 patients underwent repeat angiography. The overall restenosis rate was 21%. In the dissection group, 11 (18%) had documented restenosis and 49 (82%) did not develop restenosis. In the nondissection group, 35 (24%) had documented restenosis and 113 (76%) did not develop restenosis. These data show that patients who develop dissections at the time of TCA are no more likely to develop restenosis during follow-up.     

Luminal loss and restenosis after coronary angioplasty. The role of lipoproteins and lipids.

AIMS: Lipoproteins and lipids, especially lipoprotein(a), have been studied as risk factors for restenosis after coronary angioplasty with conflicting results. We investigated the association between serum levels of lipoprotein(a) apolipoprotein A-1, apolipoprotein B-100, total-cholesterol, high density lipoprotein-cholesterol, triglycerides, and coronary luminal loss and restenosis after angioplasty.METHODS: The lipoproteins and lipids were measured in 305 consecutive patients who underwent successful angioplasty and reangiography 20+/-3 weeks after angioplasty. Single-vessel dilatation was performed in 251 patients. Luminal loss was defined as minimal luminal diameter post-angioplasty minus minimal luminal diameter at follow-up, divided by the interpolated reference diameter of the vessel. Restenosis was defined according to three dichotomous categorical criteria: (1) >50% diameter stenosis at follow-up (2) loss of >50% of the gain achieved by angioplasty, (3) the need for target vessel revascularization.RESULTS: There was no significant association between the serum levels of lipoproteins and lipids and luminal loss. Univariate analysis did not show any significant difference in the serum levels of any of the lipoproteins and lipids between the restenosis and no-restenosis groups. Multivariate analysis revealed that only the angiographic variables (luminal gain and post-angioplasty minimal luminal diameter) were associated with luminal loss and restenosis after angioplasty.CONCLUSION: Lipoproteins and lipids were neither associated with luminal loss nor independent risk factors for restenosis after angioplasty.     

Influence of continued smoking and some biological risk factors on restenosis after percutaneous transluminal coronary angioplasty

Objectives. To identify possible biological risk factors for restenosis following successful percutaneous transluminal coronary angioplasty (PTCA) in patients having single or multivessel disease. The effect of continued smoking on restenosis was also evaluated.
Design. In this prospective smoking controlled study all subjects had a routine angiographic restudy after 6 months. The biological risk factors assessed before angioplasty were adrenaline, endothelin, fibrinogen, lipoprotein (a) and tissue plasminogen activator.
Subjects. The study population consisted of 122 patients of whom 25% were current smokers.
Main outcome measures. Angiographic restenosis was defined as at least 50% diameter stenosis on the follow-up angiogram after an initially successful procedure.
Results. Restenosis was observed in 43% of patients. The restenosis rate was significantly lower among current smokers, but they were significantly younger and also had significantly less dilated stenoses. Multivariate analysis revealed the number of dilated stenoses, the mean inflation time, post-PTCA percentage diameter stenosis and left anterior descending coronary artery to be predictive of restenosis, while continued smoking was not. When only the lesion with the greatest loss in luminal diameter of each patient was considered, the multiple linear regression analysis revealed high endothelin level to be predictive of restenosis.
Conclusions. This study revealed high endothelin levels to be predictive of luminal narrowing after angioplasty. In addition, the number of dilated stenoses, the mean inflation time, post-PTCA percentage diameter stenosis and stenosis location in the left anterior descending artery were found to be predictive of restenosis. However, continued smoking after angioplasty did not emerge as a risk factor for restenosis.     

Impact of restenosis 10 years after coronary angioplasty

Aims The aim of the study was to compare the 10-year follow-up resultsof patients with or without restenosis following single-vesselpercutaneous transluminal coronary angioplasty (PTCA). Methods and Results A total of 313 patients with successful PTCA (20% reductionin luminal diameter narrowingwithout acute complications) anda control angiography 6 months after PTCA were included in thestudy. Events during the follow-up period were defined as death,myocardial infarction, bypass surgery, or repeat PTCA. Statisticalevaluation was performed by the Fisher test, logistic regression,and life-table analysis. Restenosis (loss of >50% of the initialgain and diameter stenosis of <50%) was found in 87 (28%)patients. During follow-up, 11 patients (5%) without restenosis(group A) and 11 (13%) patients with restenosis (group B) died(P<0·05). In group A, 17 (8%) patients and in groupB, 11 (13%) patients suffered myocardial infarction (ns); 17group A (8%) patients and 25 (29%) group B patients had bypasssurgery (P<0·0001), and 34 (15%) group A patientsand 55 (63%) group B patients underwent repeat PTCA (P<0·0001).Logistic regression analysis identified restenosis as an independentrisk factor that increases the risk of death 2·8-fold(P=0·02), bypass surgery 5·6-fold (P<0·0001),and repeat PTCA 10-fold (P<0·0001). Conclusion: We conclude that patients with restenosis had a poorer long-termoutcome than patients without restenosis. Although most patientswith restenosis underwent repeat PTCA, the survival rate withoutany serious adverse events was only 59%, compared with 83% inpatients without restenosis (P<0·0001).     

Effect of prior coronary restenosis on the risk of subsequent restenosis after stent placement or directional atherectomy

Lesions that have developed restenosis after a prior intervention may be more likely to develop restenosis after subsequent percutaneous interventions. To determine if this is an independent effect, the clinical characteristics and immediate angiographic outcomes of 179 prior restenosis lesions were compared with those of 254 primary lesions after stenting or directional atherectomy. Six-month angiographic follow-up was obtained for 79% of successfully treated lesions. Univariable and muttivariable logistic regression was used to determine how binary restenosis (defined as -50% diameter stenosis at follow-up) was influenced by postprocedure luminal diameter, left anterior descending artery location, diabetes mellitus, as well as prior restenosis. At 6-month follow-up, prior restenosis lesions had a significantly smaller late diameter (1.77 vs 2.18 mm, p < 0.001), more absolute late loss (1.35 vs 1.14 mm, P = 0.051), a higher loss index (0.58 vs 0.45, p < 0.02), and a higher binary restenosis rate (37.3% vs 24.4%, P = 0.01). Whereas univariable analysis revealed that left anterior descending artery location, diabetes mellitus, postprocedure luminal diameter < 3.1 mm, and prior restenosis were each strong predictors of binary restenosis (all p < 0.02), muttivariable analysis showed that after adjustment for left anterior descending artery location, diabetes, and postprocedure luminal diameter, prior restenosis was no longer an independent predictor of restenosis (odds ratio 1.57, 95% confidence interval 0.95–2.60, P = 0.073). In conclusion, although prior restenosis lesions do show more restenosis than primary lesions, much of this effect is due to preselection of a population enriched in other known factors that predispose to restenosis.     

Effectiveness and safety of the genous endothelial progenitor cell-capture stent in acute ST-elevation myocardial infarction

The endothelial progenitor cell (EPC)-capture stent promotes endothelialization and preliminary studies have suggested its safety and feasibility in ST-elevation myocardial infarction (STEMI). Detailed late clinical follow-up and angiographic analyses are, however, limited. We sought to determine late angiographic and clinical outcomes of the Genous EPC-capture stent in primary angioplasty. EPC-capture stents were implanted during primary angioplasty in 489 consecutive patients presenting with STEMI from 2004 through 2008. The first 100 consenting patients undergoing successful stent implantation scheduled to undergo relook coronary angiography at 6 to 12 months were enrolled. Ninety-five patients with 96 lesions were analyzed independently. Mean duration of follow-up coronary angiography was 245 days. In-stent late luminal loss measured 0.87 ± 0.67 mm. Binary restenosis (defined as >50% diameter stenosis) was 28%, with diffuse in-stent restenosis (Mehran class II) as the predominant pattern. Of 27 patients with binary restenosis, 14 (52%) were symptomatic, with 10 patients undergoing target lesion revascularization. Asymptomatic patients had significantly larger reference vessel and in-stent minimal luminal diameters (2.77 ± 0.39 vs 2.54 ± 0.44 mm, p = 0.040; 2.74 ± 0.34 vs 2.31 ± 0.72 mm, p = 0.004, respectively). Follow-up late loss and diameter stenoses were also in favor of the asymptomatic group. Major adverse cardiac event rate was 16% at a mean follow-up of 34 months. There were no cases of Academic Research Consortium-defined stent thrombosis. In conclusion, implantation of the EPC-capture stent during primary angioplasty is associated with a favorable late clinical outcome but with higher than anticipated angiographic late loss.     

The Frankfurt experience in restenosis after coronary angioplasty

Three hundred and thirty-three of 356 patients underwent angiographic follow-up from 1 to 18 months (mean 5.6 months) after percutaneous transluminal coronary angioplasty (PTCA). This is a reangiography rate of 94%. Recurrence rate after the first PTCA was 15% (n = 289). Restenosis rate was defined as an increase from immediate post-PTCA stenosis of more than 30%, or the loss of at least half of the initial gain in luminal diameter. Patients who needed a second angioplasty due to restenosis (n = 30) had a restenosis rate of 33%. Patients with angioplasty in the aortocoronary bypass (n = 14) had a restenosis rate of 45%. All patients were treated before, during and at least 4 to 6 months after the procedure with 60 to 100 mg of isosorbide dinitrate daily plus 160 to 360 mg of verapamil or 100 to 150 mg of gallopamil and 1.5 g of acetylsalicylic acid. In a second retrospective study 111 of 399 patients had the acetylsalicylic acid therapy discontinued or decreased. Forty-two of them developed restenosis (38%), whereas only 49 of 288 patients who continued to receive 1.5 g aspirin developed restenosis (17%). The restenosis rate was 32% in those who received the reduced dose of aspirin. Thus, a large dose of acetylsalicylic acid given before, during and 4 to 6 months after the procedure seems to be necessary to achieve a low rate of restenosis after PTCA.     

Predictors of angiographic restenosis after coronary intervention in patients with diabetes mellitus

Background

Patients with diabetes mellitus are particularly prone to restenosis after percutaneous coronary intervention. An exploratory, nested, case-control study was undertaken to identify clinical, lesional, and procedural predictors of angiographic restenosis in these patients.

Methods

Seventy-five patients with diabetes mellitus with 86 coronary lesions were selected from a larger population of 217 patients who had undergone 6-month angiographic follow-up after a first, successful balloon angioplasty (PTCA) or stent implantation procedure. Data collection was by patient interview and review of hospital database and other medical records. All angiograms were analyzed with quantitative coronary angiography, and restenosis was defined as a ≥50% diameter reduction at the treated site. A multivariate analysis of 10 prespecified explanatory variables, derived from a literature review, was performed on a per-lesion basis.

Results

There were 45 patients (53 lesions) with restenosis and 30 patients (33 lesions) without restenosis. Univariate predictors of binary restenosis were periprocedural glycosylated hemoglobin level, vessel reference diameter, PTCA, and larger final balloon size to reference artery diameter ratio. Multiple logistic regression identified poor glycemic control (odds ratio [OR] 3.03, 95% CI 1.06-8.65, P = .038), small vessel reference diameter (OR 3.41, 95% CI 1.17-9.95, P = .025), and mode of intervention (OR 3.12, 95% CI 1.08-9.00, P = .036) as independent risk factors. Vessel reference diameter appeared to be an important effect modifier of the association between type of intervention and angiographic outcome, with stenting no longer superior to PTCA in patients with diabetes mellitus who had vessels <2.87 mm in diameter (P = .054).

Conclusion

Poor glycemic control, vessel size, and PTCA were independent predictors of restenosis in patients with diabetes mellitus. It is possible that improved periprocedural glycemic control, in addition to stenting, may reduce the restenosis rate in these patients.     

Incidence of restenosis after successful coronary angioplasty: a time-related phenomenon. A quantitative angiographic study in 342 consecutive patients at 1, 2, 3, and 4 months

Data from experimental, clinical, and pathologic studies have suggested that the process of restenosis begins very early after coronary angioplasty. The present study was performed to determine prospectively the incidence of restenosis with use of the four National Heart, Lung, and Blood Institute and the 50% or greater diameter stenosis criteria, as well as a criterion based on a decrease of 0.72 mm or more in minimal luminal diameter. Patients were recatheterized at 30, 60, 90, or 120 days after successful percutaneous transluminal coronary angioplasty (PTCA). After PTCA all patients received 10 mg nifedipine three to six times a day and aspirin once a day until repeat angiography. Of 400 consecutive patients in whom PTCA was successful (less than 50% diameter stenosis), 342 underwent quantitative angiographic follow-up (86%) by use of an automated edge-detection technique. A wide variation in the incidence of restenosis was found dependent on the criterion applied. The incidence of restenosis proved to be progressive to at least the third month for all except NHLBI criterion II. At 4 months a further increase in the incidence of restenosis was observed when defined as a decrease of 0.72 mm or more in minimal luminal diameter, whereas the criteria based on percentage diameter stenosis showed a variable response. The lack of overlap between the different restenosis criteria applied affirms the arbitrary nature of angiographic definitions currently in use. Restenosis should be assessed by repeat angiography, and preferably ascertained according to the change in absolute quantitative measurements of the luminal diameter.     

Postangioplasty restenosis rate between segments of the major coronary arteries.

Conflicting data have been published regarding the rate of postangioplasty restenosis observed in diverse segments of the coronary tree. However, these studies may be criticized for their biased selection of patients, methods of analysis, and definitions of restenosis. In the present study, 1,353 patients underwent a successful coronary dilatation of greater than or equal to 1 site. In all, 1,234 patients (91%) had a follow-up angiogram after 6 months, or earlier when indicated by symptoms. All films were processed and analyzed at the thoraxcenter core laboratory with the coronary angiography analysis system (automated contour detection). Restenosis was considered present if the diameter stenosis at follow-up was greater than 50%. No differences in restenosis rates were observed between coronary segments using this categorical definition. A continuous approach was also used; absolute changes in minimal luminal diameter adjusted for vessel size were used in order to allow comparison between vessels of different sizes (relative loss). No significant differences were observed between the coronary segments with this continuous approach. These results suggest that restenosis is a ubiquitous phenomenon without any predilection for a particular site in the coronary tree.     

Physiologic response to gain and loss in coronary minimal luminal diameter in patients treated with coronary angioplasty: prediction of restenosis on the basis of exercise capacity

BACKGROUND: The effect of percutaneous transluminal coronary angioplasty (PTCA) on physiologic measurements has previously been shown, but the relation between physiologic response and degree of change in coronary luminal diameter is not known. We studied the relation between exercise capacity and minimal luminal diameter before and after PTCA. We also explored the usefulness of measurement of attenuation in exercise capacity after PTCA to predict the likelihood of restenosis. METHODS: Bicycle exercise testing was performed 2 weeks before and 2 and 20 weeks after PTCA in 395 consecutively enrolled patients. Angiograms obtained before and after PTCA and 20 weeks afterward were analyzed by quantitative coronary angiography. Restenosis was defined as both angiographic (>/=50% diameter stenosis at follow-up angiography) and clinical (target-vessel revascularization), after successful PTCA. Exercise capacity was defined as the cumulative work performed divided by body weight (watt x minutes x kilograms(-1)). RESULTS: Exercise capacity increased 43% (P <.0001) from before PTCA to 2 weeks after PTCA (early increase) and decreased 4% (P =.01) from 2 to 20 weeks after PTCA (late decrease). The gain in minimal luminal diameter (Minimal luminal diameter after - Minimal luminal diameter before) was 0.92 +/- 0.46 mm. The loss in minimal luminal diameter (Minimal luminal diameter after PTCA - Minimal luminal diameter at follow-up examination) was 0.27 +/- 0.42 mm. Exercise capacity and minimal luminal diameter measured before PTCA were positively correlated (coefficient 3.3; R = 0.12; P =.01). Gain in minimal luminal diameter correlated with the early increase in exercise capacity (coefficient -3.8; R = 0.23; P <.0001). Loss in minimal luminal diameter correlated with the late decrease in exercise capacity (coefficient 3.3; R = 0.20; P <.0001). Multivariate logistic regression analysis revealed that the late decrease in exercise capacity was independently predictive of both angiographically (odds ratio 1.13; P <.0001) and clinically (odds ratio 1.12; P <.0001) defined restenosis. CONCLUSIONS: The results demonstrated a linear relation between the severity of coronary stenosis and exercise capacity measured before PTCA. The degree of coronary luminal enlargement achieved with angioplasty and the luminal reduction that occurred between PTCA and follow-up evaluation correlated with increases and decreases in exercise capacity. Attenuation in exercise capacity was found to be a strong predictor of restenosis.     

Pravastatin reduces restenosis after coronary angioplasty of high grade stenotic lesions: Results of SHIPS (SHIga Pravastatin Study)

Summary We conducted a multicenter prospective, randomized, double-blind, placebo-controlled trial to test whether pravastatin, a hydroxymethyl glutaryl coenzyme A reductase inhibitor, can decrease restenosis after percutaneous transluminal coronary angioplasty (PTCA). Pravastatin 10 mg twice daily was begun at least 10 days prior to elective PTCA in patients with total cholesterol less than 280 mg/dl. The end-point was a between-group comparison of the frequency of restenosis defined as a more than 50% loss of the initial gain in diameter stenosis at the PTCA site at 3 months during follow-up by automated quantitative coronary arteriography. Of 207 patients randomly assigned to study groups, 139 patients underwent PTCA; 133 procedures were successful, and 124 patients underwent follow-up angiography at 3 months, and 179 lesions (85 pravastatin, 94 placebo) in 124 patients (62 pravastatin, 62 placebo) were analyzed. The two groups were comparable for baseline characteristics. Total cholesterol decreased by 19.6% in the pravastatin group (p<0.001) but not in the placebo group. Although the restenosis rate was not different in the two groups (29.4% in pravastatin vs. 39.4% in placebo, p=0.215) as a whole, it was reduced to about one fifth (8.8%) in the pravastatin group compared with 14.8% in the placebo group (p=0.0011) when the comparison was restricted to high grade lesions (75% diameter stenosis, 34 lesions in pravastatin, 29 lesions in placebo). Pravastatin thus reduces restenosis after PTCA of high grade lesions.     

Restenosis after percutaneous transluminal coronary angioplasty (PTCA): A report from the PTCA registry of the national heart, lung, and blood institute

The results of follow-up angiography in patients from 27 clinical centers enrolled in the PTCA Registry were analyzed to evaluate restenosis after PTCA. Of 665 patients with successful PTCA, 557 (84%) had follow-up angiography (median follow-up 188 days). Restenosis, defined as an increase of at least 30% from the immediate post-PTCA stenosis to the follow-up stenosis or a loss of at least 50% of the gain achieved at PTCA, was seen in 187 patients (33.6%). The incidence of restenosis in patients who underwent follow-up angiography was highest within the first 5 months after PTCA. Restenosis was found in 56% of patients with definite or probable angina after PTCA and in 14% of patients without angina after PTCA. Twenty-four percent of patients with restenosis did not have either definite or probable angina. Multivariate analysis selected 4 factors associated with increased rate of restenosis: male sex, PTCA of bypass graft stenosis, severity of angina before PTCA and no history of MI before PTCA.     

芪参益气滴丸联合阿托伐他汀对冠状动脉内支架再狭窄的干预

目的 探讨芪参益气滴丸联合阿托伐他汀对冠状动脉内支架再狭窄的干预作用.方法 纳入冠脉内支架置入术成功的141例冠心病患者,随机分为对照组（n=30）、芪参益气滴丸组（芪参组,n=36）、阿托伐他汀组（n=36）、和联合组（阿托伐他汀＋芪参益气滴丸,n=39）,药物治疗疗程均为6个月.采用冠状动脉定量分析支架术前、术后狭窄病变管腔内径和面积指标,评价阿托伐他汀、芪参益气滴丸及联合用药对支架内再狭窄的作用.结果 共有85例患者及108处支架在术后6个月内进行冠脉造影复查.四组患者随访时间及随访率比较,差异无统计学意义（P＞0.05）.芪参组、阿托伐他汀组、联合组支架内再狭窄率均低于对照组（P＜0.05）.联合组、阿托伐他汀组在晚期内径丢失、晚期内径丢失指数均小于对照组和芪参组（P＜0.05～0.01）;在支架置入血管段最小内径、净内径获得、净内径获得指数、管腔面积净获得方面均大于对照组和芪参组（P＜0.05～0.01）.联合组晚期内径丢失、晚期内径丢失指数、再狭窄率呈小于阿托伐他汀组趋势,而支架置入血管段最小内径、净内径获得、净内径获得指数、管腔面积净获得方面呈大于阿托伐他汀组趋势,但两组上述指标差异无统计学意义（P＞0.05）.结论 芪参益气滴丸联合阿托伐他汀对支架内再狭窄的防治有协同作用.     

Chlamydia pneumoniae seropositivity predicts the risk of restenosis after percutaneous transluminal coronary angioplasty

This study was done to evaluate whether anti-Chlamydia pneumoniae seropositivity can be a predictor of restenosis after coronary intervention. Recent studies indicate that latent infection with C. pneumoniae is associated with and could possibly cause atherosclerosis. However, it is unknown whether chronic infection with this microorganism is involved in the mechanism of restenosis after percutaneous transluminal coronary angioplasty. We prospectively studied 78 consecutive patients (90 target lesions) with symptomatic coronary artery disease who underwent successful coronary intervention to a de novo lesion (conventional balloon angioplasty to 31 lesions and stent implantation to 59 lesions). At angioplasty, blood samples were collected to measure the serum level of anti-C. pneumoniae IgG to examine whether seropositive patients were prone to restenosis and whether the seropositivity could predict the risk of restenosis determined by follow-up coronary angiography performed within 6 months after the angioplasty. Restenosis, defined as more than 50% stenosis with an increase of 15% or more in the degree of stenosis from that measured on cineangiograms after angioplasty, developed in 36 of 62 seropositive patients and in 4 of 16 seronegative patients (58% vs 25%, P = 0.025). Lesions in the seropositive patients had a greater mean loss index (mean ± SD 0.75 ± 0.45 vs 0.35 ± 0.41, P < 0.001), which was defined as late loss (luminal diameter reduction at follow-up angiography) divided by acute gain (luminal diameter gain by angioplasty), in late loss (1.07 ± 0.64 mm vs 0.65 ± 0.79 mm, P = 0.019), in percentage of diameter stenosis (57% ± 20% vs 41% ± 21%, P = 0.003) and a lesser mean in minimal luminal diameter (1.18 ± 0.58 mm vs 1.67 ± 0.63 mm, P = 0.002) at follow-up angiography. In a multivariate logistic regression model, anti-C. pneumoniae IgG seropositivity was a strong independent predictor of restenosis compared to the other risk factors (odds ratio = 6.2, P = 0.01). C. pneumoniae could play an important role in the mechanism of restenosis and evaluation of the IgG seropositivity, and may help to identify patients at high risk for restenosis. Received: June 13, 2001 / Accepted: December 7, 2001     

Optimal coronary balloon angioplasty with provisional stenting versus primary stent (OCBAS): Immediate and long-term follow-up results

Objective. This study sought to compare two strategies of revascularization in patients obtaining a good immediate angiographic result after percutaneous transluminal coronary angioplasty (PTCA): elective stenting versus optimal PTCA. A good immediate angiographic result with provisional stenting was considered to occur only if early loss in minimal luminal diameter (MLD) was documented at 30 min post-PTCA angiography.Background. Coronary stenting reduces restenosis in lesions exhibiting early deterioration (>0.3 mm) in MLD within the first 24 hours (early loss) after successful PTCA. Lesions with no early loss after PTCA have a low restenosis rate.Methods. To compare angiographic restenosis and target vessel revascularization (TVR) of lesions treated with coronary stenting versus those treated with optimal PTCA, 116 patients were randomized to stent (n = 57) or to optimal PTCA (n = 59). After randomization in the PTCA group, 13.5% of the patients crossed over to stent due to early loss (provisional stenting).Results. Baseline demographic and angiographic characteristics were similar in both groups of patients. At 7.6 months, 96.6% of the entire population had a follow-up angiographic study: 98.2% in the stent and 94.9% in the PTCA group. Immediate and follow-up angiographic data showed that acute gain was significantly higher in the stent than in the PTCA group (1.95 vs. 1.5 mm; p < 0.03). However, late loss was significantly higher in the stent than the PTCA group (0.63 ± 0.59 vs. 0.26 ± 0.44, respectively; p = 0.01). Hence, net gain with both techniques was similar (1.32 ± 0.3 vs. 1.24 ± 0.29 mm for the stent and the PTCA groups, respectively; p = NS). Angiographic restenosis rate at follow-up (19.2% in stent vs. 16.4% in PTCA; p = NS) and TVR (17.5% in stent vs. 13.5% in PTCA; p = NS) were similar. Furthermore, event-free survival was 80.8% in the stent versus 83.1% in the PTCA group (p = NS). Overall costs (hospital and follow-up) were US $591,740 in the stent versus US $398,480 in the PTCA group (p < 0.02).Conclusions. The strategy of PTCA with delay angiogram and provisional stent if early loss occurs had similar restenosis rate and TVR, but lower cost than primary stenting after PTCA.     

Clinical and quantitative angiographic outcomes following elective implantation of the self-expanding Wallstent for longer coronary artery lesions--final results of the Wellstent native study

BACKGROUND: Implantation of short balloon-expandable stents provides superior clinical and angiographic outcome compared with balloon angioplasty in selected patients. The purpose of the Wellstent study was to evaluate the safety and efficacy of the self-expanding Wallstent combined with aspirin and ticlopidine in patients with stable or unstable angina related to a native coronary lesion up to 45 mm in length. METHODS: 105 patients (111 lesions) with stable (57%) or unstable (43%) angina were included in this prospective multicentre evaluation. Angiography before and after Wallstent implantation and at 6-month follow-up was analysed at the core lab using the CAAS 2 system. The primary end-point was incidence of major adverse cardiac events (MACE) at 30 days. Secondary end-points were angiographic outcome at 6 months and MACE at 6 months and 1 year. RESULTS: Acute procedural success (successful stent implantation with residual stenosis <20%) was achieved in 99%. Mean reference diameter was 3.18 &#45 0.66 mm, minimal luminal diameter was 1.00 &#45 0.50 mm pre- and 2.84 &#45 0.47 mm poststent (diameter stenosis 16 &#45 6%). The mean hospital stay was 2.2 days. At 30 days, 95% of patients were free of MACE. At 6 month and 1 year clinical follow-up, 75% and 71% of patients, respectively, remained free of MACE, the majority of which (19 of 30) were re-interventions at re-angiography. In 90% of eligible patients, MLD at follow-up was 1.65 &#45 0.75 mm (late loss 1.20 &#45 0.66 mm, loss index 0.66), diameter stenosis 42 &#45 15%, with a restenosis rate of 32%. Longer stents were associated with greater luminal loss (P = 0.001) and less-favourable clinical outcome. CONCLUSIONS: Wallstent implantation, combined with aspirin and ticlopidine, achieved excellent acute and 30 day clinical results in a heterogenous high-risk patient group. Clinical outcome at 6 months and 1 year remained good, and most adverse events were re-PTCA during follow-up angiography. The loss index of 0.66 and restenosis rate of 32%, related in part to the use of longer stents, emphasizes the continuing need for effective anti-proliferative therapy.     

The importance of acute luminal diameter in determining restenosis after coronary atherectomy or stenting.

BACKGROUND. We evaluated native coronary arteries treated by directional coronary atherectomy or balloon-expandable stent placement in an effort to derive a quantitative geometric model relating the luminal diameter immediately after intervention to that present 6 months later. The minimal luminal diameter of each lesion was measured before and immediately after intervention in 102 single Palmaz-Schatz stents and 134 directional atherectomies, 192 (81%) of which had repeat angiographic measurement of minimal luminal diameter 6 months after the intervention. The immediate enlargement in luminal diameter produced by the intervention (acute gain) and the subsequent reduction in luminal diameter from the time of intervention to 6 months of follow-up (late loss) were calculated. METHODS AND RESULTS. Luminal diameter increased from 0.69 +/- 0.40 mm to 3.11 +/- 0.64 mm (acute gain, 2.41 +/- 0.64 mm) after intervention, providing an immediate postprocedure residual stenosis of 1 +/- 14% relative to a reference diameter of 3.13 +/- 0.65 mm. At 6-month follow-up, the late luminal diameter was 1.97 +/- 0.92 mm (late loss, 1.13 +/- 0.89 mm), yielding a late diameter stenosis of 36 +/- 26%. The restenosis rate (according to the traditional definition of diameter stenosis > or = 50%) was 30%. Multivariable analysis demonstrated that late luminal diameter (p = 0.02), late percent stenosis (p = 0.04), and restenosis (according to a > 50% definition, p = 0.04) were each strongly associated with the luminal diameter present immediately after the procedure. Whereas late luminal diameter was also influenced by reference artery size and the vessel treated (left anterior descending versus right coronary artery), reference vessel size was rejected by the multivariable models of late percent stenosis and binary restenosis after they were adjusted for the effect of postprocedure luminal diameter. Once adjusted for postprocedure luminal diameter, neither late luminal diameter nor late loss was found to be independently determined by which device was used (atherectomy versus stents). Rather, late loss was determined independently by the immediate postprocedure luminal diameter (p = 0.005) and the postprocedure percent stenosis (p = 0.02). Although late loss thus increased with acute gain, the net beneficial effect of increased acute gain was maintained: Late loss was only a fraction (0.47) of acute gain, so the ability of a larger postprocedure luminal diameter to reduce the probability of subsequent restenosis was preserved. CONCLUSIONS. This quantitative model demonstrates that the late coronary lumen diameter and the probability of restenosis after Palmaz-Schatz stenting or directional atherectomy are influenced strongly by the lumen diameter present immediately after the procedure rather than by the specific device used. Although the influence of a larger acute result on reduced restenosis appears to be well established in this treatment population, the interplay among the multiple other biological influences on restenosis limits the ability to predict the probability of restenosis for the individual patient based on a large acute result alone. Future studies of restenosis, however, can further refine this multivariable quantitative model by adjusting for the effects of other clinical variables, mechanical interventions, or drug therapies in addition to the clear effect of postprocedure luminal diameter.     

N-3 fatty acids do not prevent restenosis after coronary angioplasty: results from the CART study. Coronary Angioplasty Restenosis Trial.

OBJECTIVES: The aim of the study was to investigate whether omega-3 fatty acids (n-3 FA) reduce the occurrence of restenosis after percutaneous transluminal coronary angioplasty. BACKGROUND: Meta-analyses have shown significant reduction of restenosis after coronary angioplasty upon supplementation with n-3 FA. METHODS: In a prospective, placebo-controlled, double-blind study, 500 patients were randomly allocated to treatment with n-3 FA (Omacor, Pronova AS, Oslo, Norway) 5.1 g/day or corn oil (placebo) starting at least two weeks prior to elective coronary angioplasty. The treatment was continued until restenosis evaluation by quantitative coronary angiography after six months. Stenosis was defined as a minimal luminal diameter (MLD) < 40% of the reference diameter. Successful coronary angioplasty was defined as > or = 20% acute gain in MLD and a residual stenosis < 50%. Restenosis was defined as > or = 20% late loss of diameter and stenosis > 50% or an increase in stenosis of > or = 0.7 mm. Three-hundred ninety-two patients fulfilled the criteria for initial stenosis and successful coronary angioplasty, and, except four patients who died, none were lost for follow-up. RESULTS: Restenosis occurred in 108/266 (40.6%) of the treated stenoses in the Omacor group and in 93/263 (35.4%) in the placebo group (odds ratio [OR] 1.25, 95% confidence interval [CI] [0.87-1.80] p = 0.21). In the Omacor group one or more restenoses occurred in 90/196 (45.9%) patients as compared with 86/192 (44.8%) in the placebo group (OR 1.05, 95% CI [0.69-1.59] p = 0.82). CONCLUSIONS: Supplementation with 5.1 g n-3 FA/day for six months, initiated at least two weeks prior to coronary angioplasty did not reduce the incidence of restenosis.     

Influence of residual stenosis in determining restenosis after cutting balloon angioplasty.

The cutting balloon is a new device for coronary angioplasty, which, by the combination of incision and dilatation of the plaque, is believed to minimize arterial wall trauma, the neoproliferative response, and subsequent restenosis. In this study, we sought to determine predictors of the restenosis using this technique. Seventy-seven patients underwent successful coronary angioplasty with cutting balloon alone. In 67 of these patients (87%), we performed a control angiogram at 6-month follow-up. Pre-, post-, and late angiographic results were evaluated by quantitative coronary analysis. Clinical and angiographic variables were correlated with restenosis as a binary variable and a continuous variable (late loss and late minimum luminal diameter). Univariate analysis showed that the immediate postprocedure minimum luminal diameter (MLD) was smaller in the restenotic group (defined as MLD > 50% by quantitative coronary angiography) than in the nonrestenotic group (1.90 +/- 0.47 mm vs. 2.19 +/- 0.56 mm, P < 0.05). In addition, the immediate percentage of stenosis was higher in the restenotic group than in the nonrestenotic group (37% +/- 10% vs. 27% +/- 11%, P < 0. 003). Multivariate analysis identified the immediate postcutting balloon percentage of stenosis as an independent determinant of binary restenosis (P < 0.008). When restenosis was defined as a continuous variable, the immediate postprocedure MLD was an independent predictor of late loss (P < 0.02) and of late MLD (P < 0. 0002). No clinical, preprocedure angiographic, or technical variables tested were associated with restenosis. The degree of postprocedural residual stenosis after cutting balloon angioplasty is predictive of late restenosis.