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Aims: Although hirudin is superior to unfractionated heparin for prevention of death, myocardial infarction, or refractory ischaemia in patients with non-ST-elevation acute coronary syndrome, it is not clear whether hirudin is also of benefit in acute coronary syndrome patients undergoing early percutaneous coronary intervention., Methods and Results: In the OASIS 2 trial, 10 141 patients with non-ST-elevation acute coronary syndrome were randomized to 72 h of intravenous hirudin or unfractionated heparin. Percutaneous coronary intervention was performed at the discretion of the investigator. One hundred and seventeen patients underwent percutaneous coronary intervention within the first 72 h ("early percutaneous coronary intervention"). In patients undergoing early percutaneous coronary intervention, hirudin compared with unfractionated heparin was associated with a significantly lower incidence of death or myocardial infarction at 96 h (6.4% vs 21.4%, OR 0.30; 95% CI: 0.10-0.88) and 35 days (6.4% vs 22.9%, OR 0.25; 95% CI: 0.07-0.86). In the unfractionated heparin group, death or myocardial infarction was significantly higher at 35 days in patients undergoing early percutaneous coronary intervention compared with those managed conservatively (22.9% vs 7.3%, OR 3.14, P<0.001) but this early percutaneous coronary intervention-related hazard was not observed in hirudin-treated patients (6.4% vs 6.8%, OR 0.94 P=1.0). A time-dependent covariate for percutaneous coronary intervention was not significant in a Cox regression model, suggesting a similar treatment benefit with hirudin before and after percutaneous coronary intervention. After adjustment for percutaneous coronary intervention propensity, the benefits of hirudin remained significant. There were three major bleeds in patients undergoing early percutaneous coronary intervention, all in patients randomized to hirudin., Conclusion: In patients with non-ST-elevation acute coronary syndrome undergoing early percutaneous coronary intervention, a direct thrombin inhibitor such as hirudin may be more effective than heparin in reducing the incidence of ischaemic complications., (Copyright 2001 The European Society of Cardiology.)

Background: ORG31540/SR90107A, a synthetic pentasaccharide, is a selective inhibitor of factor-Xa. It was hypothesized that prolonged factor-Xa inhibition with pentasaccharide may be an effective and safe antithrombotic co-therapy in acute myocardial infarction., Methods and Results: Patients (n=333) with evolving ST-segment elevation acute myocardial infarction were treated with aspirin and alteplase and randomized to unfractionated heparin, given intravenously during 48 to 72 h, or to a low, medium or high dose of pentasaccharide, administered daily for 5 to 7 days, intravenously on the first day, then subcutaneously. Coronary angiography was performed at 90 min and on days 5 to 7. Thrombolysis in Myocardial Infarction (TIMI) flow grade 3 rates at 90 min were similar in the four treatment groups. Among patients with TIMI 3 flow at 90 min and who did not undergo a coronary intervention (n=155), a trend towards less reocclusion of the infarct-related vessel on days 5 to 7 was observed with pentasaccharide: 0.9% vs 7.0% with unfractionated heparin (P=0.065). Also, fewer revascularizations during the 30-day follow-up period were performed in patients given pentasaccharide (39% vs 51% for unfractionated heparin;P=0.054). The primary safety end-point, the combined incidence of intracranial haemorrhage and need for blood transfusion, was identical with pentasaccharide and unfractionated heparin (7.1%). One non-fatal intracranial haemorrhage occurred in the 241 patients given pentasaccharide (0.4%)., Conclusions: In this study, pentasaccharide given together with alteplase was safe and as effective as unfractionated heparin in restoring coronary artery patency. Prolonged administration of pentasaccharide was associated with a trend towards less reocclusion and fewer revascularizations. Selective factor-Xa-inhibition seems to be an attractive therapeutic concept in patients presenting with ST-segment elevation acute myocardial infarction., (Copyright 2001 The European Society of Cardiology.)

Aims: Rotablation is a widely used technique for the treatment of complex coronary artery lesions but is so far only poorly supported by controlled studies. The Comparison of Balloon-Angioplasty versus Rotational Atherectomy study (COBRA) is a multicentre, prospective, randomized trial to compare short- and long-term effects of percutaneous transluminal coronary angioplasty (PTCA) and rotablation in patients with angiographically pre-defined complex coronary artery lesions., Methods and Results: At seven clinical sites 502 patients with pre-defined complex coronary artery lesions were assigned to either PTCA (n=250) or rotablation (n=252). Primary end-points were procedural success, 6-month restenosis rates in the treated segments, and major cardiac events during follow-up. Procedural success was achieved in 78% (PTCA), and 85% (rotablation) (P=0.038) of cases. Crossover from PTCA to rotablation was 4% and 10% vice versa (P=0.019). There was no difference between PTCA and rotablation with respect to procedure-related complications such as Q wave infarctions (2.4% each), emergency bypass surgery (1.2% versus 2.4%), and death (1.6% versus 0.4%). However, more stents were required after PTCA (14.9% versus 6.4%, P<0.002), predominantly for bailout or unsatisfactory results. Including bail-out stents as an end-point, the procedural success rates were 73% for angioplasty and 84% for rotablation (P=0.006). At 6 months, symptomatic outcome, target vessel reinterventions and restenosis rates (PTCA 51% versus rotablation 49%, P=0.33) were not different., Conclusion: Complex coronary artery lesions can be treated with a high level of success and low complication rates either by PTCA with adjunctive stenting or rotablation. The long-term clinical and angiographic outcome is comparable.

Aims: The aim of the study was to compare the 10-year follow-up results of patients with or without restenosis following single-vessel percutaneous transluminal coronary angioplasty (PTCA)., Methods and Results: A total of 313 patients with successful PTCA (> or = 20% reduction in luminal diameter narrowing without acute complications) and a control angiography 6 months after PTCA were included in the study. Events during the follow-up period were defined as death, myocardial infarction, bypass surgery, or repeat PTCA. Statistical evaluation was performed by the Fisher test, logistic regression, and life-table analysis. Restenosis (loss of > 50% of the initial gain 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 group B, 11 (13%) patients suffered myocardial infarction (ns); 17 group A (8%) patients and 25 (29%) group B patients had bypass surgery (P < 0.0001), and 34 (15%) group A patients and 55 (63%) group B patients underwent repeat PTCA (P < 0.0001). Logistic regression analysis identified restenosis as an independent risk 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-term outcome than patients without restenosis. Although most patients with restenosis underwent repeat PTCA, the survival rate without any serious adverse events was only 59%, compared with 83% in patients without restenosis (P < 0.0001).

Although several randomized trials have been performed to compare the outcomes of percutaneous transluminal coronary angioplasty (PTCA) and coronary artery bypass surgery (CABG) in patients with multivessel disease, there is little data available on angiographic follow-up results. The present substudy of the German angioplasty versus bypass surgery investigation (GABI Trial) compares the angiographic revascularization status in these two cases 6 months after treatment. Follow-up angiograms were available in 102 CABG patients and 117 PTCA patients. Although the protocol excluded patients with total occlusion, on follow-up 6 months after treatment we found total occlusion of 94 native arteries (36.9%) in the CABG group and of six arteries (2.5%) in the PTCA group (P < 0.001). The rate of occluded native vessels did not correlate significantly with the severity of the lesion before bypass surgery. In the CABG group 31 bypass grafts (12.2%) were found to be occluded at the 6 month follow-up examination (29/225 vein grafts [12.9%]; 2/30 mammary artery grafts [6.7%]). The main pathway, defined as the nutrient vessel (native vessel or bypass graft) providing the least resistance to blood flow, was narrowed by a lesion with a diameter stenosis of 70-100% for 36 target lesions (14.1%) in the CABG group and 39 target lesions (16.2%) in the PTCA group (P, ns). However, the prevalence of moderately severe lesions with a 50-69% diameter reduction of the main pathway was significantly greater in the PTCA group (44 lesions, 18.3%) than in the CABG group (19 lesions, 7.5%, P < 0.01). Thus, 6 months after randomized allocation to PTCA or CABG, we found comparable rates of high-grade lesions in the main pathways of both treatment groups. Whereas moderately severe lesions of the main pathway were predominantly seen in the PTCA group, there was marked disease progression to total occlusion in the native circulation after bypass grafting.

Percutaneous transluminal coronary angioplasty is often complicated by thrombotic abrupt vessel closure in patients with unstable angina pectoris. The present multicentre trial was performed to determine the feasibility of two-dose regimens of recombinant hirudin (r-hirudin) compared to standard heparin in patients undergoing coronary angioplasty for unstable angina, and to investigate the effects of the different treatment regimen on markers of coagulation activation. At five participating centres, 61 patients were randomly enrolled in one of two sequential groups of r-hirudin (group 1: 0.3 mg.kg-1 i.v. bolus, 0.12 mg.kg-1.h-1 i.v. infusion; 21 patients; group 2: 0.5 mg.kg-1 i.v. bolus, 0.24 mg.kg-1.h-1 i.v. infusion; 19 patients) or in a heparin control group (150 IU.kg-1 i.v. bolus, 20 IU.kg-1.h-1 i.v. infusion; 21 patients). Antithrombotic therapy was started immediately before coronary angioplasty and continued for 24 h. This was followed by a low-dose anticoagulant infusion for another 24 h (r-hirudin: 0.04 mg . kg-1 . h-1; heparin: 7 IU . kg-1 . h-1). Activated partial thromboplastin time, r-hirudin plasma concentrations by both immunological and functional assay, thrombin-hirudin complex, thrombin-antithrombin III complex, soluble fibrin, and prothrombin fragment 1 + 2 were closely monitored. The median partial thromboplastin time prolongations at 24 h vs baseline were found to be 1.9-fold and 2.3-fold in r-hirudin group 1 and dose group 2, respectively, and 3.0-fold in the heparin group. There was a dose-dependent correlation between partial thromboplastin time and the r-hirudin plasma levels (r = 0.61). In five of 21 patients of dose group 1, three of 19 patients of dose group 2, and 10/21 patients of the heparin group, partial thromboplastin time values exceeding the predefined target range prompted an interruption of the infusion. One major bleeding complication occurred in dose group 2. The functional assay for the estimation of r-hirudin plasma concentrations showed excellent correlations to the immunological technique (r = 0.99). Differences between the thrombin-hirudin complex levels could not be observed. Increased concentrations of thrombin-antithrombin III complex, soluble fibrin, and prothrombin fragment 1 + 2 were seen 4-8 h after coronary angioplasty and after reduction of the high-dose therapy in dose group 1 when compared with dose group 2 and the heparin group, respectively. Based on coagulation tests the present study showed the feasibility of a periprocedural antithrombotic regimen with r-hirudin for patients undergoing coronary angioplasty for unstable angina. In addition to the partial thromboplastin time the determination of r-hirudin plasma levels by a chromogenic substrate assay considerably improves the monitoring of therapy. The lower dose r-hirudin regimen seems to be suboptimal as periprocedural anticoagulation in coronary angioplasty patients as indicated by markers of thrombin generation and thrombin activity.

Background: A substantial proportion of patients undergoing heart catheterization for suspected coronary artery disease have normal angiograms. Coronary morphology and blood flow velocity can be assessed very accurately with intracoronary ultrasound and Doppler. The purpose of this study was to use both methods to classify further patients with suspected coronary artery disease but with coronary angiograms adjudged normal at the time., Methods and Results: In forty-four patients with suspected coronary artery disease and normal coronary angiograms, intracoronary ultrasound and intracoronary Doppler were performed in the left anterior descending and left main coronary arteries. Coronary flow reserve was obtained by calculating the ratio of the maximal coronary flow mean velocity after the intracoronary administration of 10 mg papaverine to the coronary flow mean velocity at rest. Of 44 patients, 16 (36%) (group I) were found to have normal coronary morphology by intracoronary ultrasound and normal (> 3.0) coronary flow reserve (5.3 +/- 1.8). In seven patients (16%) (group II) there were normal intracoronary ultrasonic findings but a reduced coronary flow reserve (2.1 +/- 0.4). Plaque formation was found in a total of 21 (48%) of the 44 patients; mean plaque sizes were 3.6 +/- 1.6 mm2 for those in group III (normal coronary flow reserve) and 5.0 +/- 2.3 mm2 for those in group IV (reduced coronary flow reserve). Vessel area in both of these groups (16.3 +/- 8.0 mm2 and 19.2 +/- 6.1 mm2) was significantly larger than that of group I (14.6 +/- 5.7 mm2, P < 0.01). Plaque calcification was found in 25% of those in group III and 44% of those in group IV. Thus, only 36% of the patients with normal angiograms were true normal, 48% exhibited early stage of coronary atherosclerosis, and the other 16% might be considered as syndrome X., Conclusion: Intracoronary ultrasound and Doppler can be used to differentiate further heart disease in patients with normal coronary angiograms. Only a minority were true normal. Early signs of atherosclerosis cannot be detected by coronary angiography. This may have important therapeutic and prognostic implications.

The aim of this study was to compare the morphology of stable and unstable coronary lesions using intravascular ultrasound in patients undergoing coronary balloon angioplasty and to determine whether lesion morphology had any influence on the mechanism of balloon angioplasty. Thirty three (15 stable and 18 unstable) patients undergoing single lesion percutaneous transluminal coronary angioplasty were studied with intravascular ultrasound before and after intervention. All examinations, recorded on S-VHS video tape, were studied off-line and matched sites from the point of minimum lumen area after the procedure and the corresponding site prior to intervention were compared. The morphology of lesions before intervention was noted and the mechanisms of angioplasty (vessel stretch, lesion remodelling and lesion tears) were determined by comparing pre- and post-interventional morphology and dimensions. The only significant morphological difference between stable and unstable lesions was the presence of a demarcated inner layer in unstable lesions, delimited by a fine circumferential line. This pattern was noted in 77% (14/18) of unstable lesions and in 7% (1/15) of stable lesions (P < 0.01). Unstable lesions tended to have more echolucent zones than stable lesions (72% (13/18) vs 46% (7/15), P = 0.13). The mechanisms of angioplasty were also found to differ. Whereas lesion remodelling (or 'compression') was seen in 77% (14/18) of unstable lesions, it occurred in only 13% (2/15) of stable lesions and mean lesion cross-sectional area reduction was greater in unstable lesions, - 14.8 +/- 8.3% (2.1 +/- 1.3 mm2) compared to stable lesions, - 4.1 +/- 8.4% (0.42 +/- 0.9 mm2), P < 0.01. In contrast, vessel stretch was seen more frequently in stable lesions (73%, 11/15) compared to unstable lesions (22%, 4/18) P < 0.01 and the mean increase in vessel cross-sectional area was + 13.5 +/- 6.8 (1.6 +/- 0.9 mm2) in stable lesions compared to + 5.5 +/- 5.6% (0.8 +/- 0.9 mm2) in unstable lesions, P < 0.01. Lesion tear was present to a similar degree in both groups of patients. In this observational study we found a set of echographic markers that distinguished unstable lesions. The mechanisms of angioplasty differed between stable and unstable angina, with greater lesion remodelling seen in unstable lesions and vessel stretch in stable lesions. Taken together, these findings suggest that the markers we describe may be echographic indicators of mural thrombus.

We evaluated prospectively clinical and angiographic data in 400 patients, 200 with unstable and 200 with stable angina in order to determine which clinical markers could reliably predict unstable coronary artery lesions. Comparison of the angiogram of 200 patients with unstable and 200 with stable angina revealed a high-grade lesion (42% vs 23%, P < 0.0001), complex lesion morphology (49% vs 20%, P < 0.0001) and thrombus-containing lesions (7% vs 1%, P = 0.006) as typical findings in patients with unstable angina. A high-grade lesion and/or complex lesion (including thrombotic lesions but excluding total occlusion) was found in 61% of unstable and 34% of stable patients (P < 0.0001). Clinical features including the Braunwald classification of unstable angina were then evaluated by means of a multivariate approach with regard to their ability to predict the presence of unstable coronary artery lesions. Multivariate analysis revealed an abnormal ECG as the single most predictive clinical indicator of complex lesion morphology (P < 0.0001, odds ratio 4,2). The clinical presentation of recent onset of angina was highly predictive of a high grade lesion (P = 0.0003, odds ratio 3,2). The endpoint of a high-grade and/or a complex lesion was identified by an abnormal ECG (P = 0.0015, odds ratio 3,0) and recent onset angina (P = 0.0119, odds ratio 2,5). Thus, a high grade and/or complex lesion, typical of patients with unstable angina, was best identified by the clinical feature of recent onset angina and/or abnormal ECG changes.

The purpose of the study was to evaluate prospectively the effect of a continuous perfusion balloon catheter ('High Flow CPC Mainz', Schneider/Pfizer Europe AG, CH-8052 Zurich, Switzerland) on tolerated inflation time during elective PTCA (n = 31), and its usefulness in cases of unsatisfactory morphological or functional results after PTCA (n = 42). Sixty-five patients were male, eight female; their mean age was 57.6 +/- 8.85 years. The target vessel was the LAD in 39 patients, the RCA in 29, the LCX in three, and bypass grafts in two. Seven patients had type A lesions, 44 type B and 22 type C, respectively. The target lesion was in the proximal third of the coronary artery in 41 patients, in the mid-third in 30, and in the distal third in two. Side branches were involved in 24 patients. The median size of the standard PTCA balloon was 3.00 mm and 3.5 mm for the CPC. Tolerated inflation time rose from 36 +/- 21 s to 213 +/- 108 s (P < 0.01). Additionally, the CPC catheter was used in 42 patients with symptomatic dissections (ST segment elevation, chest pain, or impaired contrast run-off) after PTCA. Wall wrapping by CPC was successful in 24 (57%) and unsuccessful in 18 (43%) patients. A significant difference was found for the inflation times tolerated between patients with successful (265 +/- 99 s) and unsuccessful wall wrapping (161 +/- 108 s; P < 0.01). Of the 18 patients with unsuccessful wall wrapping, 11 (61%) required an intracoronary stent, and six patients (30%) could be managed by medical treatment alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute occlusion of the left main coronary artery (LMCA) is a rare angiographic finding. We report five patients with acute myocardial infarction (AMI) and one patient with unstable angina, in whom reperfusion was achieved or attempted with percutaneous transluminal coronary angioplasty (PTCA). All patients had a long history of stable angina pectoris. The indication for emergency PTCA was cardiogenic shock in the five patients with MI. PTCA was successful in five of six patients. Three patients with reperfusion survived, three died. All survivors underwent coronary artery bypass grafting (CABG) and were still alive at 23 months, 3 and 8 years respectively in NYHA functional class II or III. All patients had a dominant right coronary artery, but only the survivors had moderate or extensive collateralization. Our experience and the literature review indicate that the clinical outcome of patients with acute LMCA occlusion is strongly dependent on the presence or absence of intercoronary collaterals.

Percutaneous transluminal coronary angioplasty (PTCA) was performed in 14 patients with significant left main stem stenosis following protective coronary artery bypass grafting (CABG). The procedure was successful in 13/14 patients (93%), achieving a decrease in mean diameter stenosis from 74% +/- 7% to 31% +/- 12% (P less than 0.01). Accordingly, the absolute stenosis diameter increased from 0.9 mm +/- 0.3 mm to 2.4 mm +/- 0.5 mm (P less than 0.01). Dissection of the left main stem artery and a transient significant fall of blood pressure each occurred in one patient. No other serious complications were noted. Eight of 13 patients (62%) with successful PTCA underwent control angiography. Restenosis had occurred in 3 of 8 patients (38%) with total occlusion of the left main stem in 1 patient. All bypass grafts were found to be patent at follow-up. Clinical evaluation in all 14 patients revealed no serious events (death, myocardial infarction, repeat revascularization procedure) during a mean follow-up period of 27 months (range 6-39 months). PTCA of the left main stem following CABG can be considered a relatively safe and effective procedure with a marked restenosis-rate but beyond that, an uncomplicated long-term follow-up.

Acute results and follow-up data over a period of 36 months after attempted PTCA in 406 patients with stable angina and 202 patients with unstable angina are reported. The rate of acute complications (death, myocardial infarction and bypass grafting (CABG) amounted to 1.5% in stable and 6.4% in unstable patients (P less than 0.005). Within the first week after PTCA a significantly lower percentage (1.7% vs 10.4%) of cardiac events (death, myocardial infarction, CABG and repeat PTCA) was observed in the stable group (P less than 0.001). During a 12-month follow-up period, another 16.3% of the patients in the stable group and 30.7% of unstable patients suffered a new cardiac event (P less than 0.001). The long-term follow-up of 36 months revealed no significant difference in the event rate between stable and unstable patients (5.4% in both groups). The cumulative rate of myocardial infarction within 3 years after PTCA was significantly lower (3.7% vs 9.4%) in the stable group (P less than 0.005). The cumulative mortality amounted to 3.0% in stable and 6.4% in unstable patients (P less than 0.05) and the incidence of repeated PTCA was 8.1% and 19.3% respectively (P less than 0.001). The crossover rate to CABG was 10.1% in stable and 17.8% in unstable patients (P less than 0.01). The total rate of any cardiac event thus amounted to 24.9% in stable and 53.0% in unstable patients (P less than 0.001) within a 3-year follow-up period. At the end of follow-up, 74% of the stable patients were asymptomatic, compared with 60% of unstable patients (P less than 0.01). 45% of the stable group patients and 28% of the unstable patients were not on antianginal treatment (P less than 0.01). We conclude that PTCA in unstable angina carries a markedly enhanced risk of acute complications and cardiac events in the early phase after PTCA. In the long run, patients with stable angina have a better quality of life with regard to medical treatment and angina symptoms.