Postprocedural PAI-1 activity is a risk marker of subsequent clinical restenosis in patients both with and without stent implantation after elective balloon PTCA.

Stent implantation after balloon dilation of coronary arteries has improved clinical prognosis in patients undergoing transluminal coronary angioplasty (PTCA), but late restenosis remains a relevant problem. A previous study has indicated that PAI-1 activity changes immediately after PTCA without stent implantation are predictive of clinical restenosis. The present study was aimed to investigate the early PAI-1 changes and fibrin formation in patients undergoing elective PTCA with stent implantation. PAI-1 activity and D-dimer plasma levels were evaluated in two groups of patients (G1 underwent only elective balloon PTCA and G2 underwent elective PTCA with stent implantation) before and after the procedure. At the end of the procedure, PAI-1 activity significantly decreased, while D-dimer levels significantly increased in both groups. Post-PTCA D-dimer levels in the group with stent implantation were significantly higher than in the other group (P<.05). In both groups of patients, the post-PTCA PAI-1 activity was higher in patients with subsequent clinical recurrence with restenosis (P<.005 in G1 and P<.0005 in G2) than in those without, whereas no differences were found in D-dimer levels. In conclusion, our results demonstrate that fibrin formation assessed by D-dimer levels is enhanced by stent implantation. However, this behaviour is not related, differently from PAI-1 changes, to subsequent occurrence of clinical restenosis.

Transferring patients for direct coronary angioplasty: a retrospective analysis of 135 unselected patients with acute myocardial infarction.

BACKGROUND: Direct coronary angioplasty (PTCA) represents the most effective treatment for acute myocardial infarction. However, only a minority of patients are initially admitted to hospitals with direct PTCA facilities available 24 hours daily. The safety and benefits of transfer direct PTCA are debated, and we have no data about the early return of patients to the admission hospital. METHODS: We report our experience with transfer direct PTCA in unselected patients with acute myocardial infarction, and the early post-procedural return to the referring hospitals. RESULTS: One hundred and thirty-five unselected patients with acute myocardial infarction were referred to our center for direct PTCA during 1998. The majority of patients (n = 93, 69%, group T) were initially admitted to a primary hospital whereas the rest (n = 42, 31%, group NT) were directly admitted to our hospital. One hundred and thirty-four patients underwent coronary angiography, and direct PTCA was attempted in 126 patients. The median time interval between admission and direct PTCA was higher in group T (60 vs 40 min, p < 0.001). Only 3 patients (3.2%) had severe complications during transfer to our center: 1 patient with cardiogenic shock died, and 2 patients had ventricular fibrillation. The procedural and in-hospital outcomes of both groups were similar. The early post-procedural transfer to the referring hospital was possible in 88% of patients; no complications occurred during the transfer. The incidences of cardiac mortality at 6 months and at long-term follow-up were 3.4 and 5.1% respectively. CONCLUSIONS: In our experience, interhospital transfer for direct PTCA in unselected patients with acute myocardial infarction is feasible and safe. The early return to the admission hospital is safe and does not negatively influence the in-hospital outcome.

An angiographic evaluation of restenosis rate at a six-month follow-up of patients with ST-elevation myocardial infarction submitted to primary percutaneous coronary intervention.

BACKGROUND: Percutaneous coronary intervention (PCI) is considered to be the optimal type of revascularization in patients with ST-segment elevation myocardial infarction (STEMI). However, the long-term effectiveness of this procedure can be reduced by restenosis. This investigation was aimed at a prospective evaluation, in a group of STEMI patients of "the real world" (not involved in randomised trials), of the angiographic restenosis rate at a 6-month follow-up, and at identifying the relationship between restenosis and the patients' characteristics. MATERIALS AND METHODS: Our study population consisted of 123 patients with STEMI submitted to primary PCI to then undergo stress echocardiography 3 months after PCI and an angiographic evaluation at a 6-month follow-up. RESULTS: a) In real life the restenosis rate is quite high (42.3%); b) no correlation was found between patients' clinical characteristics and restenosis; c) restenosis rate was higher in patients with bare metal stents than in those with drug-eluting stents (55.8% vs. 11.1%; p<0.001); in patients with longer stents (21.6+/-8.62 vs 18.1+/-6.34 mm, p=0.015) and when more than one stent was implanted. Moreover, a consistent number of patients showed restenosis though asymptomatic. CONCLUSIONS: Our data suggest that primary PCI is associated with a high incidence of angiographic restenosis. No correlation was found between patients' clinical characteristics and restenosis. The length and the number of implanted stents seem to be associated with a more probable restenosis at six-month angiographic evaluation. Drug-eluting stent implantation seems to be associated with a lower incidence of restenosis even in STEMI patients.

Relevance of post-methionine homocysteine and lipoprotein (a) in evaluating the cardiovascular risk in young CAD patients.

BACKGROUND: Aims of our study were to evaluate the prevalence of high lipoprotein (a) [Lp(a)] and homocysteine levels - both in the fasting state (FHcy) and post-methionine (PMHcy) - in young coronary artery disease (CAD) patients, and to investigate the role of genetic and environmental factors for hyperhomocysteinaemia. MATERIALS AND METHODS: We studied 140 patients with angiographically documented CAD (24 women

Advances in antithrombotic therapy of acute myocardial infarction.

The aim of the acute treatment of myocardial infarction is to restore, as promptly as possible, blood flow in the culprit vessel. Thrombolysis is a cornerstone of treatment, and direct coronary angioplasty (PTCA) is emerging as a valuable or even better alternative reperfusion strategy. The activation of hemostasis after plaque disruption, thrombolysis, or PTCA represents a strong rationale for the use of antithrombotic drugs. The results of the ISIS-2 trial and the data from the Antiplatelet Trialists' Collaboration indicated that aspirin is mandatory in patients with acute myocardial infarction and for secondary prevention. Recently, the efficacy of abciximab and other glycoprotein IIb/IIIa inhibitors was proven in the treatment of acute coronary syndromes and after PTCA, and their early use in patients with acute myocardial infarction is presently under evaluation. Anticoagulation with heparin appears to be only slightly effective in acute myocardial infarction not treated with thrombolysis; however, a rationale exists for its use in patients undergoing percutaneous and/or surgical revascularization and in conjunction with fibrin-specific thrombolytic agents. Further studies are under way on the possible usefulness of low-molecular-weight heparin. Direct antithrombin agents (hirudin, hirulog, and others) have been recently studied as an adjunct to thrombolysis. The data from these studies indicate the presence of a narrow therapeutic window, with only marginal advantage over heparin; studies with newer compounds are ongoing. Aspirin is still a mandatory drug in patients with acute myocardial infarction; the most promising agents in this setting seem to be glycoprotein IIb/IIIa inhibitors. Heparin and low-molecular-weight heparins are indicated in selected cases, and further studies are needed to assess the value of newer direct thrombin inhibitors.

Angiotensin converting enzyme DD genotype affects the changes of plasma plasminogen activator inhibitor-1 activity after primary percutaneous transluminal coronary angioplasty in acute myocardial infarction patients.

Angiotensin converting enzyme (ACE) DD genotype, and plasminogen activator inhibitor (PAI-1) 4G/4G genotype have been reported to affect PAI-1 activity in control subjects and atherosclerotic patients, but no data are available on the influence of angiotensin II type 1 receptor (AT1R) A1166C polymorphism on the inhibitor levels. The degree of fibrinolytic activation after percutaneous transluminal coronary angioplasty (PTCA) has been found to affect the risk of restenosis. The aim of this study was to investigate the possible influence of ACE I/D, AT1R A1166C, and PAI-1 4G/5G polymorphisms on the changes of PAI-1 activity after primary successful percutaneous transluminal angioplasty. In 29 consecutive acute myocardial infarction patients, undergoing primary successful angioplasty, genotyping of ACE I/D, AT1R A1166C, and PAI-1 4G/5G polymorphisms was performed by polymerase chain reaction and restriction fragment length polymorphism analysis, and PAI-1 plasma activity (chromogenic method) was assessed before and after angioplasty. Following angioplasty, PAI-1 activity increased in 10 of 29 patients and decreased or remained unchanged in 19 of 29. ACE DD genotype was significantly (P = 0.04) associated with an increase of PAI-1 activity post angioplasty (OR DD/ID+II = 6.5, CI 95% 4.83-8.22). Whereas no effect of PAI-1 4G/5G and AT1R A1166C polymorphisms on PAI-1 response to angioplasty was demonstrated, these data suggest that renin-angiotensin system genes are involved in the regulation of the fibrinolytic response to balloon injury, possibly affecting angiotensin converting enzyme activity. This interaction between the renin-angiotensin system and hemostasis may be a mechanism by which ACE DD genotype affects the risk of restenosis after percutaneous transluminal angioplasty.