Characteristics and prognosis of patients with angiographic stent thrombosis: comparison between drug-eluting and bare-metal stents.

INTRODUCTION: Conflicting data exist on the risk of stent thrombosis with drug-eluting stents (DES) versus bare-metal stents (BMS). Little is known about the potential different characteristics and outcomes of DES versus BMS thrombosis. OBJECTIVE: To compare the characteristics, timing and outcomes of patients with angiographic stent thrombosis according to type of stent implanted. METHODS: The population comprised consecutive patients who underwent BMS or DES implantation (January 2003-April 2007) at Pitié-Salpêtrière Hospital. Data from patients with and without a stent thrombosis were compared to identify predictors of thrombosis. Timing of thrombosis (acute,<24 hours; subacute,<30 days; late,>30 days; very late,>1 year), clinical, angiographic and procedural characteristics, and outcomes were compared between patients with a BMS or DES thrombosis. RESULTS: A total of 3579 patients received a BMS (2815 lesions, 2318 patients) or a DES (1536 lesions, 1261 patients). Documented angiographic stent thrombosis occurred in 52 (1.4%) patients, 16 (1.3%) with a DES and 36 (1.6%) with a BMS. Rates of acute (0.1% versus 0.2%), subacute (1% versus 0.7%), late (both 0.2%) and very late (both 0.2%) thrombosis were similar in patients with BMS and DES thrombosis. Factors predictive of stent thrombosis were similar, including left ventricular failure (P<0.0001), initial percutaneous coronary intervention (PCI) for acute myocardial infarction (P<0.0001), multivessel PCI (P<0.0001), and balloon dilatation before stenting (P<0.04). Eleven (21%) cases of BMS (n=8, 22%) or DES (n=3, 19%) thrombosis arose soon after stopping antiplatelet therapy. Thirteen of 52 (25%) patients died a few hours after the event. Twenty-seven (52%) major adverse cardiac events occurred at 18 months, 7 in patients with a DES and 20 in those with a BMS (44% versus 55%, P=NS). These included 16 deaths (31%), 7 repeat PCIs and 4 myocardial infarctions. There were no independent predictive factors of death after stent thrombosis. CONCLUSIONS: BMS and DES thrombosis are similar in terms of timing of thrombosis, characteristics and outcomes, and share the same risk of late thrombosis after interruption of antiplatelet therapy.

[The value of active stents for coronary angioplasty in patients with chronic renal failure]. / Intérêt du stent actif dans l'angioplastie coronaire chez l'insuffisant rénal chronique.

UNLABELLED: The risk of intra-stent restenosis has diminished considerably with the advent of endoprostheses which actively release sirolimus or paclitaxel. Patients with chronic renal failure constitute a high cardiovascular risk population, in whom the incidence of coronary heart disease is particularly high, representing one of the principal causes of death. The aim of this study, which included 152 patients, was to quantify the value of active stents for coronary angioplasty in patients with chronic renal failure. Thirty eight patients with chronic renal failure who underwent angioplasty with active stents were matched for age, sex and the presence of diabetes with 3 other groups of patients: one group with active stents but without renal failure, one group with inactive stents and no renal failure, and one group with inactive stents and chronic renal failure. The average follow up was 16 +/- 5 months. The acute stent thrombosis rate (2%) was not elevated in cases of renal failure nor after active stent implantation. Chronic renal failure significantly increased the mortality rate 16 months after angioplasty, whichever type of stent was used: 8 versus 2% deaths in patients with an inactive stent (p = 0.001). In renal failure, the risk of death was lower with an active stent (8 vs 26% with an inactive stent, p<0.05). Similarly, there was a non-significant trend towards a lower risk of death and/or infarction in renal failure after active stents (8 vs 21% with an inactive stent, NS). CONCLUSIONS: In this study, coronary angioplasty with an active stent in patients with chronic renal failure was associated with a lower mortality rate compared with inactive stents, with no increase in the risk of acute thrombosis.

[Antithrombotics in pre-hospital phase of acute coronary syndromes]. / Antithrombotiques durant la phase préhospitalière des syndromes coronaires aigus.

Antithrombotic therapies are the corner stone of acute coronary syndrome management. We have the proof that many of them should be initiated during the prehospital care because their clinical benefit is time-dependent. The hypothesis that anticoagulation therapy is an effective treatment of STEMI, which benefit is time-dependent, is now validated. It is also fair to affirm that GP lIb/IIIa receptor inhibitors are the adjuvant therapy of choice for primary PCI. Indeed, these medications reduce short-term and long-term mortality. This clinical benefit is time dependent. Clopidogrel therapy is probably also a medication of the prehospital phase. It is well established now that the biological efficacy of this pro drug is loading dose dependent. It is also demonstrated that its clinical efficacy depends on the time delay between symptom onset and initiation of the therapy. However, the clinical benefit of prehospital administration remains to be established.

Impact of prior use or recent withdrawal of oral antiplatelet agents on acute coronary syndromes.

BACKGROUND: Oral antiplatelet agents (OAAs) can prevent further vascular events in cardiovascular disease. How prior use or recent discontinuation of OAA affects clinical presentation of acute coronary syndromes (ACS) and clinical outcomes (death, myocardial infarction [MI]) is unclear. METHODS AND RESULTS: We studied and followed up for up to 30 days a cohort of 1358 consecutive patients admitted for a suspected ACS; of these, 930 were nonusers, 355 were prior users of OAA, and 73 had recently withdrawn OAA. Nonusers were at lower risk, more frequently presented with ST-elevation MI on admission, and more frequently had Q-wave MI at discharge than prior users (36.6% versus 17.5%, P<0.001; and 47.8% versus 28.2%, P<0.001, respectively). However, there was no difference regarding the incidence of death or MI at 30 days between nonusers and prior users (10.3% versus 12.4%, P=NS). In addition, prior users experienced more major bleeds within 30 days compared with nonusers (3.4% versus 1.4%, respectively; P=0.04). Recent withdrawers were admitted on average 11.9+/-0.8 days after OAA withdrawal. Interruption was primarily a physician decision for scheduled surgery (n=47 of 73). Despite a similar cardiovascular risk profile, recent withdrawers had higher 30-day rates of death or MI (21.9% versus 12.4%, P=0.04) and bleedings (13.7% versus 5.9%, P=0.03) than prior users. After multivariate analysis, OAA withdrawal was found to be an independent predictor of both mortality and bleedings at 30 days. CONCLUSIONS: Among ACS patients, prior users represent a higher-risk population and present more frequently with non-ST-elevation ACS than nonusers. Although patients with a recent interruption of OAA resemble those chronically treated by OAA, they display worse clinical outcomes.

Anti-Xa activity relates to survival and efficacy in unselected acute coronary syndrome patients treated with enoxaparin.

BACKGROUND: Low-molecular-weight heparin (LMWH) is recommended in the treatment of unstable angina (UA)/non-ST-segment-elevation myocardial infarction (NSTEMI), but no relationship has ever been shown between anticoagulation levels obtained with LMWH treatment and clinical outcomes. METHODS AND RESULTS: In all, 803 consecutive patients with UA/NSTEMI were treated with subcutaneous enoxaparin and were followed up for 30 days. The recommended dose of enoxaparin of 1 mg/kg BID was used throughout the population except when physicians decided on dose reduction because of a history of a recent bleeding event or because of a high bleeding risk. Anti-factor Xa activity was >0.5 IU/mL in 93% of patients; subtherapeutic anti-Xa levels (<0.5 IU/mL) were associated with lower doses of enoxaparin. The 30-day mortality rate was significantly associated with low anti-Xa levels (<0.5 IU/mL), with a >3-fold increase in mortality compared with the patients with anti-Xa levels in the target range of 0.5 to 1.2 IU/mL (P=0.004). Multivariate analysis revealed low anti-Xa activity as an independent predictor of 30-day mortality at least as strong as age, left ventricular function, and renal function. In contrast, anti-Xa activity did not predict major bleeding complications within the range of anti-Xa levels observed in this study. CONCLUSIONS: In this large unselected cohort of patients with UA/NSTEMI patients, low anti-Xa activity on enoxaparin treatment is independently associated with 30-day mortality, which highlights the need for achieving at least the minimum prescribed anti-Xa level of 0.5 IU/mL with enoxaparin whenever possible.

Subcutaneous enoxaparin with early invasive strategy in patients with acute coronary syndromes.

BACKGROUND: Subcutaneous enoxaparin during at least 48 hours provides adequate anticoagulation and good clinical results in patients with non-ST-segment elevation acute coronary syndromes undergoing percutaneous coronary intervention (PCI). METHODS: In this nonrandomized retrospective study, we compared 347 patients with non-ST-segment elevation acute coronary syndromes who underwent rapid PCI after only 2 injections of subcutaneous enoxaparin (EI, n = 117) to those referred later to the catheterization laboratory with >or=3 injections (DI, n = 230). We measured anti-Xa at the time of PCI and evaluated bleeding and major ischemic events (death/myocardial infarction) at 30 days. RESULTS: Patients in the EI group more frequently received glycoprotein IIb/IIIa inhibitors and clopidogrel preceding PCI than did patients in the DI group (58.1% vs 31.7%, P <.0001 for glycoprotein IIb/IIIa inhibitors and 68.4% vs 40.4% for clopidogrel pretreatment, P <.0001, respectively). The anti-Xa activity measured at the time of catheterization (0.92 +/- 0.04 U/mL vs 0.96 +/- 0.02 U/mL, EI vs DI, P =.25) and the injection-to-catheterization times (5.6 +/- 0.2 h vs 5.2 +/- 0.1 h, EI vs DI, P =.17) were similar in both groups. The 30-day bleeding rates of 1.7% and 4.8% in the EI and DI strategies were found to be equivalent with a significant non-inferiority test for the EI strategy (P <.05). There was a nonsignificant trend for less death or myocardial infarction at 30 days in the EI group compared to the DI group (4.3% vs 7.0%, non-inferiority test not significant). CONCLUSION: A rapid invasive strategy with only 2 subcutaneous injections of enoxaparin provides similar levels of anticoagulation, and is associated with a favorable trend for ischemic events and with safety equivalent to a more prolonged "upstream" treatment with enoxaparin.

Acute release of plasminogen activator inhibitor-1 in ST-segment elevation myocardial infarction predicts mortality.

BACKGROUND: A few studies have suggested that von Willebrand factor (vWF) or plasminogen activator inhibitor-1 (PAI-1) can be associated with outcomes of acute coronary syndromes. The present study was designed to assess the acute release of these markers in ST-segment elevation myocardial infarction (STEMI) and their relations to death. METHODS AND RESULTS: In 153 consecutive patients with STEMI, vWF and PAI-1 antigens were measured on admission (H0) and 24 hours later (H24). At 30 days, the death rate was 7.2%. Heart failure (Killip stage > or =3) on admission was present in 13.7% of patients. The acute release of PAI-1 (H24-H0, in ng/mL) and of vWF (H24-H0, in %) was dramatically higher in patients who died than in those who survived (46.9+/-26.3 versus -0.6+/-2.8 ng/mL, P=0.0001 and 65.8+/-20.0% versus 10.0+/-5.1%, P=0.004 for PAI-1 and vWF, respectively) and in patients developing heart failure compared with those without (24.8+/-10.1 versus -1.1+/-3.3 ng/mL, P=0.004 and 47.3+/-11.0% versus 8.1+/-5.6%, P=0.005 for PAI-1 and vWF, respectively). The release of PAI-1 correlated weakly with the left ventricular ejection fraction (R=-0.195, P=0.01) and the peak of troponin (R=0.149, P=0.045). Postangioplasty TIMI-3 flow and the acute release of PAI-1 were the only 2 independent predictors of death at 30 days. CONCLUSIONS: The acute release of vWF and PAI-1 over the first 24 hours of STEMI is associated with death and heart failure. The acute rise of PAI-1 is also a strong independent predictor of death at 30 days.

[Role of glycoprotein IIb/IIIa inhibitors in the management of acute coronary syndromes]. / Intérêt de la prise en charge précoce des syndromes coronaires aigus par les anti-GPIIb/IIIa.

Antiplatelet therapy is a cornerstone in the medical management of acute coronary syndromes. Three classes of antiplatelet drugs are available in this setting: acetylsalicylic acid, thienopyridines, and glycoprotein IIb/IIIa antagonists. During the last ten years, numerous clinical trials have been conducted in large populations of patients suffering from acute coronary syndromes. Further investigations are in progress. In the light of these results, the respective roles of the different antiplatelet drugs have been more precisely defined, in terms of class preference as well as in terms of the combination of several antiplatelet drugs and of antiplatelet drugs with other therapies, including non fractionated--or low molecular weight--heparin and non-invasive or invasive revascularisation procedures. In the present article, we review the results of the major published or non published trials that addressed the role of glycoprotein IIb/IIIa antagonists in the management of acute coronary syndromes. Based on these results, the current therapeutic guidelines for clinical practice issued by the American and European cardiology societies are given in the conclusion, with their level of evidence.

[Non-ST acute coronary syndromes]. / Syndrome coronaire aigu sans--ST.

Acute coronary syndromes are the first cause of death in France. Unstable angina is the most frequent acute coronary syndrome. Risk stratification to predict morbimortality and the risk of major hemorrhage is the key step of the medical approach. Combined antithrombotic therapy (aspirine + clopidogrel + LMWH) has led to a substantial reduction of major coronary events with a good tolerance because of the short duration of such aggressive strategy. This combined antithrombotic also allowed to increase the benefit of an early invasive strategy including coronary angiogram with stent percutaneous coronary intervention.

Unprotected left main coronary artery stenting: correlates of midterm survival and impact of patient selection.

BACKGROUND: The study served to present the in-hospital and six-month clinical outcome and also the long-term survival data of a consecutive series of patients undergoing stenting for unprotected left main coronary artery (LMCA) disease. METHODS: Revascularization with coronary bypass surgery has been generally recommended for treatment of left main coronary stenosis. Improvements in angioplasty and coronary stent techniques and equipment may result in the wider applicability of a percutaneous approach. A total of 92 consecutive patients underwent unprotected LMCA stenting between March 1994 and December 1998. For the initial 39 patients (group I) angioplasty was performed only when surgical revascularization was contraindicated. The remaining 53 patients (group II) also included patients in whom surgery was feasible. Patients were followed for 7.3 +/- 5.8 months (median 239 days; range 49 to 1,477 days). RESULTS: Compared to group I, group II patients had higher left ventricular ejection fraction (60 +/- 12% vs. 51 +/- 16%, p < 0.01), less severe LMCA stenosis (68 +/- 12% vs. 80 +/- 10%, p < 0.001), lower surgical risk score (13 +/- 7 vs. 20 +/- 7, p < 0.001), and had angioplasty more often performed via the radial approach (88% vs. 23%, p < 0.001) with smaller guiding catheters (6F: 49% vs. 15%; 8F: 2% vs. 77%, p < 0.001). The procedural success rate was 100%. In-hospital mortality was 4% (4 deaths, 3 cardiac). During follow-up there were six deaths, 13 patients required repeat percutaneous transluminal coronary angioplasty (4 LMCA), and two required coronary artery bypass graft surgery. Estimated survival (+/- SEE) was 89 +/- 6.3% at 500 days and 85 +/- 12% at 1,000 days post-stenting. Overall mortality was 3.8% in group II and 20.5% in group I (p < 0.02). CONCLUSIONS: Coronary stenting can be performed safely in high-risk individuals with acceptable intermediate-term outcome. It may be feasible to broaden the application of this technique in selected patients needing revascularization for left main coronary disease.

Enoxaparin in unstable angina patients with renal failure.

The dosage of the subcutaneous low molecular weight heparin enoxaparin in unstable angina patients undergoing coronary angiogram and coronary angioplasty depends clearly on the renal function. It should be significantly reduced to 64% of the standard dose (1 mg/kg per 12 h) in patients with severe renal failure (creatinine clearance<30 ml/min) to provide a safe anticoagulant profile.

Platelet glycoprotein IIb/IIIa inhibition with coronary stenting for acute myocardial infarction.

BACKGROUND: When administered in conjunction with primary coronary stenting for the treatment of acute myocardial infarction, a platelet glycoprotein IIb/IIIa inhibitor may provide additional clinical benefit, but data on this combination therapy are limited. METHODS: We randomly assigned 300 patients with acute myocardial infarction in a double-blind fashion either to abciximab plus stenting (149 patients) or placebo plus stenting (151 patients) before they underwent coronary angiography. Clinical outcomes were evaluated 30 days and 6 months after the procedure. The angiographic patency of the infarct-related vessel and the left ventricular ejection fraction were evaluated at 24 hours and 6 months. RESULTS: At 30 days, the primary end point--a composite of death, reinfarction, or urgent revascularization of the target vessel--had occurred in 6.0 percent of the patients in the abciximab group, as compared with 14.6 percent of those in the placebo group (P=0.01); at 6 months, the corresponding figures were 7.4 percent and 15.9 percent (P=0.02). The better clinical outcomes in the abciximab group were related to the greater frequency of grade 3 coronary flow (according to the classification of the Thrombolysis in Myocardial Infarction trial) in this group than in the placebo group before the procedure (16.8 percent vs. 5.4 percent, P=0.01), immediately afterward (95.1 percent vs. 86.7 percent, P=0.04), and six months afterward (94.3 percent vs. 82.8 percent, P=0.04). One major bleeding event occurred in the abciximab group (0.7 percent); none occurred in the placebo group. CONCLUSIONS: As compared with placebo, early administration of abciximab in patients with acute myocardial infarction improves coronary patency before stenting, the success rate of the stenting procedure, the rate of coronary patency at six months, left ventricular function, and clinical outcomes.

Long-term (> or =8 years) outcome after Palmaz-Schatz stent implantation.

The purpose of this single-center study was to evaluate the long-term (> or =8 years) outcome of Palmaz-Schatz intracoronary stenting and to identify independent predictors of outcome. Although short-term results of Palmaz-Schatz intracoronary stenting have been promising, with a reduction in both angiographic restenosis and clinical cardiac events up to 3 years, longer-term follow-up has not been established. We analyzed clinical outcome in 426 consecutive patients at least 8 years after coronary stenting. Demographic, clinical, and procedural predictors of restenosis, survival, and event-free survival, defined as freedom from death, myocardial infarction (MI), and coronary revascularization (target stented site, target vessel, and any revascularization) were analyzed. Before discharge, 28 patients (6.6%) sustained at least 1 major cardiovascular event: 3 deaths (0.7%), 18 MIs (4.2%), and 17 repeat revascularizations. Surviving patients were followed for 8.9 years (interquartile range 8.4 to 9.4). After discharge, 59 patients (13.9%) died, 47 (11.1%) sustained an MI, and 188 (44.4%) underwent coronary revascularization. The 8-year event-free survival (freedom from death, freedom from death/MI/target-stented site revascularization, and freedom from death/MI/any coronary revascularization) was (mean +/- SE) 0.86 +/- 0.01, 0.62 +/- 0.03, and 0.47 +/- 0.02, respectively. Unstable angina, lower left ventricular ejection fraction, and saphenous vein graft stenting were found to be independent predictors of death during follow-up. Hypertension, unstable angina, multivessel disease, and multiple stent implantation were found to be independent predictors of the composite of death/MI/any coronary revascularization during follow-up. This study provided a useful assessment of very long-term outcome in survival, event-free survival, and predictors of major cardiac events 8 to 10 years after Palmaz-Schatz stent implantation.

Effects of Abciximab on the architecture of platelet-rich clots in patients with acute myocardial infarction undergoing primary coronary intervention.

BACKGROUND: Abciximab plus aspirin improves the TIMI 3 flow rate of the infarct-related artery in patients treated with either percutaneous coronary intervention or thrombolysis. The present study investigated whether the reperfusion efficacy of abciximab relates to modifications of clot architecture in patients admitted for acute myocardial infarction (AMI). METHODS AND RESULTS: A total of 23 AMI patients in the Abciximab before Direct angioplasty and stenting in Myocardial Infarction Regarding Acute and Long term follow-up (ADMIRAL) trial received, in a double-blind fashion, either abciximab (n=13) or placebo (n=10) before primary stenting. Viscoelastic (G' in dyne/cm(2)) and morphological (mean platelet aggregate surface area [SAG] in micrometer(2)) indexes of ex vivo platelet-rich clots (PRC) were assessed in a double-blind fashion before and after the bolus administration of abciximab or placebo. G' and SAG reflect the mechanical and morphological impact of activated platelets on the PRC fibrin network, respectively. Abciximab administration reduced G' by 63% (P=0.0001) and SAG by 65% (P=0.0007), and no effect was seen in the placebo group. These abciximab-related changes increased fibrin exposure as a consequence of the platelet-aggregate surface reduction and may have improved endogenous fibrinolysis. These effects were identified in all patients, independent of previous heparin administration. CONCLUSIONS: Abciximab dramatically reduces platelet aggregate size and increases the fibrin accessibility of ex vivo PRC in AMI patients. These modifications could participate in the better coronary artery patency observed with abciximab.

[Use of heparin in unstable angina and non-Q-wave infarction]. / Utilisation des héparines dans l'angor instable et l'infarctus sans onde Q.

The limitations of conventional treatment by non-fractionated heparin (NFH) in unstable angina and non-Q wave infarction with a serious adverse event rate (infarction and/or death) of 7 to 9% at 30 days have led to research in the use of low molecular weight heparin (LMWH). In 1995, Gurfinkel et al reported the superiority of the association aspirin-LMWH (Nadroparine) over a more classical treatment with aspirin alone or the association of aspirin-NFH in unstable angina and non-Q wave infarction. In 1996, the FRISC trial confirmed the value of LMWH (Dalteparine). However, this trial compared the LMWH with placebo. In 1997, the FRIC trial showed that dalteparine was equivalent to NFH. However, the ESSENCE and TIMI 11B trials reported the superiority of LMWH (Enoxaparine) over NFH in unstable angina and non-Q wave infarction. Compared with NFH, a significant 20% reduction in the composite criterion (death-non-fatal infarction) was observed with enoxaparine from the 2nd day up to day 43, without an increase in serious haemorrhagic complications. More recently, FRISC II showed the value and indicated the duration of treatment of LMWH, dalteparine, with respect to the chosen "invasive" or "non-invasive" strategies of revascularisation. The subcutaneous administration, absence of biological controls, the predictability of the anticoagulation and the better tolerance of the LMWH are powerful arguments in favour of their use in unstable angina and non-Q wave infarction. Thus, the LMWH have taken their place in the treatment of unstable coronary disease where the therapeutic arsenal is in constant evolution.

Percutaneous coronary intervention after subcutaneous enoxaparin pretreatment in patients with unstable angina pectoris.

BACKGROUND: Subcutaneous low-molecular-weight (LMW) heparins can effectively replace unfractionated heparin in patients with unstable angina or non-Q-wave myocardial infarction. However, the optimal anticoagulation strategy for these patients when they require cardiac catheterization is still unclear. Therefore, we evaluated a new and simple strategy of anticoagulation in these patients. METHODS AND RESULTS: A total of 451 consecutive patients with unstable angina/non-Q-wave myocardial infarction were treated for at least 48 hours with subcutaneous injections of enoxaparin (1 mg [100 IU]/kg every 12 hours, cycled at 6 AM and 6 PM). Of this unselected population, 293 patients (65%) underwent a coronary angiography within 8 hours of the morning LMW heparin injection, followed by immediate percutaneous coronary intervention (PCI) in 132 patients (28%). PCI was performed without any additional bolus of unfractionated/LMW heparin and without coagulation monitoring. Anti-Xa activity at the time of catheterization was 0.98+/-0.03 IU/mL, was >0.5 IU/mL in 97.6% of patients, and did not relate to the LMW heparin injection-to-catheterization time. There were no in-hospital abrupt closures or urgent revascularizations after PCI. The death/myocardial infarction rate at 30 days was 3.0% in the PCI group (n=132) but 6.2% in the whole population (n=451) and 10.8% in the patients not undergoing catheterization (n=158). The 30-day major bleeding rate was 0.8% in the PCI group, which was comparable to that of patients without catheterization (1.3%). CONCLUSIONS: PCI within 8 hours of the last enoxaparin subcutaneous injection seems to be safe and effective. The safety of subcutaneous LMW heparin in combination with platelet glycoprotein IIb/IIIa blockade awaits further study.

[Review and future perspectives on low-molecular-weight heparin]. / Acquis et perspectives des héparines de bas poids moléculaire.

Low molecular weight heparins appear to be a better choice in patients with unstable angina than unfractionated heparin. Their favourable pharmacokinetic profile allows an excellent predictable dose-response with a subsequent rapidly effective and stable anticoagulation, which is ideal in the setting of percutaneous coronary intervention. Although direct comparisons between LMWH and UH are limited, substantial evidence exists that patients receiving LMWH can be safely brought to cardiac catheterization. Therefore, previous concern regarding transitioning such therapy from the medical service to the cardiac catheterization laboratory should not impede the upstream use of these agents. Direct i.v. injection of LMWH in the setting of elective PCI have also been shown to be safe and effective. Although UH remains an option in conjunction with GP IIb/IIIa inhibitors, there is substantial evidence that LMWH and GP IIb/IIIa inhibitor therapy can be used safely in combination. Patients with either chronic renal failure, mechanical valves or atrial fibrillation are other important issues which deserve additional prospective evaluation of the safety and the efficacy of LMWH. Development of a biological assay for monitoring either LMWH or GP IIb/IIIa receptor antagonists is another important issue in the setting of antithrombotic combinations which are now commonplace.

[Percutaneous angioplasty of unprotected left main coronary disease with implantation of systematic stenting. Immediate and mid-term results]. / Angioplastie percutanée du tronc commun de la coronaire gauche non protégé avec implantation systématique d'une endoprothèse. Résultats immédiats et à moyen terme.

The authors report the immediate and medium term results of percutaneous angioplasty of unprotected left main coronary disease with systematic stenting. Between March 1994 and December 1998, out of 6,006 patients undergoing coronary angioplasty, 92 had significant unprotected left main stem disease. The majority of patients was male (74 men, 80%) with an average age of 74.3 +/- 8.1 years. Between March 1994 and October 1996, only patients with a surgical contraindication were treated by angioplasty (n = 39). After October 1996, the indications were extended to patients who did not have surgical contraindications (n = 53). During the hospital phase, 4 patients (4%) died (ventricular arrhythmia: 1, cardiogenic shock: 2, gastro-intestinal haemorrhage: 1). No non-fatal infarction with or without Q waves were observed, and no emergency coronary bypass surgical procedures were required. The angiographic success rate was 100%. During follow-up (7.3 +/- 5.8 months), 6 other patients died, 13 required a repeat coronary angioplasty, 4 for restenosis of the left main coronary artery, and 2 underwent coronary bypass surgery. The actuarial survival rate was 89 +/- 5% at 1 year and 85 +/- 17% at 3 years. Percutaneous angioplasty for unprotected left main coronary disease with systematic stenting was performed with acceptable hospital and medium term results.

Effect of prior exposure to Chlamydia pneumoniae, Helicobacter pylori, or cytomegalovirus on the degree of inflammation and one-year prognosis of patients with unstable angina pectoris or non-Q-wave acute myocardial infarction.

Inflammation and chronic infections may be important features in the pathogenesis of acute coronary syndromes. We describe 6 systemic markers of inflammation in patients with unstable angina or non-Q-wave myocardial infarction and the relations between these markers, seropositivity to chronic infections, and prognosis. C-reactive protein (CRP), serum amyloid A protein (SAA), fibrinogen, interleukin-6 (IL-6), neopterin, procalcitonin, and serum antibody levels to Chlamydia pneumoniae, Helicobacter pylori, and cytomegalovirus were measured on admission and 48 hours later. One-year clinical follow-up was performed. Plasma levels of acute phase reactants were all elevated on admission and increased further at 48 hours: CRP from 10.1 +/- 2.1 mg/L at baseline to 26.6 +/- 5.1 mg/L at 48 hours (p <0.001); SAA from 27.3 +/- 8.5 to 93.1 +/- 23.2 mg/dl (p <0.005); fibrinogen from 3.2 +/- 0.1 to 3.8 +/- 0.1 g/L (p <0.0001); whereas initial high levels of IL-6 tended also to increase from 9.8 +/- 2 to 15.3 +/- 3.1 pg/ml (p = NS). In contrast, neopterin and procalcitonin remained unchanged. We found no association between levels of each inflammatory marker and the serologic status. Furthermore, levels of inflammatory proteins in patients seronegative to all 3 agents were comparable to those of patients seropositive to 2 or 3 infectious agents. The composite end points of death, myocardial infarction, recurrent angina, or revascularization at 1-year follow-up did not differ according to the serologic status. Thus, in patients with acute coronary syndromes, the acute phase proteins increased over the first 2 days of hospitalization. This initial inflammatory reaction as well as the 1-year clinical outcome did not differ according to the initial serologic status of Chlamydia pneumoniae, Helicobacter pylori, or cytomegalovirus.

Long-term clinical outcome after endoluminal reconstruction of diffusely degenerated saphenous vein grafts with less-shortening wallstents.

OBJECTIVES: This study was designed to evaluate the immediate and long-term clinical results of patients undergoing endoluminal reconstruction in diffusely degenerated saphenous vein grafts (SVGs) with elective implantation of one or more less-shortening Wallstents. BACKGROUND: The optimal treatment strategy for patients with diffusely degenerated SVGs is controversial. Endoluminal reconstruction by stent implantation is one proposed strategy; however, there are few data regarding long-term clinical outcome. METHODS: Between May 1995 and September 1998, 6,534 consecutive patients underwent angioplasty in our institution, including 440 who were treated for SVG lesions. Of these, 126 (115 men, 11 women, median age 69.5 years, range: 33-86 years) with old SVGs (mean age: 13+/-5 years) diffusely degenerated stenosed or occluded (mean lesion length: 27+/-12 mm) were treated electively with implantation of one or multiple (total 197) less-shortening Wallstents. RESULTS: Before discharge, 13 patients (10.3%) sustained at least one major cardiovascular event, including 4 deaths (3.2%), 11 myocardial infarctions (MI) (8.7%), and 3 repeat revascularizations (target vessel = 1, nontarget vessel = 2, 2.4%). Surviving patients were followed for 22+/-11 months: 13 patients (11.1%) died, 11 (9.4%) sustained an MI, 37 underwent angioplasty (31.6%), and 4 (3.4%) underwent bypass surgery. The estimated three-year event-free survival rates (freedom from death, and freedom from death/MI/target vessel revascularization) were (mean +/- SE) 81.1+/-7.8% and 43.2+/-18.5%, respectively. CONCLUSIONS: The long-term clinical outcome of patients undergoing endoluminal reconstruction in diffusely degenerated SVG is relatively poor, mainly because of a high incidence of death or MI and the frequent need for repeat angioplasty. It is unlikely that percutaneous intervention alone will provide a satisfactory or definitive solution for these patients.