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G Dangas

Publications and source records attributed to G Dangas.

At least 73 records · Page 4Linked to original sources
PubMed1999

Effects of platelet glycoprotein IIb/IIIa inhibition with abciximab on thrombin generation and activity during percutaneous coronary intervention.

BACKGROUND: Antagonists of the platelet glycoprotein IIb/IIIa decrease acute ischemic complications after percutaneous coronary interventions (PCI). Abciximab (c7E3 Fab, ReoPro) has been reported to decrease thrombin generation in vitro. We investigated in vivo the effect of abciximab therapy on thrombin generation, thrombin activity, and the activated clotting time (ACT) during PCI. METHODS: We studied 32 consecutive patients who underwent PCI for unstable coronary syndromes. Group I (n = 11) was treated with heparin plus aspirin, and group II (n = 21) was treated with heparin plus aspirin plus standard-dose abciximab, administered 5 minutes after the initial heparin bolus. Patients received a standardized heparin bolus at time 0, and arterial blood specimens for prothrombin fragment F1.2, fibrinopeptide A (FPA), and ACT were obtained from the guiding catheter at 5 minutes, 10 minutes (ACT only), 20 minutes, and at the end of the PCI. Standard-dose abciximab was administered in group II only. Each patient served as his or her own control, and the changes against the baseline were compared between the 2 groups. RESULTS: There were no significant differences between the 2 groups regarding baseline characteristics, hematocrit, and platelet count. Group I patients had higher ACT and lower F1.2 and FPA compared with group II at baseline. Subsequent measurements demonstrated a gradual decrease in FPA and F1.2 in group II; the end of procedure versus baseline changes that occurred in F1.2 were significantly different compared with group I (decrease of 0.59 +/- 0.22 nmol/L in group II vs increase of 0.22 +/- 0.3 nmol/L in group I, P =.04), and a trend in the same direction was evident for FPA changes (decrease of 1.46 +/- 1.16 ng/mL in group II vs increase of 2.25 +/- 1.58 ng/mL in group I, P =.07). The ACT response to abciximab was variable, but a 6.3% increase (+20 sec) in ACT was documented 5 minutes after abciximab bolus in group II compared with the 3.4% decrease (-10 sec) observed in group I at the same time point (P =.1). CONCLUSION: Addition of abciximab to heparin plus aspirin during PCI was associated with a significant decrease in thrombin generation and a borderline decrease in thrombin activity.

Abciximab↗
PubMed1999

Pravastatin therapy in hyperlipidemia: effects on thrombus formation and the systemic hemostatic profile.

OBJECTIVES: The study sought to determine the effects of lipid-lowering with pravastatin on the systemic fibrinolytic profile and on thrombus formation under dynamic flow conditions. BACKGROUND: Lowering cholesterol (C) decreases clinical events in coronary artery disease (CAD) patients, but an analysis of the effects of lipid-lowering on the entire hemostatic and thrombotic profile has not been conducted. METHODS: We prospectively studied 93 stable patients with untreated low-density lipoprotein cholesterol (LDL-C) >145 mg/dl. The CAD patients received pravastatin, and non-CAD patients were randomized to pravastatin versus placebo (double-blind). Thrombus formation upon an injured vascular surface was assessed in a substudy of 40 patients with a previously validated ex vivo perfusion chamber system. Systemic hemostatic markers and thrombus formation were evaluated at baseline, three and six months. RESULTS: Placebo produced no changes in either the lipid profile, any of the hemostatic markers, or the ex vivo thrombus formation. Both pravastatin groups (CAD and non-CAD) showed decreased LDL-C by 30% within 6 weeks (188 to 126 mg/dl, p < 0.001 vs. baseline), and decreased plasminogen activator inhibitor-1 at 3- and 6-month follow-up compared to baseline (15% to 18% decrease at 3 months and 21% to 23% at 6 months). For the tissue plasminogen activator antigen, CAD and non-CAD groups showed significant decreases at 6 months compared to baseline (10% and 13%, respectively). No significant changes were observed with treatment in d-dimer, fibrinopeptide A, prothrombin fragment F1.2, factor VIIa, von Willebrand factor, or C-reactive protein. Fibrinogen levels were significantly increased at 6 months compared to baseline, though still below the upper normal limit. In the perfusion chamber substudy, there was a decrease in thrombus area in non-CAD patients treated with pravastatin at both 3 and 6 months compared to baseline (by 21% and 34%, respectively). The CAD patients showed decreases in thrombus formation by 13% at 3 months, and by 16% at 6 months. The change in LDL-C- correlated modestly with the change in thrombus formation (r = 0.49; p < 0.01). CONCLUSIONS: Pravastatin therapy significantly decreased thrombus formation and improved the fibrinolytic profile in patients with and without CAD. These early effects may, in part, explain the benefit rendered in primary and secondary prevention of CAD.

Aged↗
PubMed1999

Creatine kinase-MB elevation after coronary intervention correlates with diffuse atherosclerosis, and low-to-medium level elevation has a benign clinical course: implications for early discharge after coronary intervention.

OBJECTIVES: The study evaluated the incidence and predictors of creatine kinase-MB isoenzyme (CK-MB) elevation after successful coronary intervention using current devices, and assessed the influence on in-hospital course and midterm survival. BACKGROUND: The CK-MB elevation after coronary intervention predominantly using balloon angioplasty correlates with late cardiac events of myocardial infarction (MI) and death. Whether CK-MB elevation after nonballoon devices is associated with an adverse short and midterm prognosis is unknown. METHODS: The incidence and predictors of CK-MB elevation after coronary intervention were prospectively studied in 1,675 consecutive patients and were followed for in-hospital events and survival. RESULTS: CK-MB elevation was detected in 313 patients (18.7%), with 1-3x in 12.8%, 3-5x in 3.5% and >5x normal in 2.4% of patients. Procedural complications or electrocardiogram changes occurred in only 49% of the CK-MB-elevation cases; CK-MB elevation was more common after nonballoon devices (19.5% vs. 11.5% after percutaneous transluminal coronary angioplasty; p < 0.01). Predictors of CK-MB elevation on multivariate analysis were diffuse coronary disease (p = 0.02), systemic atherosclerosis (p = 0.002), stent use (p = 0.04) and absence of beta-blocker therapy (p = 0.001). Adverse in-hospital cardiac events were more frequent in patients with >5x CK-MB elevation, with no significant difference between 1-5x CK-MB elevation versus normal CK-MB group. During a mean follow-up of 13 +/- 3 months, the incidence of death in the CK-MB-elevation group was 1.6% versus 1.3% in the normal CK-MB group (p = NS). CONCLUSIONS: The CK-MB elevation after coronary intervention was observed even in the absence of discernible procedural complications and was more common in patients with diffuse atherosclerosis. In-hospital clinical events requiring prolonged monitoring were higher in >5x CK-MB-elevation patients only. Midterm survival of CK-MB-elevation patients was similar to those with normal CK-MB. Our prospective analysis shows a lack of adverse in-hospital cardiac events and suggests that early discharge of stable 1-5x normal CK-MB-elevation patients after successful coronary intervention is safe.

Aged↗
PubMed1999

Platelet glycoprotein IIb/IIIa antagonists in percutaneous coronary revascularization.

Coronary dissections and intracoronary thrombosis are the most important determinants of acute and subacute complications occurring during coronary interventions. Stents have proved efficacious to repair coronary dissections. The formation of intracoronary thrombi during percutaneous coronary intervention (PCI), the other main pathogenic mechanism for acute complications of PCI, has also been implicated in the pathogenesis of long-term ischemic outcomes. To reduce intracoronary thrombosis, all PCIs have been historically performed during intense short-term anticoagulation with the combination of unfractionated heparin plus aspirin. Compelling data on the central role of platelets in arterial thrombosis have made apparent the need for more potent antiplatelet agents for the treatment of patients undergoing PCI.

Abciximab↗
PubMed1999

The effect of early postinfarction revascularization of asymptomatic patients on left ventricular remodeling.

BACKGROUND: Patients with angina after a Q-wave myocardial infarction benefit from elective revascularization, but it is not known whether asymptomatic patients, including those with a totally occluded infarct-related artery, improve after revascularization. OBJECTIVE: To determine the effect of early postinfarction revascularization of asymptomatic patients on left ventricular remodeling. METHODS: We prospectively studied 31 consecutive asymptomatic patients (aged 57 +/- 2 years, 24 with anterior infarcts) after Q-wave myocardial infarction with > or = 70% stenosis of the infarct-related artery (IRA) who underwent early elective revascularization (days 4-10 after myocardial infarction). Group I consisted in patients with a totally occluded IRA (n = 10), and group II consisted in patients with a patent, though stenosed, IRA (n = 21). Resting echocardiography and low-dose dobutamine echocardiography were performed at baseline (day 3 +/- 1), and rest echocardiography was repeated after an 8-week follow-up. Significant myocardial viability was defined as > or = 2 wall segments improved (in a 16-segment model of left ventricle) versus baseline, and significant functional recovery as > or = 2 segments improved versus baseline on follow-up examination. Left ventricular end-systolic volume indices (ESVI) and end-diastolic volume indices and ejection fractions were measured by using a modified version of Simpson's rule (using apical two-chamber and four-chamber views). RESULTS: The left ventricular ESVI of patients in group I had decreased by 4.2 +/- 1.9 ml/m2, whereas for patients in group II the left ventricular ESVI had increased by 4.2 +/- 1.7 ml/m2 (P = 0.006). Similarly, the left ventricular end-diastolic volume index had decreased by 0.7 +/- 2.4 ml/m2 versus baseline at follow-up for patients in group I and increased by 7.8 +/- 2.1 ml/m2 for patients in group II (P = 0.02). The left ventricular ejection fraction increased by 7.3 +/- 3% for patients in group I and decreased by 0.4 +/- 2% for patients in group II (P = 0.04). CONCLUSION: There is less global left ventricular remodeling, a potentially deleterious process, after elective revascularization early after Q-wave myocardial infarction in asymptomatic patients who had had a totally occluded IRA before revascularization than there is in patients who had already had a patent, though stenosed, IRA before revascularization. These results suggest that restoration of patency of IRA after a Q-wave myocardial infarction is beneficial even for asymptomatic patients.

Coronary Disease↗
PubMed1999

Angina pectoris in severe aortic stenosis.

We studied the value of angina pectoris as a predictor of significant coronary artery disease (CAD) in very elderly patients with severe aortic stenosis (AS). The study population consisted of patients with age at least 70 years who were referred for balloon aortic valvuloplasty (n = 90 patients). Routine coronary angiography was performed before the valvular intervention. Patients were grouped according to the presence or absence of angina pectoris. Of the patients with angina pectoris, 78% had obstructive (>50% diameter stenosis) CAD on coronary angiogram, while only 17% of patients without angina pectoris had obstructive CAD (p < 0.01). Angina pectoris had a sensitivity of 78% and a specificity of 82% for prediction of obstructive CAD. This suggests that in elderly patients with severe AS, the presence of angina pectoris is a strong determinant of CAD, and the absence of angina strongly suggests absence of obstructive CAD. In a very elderly population, appropriate decision-making with respect to AS management should not await diagnostic coronary angiography.

Aged↗
PubMed1999

Coronary artery stents: appropriate use of adjunctive pharmacotherapy to prevent stent thrombosis.

In 1986, the first metallic stent was implanted inside a human coronary artery in order to reduce the incidence of abrupt vessel occlusion and restenosis after percutaneous coronary balloon angioplasty. Little was known at that time regarding the adequate anticoagulation regimen needed and the initial enthusiasm was soon marred by a high rate of thrombotic stent closure that usually occurred 2 days to 4 weeks after stent implantation. Antithrombotic drugs such as heparin, aspirin (acetylsalicylic acid), low molecular weight heparins, dextran, dipyridamole and warfarin (coumadin) were incorporated in a series of trials which reduced the risk of stent thrombosis, but increased substantially the rate of bleeding complications and the length of hospitalisation. The greatest breakthrough came with the improvement in stent deployment techniques using intravascular ultrasound-guided, high-pressure balloon inflation inside the stent, and the understanding of the central role of platelet activation in stent thrombosis. These 2 factors have led to 'optimal stent deployment' with high-pressure ballooning after stent deployment and the simultaneous use of more potent antiplatelet agents in conjunction with aspirin. Newly developed selective inhibitors of the platelet glycoprotein IIb/IIIa receptor and new stent designs have also recently been integrated into clinical practice and are currently being evaluated in clinical trials.

Adjuvants, Pharmaceutic↗
PubMed1999

The role of platelet glycoprotein IIb/IIIa antagonists in percutaneous coronary revascularization procedures.

Platelet activation occupies a central role in arterial thrombosis after vascular injury, and the platelet glycoprotein GPIIb/IIIa integrin mediates the final common pathway for platelet aggregation. Agents of the recently developed pharmacologic class of inhibitors of the platelet GPIIb/IIIa receptor have been shown to decrease ischemic complications after coronary revascularization procedures. However, several issues need to be determined with respect to their specific indications, dosage, and combination with other antithrombotic therapies. Intracoronary thrombus formation during percutaneous coronary interventions (PCI) is the main pathogenic mechanism of the acute complications of PCI, but has also been implicated in the pathogenesis of their long-term results. In order to target intracoronary thrombosis, all PCIs have been performed during intense short-term anticoagulation with combination of unfractionated heparin plus aspirin. Compelling data on the central role of platelets in arterial thrombosis have made apparent the need for more potent antiplatelet agents for the treatment of patients undergoing PCI.

Angioplasty, Balloon, Coronary↗
PubMed1999

Primary mechanical reperfusion in acute myocardial infarction: the United States experience.

Achievement of infarct-related artery (IRA) patency with thrombolytic agents has improved the clinical outcome of patients with acute myocardial infarction (MI). Primary angioplasty (PTCA) for direct IRA reperfusion may further improve patient outcome by overcoming several limitations of thrombolytic therapy, e.g. by decreasing the risk of haemorrhagic stroke, increasing the achievement of brisk antegrade flow, decreasing the risk of IRA reocclusion, and allowing early identification of patients who need surgical revascularization. In the PAMI-1 randomized trial, primary PTCA was superior to thrombolytic therapy. The GUSTO-IIb angioplasty substudy supported the same conclusion but with a narrower margin of benefit from PTCA. In order to further improve the outcome of primary mechanical reperfusion, routine intra-aortic balloon pump (IABP) insertion in high-risk MI patients and primary stenting have been evaluated. In PAMI-2, there was no major clinical benefit in routine IABP insertion during primary PTCA in high-risk patients. In contrast, primary stenting appears to offer significant advantages over PTCA, especially by decreasing the need for subsequent IRA revascularization procedures as shown in the recent PAMI Stent Randomized Trial. Adjunctive pharmacotherapy with potent antiplatelet agents in acute MI is being evaluated both in combination with thrombolytic therapy, and with primary PTCA and stenting. Finally, meaningful consideration of cost-effectiveness and health policy guidelines is warranted to optimize the appropriate management of MI patients in the current era, given the increasingly complex and expensive therapeutic strategies available.

Angioplasty, Balloon, Coronary↗
PubMed1999

Intra-arterial reteplase for the treatment of acute limb ischemia.

The removal of urokinase from the market has created a dilemma for interventionists and vascular surgeons treating patients with acute limb threatening ischemia due to arterial thrombosis or embolization. Reteplase is a newer, fibrin-specific thrombolytic agent with properties that make it an attractive alternative to urokinase. We report two cases of successful treatment of acute, limb threatening ischemia with intra-arterial Reteplase therapy.

Acute Disease↗
PubMed1999

Glycoprotein IIb/IIIa Receptor Inhibitors During Primary Angioplasty for Acute Myocardial Infarction.

Platelet glycoprotein IIb/IIIa receptors are the final common pathway leading to platelet aggregation and coronary thrombosis during acute myocardial infarction (AMI). Therefore, they are ideal candidates for pharmacologic intervention. The recent development of glycoprotein IIb/IIIa receptor antagonists has led to several studies that have shown the benefits and efficacy of these agents in the treatment of acute coronary syndromes and in the setting of percutaneous intervention. To date, six published trials have examined the safety and efficacy of intravenous abciximab, a mouse/human chimeric version of the 7E3 antibody, as an adjunct to primary mechanical reperfusion in patients with AMI. In this article, we review these trials, as well as new studies currently underway that will provide further information on the long-term benefits of combining these pharmacologic agents and stenting in the treatment of AMI.

Journal Article↗
PubMed1998

A prolonged QRS duration on surface electrocardiogram is a specific indicator of left ventricular dysfunction [see comment].

OBJECTIVE: We sought to determine whether a prolonged QRS-interval duration is associated with decreased left ventricular (LV) systolic function. BACKGROUND: The 12-lead electrocardiogram (ECG) is a routine test for suspected cardiac disease. Although several scoring systems have been devised to estimate LV systolic function, no studies have examined the direct relationship between QRS duration alone and LV systolic function. METHODS: We analyzed the standard 12-lead surface ECG of 270 consecutive patients, referred for radionuclide ventriculography. Patients (n = 44) with bundle branch blocks, atrial flutter or fibrillation, pacemaker rhythm, recent myocardial infarction or bypass surgery, and patients on antiarrhythmic drugs were excluded. In the remaining patients (n = 226), we correlated the QRS duration on standard resting ECG, and the resting LV ejection fraction (EF), end-systolic and end-diastolic counts (ESC and EDC, respectively; LV volume indices), as obtained by radionuclide angiography. We used a multivariate analysis to identify independent predictors of reduced ventricular function entering QRS duration, the previously described R-wave score and clinical variables in our model. RESULTS: The QRS duration in the abnormal EF group was significantly longer than in the normal EF group (0.102 vs. 0.091 s, p < 0.0001). A QRS duration >0.10 s was highly specific (83.6%), but modestly sensitive (43.8%), for the prediction of abnormal EF. Furthermore, an abnormal EF was predicted with incrementally increased specificity (83.6% to 99.3%) and a corresponding decrease in sensitivity (43.8% to 13.8%) for each 0.01-s increase in the definition of prolonged QRS (from >0.10 to >0.12 s). Accordingly, the positive likelihood ratio for the prediction of decreased LV function was increased from 2.67 to 19.7 as the definition of prolonged QRS duration was increased from >0.10 to >0.12 s. In the multivariate analysis, a prolonged QRS duration and a low R-wave score were the only independent predictors of decreased LV systolic function. CONCLUSIONS: Prolonged QRS duration (>0.10 s) obtained from a standard resting 12-lead ECG is a specific, but relatively insensitive indicator of decreased LV systolic function. Further prolongation of the QRS had a higher specificity for decreased LV EF and a higher positive likelihood ratio for predicting abnormal LV EF.

Arrhythmias, Cardiac↗
PubMed1998

Rotational atherectomy for in-stent restenosis: acute and long-term results of the first 100 cases.

OBJECTIVES: This study evaluated the clinical safety and long-term results of rotational atherectomy (RA) followed by low-pressure balloon dilatation (percutaneous transluminal coronary angioplasty [PTCA]) for the treatment of in-stent restenosis (ISR). BACKGROUND: In-stent restenosis is associated with a high incidence of recurrence after interventional treatment. Because ISR is due to neointimal hyperplasia, rotational ablation may be a more effective treatment than PTCA. METHODS: Between November 1995 and November 1996, 100 consecutive patients with first-time ISR were treated by RA. Quantitative coronary angiography and intravascular ultrasound (IVUS) were used to analyze the acute procedural results. The incidence of repeat in-stent restenosis and target vessel revascularization (TVR) at follow-up was determined. RESULTS: Procedural success without any major in-hospital complications was achieved in 100% of cases. Slow flow was observed in 3% and creatine kinase-MB enzyme elevation >3x normal occurred in 2%. The mean burr-to-artery ratio was 0.68+/-0.18 and adjuvant balloon dilatation was performed at 4.2+/-2.1 atm. Minimum luminal diameter increased from 0.86+/-0.28 mm to 1.89< or =0.21 mm after RA and to 2.56+/-0.29 mm after adjunct PTCA. Quantitative IVUS analysis showed that 77% of the luminal gain occurred due to rotational ablation of the restenotic tissue and only 23% occurred after adjunct balloon dilation, and further stent expansion did not contribute to the luminal enlarge. ment. At a mean follow-up of 13+/-5 months, repeat in-stent restenosis occurred in 28% of patients with TVR of 26%. Univariate predictors of repeat restenosis were burr-to-artery ratio <0.6, ISR in <90 days of stenting, ostial lesion, stent for a restenotic lesion and diffuse type ISR. CONCLUSIONS: Rotational atherectomy is a safe and feasible technique for treatment of ISR and is associated with a relatively low recurrent restenosis in comparison to historical controls of balloon angioplasty.

Angioplasty, Balloon, Coronary↗
PubMed1998

Lipoprotein(a) and inflammation in human coronary atheroma: association with the severity of clinical presentation.

OBJECTIVES: The purpose of this study was the investigation of the in vivo role of lipoprotein(a) [Lp(a)] and inflammatory infiltrates in the human coronary atherosclerotic plaque and their correlation with the clinical syndrome of presentation. BACKGROUND: Lipoprotein(a) is an atherogenic and thrombogenic lipoprotein, and has been implicated in the pathogenesis of acute coronary syndromes. Lipoprotein(a) induces monocyte chemoattraction and smooth muscle cell activation in vitro. Macrophage infiltration is considered one of the mechanisms of plaque rupture. METHODS: This study of atherectomy specimens investigated the in vivo role of Lp(a) at different stages of the atherogenic process, and its relationship with macrophage infiltration. We examined coronary atheroma removed from 72 patients with stable or unstable angina. Specimens were stained with antibodies specific for Lp(a), macrophages (KP-1), and smooth muscle cells (alpha-actin). Morphometric analysis was used to quantify the plaque areas occupied by each of the three antigens, and their colocalization. RESULTS: All specimens had localized Lp(a) staining; the mean fractional area was 58.2%. Ninety percent of the macrophage areas colocalized with Lp(a) positive areas, whereas 31.3% of the smooth muscle cell areas colocalized with Lp(a) positive areas. Patients with unstable angina (n = 46) had specimens with larger mean plaque Lp(a) areas than specimens from stable angina patients (n = 26): 64.4% versus 47.7% (p = 0.004). Unstable angina patients with rest pain (n = 28) had greater mean plaque Lp(a) area than unstable angina patients with crescendo exertional pain (n = 18): 71.1% versus 52.4% (p < 0.001). Mean KP-1 area was 31.2% in unstable rest angina versus 18.3% in stable angina (p = 0.05); alpha-actin area was greater in stable (48.5%) and crescendo exertional angina (48.8%) than in rest angina (30.4%). The strongest correlation between plaque KP-1 and Lp(a) area was in unstable rest angina (r = 0.88, p < 0.001), and between alpha-actin and Lp(a) areas in the crescendo exertional angina (r = 0.62, p < 0.01). CONCLUSIONS: Lipoprotein(a) is ubiquitous in human coronary atheroma. It is detected in larger amounts in tissue from culprit lesions in patients with unstable compared to stable syndromes, and has significant colocalization with plaque macrophages. A correlation of plaque alpha-actin and Lp(a) area suggests a role of Lp(a) in plaque growth.

Angina Pectoris↗
PubMed1998

Histopathological correlates of early arterial recoil following directional coronary atherectomy.

Elastic recoil has been implicated in the pathophysiology of restenosis after conventional balloon angioplasty alone. Directional atherectomy may attenuate arterial recoil by removing the internal elastic lamina and medial smooth muscle cells and altering the vessel wall architecture. This study sought to evaluate early recoil after directional atherectomy and its relation with excision of deep arterial wall structures. We prospectively evaluated the correlation of the histopathologic evidence of media or adventitia as assessed in the atheroma retrieved during the procedure with the early changes in minimal lumen diameter after directional atherectomy followed by adjunct balloon dilatation in 50 consecutive cases. Recoil was assessed by routinely performed 1- and 15-min postprocedure angiograms, and patients were divided into two groups according to the absence (group I, n = 26) or presence (group II, n = 24) of recoil. The mean changes in minimal luminal diameter between 1 and 15 min was +0.22 mm in group I and -0.14 mm in group II. The absence of recoil was strongly associated with evidence of media tissue in the pathologic analysis as compared with cases with recoil (42 vs. 18%, respectively; p = 0.02). Similarly, retrieval of adventitia was seen exclusively in the group without recoil (15 vs. 0%; p = 0.06). Vessels that underwent recoil had significantly larger reference and immediate postprocedure minimal luminal diameters (3.62 +/- 0.57 and 3.02 +/- 0.45 mm, respectively) as compared with arteries with no recoil (3.28 +/- 0.35 and 2.75 +/- 0. 43 mm, respectively; p < 0.05 for both). Therefore, early luminal changes, likely related to elastic recoil, correlated with excision of deep wall structures during directional atherectomy. Arteries that showed recoil were larger, possibly due to thicker muscular layer and/or larger plaque burden as compared with arteries that did not recoil. Thus, optimal tissue debulking during directional atherectomy appears to attenuate recoil, providing an additional insight into the mechanism of action of this percutaneous revascularization device.

Angioplasty, Balloon, Coronary↗
PubMed1998

Directional coronary atherectomy in acute myocardial infarction.

Balloon angioplasty (percutaneous transluminal coronary angioplasty, PTCA) is an established common strategy in the treatment of acute myocardial infarction (MI) with high success rates but a 5-10% incidence of reclosure/reinfarction due to thrombus and/or intimal flaps. Directional coronary atherectomy (DCA) by removing plaque/thrombus and achieving larger postprocedural luminal diameter may further decrease the incidence of reclosure/reinfarction, with a resultant better in-hospital outcome in this setting. We analyzed the clinical, procedural and in-hospital outcome of patients who underwent DCA or PTCA within 48 h of MI. Long lesions (>20 mm), large angiographic intracoronary thrombus, lesions in a bend, heavy calcification, and vessel diameter <3.0 mm were excluded from the study. Although slow flow occurred more frequently during DCA (17 vs. 9% during PTCA, p = 0.04), procedural success (<50% final diameter stenosis with TIMI-3 flow) was achieved in 96% of DCA and 92% of PTCA group (nonsignificant). Acute closure occurred in 9% of the PTCA group versus 2% of the DCA (p = 0.05), and the composite endpoint of in-hospital reinfarction, reintervention, bypass surgery or death was present in 9% of PTCA cases versus none of DCA cases (p = 0.03). There were no major peripheral vascular complications requiring surgery in either group. Therefore, DCA appears safe and effective in selected patients with recent MI, and is associated with a low incidence of major clinical complications.

Aged↗
PubMed1998

Administration of abciximab during percutaneous coronary intervention reduces both ex vivo platelet thrombus formation and fibrin deposition: implications for a potential anticoagulant effect of abciximab.

Abciximab (c7E3 Fab, ReoPro), a platelet glycoprotein (GP) IIb/IIIa inhibitor, decreases acute ischemic complications after percutaneous coronary interventions. Recently, abciximab was shown to decrease thrombin generation in vitro in a static system. To assess whether abciximab can decrease fibrin formation in blood from patients, we quantified both platelet thrombi and fibrin deposition by using an ex vivo flow chamber model. We prospectively studied 18 consecutive patients who underwent percutaneous interventions for unstable coronary syndromes. Blood was perfused directly from the patient through an ex vivo perfusion chamber at a high shear rate, thus mimicking mildly stenosed coronary arteries. Perfusion chamber studies were performed when patients were being treated with heparin plus aspirin before the procedure (baseline) and then repeated after the procedure, when patients were on either aspirin plus heparin alone (group 1, no abciximab, control) or aspirin plus heparin plus abciximab (group 2, abciximab treated). Each patient served as his or her own control. Specimens were stained with combined Masson's trichrome-elastin and antibodies specific for fibrinogen, fibrin, and platelet GP IIIa. Total thrombus area and areas occupied by platelet aggregates and fibrin layers were quantified by planimetry. Group 1 demonstrated no significant change in thrombus area before versus after the procedure; in contrast, treatment with abciximab reduced total thrombus area by 48% in group 2 (after the procedure versus baseline, P=0.01). This decline was due to significant reductions in both platelet aggregates (55%, P=0.005) and fibrin layers (45%, P=0.03). The addition of abciximab to heparin and aspirin in patients undergoing coronary interventions significantly decreases ex vivo thrombus formation on an injured vascular surface. Treatment with abciximab appears to reduce both the platelet and the fibrin thrombus components. This finding supports a potential role for GP IIb/IIIa receptor blockade in decreasing fibrin formation in addition to inhibition of platelet aggregation. Thus, potent inhibitors of GP IIb/IIIa may also act as anticoagulants.

Abciximab↗