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At least 235 records · Page 13Linked to original sources
PubMed2004

A dose-finding study of fondaparinux in patients with non-ST-segment elevation acute coronary syndromes: the Pentasaccharide in Unstable Angina (PENTUA) Study.

OBJECTIVES: In this dose-finding study, we sought to compare fondaparinux with enoxaparin in patients with acute coronary syndromes (ACS). BACKGROUND: Fondaparinux is a synthetic pentasaccharide that selectively inhibits activated clotting factor X. It has been demonstrated as effective in preventing thromboembolic complications in orthopedic surgery. METHODS: Four doses fondaparinux (2.5, 4, 8, or 12 mg once daily) and enoxaparin (1 mg/kg twice daily) were compared, both given for three to seven days, in patients with ACS without persistent ST-segment elevation. RESULTS: The rates of the combined primary end point of death, myocardial infarction, or recurrent ischemia after nine days were 27.9%, 35.9%, 34.7%, 30.3%, and 35.7% in patients allocated to fondaparinux doses of 2.5, 4, 8, and 12 mg and enoxaparin, respectively (p = NS). In the per-protocol analysis (929 patients who received adequate study drug and had adequate ST-segment monitoring), these figures were 30.0%, 43.5%, 41.0%, 34.8%, and 40.2%. Again, no dose response was observed. The lowest event rates were observed in the 2.5-mg fondaparinux group, which had significantly lower rates than the enoxaparin group as well as for 4 and 8 mg fondaparinux in the per-protocol analysis (p < 0.05). Bleeding rates were low and not different among the patient groups. No differences were observed in fondaparinux concentrations in patients with or without death, myocardial infarction, recurrent ischemia, or bleeding events. CONCLUSIONS: This dose-finding study revealed no dose response for different fondaparinux doses ranging from 2.5 to 12 mg subcutaneously and suggests that the efficacy and safety of fondaparinux may be similar to that of enoxaparin. Further studies with fondaparinux in ACS might include the lowest dose (2.5 mg) investigated in this study.

Acute Disease↗
PubMed2004

Lack of efficacy of clopidogrel pre-treatment in the prevention of myocardial damage after elective stent implantation.

OBJECTIVES: The object of this study was to determine the effect of pre-treatment with clopidogrel in patients undergoing elective stent implantation. BACKGROUND: The treatment of patients with adenosine diphosphate receptor blockers after percutaneous coronary intervention (PCI) with stent implantation has been shown to decrease the incidence of subacute stent thrombosis. Furthermore, non-randomized studies on pre-treatment with clopidogrel among patients undergoing stent implantation have suggested a reduction in myocardial damage and clinical events. The effect of pre-treatment with clopidogrel has been studied in only a few randomized trials. METHODS: In a randomized trial, three days of pre-treatment with clopidogrel was compared with standard post-procedural treatment in 203 patients undergoing elective stent implantation. The primary end point was a rise in troponin I or creatine kinase-MB fraction (CK-MB) serum levels at 6 to 8 and 16 to 24 h after PCI. Secondary end points were death, stroke, myocardial infarction, coronary bypass grafting, repeated PCI, and subacute stent thrombosis at one and six months after PCI. RESULTS: No difference was found between non-pre-treated and pre-treated patients in the post-procedural elevation of troponin I (42 [43.3%] vs. 48 [51.1%], respectively, p = 0.31) or CK-MB (6 [6.3%] vs. 7 [7.4%], respectively, p = 0.78). Adjustment for possible confounding factors did not change these findings. Patient follow-up at one and six months showed no significant difference between the treatment groups in death, stroke, myocardial infarction, coronary artery bypass grafting, repeated PCI, or subacute stent thrombosis. CONCLUSIONS: In this randomized study, no beneficial effect of pre-treatment with clopidogrel on post-procedural elevation of troponin I and CK-MB or on clinical events after one and sixth months could be demonstrated. The study suggests that among patients with stable coronary syndromes in whom coronary stent implantation is planned, pre-treatment may not be beneficial in reducing early myocardial damage.

Aged↗
PubMed2004

The additive value of tirofiban administered with the high-dose bolus in the prevention of ischemic complications during high-risk coronary angioplasty: the ADVANCE Trial.

OBJECTIVES: We sought to determine the safety and efficacy of high-dose bolus (HDB) tirofiban in high-risk patients undergoing percutaneous coronary intervention (PCI). BACKGROUND: The use of HDB tirofiban in the catheterization laboratory is controversial. In particular, in patients with acute coronary syndromes undergoing PCI, there is no evidence that tirofiban administered in the catheterization laboratory is superior to heparin alone. This finding probably reflects the suboptimal platelet inhibition when tirofiban is employed at RESTORE (Randomized Efficacy Study of Tirofiban for Outcomes and Restenosis) regimen. METHODS: A total of 202 patients (mean age 69 +/- 8 years; 137 males [68%]) undergoing high-risk PCI, pretreated with thienopyridines, were consecutively randomized to HDB tirofiban (25 microg/kg/3 min, and infusion of 0.15 microg/kg/min for 24 to 48 h) or placebo immediately before the procedure and then followed for a median time of 185 days (range 45 to 324 days) for the occurrence of the primary composite end point of death, myocardial infarction, target vessel revascularization (TVR), and bailout use of glycoprotein (GP) IIb/IIIa inhibitors. RESULTS: The cumulative incidence of the primary end point was 35% and 20% in placebo and HDB tirofiban groups, respectively (hazard ratio 0.51, 95% confidence interval 0.29 to 0.88; p = 0.01). This difference was mainly due to the reduction of myocardial infarction and bailout use of GP IIb/IIIa inhibitors, with no significant effect on TVR or death. The safety profile did not differ between tirofiban and placebo. CONCLUSIONS: The use of tirofiban, when administered at HDB, is safe and significantly reduces the incidence of ischemic/thrombotic complications during high-risk PCI.

Acute Disease↗
PubMed2004

Clinical, angiographic, and intravascular ultrasound characteristics of early saphenous vein graft failure.

OBJECTIVES: We sought to examine saphenous vein graft (SVG) lesions that fail within the first year after operation. BACKGROUND: Saphenous vein grafts remain patent for approximately 10 years; however, up to 15% to 20% of SVGs become occluded within the first year. METHODS: We studied 100 patients who underwent percutaneous coronary intervention (PCI) for early (<1 year post-implantation) SVG failure lesions and compared them with a diabetes- and hypercholesterolemia-matched cohort of late SVG failures (>1 year). Coronary angiography and intravascular ultrasound images were analyzed. RESULTS: The majority of patients in both groups were males who presented with unstable angina; 36% were diabetic. Graft ages were 6.0 +/- 2.9 months and 105.4 +/- 50.8 months, respectively. The early SVG failure lesion location was more often ostial or proximal (62% vs. 42%, respectively). Early SVG failures were angiographically smaller than late failures (reference: 2.47 +/- 0.86 mm vs. 3.26 +/- 0.83 mm, p < 0.001) but had similar lesion lengths. Intravascular ultrasound showed that early failure lesions had smaller proximal and distal reference lumen areas (7.3 +/- 6.8 mm2 vs. 10.6 +/- 3.8 mm2, p = 0.026) and greater reference plaque burden than late failures (52.3% vs. 36.1%, p < 0.001). After PCI, 20.6% of early and 30.6% of late failure lesions had creatine kinase-myocardial band (CK-MB) greater than twice normal. CONCLUSIONS: Early SVG failure is mostly proximal or ostial, lesions appear focal, and early SVGs appear smaller than late SVGs. Intravascular ultrasound shows significant reference segment plaque burden, suggesting more severe, diffuse SVG disease.

Aged↗
PubMed2004

Differential mortality risk of postprocedural creatine kinase-MB elevation following successful versus unsuccessful stent procedures.

OBJECTIVES: This study was designed to evaluate the effect of periprocedural myocardial infarction (MI) on mortality according to success of the stent procedure. BACKGROUND: The mortality effect of periprocedural MI relative to successful versus unsuccessful procedures has not been examined. METHODS: All-cause mortality during the first year was evaluated prospectively among 5,850 patients from coronary stent clinical trials. Myocardial infarction was classified according to creatine kinase-MB level as type 1 (>1 but <3 times normal), type 2 (>or=3 but 8 times normal or Q-wave MI). Procedures were classified as successful unless there was a final diameter stenosis >50%; final Thrombolysis In Myocardial Infarction flow grade <3; final National Heart, Lung, and Blood Institute dissection grade >or=D; repeat revascularization within 24 h; or stent thrombosis within 24 h. RESULTS: Myocardial infarction was more frequent after unsuccessful procedures (69.6% vs. 20.4%, p < 0.001). Mortality during the first year was higher in patients with MI (2.8% vs. 1.7%, p = 0.01), but the effect was significant only for type 3 MI (4.7% vs. 1.7%, p = 0.008). Moreover, the mortality difference for any MI was confined to patients with unsuccessful procedures (13.1% vs. 0%, p = 0.03), with no significant effect among patients with otherwise successful procedures (2.1% vs. 1.7%, p > 0.20). The independent predictors of mortality were unsuccessful procedure (p < 0.001), diabetes mellitus (p = 0.001), history of prior MI (p = 0.003), multivessel disease (p = 0.006), and advancing age (p < 0.001), but not periprocedural MI. CONCLUSIONS: The association of periprocedural MI with increased mortality during the first year following stent placement was confined to patients with unsuccessful procedures.

Aged↗
PubMed2005

Cardiovascular manifestations of moderate to severe carbon monoxide poisoning.

OBJECTIVES: We describe the cardiovascular manifestations of carbon monoxide (CO) poisoning. BACKGROUND: Carbon monoxide poisoning is a common cause of toxicologic morbidity and mortality. Although the neurologic sequelae of CO poisoning have been well described, the cardiovascular consequences are limited to isolated case reports. METHODS: We reviewed the cardiovascular manifestations of 230 consecutive patients treated for moderate to severe CO poisoning in the hyperbaric oxygen chamber at Hennepin County Medical Center (HCMC), a regional center for treatment of CO poisoning. RESULTS: The mean age was 47.2 years with 72% men. Ischemic electrocardiogram (ECG) changes were present in 30% of patients, whereas only 16% had a normal ECG. Cardiac biomarkers (creatine kinase-MB fraction or troponin I) were elevated in 35% of patients. In-hospital mortality was 5%. CONCLUSIONS: Cardiovascular sequelae of CO poisoning are frequent, with myocardial injury assessed by biomarkers or ECG in 37% of patients. Patients admitted to the hospital with CO poisoning should have a baseline ECG and serial cardiac biomarkers.

Adult↗
PubMed2005

Aspirin and clopidogrel drug response in patients undergoing percutaneous coronary intervention: the role of dual drug resistance.

UNLABELLED: We evaluated the response to clopidogrel among aspirin-resistant versus aspirin-sensitive patients undergoing elective coronary stenting. Patients (n = 150) treated with aspirin but not clopidogrel had blood samples drawn at baseline and 24 h after clopidogrel loading. Depending on the definition used, 9% to 15% were resistant to aspirin and 24% to clopidogrel. About half of the aspirin-resistant patients were also resistant to clopidogrel. As a group, aspirin-resistant patients had lower response to clopidogrel (assessed by platelet aggregation and activation markers) than aspirin-sensitive patients. Both aspirin- and clopidogrel-resistant patients had higher incidence of creatine kinase-MB elevation than the respective sensitive patients. OBJECTIVES: We sought to evaluate the response to clopidogrel among aspirin-resistant versus aspirin-sensitive patients undergoing percutaneous coronary intervention (PCI). BACKGROUND: Wide variability has been reported in response to aspirin and clopidogrel. There are limited data on the simultaneous responses to both drugs. METHODS: Elective PCI patients (n = 150) who received aspirin for > or = 1 week but not clopidogrel were included. All patients received bivalirudin during PCI. Blood samples were drawn at baseline and 20 to 24 h after a 300-mg clopidogrel dose. Aspirin resistance was defined by > or = 2 of 3 criteria: rapid platelet function analyzer-ASA score > or = 550, 5 micromol/l adenosine diphosphate (ADP)-induced aggregation > or = 70%, and 0.5 mg/ml arachidonic acid-induced aggregation > or = 20%. Clopidogrel resistance was defined as baseline minus post-treatment aggregation < or = 10% in response to 5 and 20 micromol/l ADP. RESULTS: Nineteen (12.7%) patients were resistant to aspirin and 36 (24%) to clopidogrel. Nine (47.4%) of the aspirin-resistant patients were also clopidogrel resistant. Aspirin-resistant patients were more likely to be women and have diabetes than were aspirin-sensitive patients. They also had lower response to clopidogrel, assessed by platelet aggregation and activation markers (flow cytometry-determined PAC-1 binding and P-selectin expression). Elevation of creatine kinase-myocardial band after stenting occurred more frequently in aspirin-resistant versus aspirin-sensitive patients (38.9% vs. 18.3%; p = 0.04) and in clopidogrel-resistant versus clopidogrel-sensitive patients (32.4% vs. 17.3%; p = 0.06). CONCLUSIONS: Aspirin-resistant patients as a group have reduced response to clopidogrel. Furthermore, we have identified a unique group of dual drug-resistant patients who may be at increased risk for thrombotic complications after PCI.

Aged↗
PubMed2006

Frequency and clinical implications of discordant creatine kinase-MB and troponin measurements in acute coronary syndromes.

OBJECTIVES: We sought to evaluate the association between discordant cardiac marker results and in-hospital mortality and treatment patterns in patients with non-ST-segment elevation acute coronary syndromes (NSTE ACS). BACKGROUND: Creatine kinase-MB (CK-MB) and cardiac troponins (cTn) are often measured concurrently in patients with NSTE ACS. The significance of discordant CK-MB and cTn results is unknown. METHODS: Among 29,357 ACS patients in the CRUSADE initiative who had both CK-MB and cTn measured during the first 36 hours, we examined relationships of four marker combinations (CK-MB-/cTn-, CK-MB+/cTn-, CK-MB-/cTn+, and CK-MB+/cTn+) with mortality and American College of Cardiology/American Heart Association guidelines-recommended acute care. RESULTS: The CK-MB and cTn results were discordant in 28% of patients (CK-MB+/cTn-, 10%; CK-MB-/cTn+, 18%). In-hospital mortality was 2.7% among CK-MB-/cTn- patients; 3.0%, CK-MB+/cTn-; 4.5%, CK-MB-/cTn+; and 5.9%, CK-MB+/cTn+. After adjustment for other presenting risk factors, patients with CK-MB+/cTn- had a mortality odds ratio (OR) of 1.02 (95% confidence interval [CI] 0.75 to 1.38), those with CK-MB-/cTn+ had an OR of 1.15 (95% CI 0.86 to 1.54), and those with CK-MB+/cTn+ had an OR of 1.53 (95% CI 1.18 to 1.98). Despite variable risk, patients with CK-MB+/cTn- and CK-MB-/cTn+ were treated similarly with early antithrombotic agents and catheter-based interventions. CONCLUSIONS: Among patients with NSTE ACS, an elevated troponin level identifies patients at increased acute risk regardless of CK-MB status, but an isolated CK-MB+ status has limited prognostic value. Recognition of these risk differences may contribute to more appropriate early use of antithrombotic therapy and invasive management for all cTn+ patients.

Aged↗
PubMed2006

Elevated placental growth factor levels are associated with adverse outcomes at four-year follow-up in patients with acute coronary syndromes.

OBJECTIVES: This study sought to evaluate the predictive value of baseline placental growth factor (PlGF) for long-term cardiovascular events in acute coronary syndromes (ACS). BACKGROUND: A biomarker of vascular inflammation, PlGF is identified as a powerful predictor for short-term outcome in patients with ACS. METHODS: In 544 patients who were enrolled in the placebo arm of the c7E3 Fab Anti Platelet Therapy in Unstable REfractory angina (CAPTURE) trial, PlGF levels were determined as well as markers of myocardial necrosis (troponin T [TnT]), general inflammation (high-sensitivity C-reactive protein [hsCRP]), and platelet activation (soluble CD40 ligand [sCD40L]). Cox proportional hazard regression analyses were applied to evaluate the relationship between biomarkers and the occurrence of all-cause death or non-fatal myocardial infarction during a median follow-up period of four years. RESULTS: Patients with PlGF levels in the fourth and fifth quintile (>27 ng/l) had higher mortality than those with lower levels (10.8% vs. 3.2%; hazard ratio [HR], 3.3; 95% confidence interval [CI], 1.6 to 7.1), as well as a higher incidence of the composite end point of death or myocardial infarction (27.6% vs. 11.3% events; HR, 2.6; 95% CI, 1.7 to 3.9). The relationship between PlGF and the composite end point remained significant after adjustment for TnT, sCD40L, and hsCRP (adjusted HR, 3.3; 95% CI, 2.0 to 5.4). CONCLUSIONS: In patients with ACS, elevated plasma levels of PlGF are associated with adverse cardiac outcomes during long-term follow-up. These data suggest that PlGF as a more specific marker of vascular inflammation should be considered for risk stratification of patients with ACS rather than general markers of inflammation.

Abciximab↗
PubMed2006

Effect of clopidogrel with and without eptifibatide on tumor necrosis factor-alpha and C-reactive protein release after elective stenting: results from the CLEAR PLATELETS 1b study.

OBJECTIVES: This study was performed to compare the effects of antiplatelet regimens on early inflammation and cardiac marker release after elective stenting. BACKGROUND: Few data exist regarding the comparative effects of specific antiplatelet regimens on early inflammation marker release after stenting. METHODS: In a 2 x 2 factorial randomized investigation, patients undergoing stenting were treated with either clopidogrel alone (300 mg or 600 mg; n = 60) or clopidogrel with eptifibatide (n = 60). Platelet aggregation (5 and 20 muM adenosine diphosphate [ADP]), ADP-stimulated expression of active glycoprotein (GP) IIb/IIIa, and platelet-bound P-selectin, tumor necrosis factor (TNF)-alpha, C-reactive protein (CRP), and cardiac markers were measured. RESULTS: Compared with a strategy of clopidogrel alone, clopidogrel + eptifibatide reduced the release of cardiac markers. A marked reduction in platelet aggregation and active GP IIb/IIIa expression (p < or = 0.001) with clopidogrel + eptifibatide was associated with a decrease in CRP and TNF-alpha release (p < or = 0.001). CONCLUSIONS: A strategy of clopidogrel with GP IIb/IIIa blockade resulted in superior inhibition of inflammation and cardiac marker release, which was accompanied by superior platelet inhibition immediately after percutaneous coronary intervention compared with a strategy of clopidogrel alone. The mechanistic and clinical implications of attenuated periprocedural inflammation and myocardial necrosis with a strategy of GP IIb/IIIa inhibition warrant further investigation.

Aged↗
PubMed2006

Value of platelet reactivity in predicting response to treatment and clinical outcome in patients undergoing primary coronary intervention: insights into the STRATEGY Study.

OBJECTIVES: The purpose of this study was to evaluate the value of platelet reactivity (PR) in predicting the response to treatment and outcome in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention assisted by glycoprotein (GP) IIb/IIIa inhibition. BACKGROUND: There is limited prognostic information on the role of spontaneous or drug-modulated PR in STEMI patients. METHODS: The PR was measured with Platelet Function Analyzer (PFA)-100 and light transmission aggregometry (LTA) using adenosine diphosphate as agonist in 70 consecutive STEMI patients at entry (PR-T0), 10 min after GP IIb/IIIa bolus (PR-T1), and discharge (PR-T2) and in 30 stable angina (SA) patients (PR-SA). Complete platelet inhibition (CPI) was based on closure time >300 s by PFA-100 and percentage inhibition of platelet aggregation >95% by LTA. Clinical, electrocardiographic, and angiographic responses to treatment during 1-year follow-up were collected. RESULTS: According to both techniques, PR-T0 was higher than: 1) PR-T2 and PR-SA; 2) in those without CPI at T1; and 3) in patients with final Thrombolysis In Myocardial Infarction (TIMI) flow grade <3. The PR-T0 assessed with PFA-100 correlated with: 1) corrected TIMI frame count (r = -0.6, p < 0.001); 2) ST-segment resolution (r = 45, p < 0.001); and 3) creatine kinase-MB (r = -0.47, p < 0.001). At 1 year, patients with high PR-T0 showed an adjusted 5- to 11-fold increase in the risk of death, reinfarction, and target vessel revascularization (hazard ratio [HR] 11, 95% confidence interval [CI] 1.5 to 78 [p = 0.02] in PFA-100; HR 5.2, 95% CI 1.1 to 23 [p = 0.03] in LTA). CONCLUSIONS: The PR at entry affects response to GP IIb/IIIa inhibition, mechanical treatment, and long-term outcome in STEMI patients undergoing primary intervention.

Abciximab↗
PubMed2005

Early negative T waves and viable myocardium in patients with a first ST-elevation acute coronary syndrome.

Deep negative T waves (NTW) are a frequent finding following acute ST-segment elevation coronary syndromes but its possible relation with the status of regional contractility remains unclear. We studied 52 patients with a first ST-elevation acute coronary syndrome with or without NTW in anterior leads (> or =3 mm in > or=3 leads) and assessed the ejection fraction and regional myocardial contractility by contrast left ventriculography at baseline and during a low-dose dobutamine test (10 microg/kg per minute). Ejection fraction and regional contractility tended to be more preserved in patients with NTW, but dobutamine increased regional contractility in the jeopardized area in most patients with or without NTW and the improvement was similar in those either with or without enzyme elevation. In conclusion, deep NTW after ST-elevation acute coronary syndromes tends to be associated with a more preserved myocardium but it is neither a sensitive nor a specific marker of viable myocardium.

Angina Pectoris↗