Tirofiban-induced diffuse alveolar hemorrhage: after primary angioplasty

Platelets play an important role in the development of acute coronary syndromes. Evidence indicates that platelet-inhibiting drugs, such as glycoprotein IIb/IIIa inhibitors, can be beneficial when they are administered at the time of primary percutaneous coronary intervention for acute ST-segment-elevation myocardial infarction. However, an associated increase in the risk of bleeding is well documented. Diffuse alveolar hemorrhage is a rare but life-threatening and underdiagnosed complication of therapy with glycoprotein IIb/IIIa inhibitors. Diffuse alveolar hemorrhage can easily be mistaken for acute pulmonary edema, a condition commonly seen in patients with acute coronary syndrome. Physicians need to be aware of this diagnostic dilemma, because early treatment increases the chance that the patients will survive.Herein, we report the fatal outcome of diffuse alveolar hemorrhage in a 73-year-old man who presented with acute ST-segment-elevation myocardial infarction and was treated with tirofiban in conjunction with primary percutaneous coronary intervention. In addition, we review the medical literature pertaining to the sequelae of glycoprotein IIb/IIIa inhibitor therapy in the presence of diffuse alveolar hemorrhage.     

Ipsilateral intracerebral hemorrhage following carotid stent-assisted angioplasty: a manifestation of hyperperfusion syndrome--a case report

A case of hyperperfusion syndrome manifested as intracerebral hemorrhage following carotid stent-assisted angioplasty while using intravenous abciximab is described. Review of literature regarding hyperperfusion syndrome in patients undergoing carotid artery revascularization is presented. Possible mechanisms of hyperperfusion and the role of arterial hypertension, anticoagulation, and antiplatelet treatment in the genesis of hyperperfusion syndrome are discussed. Widening use of percutaneous carotid revascularization necessitates physicians' awareness of early recognition of this complication.     

Intracranial hemorrhage after coronary thrombolysis with tissue plasminogen activator.

PURPOSE AND METHODS: We analyzed the clinical, laboratory, and radiologic data in nine patients who sustained an intracranial hemorrhage (ICH) after receiving intravenous recombinant tissue plasminogen activator (rt-PA) and heparin for treatment of acute myocardial infarction (MI). Our purpose was to delineate the clinical and radiologic features of the ICHs, as well as to determine their potential risk factors and mechanisms. RESULTS: Among 1,700 patients with an acute MI treated with an investigational two-chain rt-PA, duteplase (Burroughs Wellcome Co., Research Triangle Park, NC), nine (0.53%) developed symptomatic ICH. Neurologic symptoms occurred between 7 and 96 hours after onset of rt-PA therapy. All patients received heparin concomitantly for prevention of coronary reocclusion. The activated partial thromboplastin times (aPTTs) in five of eight (63%) patients at onset of ICH were excessively prolonged (greater than two times control); hypofibrinogenemia occurred in only one of five (20%) patients tested; and thrombocytopenia was present in only one of the nine (11%) patients. Fibrin degradation products (FDPs) were elevated in all five patients tested. Minor hemorrhage (not requiring transfusion) outside the central nervous system occurred in five of the nine patients with ICH. The ICHs were often of lobar location and of moderate to large size. They occurred at multiple sites in three patients, and were fatal in four instances (44%). CONCLUSIONS: The incidence of ICH in this series was low, and consistent with figures reported from studies with alteplase in patients with acute MI. The mechanisms of these hemorrhages remain unclear; while hypofibrinogenemia was not a uniform finding, excessive prolongation of the aPTT and elevated FDPs may have contributed to the occurrence of ICH in some patients. Still unidentified local cerebrovascular factors may play an additional role in causing ICH. In order to further clarify the mechanisms of ICH in the setting of thrombolytic therapy, prospective data collection on probable risk factors for ICH in patients with acute MI treated with rt-PA will be required.     

Bilateral carotid angioplasty and stenting.

Bilateral carotid stenosis is generally treated by staged stenting procedure and rarely simultaneously due to concerns about hemodynamic impairment from stimulation of the carotid sinus baroreflex (severe bradycardia, hypotension) and the risk of cerebral hyperperfusion syndrome. Most of the accounts of bilateral carotid stenting are of small series. The aim of this study was to evaluate the feasibility and safety of simultaneous bilateral carotid angioplasty and stenting (CAS) in comparison with staged procedure. We retrospectively analyzed the procedural outcome and complications of bilateral CAS done between February 1995 and June 2004 in a consecutive series of 57 high-risk patients. Mean age was 64 +/- 9 years (male, 43; female 14). One hundred fifteen arteries were treated (one patient had bilateral internal carotid artery stenosis associated to an ostial common carotid artery stenosis). Thirty-nine patients were symptomatic (70%). Thirty-six patients had severe coronary artery disease. Seventeen patients underwent a simultaneous bilateral CAS (group 1), 40 in a staged manner (group 2). Among these 40 patients 10 were treated with a time interval of 24 hr, while the 30 other ones were treated with a time interval of 2 days to 2 months. A neuroprotection device was used in the last 42 patients. There was technical success in all patients and transient bradycardia and/or hypotension in 25 patients (44%). There was no prolonged bradycardia or hypotension. At 30 days, we observed in group 1 (simultaneous bilateral CAS) no transient ischemic attack (TIA), no minor stroke, one (5.8%) major stroke (hyperperfusion syndrome with brain hemorrhage leading to death in a patient under IIb/IIIa inhibitors), one myocardial infarction leading to death, and two (11.7%) death/stroke/myocardial infarction; in group 2 (staged procedure), two (5%) TIAs, no minor stroke, no major stroke, and one (2.5%) hyperperfusion syndrome with rapid recovery. Among the 10 patients treated with a time interval of 24 hr, we observed one TIA. Among carefully selected patients, bilateral CAS is feasible simultaneously or the day after, with a safety and complication rate comparable to that of large published series of CAS or endarterectomies in high-risk patients. Nevertheless, careful monitoring of the patient, blood pressure, and heart rate is mandatory to avoid complications related to hyperperfusion syndrome. Routine use of neuroprotection device and meticulous technique should improve the outcomes of bilateral CAS.     

Restenosis after transluminal coronary angioplasty: a risk factor analysis

In order to determine the relationship of restenosis following percutaneous transluminal coronary angioplasty (PTCA) to risk factors such as hypercholesterolemia, hyperglycemia, smoking, and weight, we performed a univariate analysis to test the association of these variables with restenosis in 723 patients who had percutaneous transluminal coronary angioplasty and follow-up catheterization. Cholesterol levels were higher in younger and female subjects (less than 0.0001). Initial cholesterol did not predict restenosis, and follow-up cholesterol levels showed an inverse relationship with restenosis (P less than .02). There was a trend (P less than .09) toward decreased restenosis in those who were active smokers at the time of follow-up catheterization. No differences were seen in diabetics with hyperglycemia, in both treated and untreated groups (P = NS). A stepwise multiple logistic regression was used to simultaneously test the association of the above risk factor variables to restenosis. None of the interactions were found to be significant, except cholesterol at follow-up (P = .001). Therefore, the status of serum cholesterol, blood sugar, smoking, and weight during the time of PTCA and at follow-up catheterization may be unimportant in predicting restenosis. Thus, we conclude 1) that to better determine the effect of these variables on restenosis, they should be estimated at times other than follow-up and 2) that the pathophysiological mechanism of restenosis may have different risk factors than progression of atherosclerotic coronary artery disease.     

颈动脉支架置入术后3年随访结果分析

目的探讨颈动脉支架置入术(CAS)在预防脑梗死方面的远期效果。方法选择接受颅外段CAS患者55例,定期随访3年。根据CAS后发生缺血性脑血管事件(4例)和未发生缺血性脑血管事件(51例)进行比较。并分析CAS后血管再狭窄情况。结果在55例完成3年随访的CAS患者中,4例(7.3%)出现了终点事件的患者均为脑梗死。其中3例患者缺血事件对应的脑梗死在支架置入同侧,1例患者缺血事件对应的脑梗死在支架置入对侧。单因素分析发现,年龄>75岁、高血压史、有两个以上脑血管病危险因素、术后未系统服用抗血小板药物、术前有多次脑梗死病史的患者术后容易发生缺血性脑血管事件(P<0.05)。3年随访观察,有3例(5.5%)发生了再狭窄。结论 CAS能有效降低动脉粥样硬化性颈动脉狭窄患者脑卒中发生风险。CAS后中远期再狭窄率较低。     

Predictors of infarct size after primary coronary angioplasty in acute myocardial infarction from pooled analysis from four contemporary trials

Determinates of infarct size in patients with acute myocardial infarction (AMI) undergoing percutaneous coronary intervention (PCI) have been incompletely characterized, in part because of the limited sample size of previous studies. Databases therefore were pooled from 4 contemporary trials of primary or rescue PCI (EMERALD, COOL-MI, AMIHOT, and ICE-IT), in which the primary end point was infarct size assessed using technetium-99m sestamibi single-photon emission computed tomographic imaging, measured at the same core laboratory. Of 1,355 patients, infarct size was determined using technetium-99m sestamibi imaging in 1,199 patients (88.5%), at a mean time of 23 +/- 15 days. Median infarct size of the study population was 10% (interquartile range 0% to 23%; mean 14.9 +/- 16.1%). Using multiple linear regression analysis of 18 variables, left anterior descending infarct artery, baseline Thrombolysis In Myocardial Infarction grade 0/1 flow, male gender, and prolonged door-to-balloon time were powerful independent predictors of infarct size (all p <0.0001). Other independent correlates of infarct size were final Thrombolysis In Myocardial Infarction grade <3 flow (p = 0.0001), previous AMI (p = 0.005), symptom-onset-to-door time (p = 0.021), and rescue angioplasty (p = 0.026). In conclusion, anterior infarction, time to reperfusion, epicardial infarct artery patency before and after reperfusion, male gender, previous AMI, and failed thrombolytic therapy were important predictors of infarct size after angioplasty in patients with AMI assessed using technetium-99m sestamibi imaging and should be considered when planning future trials of investigational drugs or devices designed to enhance myocardial recovery.     

Intracranial hemorrhage and hyperperfusion syndrome following carotid artery stenting: risk factors, prevention, and treatment

OBJECTIVES: The study defined the incidence of cerebral hyperperfusion syndrome and intracranial hemorrhage (ICH) and the risk factors for their development following carotid artery stenting (CAS). BACKGROUND: Hyperperfusion syndrome and ICH can complicate carotid revascularization, be it endarterectomy or CAS. Although extensive effort has been devoted to reducing the incidence of ischemic stroke complicating CAS, little is known about the incidence, etiology, and prevention strategies for hyperperfusion and ICH following CAS. METHODS: We retrospectively reviewed the prospective database of 450 consecutive patients who were treated with CAS in our department to identify patients who developed hyperperfusion syndrome and/or ICH. RESULTS: The mean age of the patients was 72.7 +/- 10.9 years, and the mean diameter narrowing was 84 +/- 12.8%. Five (1.1% [95% confidence interval 0.4% to 2.6%]) patients developed hyperperfusion. Three (0.67%) of the five developed ICH. Two of these patients died (0.44%). Symptoms developed within a median of 10 h (range, 6 h to 4 days) following stenting. All five patients had correction of a severe internal carotid stenosis (mean 95.6 +/- 3.7%) with a concurrent contralateral stenosis >80% or contralateral occlusion and peri-procedural hypertension. These same risk factors are involved in cerebral hyperperfusion following carotid endarterectomy. The use of platelet glycoprotein IIb/IIIa receptor blockers did not appear to increase the risk ICH. CONCLUSIONS: The hyperperfusion syndrome occurs infrequently following CAS, and ICH occurs in 0.67% of patients. Patients with severe bilateral carotid stenoses may be predisposed to ICH, particularly if there is concurrent arterial hypertension. Patients with these factors may require more intensive hemodynamic monitoring after CAS, including prolongation of hospitalization in some cases.     

Blood pressure control after bilateral carotid angioplasty in a patient with severe hypertension-Case report

Carotid artery angioplasty with stenting is an effective treatment for carotid artery stenosis, but is frequently associated with acute transient hemodynamic changes. We present the case of a 73-year-old female patient with long-standing refractory hypertension who remained normotensive during a three-year follow-up after undergoing staged bilateral carotid angioplasty.     

高危症状性颈动脉狭窄支架成形术的疗效分析

目的分析颈动脉支架成形术治疗高危症状性颈动脉狭窄的有效性和安全性。方法对20例高危症状性颈动脉狭窄患者进行颈动脉支架成形术治疗,其中男12例,女8例;年龄为62～76岁,平均69岁。其中短暂性脑缺血发作11例,脑梗死9例。对所有患者均行全脑血管造影,显示颈动脉狭窄率均〉70％,其中一侧颈动脉重度狭窄9例（2例为颈动脉剥脱术后再狭窄）;双侧颈动脉重度狭窄6例;一侧颈动脉闭塞,另--N重度狭窄5例（1例为鼻咽癌放疗术后）。对所有患者使用脑保护装置,并均采用预扩张,预扩张后均使用自膨式支架。结果技术成功率为100％,残余狭窄率均〈30％。所有患者术中均出现不同程度的短暂性心率、血压下降,1例患者出现了微栓子栓塞,无其他严重并发症;其余患者围手术期内无缺血性卒中发作。术后复查颈动脉超声见,显示狭窄明显改善。结论颈动脉支架治疗高危症状性颈动脉狭窄创伤小,围手术期并发症少,是安全、有效的。     

Intracranial hemorrhage after use of tissue plasminogen activator for coronary thrombolysis

Tissue plasminogen activator (tPA), an approved coronary thrombolytic agent, can cause serious bleeding. We report the cases of six patients with intracranial hemorrhage after tPA treatment for acute myocardial infarction. None of the patients were hypertensive at admission, and only one was hypertensive during therapy. Intravenous tPA, 100 mg, was followed by continuous intravenous heparin infusion; intracranial hemorrhage occurred between 2 and 14 hours after tPA infusion ended and between 3 and 17 hours after heparin therapy was started. The partial thromboplastin time (PTT) was excessively prolonged (from 81 s to more than 150 s) in all patients at onset of intracranial hemorrhage. The intracerebral hematomas were predominantly of lobar location, and two patients had multiple simultaneous hemorrhages. Four patients died from massive intracranial hemorrhage; the mechanism for these hemorrhages was unclear. Factors possibly related to hemorrhage include a systemic fibrinolytic state or a platelet anti-aggregant effect produced by tPA and enhanced hemorrhagic tendency caused by the combined effects of tPA and heparin. Local vascular changes at the bleeding site remain as potential contributing factors for isolated intracranial hemorrhage.     

Sirolimus-eluting versus paclitaxel-eluting stent in primary angioplasty: a pooled patient-level meta-analysis of randomized trials

Large interests have been focused on the role of drug-eluting stents in the setting of ST-segment elevation myocardial infarction (STEMI) and concerns have emerged regarding an higher risk of stent thrombosis. Aim of the current study was to perform a meta-analysis using individual patient data to evaluate the long-term safety and effectiveness of sirolimus-eluting stent (SES) as compared to paclitaxel-eluting stent (PES) in patients undergoing primary percutaneous coronary intervention (PCI) for STEMI. The literature was scanned by formal searches of electronic databases (MEDLINE and CENTRAL). We examined all completed randomized trials of SES versus PES for STEMI. No language restriction was applied. Primary study endpoint was the occurrence of major adverse cardiac events (MACE). Secondary endpoints were the occurrence of death, reinfarction, stent thrombosis, target-vessel revascularization (TVR). Individual patient data were obtained from 4 out of 5 trials identified, including a total of 1,000 patients, 504 (50.4 %) randomized to SES and 496 (49.6 %) randomized to PES. At long-term follow-up (1,021 [372–1,351] days), no difference was observed between SES and PES in terms of TVR (10 vs 11.6 %, HR [95 % CI 0.73 [0.45–1.16], p = 0.18, p het = 0.92]) (primary endpoint) or death (9.4 vs 10.4 %, HR [95 % CI 0.95 [0.58–1.54], p = 0.82, p het = 0.89]), reinfarction (8.2 vs 10.4 %, HR [95 % CI 0.91 [0.53–1.57], p = 0.73, p het = 0.83]), stent thrombosis (7.4 vs 4.6 %, HR [95 % CI 1.04 [0.55–2.05], p = 0.92, p het = 0.65]), and MACE (10 vs 13.6 %, HR [95 % CI 0.86 [0.63–1.18], p = 0.36, p het = 0.84]) (secondary endpoints). The present pooled patient-level meta-analysis demonstrates that, among STEMI patients undergoing primary PCI, SES and PES are associated with a similar outcome at long-term follow-up, in terms of death, reinfarction, stent thrombosis, TVR and MACE.