Coronary Artery Stent Thrombosis Research Articles

Stent Thrombosis: Understanding and Managing a Critical Problem

Coronary artery stent thrombosis (ST), defined as the thrombotic occlusion of a stented segment, is an infrequent but serious complication of percutaneous coronary intervention (PCI). The clinical consequences of ST are severe, because acute stent occlusion results in myocardial infarction and death in up to 45% of cases. Specific patient and procedural characteristics increase the risk of ST, but optimized interventional techniques and antiplatelet therapies have the potential to decrease ST and improve cardiovascular outcomes following PCI.

Intravenous tissue plasminogen activator, ischemic stroke, and the risk of Kounis Syndrome

Sir, We have read with great interest the report by Sweda et al that was published in this Journal. It described two patients who developed acute myocardial infarction (MI) following intravenous tissue plasminogen activator (tPA) for acute ischemic stroke.[1] The authors of this report speculated that fragmentation and lysis of any intracardiac thrombus may have resulted in embolization of coronary arteries and development MI after use of tPA. They did not exclude any remote possibility of coincidental occurrence of two atherosclerotic events MI and ischemic stroke. However, both patients died from fatal cardiac arrhythmia. Postmortem examination was not carried out. The first patient had a history of hypertension and the second patient had a history of hypertension, ischemic heart disease, kidney disease, and diabetes. Both patients developed hypotension, with breathlessness the first, and cardiovascular collapse the second, following the intravenous administration of tPA. Although the classical symptoms and signs of an allergic, anaphylactic, or anaphylactoid reaction were not described, and therefore such a work up was not performed, these two patients could have suffered type II variant of Kounis syndrome.[2] This syndrome is defined today as the concurrence of acute coronary syndromes with conditions associated with mast cell activation, involving interrelated and interacting inflammatory cells. These inflammatory cells namely mast cells, T-cells, and macrophages activate each other via multidirectional stimuli and behave as a ball of thread. These cells can release inflammatory mediators capable to induce coronary events. Platelets with high and low affinity IgE receptors are involving also in this process.[3] Three variants of this syndrome have been described.[4] Type I variant, which includes patients with normal coronaries in whom the allergic insult can induce either coronary artery spasm or coronary artery spasm progressing to acute myocardial infarction. Type II variant, which includes patients with culprit but quiescent pre-existing coronary disease in whom the allergic insult can induce either coronary artery spasm or plaque erosion or rupture manifesting as acute myocardial infarction. Type III variant, which includes patients with coronary artery stent thrombosis in whom aspirated thrombus specimens demonstrate the presence of eosinophils and mast cells. Allergic reactions with the use of fibrinolytics have been described in the literature, more often with streptokinase but also with the use of tPA.[5] True and obvious anaphylactic reactions to tPA are rare but anaphylactoid reactions occur in up to 0.002% of patients treated for acute MI and from 1.5% to 1.9% those treated for acute ischemic stroke.[6] Therefore, Kounis syndrome should be always being considered in such occasions, because this syndrome is not a rare disease but is a rarely diagnosed condition.[4]

Acute Multi-Vessel Coronary Stent Thrombosis

Coronary artery stent thrombosis is a rare but often fatal complication associated with percutaneous coronary intervention (PCI) using both bare-metal stents and drug-eluting stents. Although strict adherence to dual anti-platelet therapy (aspirin plus clopidogrel) minimizes this risk, stent thrombosis will still occur in rare patients, leading to acute, subacute, or late life-threatening acute coronary syndromes. To present a rare case of acute stent thrombosis involving multiple vessels to increase awareness of this life-threatening condition among emergency physicians, and to review the current guidelines for anti-platelet therapy in this patient population. A 52-year-old man who underwent PCI using drug-eluting stents in two separate coronary vessels presented to the Emergency Department within 2 h of discharge from the hospital with chest pain, dynamic electrocardiogram changes, and elevated cardiac markers. Despite compliance with the current recommendations for post-PCI anti-platelet therapy, urgent repeat catheterization revealed total thrombotic occlusion of both stents, requiring urgent repeat intervention. Despite patient compliance with the currently recommended anti-platelet regimen after stent therapy for coronary artery disease, acute stent thrombosis remains a rare but life-threatening risk in both the immediate and delayed post-intervention period. In addition, premature cessation of this anti-platelet therapy stands as the greatest risk factor for such thrombotic events. This case is presented to inform emergency physicians of the current post-PCI anticoagulation recommendations to help mitigate the risk of such complications.

Caution: Maintain Anti-Platelet Therapy in Patients with Coronary Artery Stents

Caution: Maintain Anti-Platelet Therapy in Patients with Coronary Artery Stents

Acute coronary artery stent thrombosis following rapid renewal of functional platelets: Implications for intensified antiplatelet therapy

Acute coronary artery stent thrombosis following rapid renewal of functional platelets: Implications for intensified antiplatelet therapy -

Coronary Artery Stent Thrombosis Associated with Heparin‐Induced Thrombocytopenia: Case Report and Review of the Literature

The diagnosis of an acute coronary syndrome associated with heparin-induced thrombocytopenia is an increasingly recognized complication of heparin exposure. We describe a case of an acute myocardial infarction 2 weeks after elective aortobifemoral bypass surgery, subsequent subacute coronary artery stent thrombosis, and the treatment strategies available.

Clopidogrel Resistance and Aspirin Resistance - a Cause of Coronary Artery Stent Thrombosis?.

Background: Occlusions of coronary artery stents are a seldom but often fatal complication after coronary artery intervention. With aggressive platelet inhibition therapy (combination of Aspirin (ASS) and clopidogrel) a reduction of stent thrombosis to less than 2% was achieved. The inhibition of platelet function has great interindividual variability and resistance against ASS and/or clopidogrel were previously described. Therefore we studied the relation between coronary artery stent thrombosis and insufficient inhibition of platelet function in patients after coronary artery intervention.Methods: Between 2000 and 2003 we examined 20 patients (pts) with coronary artery stent thrombosis within 4 weeks after coronary artery intervention. All patients received a clopidogrel loading dose of 300mg followed by 75mg/die and ASS 100mg/die. Platelet inhibition was studied by light transmittance aggregometry in platelet rich plasma (Aggregometer PAP 4, moelab inc.). Aggregation was recorded as the maximum percentage change in light transmittance from baseline using platelet poor plasma as a reference. We defined ASS resistance as platelet aggregation > 30% after induction with 0,5mg/ml arachidonic acid and clopidogrel resistance as platelet aggregation > 30% after induction with 20 μmol ADP. We compared these pts with 20 pts without stent thrombosis within 4 weeks after coronary artery intervention.Results: In the group with coronary artery stent thrombosis we found 13/20 patients with insufficient platelet inhibition. 2/20 pts in this group were resistent against both ASS and clopidogrel. In 2/20 pts we observed ASS resistance and in 9/20 pts clopidgrel resistance. In the group of patients without stent thrombosis we found only 1/20 pt with ASS resistance and 1/20 pt with clopidogrel resistance.Conclusions: Insufficient platelet inhibition could be one cause of early stent thrombosis after coronory artery intervention. Platelet function testing is able to detect insufficient platelet inhibition and early testing could be an instrument to prevent coronary artery stent thrombosis.

Are There Two Distinct Mechanistic Pathways That Explain the Varying Clinical Presentations, Laboratory Findings, and Outcomes of Thienopyridine-Associated Thrombotic Thrombocytopenic Purpura (TTP)?.

Introduction: The antiplatelet agents ticlopidine and clopidogrel are thienopyridine derivatives that are commonly used for secondary prevention of cerebrovascular events, prevention of coronary artery stent thrombosis, and for treatment of acute coronary syndrome. While these chemically related agents are the first and third most common causes of drug-associated TTP respectively, clinical presentations, laboratory findings, and outcomes suggest that there may be two distinct mechanistic pathways.Methods: Clinical and laboratory data for 60 cases of ticlopidine-associated TTP and 35 cases of clopidogrel associated TTP were reviewed.Results: Type 1 thienopyridine-associated TTP, characterized by onset of disease > 5 days after drug initiation, occurred in 98% of the ticlopidine patients versus 63% of the clopidogrel patients. Laboratory studies identified severe deficiency of ADAMTS13 activity and the presence of IgG inhibitors in 7 ticlopidine (Tsai, et al.; Annals of Internal Medicine, 2000) and 2 clopidogrel (Bennett, et al.; NEJM, 2000) patients. Survival was 68% in the ticlopidine patients versus 91% in the clopidogrel patients. Type 2 thienopyridine-associated TTP, consisting of TTP onset within 5 days of drug initiation, occurred in 2% of the ticlopidine patients versus 37% of the clopidogrel patients. Laboratory studies failed to identify deficient ADAMTS13 activity or the presence of IgG inhibitors in 1 clopidogrel patient (Zheng, et al.; Blood, 2004). Survival was 0% in the ticlopidine patients versus 38% in the clopidogrel patients.Conclusion: The proposed type 1 and type 2 thienopyridine-associated TTP may be distinguished on the basis of clinical presentation, ADAMTS13 levels, and outcome. Type 1 thienopyridine-associated TTP—characterized as occurring after > 5 days of thienopyridine treatment, severely deficient ADAMTS13 activity and presence of IgG inhibitors, and high survival rates with plasmapheresis—is more likely to occur in patients receiving ticlopidine. Type 2 thienopyridine-associated TTP—characterized as occurring within 5 days of thienopyridine therapy initiation, normal ADAMTS13 activity and undetectable IgG inhibitors, and poor survival rates despite plasmapheresis—is more likely to occur in patients receiving clopidogrel. Additional confirmatory studies on larger numbers of patients are needed.

Coronary artery stent thrombosis associated with exercise testing

Chest pain following coronary artery stenting is common, yet finding the cause can be difficult. Exercise testing has long been used in the assessment of chest pain, but its usefulness in patients who have recently undergone coronary artery stenting is in doubt. A case of exercise testing appearing to precipitate acute stent thrombosis in a patient several weeks post-coronary artery stenting is reported and compared to a similar case in the literature. The role of exercise testing in the assessment of chest pain early after coronary artery stenting is then reviewed.

Antiplatelet agents in the prevention of cardiovascular morbidity and mortality in older patients with vascular disease.

Antiplatelet drugs have been demonstrated to reduce the incidence of myocardial infarction (MI), stroke or vascular death in patients with vascular disease. There are no data suggesting that antiplatelet therapy acts differently in older people than in younger people and recommendations based on randomised clinical trials are probably generalisable to older people. Aspirin (acetylsalicylic acid) has been shown to reduce the incidence of non-fatal MI, nonfatal stroke and vascular death in patients with acute MI, a previous MI, angina pectoris or peripheral occlusive arterial disease (POAD), and to reduce cardiovascular morbidity and mortality in patients with a prior ischaemic stroke or transient ischaemic attack (TIA). It has also been shown to reduce the incidence of thrombus formation after coronary artery bypass graft surgery and percutaneous transluminal angioplasty, and in patients with atrial fibrillation and heart valve replacements. Deep vein thrombosis and pulmonary embolism after surgery are also prevented by aspirin. The available data allows the following recommendations to be made. Aspirin 160 to 325 mg daily should be administered to older men and women without contraindications to aspirin who have acute MI, prior MI, unstable or stable angina pectoris, ischaemic stroke, TIA or POAD, and continued indefinitely to reduce the risk of MI, stroke or vascular death. Aspirin should be started in patients before or immediately after revascularisation, and after heart valve replacement. Older men and women with nonvalvular atrial fibrillation who have contraindications to oral anticoagulant therapy but no contraindications to aspirin should be treated with aspirin 325 mg daily. It is reasonable to treat older men and women without contraindications to aspirin with aspirin 160 to 325 mg daily if they are at high risk for developing new coronary events. The incidence of stroke, MI or vascular death in patients after a stroke or TIA is reduced by ticlopidine. Therefore, ticlopidine 250 mg twice daily may be used in older men and women with a history of stroke or TIA who do not respond to or who cannot tolerate aspirin. Patients at high risk for coronary artery stent thrombosis benefit from combined therapy with aspirin plus ticlopidine. The annual incidence of ischaemic stroke, MI or vascular death was significantly reduced by clopidogrel in the Clopidogrel versus Aspirin in Patients at Risk of Ischemic Events (CAPRIE) trial. Therefore, clopidogrel 75 mg daily may be used in older men and women with symptomatic atherosclerosis who do not respond to or who cannot tolerate aspirin to reduce the incidence of ischaemic stroke, MI or vascular death. It should be noted that the acquisition cost for either ticlopidine or clopidogrel is considerably greater than that for aspirin. Most data indicate that the combination of aspirin and dipyridamole is not more effective than aspirin alone in preventing vascular events, and available data do not support the use of sulfinpyrazone in patients with vascular disease.

Usefulness of abciximab for treatment of early coronary artery stent thrombosis

The clinical and angiographic outcomes of 10 patients who received abciximab as part of their therapy for early stent thrombosis was compared with 25 patients (using historical controls) who received conventional therapy. Although the angiographic outcome and the incidence of myocardial infarction in both groups was similar, there were no deaths or referral for emergency coronary bypass surgery in the abciximab-treated group versus 3 deaths and 10 referrals for emergency bypass surgery in the conventionally treated group.

Multivessel Palmaz-Schatz Stenting: Early Results and One-Year Outcome

Objectives. To determine whether the benefits outlined in Backgroundmight extend to patients with multivessel disease, we examined the short- and long-term outcome of multivessel Palmaz-Schatz stenting.Background. Percutaneous transluminal coronary angioplasty (PTCA) has become the dominant treatment for most patients with single-vessel coronary artery disease and has emerged as an alternative treatment for selected patients with multivessel coronary artery disease. Although multivessel angioplasty has excellent early results and low procedural complication rates, long-term outcome is tempered by the frequent need for repeat revascularization. In patients with single-vessel coronary artery disease, Palmaz-Schatz stenting has been shown to have a higher success rate and a lower restenosis rate than conventional PTCA.Methods. A total of 103 patients (mean age 64 ± 11 years, 78 men and 25 women) underwent stenting of 212 vessels (saphenous vein graft [53%], left anterior descending coronary artery [20%], left circumflex artery [12%] and right coronary artery [15%]). In 88 patients (85%), multivessel stenting was performed during the same procedure, whereas the remaining 15 patients (15%) had staged multivessel stenting within 1 week of the index stent. Stenting involved only native coronary arteries in 33 patients and only vein grafts in 51 patients.Results. Angiographic success was achieved in 102 patients (99%). Major complications developed in three patients: one patient died, and two patients had Q wave myocardial infarction, with no emergency coronary artery bypass graft surgery or stent thrombosis. Eleven additional patients (11%) developed non–Q wave myocardial infarction, and nine patients (9%) had local vascular complications requiring surgical repair. Clinical follow-up was available in all patients at a mean of 13 ± 8 months. At 1 year, survival was 98%, with an event-free survival rate of 80%, reflecting predominantly repeat revascularization (17% overall, with 9% target site revascularization). Multivessel native coronary stenting resulted in a higher event-free survival rate and a lower probability of repeat revascularization than did multivessel saphenous vein graft stenting.Conclusions. In selected patients, multivessel Palmaz-Schatz stenting is technically feasible and carries both excellent early results and favorable 1-year clinical outcome.(J Am Coll Cardiol 1997;30:180–5)