Hypersensitivity Cases Associated With Drug-Eluting Coronary Stents

Nebeker, Jonathan R.; Virmani, Renu; Bennett, Charles L.; Hoffman, Joseph G.; Samore, Matthew H.; Alvarez, Jorge Iván; Davidson, Charles J.; McKoy, June M.; Raisch, Dennis W.; Whisenant, Brian; Yarnold, Paul R.; Belknap, Steven M.; West, Dennis P.; Gage, Jonathan E.; Morse, Richard E.; Gligoric, Gordana; Davidson, Laura; Feldman, Marc D.

doi:10.1016/j.jacc.2005.07.071

Cited by 539 publications

(85 citation statements)

References 14 publications

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“…Further support of hypersensitivity reactions after DES implantation comes from the Research on Adverse Drug Events and Reports (RADAR) registry, with 17 of 5783 cases reporting hypersensitivity symptoms probably or certainly related to DES. 20 Although these previous reports were limited to either autopsy series or clinical case descriptions, the present study corroborates these findings in vivo in patients presenting with very late ST undergoing emergency PCI. Thrombus aspirates harvested from very late ST segments showed signs of infiltration with neutrophils, lymphocytes, macrophages, and eosinophils, which was accompanied by IVUS evidence of vessel remodeling.…”

Section: Cook Et Al Histopathology Of Very Late St Thrombus Aspiratessupporting

confidence: 88%

Correlation of Intravascular Ultrasound Findings With Histopathological Analysis of Thrombus Aspirates in Patients With Very Late Drug-Eluting Stent Thrombosis

et al. 2009

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Background-Intravascular ultrasound of drug-eluting stent (DES) thrombosis (ST) reveals a high incidence of incomplete stent apposition (ISA) and vessel remodeling. Autopsy specimens of DES ST show delayed healing and hypersensitivity reactions. The present study sought to correlate histopathology of thrombus aspirates with intravascular ultrasound findings in patients with very late DES ST. Methods and Results-The study population consisted of 54 patients (28 patients with very late DES ST and 26 controls).Of 28 patients with very late DES ST, 10 patients (1020Ϯ283 days after implantation) with 11 ST segments (5 sirolimus-eluting stents, 5 paclitaxel-eluting stents, 1 zotarolimus-eluting stent) underwent both thrombus aspiration and intravascular ultrasound investigation. ISA was present in 73% of cases with an ISA cross-sectional area of 6.2Ϯ2.4 mm 2 and evidence of vessel remodeling (index, 1.6Ϯ0.3). Histopathological analysis showed pieces of fresh thrombus with inflammatory cell infiltrates (DES, 263Ϯ149 white blood cells per high-power field) and eosinophils (DES, 20Ϯ24 eosinophils per high-power field; sirolimus-eluting stents, 34Ϯ28; paclitaxel-eluting stents, 6Ϯ6; P for sirolimus-eluting stents versus paclitaxel-eluting stentsϭ0.09). The mean number of eosinophils per high-power field was higher in specimens from very late DES ST (20Ϯ24) than in those from spontaneous acute myocardial infarction (7Ϯ10), early bare-metal stent ST (1Ϯ1), early DES ST (1Ϯ2), and late bare-metal stent ST (2Ϯ3; P from ANOVAϭ0.038). Eosinophil count correlated with ISA cross-sectional area, with an average increase of 5.4 eosinophils per high-power field per 1-mm 2 increase in ISA cross-sectional area. Conclusions-Very

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Section: Cook Et Al Histopathology Of Very Late St Thrombus Aspiratessupporting

confidence: 88%

Correlation of Intravascular Ultrasound Findings With Histopathological Analysis of Thrombus Aspirates in Patients With Very Late Drug-Eluting Stent Thrombosis

et al. 2009

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“…Histopathological analysis revealed aneurysmal dilatation of the vessel wall within the stented segment with evidence of stent malapposition and thick fibrin thrombus between the stent and the arterial wall. Clinical evidence of hypersensitivity reactions stems from a registry, 58 with 17 of 5783 patients reporting hypersensitivity symptoms probably or certainly related to DES.…”

Section: Pathogenesis Of Stmentioning

confidence: 99%

Late Coronary Stent Thrombosis

2007

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Introduced Ͼ20 years ago, 1 coronary artery stents have improved the safety and particularly the efficacy of percutaneous coronary interventions (PCIs). 2 Abrupt vessel closure, complicating 6% to 8% of balloon angioplasty procedures, was associated with a 5% mortality, 40% rate of myocardial infarction (MI), and 40% rate of emergency coronary artery bypass grafting. 3 Stents significantly reduced these adverse events (Figure 1). 4,5 The reduction of restenosis afforded by bare metal stents (BMS) was modest (30% to 40%). Repeat revascularization still occurred in 15% to 20% of cases. 6 Drug-eluting stents (DES) with antiproliferative drugs attached via polymers on the stent surface to minimize smooth muscle proliferation have reduced restenosis and rates of target lesion revascularization by 50% to 70% compared with BMS across nearly all lesion and patient subsets. 7 Initially 8 and again more recently, 9 -16 safety concerns were raised about DES, particularly about late stent thrombosis (ST). Historical PerspectiveST was a bane of stent implantation from the beginning. The initial experience with Wallstents in the late 1980s was overshadowed by ST rates approaching 24%. 17 Subsequent series with Palmaz-Schatz and Gianturco-Roubin stents (still predominantly bailout stenting) observed ST in 6% to 12% of cases. 4,18 The postprocedural antithrombotic regimen at the time consisted of aspirin, often in conjunction with oral anticoagulation. Dual antiplatelet therapy of aspirin and the thienopyridine ticlopidine in conjunction with a shift from bailout to elective stenting resulted in a significant reduction of ST to Ͻ2%. 5,19 Earlier oral antiplatelet drug loading and glycoprotein IIb/IIIa antagonists further diminished ST. Table 1 provides an overview of ST reported in contemporary trials of BMS and DES, ranging from 0.1% to 3.1%. 11,20 -38 The wide range in the incidence of ST across trials with both BMS and DES is explained by differences in definitions, length of follow-up, antithrombotic drug regimens, and complexity of patients and lesions.

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“…Several hundred cases of hypersensitivity reactions related to drug-eluting stents (DES) have been reported, some of which were fatal. 85 Based on human autopsy series, DES late/very late stent thrombosis is caused by impaired arterial healing (with characteristic incomplete re-endothelialisation, persistent fibrin deposition and macrophage infiltration) when compared with bare metal stents. 86 Autopsies confirmed inflammatory cell infiltrates (plasma cells, macrophages, eosinophils and lymphocytes) that permeate all three vascular wall layers, a histopathological picture very similar to Kounis type I and type II.…”

Section: Hypersensitivity-induced Coronary Stent Thrombosis (Kounis Tmentioning

confidence: 99%

“…8 Three variants have been described (Table 2). 9,16,85 Transthoracic or trans-oesophageal echocardiography can reveal regional wall motion abnormalities suggestive of acute coronary syndromes, and can help distinguish between other causes of chest pain and/or hypotension (such as aortic dissection, pericarditis, pericardial effusion and pulmonary embolism).…”

Section: Clinical Variantsmentioning

confidence: 99%

Kounis syndrome: a narrative review

Fourie

2016

Southern African Journal of Anaesthesia and Analgesia

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Inflammatory mediators released from activated mast cells and basophils during hypersensitivity reactions have direct pathological effects on the myocardium and coronary vasculature. It was traditionally thought that cardiovascular signs and symptoms in anaphylaxis are largely due to peripheral vasodilation and increased vascular permeability. However, there is extensive evidence of primary cardiac involvement during hypersensitivity reactions, most notably coronary vasoconstriction as well as atherosclerotic plaque erosion and rupture, leading to angina pectoris and acute coronary syndromes. Furthermore, mast cells are well established as effector cells in atherosclerosis, through their effects on atherosclerotic plaque progression and destabilisation. It was noted over 30 years ago that cardiac patients have a markedly higher concentration of biologic amines (especially histamine) in their coronary vasculature, and, additionally, are hyper-reactive to the effects thereof. This is borne out by the disproportionate mortality rate of those with cardiac disease that suffer a hypersensitivity reaction. Kounis syndrome refers to angina pectoris or an acute coronary syndrome secondary to a hypersensitivity reaction, with the subtypes dependent on the underlying state of the coronaries and presence of a drug-eluting stent or not. This review will focus mainly on the aetiology, pathophysiology, diagnoses and treatment of this important syndrome.

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Hypersensitivity Cases Associated With Drug-Eluting Coronary Stents

Abstract: The FDA reports and autopsy findings suggest that DES may be a cause of systemic and intrastent hypersensitivity reactions that, in some cases, have been associated with late thrombosis and death.

Cited by 539 publications

References 14 publications

Correlation of Intravascular Ultrasound Findings With Histopathological Analysis of Thrombus Aspirates in Patients With Very Late Drug-Eluting Stent Thrombosis

Correlation of Intravascular Ultrasound Findings With Histopathological Analysis of Thrombus Aspirates in Patients With Very Late Drug-Eluting Stent Thrombosis

Late Coronary Stent Thrombosis

Kounis syndrome: a narrative review

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