Failed percutaneous coronary intervention: A decade of experience in 21,000 patients

Mattichak, Stephen J.; Dixon, Simon; Shannon, Francis; Boura, Judith; Safian, Robert D.

doi:10.1002/ccd.21274

Cited by 21 publications

(19 citation statements)

References 38 publications

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“…330,331 The need for emergency CABG is mainly confined to patients with a large, evolving MI due to iatrogenic vessel occlusion that cannot be salvaged percutaneously, or in patients with recurrent cardiac tamponade after pericardiocentesis following PCI-related vessel rupture. 330,332,333…”

Section: Acute Percutaneous Coronary Intervention Failurementioning

confidence: 99%

2018 ESC/EACTS Guidelines on myocardial revascularization

Neumann¹,

Ahlsson²,

Alfonso³

et al. 2018

European Heart Journal

5,029

2,078

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Section: Acute Percutaneous Coronary Intervention Failurementioning

confidence: 99%

2018 ESC/EACTS Guidelines on myocardial revascularization

Neumann¹,

Ahlsson²,

Alfonso³

et al. 2018

European Heart Journal

5,029

2,078

View full text Add to dashboard Cite

“…No or slow reflow after successful PCI is an often-unexpected complication in 0.5% to 1% of patients, 52,53 reflects an impairment of microcirculatory blood flow, and carries an adverse prognosis. 54,55 Often, coronary microembolization is simplistically assumed to be the cause of no/slow reflow.…”

Section: No-reflow Phenomenonmentioning

confidence: 99%

Coronary Microembolization

et al. 2009

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Abstract-Coronary microembolization from the erosion or rupture of a vulnerable atherosclerotic plaque occurs spontaneously in acute coronary syndromes and iatrogenically during percutaneous coronary interventions. Typical consequences of coronary microembolization are microinfarcts with an inflammatory response, contractile dysfunction, and reduced coronary reserve. Apart from transient elevations of creatine kinase and troponin, microemboli can be visualized by intracoronary Doppler and the resulting microinfarcts by late-enhancement nuclear magnetic resonance. Statins, antiplatelet agents, and coronary vasodilators protect against microembolization and microinfarction when started before percutaneous coronary interventions. Distal protection devices can retrieve atherothrombotic debris and prevent its embolization into the microcirculation, but their effect on clinical outcome has been disappointing so far, except for saphenous vein bypass grafts. Devices for aspiration of thrombi and thrombus-derived vasoconstrictor, thrombogenic, and inflammatory substances, however, reduce thrombus burden, improve perfusion, and provide protection in patients with acute myocardial infarction. Key Words:he rupture of an atherosclerotic plaque in an epicardial coronary artery does not always result in complete thrombotic coronary occlusion and impending myocardial infarction; milder forms of plaque rupture may leave some residual blood flow and result in the washout of atherothrombotic debris into the coronary microcirculation and its subsequent embolization. Coronary microembolization became a focus of attention about a decade ago with the awareness that coronary microembolization and its sequelae are a frequent iatrogenic complication of percutaneous coronary interventions (PCIs). 1,2 However, coronary microembolization was recognized much earlier as being the underlying pathophysiological event in sudden death of patients with unstable angina. [3][4][5][6] The present review summarizes and updates the pathophysiology of coronary microembolization and the clinical evidence for its diagnosis and its prevention.The incidence of coronary microembolization is difficult to judge. Spontaneous coronary microembolization occurs, but most likely, only the tip of the iceberg is recognized. Periprocedural coronary microembolization occurs on average in 25% of all PCIs, but its incidence ranges from 0% to 70%, in part depending on the method of its assessment. 7 The incidence of periprocedural coronary microembolization depends on factors related to the clinical condition of the patient, notably preexisting kidney disease or underlying unstable angina; factors related to the length 8 or complexity of the lesion; and finally, factors related to the procedure, notably the use of a stent rather than percutaneous transluminal coronary angioplasty, the number and duration of inflations, and particularly the use of atherectomy and rotablation. 7 In patients with an acute myocardial infarction, an angiographic distal filling defect occurred ...

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“…17 As we have previously reported, 18 the no-/ slow-flow phenomenon occurs more frequently in patients with ruptured plaque at the target lesion of PCI than in patients without it; and distal embolization of plaque debris is detected more frequently in those patients. Therefore, embolization of plaque debris may be an important cause of the no-/slow-flow phenomenon, which has been associated with deterioration of left ventricular function and worsening of clinical outcome.…”

Section: Factors Associated With Embolizationmentioning

confidence: 60%