Intravascular Platelet Aggregation in the Heart Induced by Norepinephrine

Haft, Jacob I.; Kranz, Paul; Albert, Frank; Fani, K

doi:10.1161/01.cir.46.4.698

Cited by 136 publications

(44 citation statements)

References 28 publications

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“…46 -48 Intracoronary ADP or intravenous norepinephrine can induce microembolization by platelet aggregates and subsequent microinfarcts in pigs and dogs, respectively. 49,50 Apparently, an ideal animal model of coronary microembolization that originates from spontaneous plaque rupture 51 and includes both the physical and bioactive properties of microemboli as seen in patients with coronary microembolization does not exist.…”

Section: Animal Models Of Coronary Microembolizationmentioning

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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Section: Animal Models Of Coronary Microembolizationmentioning

confidence: 99%

Coronary Microembolization

et al. 2009

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“…6 -11 Experimental models were also made by injecting adenosine-diphosphate or catecholamine to induce platelet aggregation in coronary microcirculation in pigs. [12][13] However, injecting microspheres with unique sizing would only occlude respective vessels with comparable sizes, while thrombotic debris in patients might vary greatly in sizing and affect vessels with different diameters. Models using adenosine diphosphate or catecholamine could mimic the platelet aggregation process during coronary microthrombosis but could not reflect the influences of various embolism components of atherosclerotic plaques.…”

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confidence: 99%

Establishment and Characterization of an Experimental Model of Coronary Thrombotic Microembolism in Rats

Bai

et al. 2010

The American Journal of Pathology

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To establish a model of coronary thrombotic microembolism in rats, either automicrothrombotic particulates (CM group) or saline control (SHAM group) was injected into temporarily clamped aortas of male Sprague-Dawley rats. After automicrothrombotic particulate injection, serum c-troponin I and von Willebrand factor levels, the no-flow area as evaluated by Thioflavin S, myocardial leukocyte infiltration levels, myocardial expressions of tumor necrosis factor ␣ and interleukin-6, the percentage of arterioles obstructed by thrombosis, and myocardial fibrosis were all significantly increased whereas cardiac function as evaluated by echocardiography and hemodynamic measurements were significantly reduced compared with the sham group. Thus, aortic automicrothrombotic particulate injection could induce coronary microembolism in rats, and this model could be of value in improving the understanding of pathophysiology of coronary microembolism. Atherosclerotic plaque rupture is a key event in the pathogenesis of acute coronary syndrome and during coronary interventions.1 It does not always result in complete thrombotic occlusion of the epicardial coronary artery with subsequent impending myocardial infarction, but may in milder forms result in the embolization of atherosclerotic and thrombotic debris into the coronary microcirculation, which has recently been identified as a potential cause of no-reflow phenomenon, myocardium ischemia, and myocardial infarctlet. Atherosclerotic embolization in the microvasculature is associated with adverse prognosis. [1][2][3][4] Research results derived from suitable experimental models of coronary microembolism would help clinicians to understand the underlying pathological mechanisms and to develop effective therapies of coronary microembolism induced by atherosclerotic embolization in the microvasculature.5 Until now, plastic microspheres ranging from 20 to 900 m in diameter were injected into the coronary microcirculation to establish the coronary microembolism models in dog, swine and sheep.6 -11 Experimental models were also made by injecting adenosine-diphosphate or catecholamine to induce platelet aggregation in coronary microcirculation in pigs.12-13 However, injecting microspheres with unique sizing would only occlude respective vessels with comparable sizes, while thrombotic debris in patients might vary greatly in sizing and affect vessels with different diameters. Models using adenosine diphosphate or catecholamine could mimic the platelet aggregation process during coronary microthrombosis but could not reflect the influences of various embolism components of atherosclerotic plaques. Therefore, established coronary microembolism models could only partly mimic the in vivo situation of coronary microthrombosis. In the present study, we showed that coronary microembolism could be induced by intraaortic injection of automicrothrombotic particulates varying in sizing in rats. Increased myocardial inflammatory cells infiltration and fibrosis as well as reduced cardiac function w...

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“…Also, amphetamine stimulates release of norepinephrine and blockade of reuptake at the sympathetic synaptic receptors, resulting acute ventricular dysfunction. Therefore, high catecholamine levels after exposure to amphetamine may trigger thrombosis by acute ventricular dysfunction and hypercoagulable status [9,14]. Echocardiography is useful in the diagnosis of LV thrombus, and it appears as an echo dense mass with definite margin during the whole course of systole and diastole.…”

Section: Discussionmentioning

confidence: 99%