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Acute Coronary Syndrome

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Hybrid CCTA/IVUS: breaking the traditional boundaries of coronary imaging - Figure 1

Eur. Heart J. (2012) 33 (8), 941; 10.1093/eurheartj/ehs006

Conceptual graphics illustrating how invasive and non-invasive imaging modalities could combine to provide an integrated assessment of microanatomical and biological features of an unstable coronary plaque. CCTA, CT coronary angiography; IVMR, intravascular magnetic resonance; IVUS, intravascular ultrasound; NIRF, near-infrared fluoroscopy; NIRS, near-infrared spectroscopy; OCT, optical coherence tomography.


Mechanical circulatory support in cardiogenic shock

Eur Heart J (2014) 35 (3): 156-167; 10.1093/eurheartj/eht248

Percutaneous assist devices in cardiogenic shock. (A) Intra-aortic balloon counterpulsation; (B) Impella® pump; (C) TandemHeartT™; (D) extracorporeal membrane oxygenation (ECMO). Modified from Thiele et al.


Contrast-induced nephropathy: the sin of primary percutaneous coronary intervention? - Figure 1

Eur Heart J (2014) 35 (23): 1504-1506; 10.1093/eurheartj/ehu126

Physiopathology of contrast-induced nephropathy in acute myocardial infarction.


Anti-inflammatory therapies in acute coronary syndromes: is IL-1 blockade a solution?

Eur Heart J (2014) 36 (6): 337-339 - 10.1093/eurheartj/ehu369

Schematic representation of acute and chronic inflammation in heart disease


Neutrophil extracellular traps: a new source of tissue factor in atherothrombosis

Eur Heart J (2014) - 10.1093/eurheartj/ehv105 [In Press]

Neutrophils contribution to thrombosis via tissue factor-bearing neutrophil extracellular traps release. Neutrophil activation in response to an inflammatory stimuli (infectious or not) induces tissue factor formation and neutrophil extracellular traps extrusion. Neutrophil extracellular traps are composed of chromatin decorated with granular proteins and functional tissue factor capable of promoting thrombin generation (favoring systemic vein thrombosis) and platelet activation. At the culprit coronary site, generated thrombin boosts platelet activation which, in turn, enhances neutrophil extracellular trap-bound tissue factor release favoring thrombus growth on the ruptured atherosclerotic plaque.


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