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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.


More transparency for a therapeutic window in platelet P2Y12 inhibition?

Eur. Heart J. (2015), 36 (27), 1714-1717, Fig 1; 10.1093/eurheartj/ehv137 - click here to view abstract

Depiction of accumulation of activated platelets at a site of endothelial injury and the underlying platelet activation mechanisms and modes of actions of antiplatelet therapies.


Requiem for the ‘vulnerable plaque’

Eur. Heart J. (2015), 36 (43), 2984-2987, Fig 1; 10.1093/eurheartj/ehv349 - click here to view abstract

Contrasts between superficial erosion and fibrous cap rupture as causes of arterial thrombosis. LDL, low-density lipoprotein.


Genetic testing to guide therapy? Not for ticagrelor!

Eur. Heart J. (2015), Fig 1; 10.1093/eurheartj/ehv229 - click here to view abstract

Absorption and metabolism of P2Y12 receptor antagonists. Hatched symbols mean prodrugs, dashed line means a reversible inhibition.


Look beyond what seems obvious: thrombus burden after aspiration thrombectomy

Eur. Heart J. (2015), Fig 1; 10.1093/eurheartj/ehv231 - click here to view abstract

During balloon angioplasty, thrombus is mechanically mobilized, squeezed to the vessel wall, and may embolize downstream.


Risk stratification in acute myocardial infarction with multiparametric cardiac magnetic resonance imaging: getting to the core of the matter

Eur. Heart J. (2015),  Fig 1; 10.1093/eurheartj/ehv517 - click here to view abstract

Tissue subtypes in acute myocardial infarction as identified by cardiovascular magnetic resonance (CMR). The most common existing and novel CMR sequences are shown, with the corresponding tissue subtypes that each sequence has been shown to detect.


Morphine in myocardial infarction: balancing on the tight rope

Eur. Heart J. (),  (), -, Fig 1; 10.1093/eurheartj/ehv546 - click here to view abstract

(A) Tentative interactions between morphine and platelet inhibitors. (B) Tentative confounding factor between morphine and platelet inhibitors. BP, blood pressure; GI, gastrointestinal.


Ischaemic risk and bleeding risk in acute coronary syndrome: still inseparable

Eur. Heart J. (2015), Fig 1; 10.1093/eurheartj/ehv638 - click here to view abstract

Growth differentiation factor-15 (GDF-15) riskometer predicting recurrent ischaemic events and major bleeding in acute coronary syndrome (see text for details).


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