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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).

Pathophysiology of ST-segment elevation myocardial infarction: novel mechanisms and treatments

Eur. Heart J. (2016) 37(16) doi: 10.1093/eurheartj/ehv592 - Click here to view the abstract

Critical determinants of myocardial infarction injury. The overlapping of vulnerable plaque and thrombogenic blood are critical determinants for myocardial infarction occurrence and extension. In addition, myocardium vulnerability, which is largely due to coronary microvascular dysfunction, contributes to extension and severity of ischaemic injury. In the most severe form (known as no-reflow), structural and functional impairment sustain vascular obstruction. Endothelial dysfunction triggers leukocyte and platelet activation/interaction, whereas thrombus debris may worsen the obstruction. Furthermore, cardiomyocyte swelling, interstitial oedema, and tissue inflammation promote extravascular compression.

Pathophysiology of ST-segment elevation myocardial infarction: novel mechanisms and treatments

Eur. Heart J. (2016) 37(16) doi: 10.1093/eurheartj/ehv592 - Click here to view the abstract

(A) Myocardial infarction and time course of oedema. Mean percentage of left ventricular volume positive for myocardial oedema at each time point. The volume of oedema remained stable in the first week after the event with a significant decrease at 15–17 days with near resolution by 6 months (with kind permission from reference Dall'Armellina et al.41). (B and C) Representative cardiac magnetic resonance images. In the column B, T2-weighted image (upward row) shows oedema in the anterior wall; the acute late gadolinium enhancement shows compact enhancement (middle row), which is reduced in size by 6 months (bottom row). In another example (column C), oedema imaging confirms acute injury (upward row). Late gadolinium enhancement present in the acute phase persists without significant alteration to the 6-month time point (middle and bottom row) (with kind permission from reference: Dall'Armellina et al.).

Histopathological thrombus analysis in patients with stent thrombosis: what are the missing pieces in the puzzle?

Eur. Heart J. (2016) 37(19) doi: 10.1093/eurheartj/ehw036 - Click here to view the abstract


Schematic figure summarizing the main findings of the PRESTIGE study: (i) no difference in thrombus composition depending on stent type and implant duration; (ii) predominance of leucocytes/neturophils in stent thrombosis compared with acute myocardial infarction aspirates and similar eosinophilic cell counts. Whether various well-characterized causes of stent thrombosis (i.e. neoatherosclerosis, hypersensitivity, malapposed and uncovered stent struts, and underexpansion) display similar thrombus composition remains unaddressed by this study. BMS, bare metal stent; DES, drug-eluting stent; NET, neutrophil extracellular trap.

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