This review summarizes the most recent developments in providing advanced supportive measures for cardiopulmonary resuscitation, and the results obtained using these new therapies in patients with cardiac arrest caused by acute myocardial infarction (AMI). Also detailed are new approaches such as extracorporeal cardiopulmonary resuscitation (ECPR), intra-arrest percutaneous coronary intervention, or the regional models for systems of care aiming to reduce the critical times from cardiac arrest to initiation of ECPR and coronary revascularization.

show that in 2012, 31% of all deaths were caused by cardiovascular disease, from which 7.4 million were due to coronary heart disease. 2 Acute coronary syndromes (ACS)are among the most severe complications of atherosclerosis, and the majority, although not all, take place due to atheromatous plaque rupture and subsequent thrombosis.3 Vulnerable atheromatous plaquesThe genesis of the atheroma is triggered by the appearance of a discontinuity in the endothelial layer, followed by an array of complex mechanical, biochemical, and biological mechanisms that will eventually lead to plaque formation. [4][5][6] The formed atherosclerotic plaque will undergo several pathophysiological changes, including the excessive accumulation of oxidized LDL-cholesterol, enhanced local inflammation, smooth muscle cell proliferation, and extracellular matrix degradation, which will eventually lead to its progression and destabilization. This paper presents the main characteristics of plaque vulnerability, the role of CCTA in the assessment of vulnerable plaques, and automatic segmentation techniques of the coronary artery tree based on CT angiography images. A detailed inventory of existing methods is given, representing the state-of-the-art of computational methods applied in vascular system segmentation, focusing on the current applications in acute coronary syndromes.

Ca ++ mPT pore damage leads to ↑ Ca ++ in the mitochondria (M), where Ca ++ pumps ↓H + and ↑pH, through the disordered depolarization ↓electric potential of the internal M membrane, ATP synthesis is also afect, which is manifested by a mitochondrial energy deficit (MED). MED provoke→ cell hypo -anergy→oxidative stress, OS→ collapse M→M swells → osmotic demyelination→membrane rupture M→detritus mass output with large molecule in intermembrane space M→in cell cytosol→apoptosis-inducing factor→cytochrome C→which are the predictors of programmed cell death. Contributing to the increase in blood pressure to OS not only hyperadrenalinemia, but also the reduction of the effect of vasorelaxation by NO, which ↓ as it becomes becomes a trap for the excess oxygen free radicals, especially for oxygen superoxide. Triphosphoric acid (ATP), donated, as an energetic carrier, mitochondrial permeability transition pore-dependent Ca++uniporter, mPT pore, restores the disorder of electrical cardiac potentials: ↓Conductivity, ↑refractoriness of the atrioventricular node, ↓sinus nodule automatism, and primary hypertension, caused by MED and, further, manifested by the microcirculatory and mitochondrial distress syndrome. Simultaneously, ATP influences: Mitochondrial ATP-dependent potassium channel, mitoKATP; acetylcholinedependent potassium channel, KACh cholinergic-M receptor; receptors: Adenosine A1; and purine P2. M myocardial cells create mesh nets that limit the disordered energy flow in the reduced M space, avoiding damage to the entire heart muscle. As a result, M also plays the role of the electroconductivity switch, which protects the heart from the extent of the damage of a "short circuit" in area necrotizing myocardiocytes and M hypoanergic. Hence, the anti-arrhythmogenic effect of ATP-energetic

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