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Books on the topic 'Atherosclerotic plague'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

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1

George, Sarah J., and Johnson Jason. Atherosclerosis: Molecular and cellular mechanisms. Wiley-VCH, 2010.

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2

Virmani, Renu, Jagat Narula, Martin B. Leon, and James T. Willerson, eds. The Vulnerable Atherosclerotic Plaque. Blackwell Publishing, 2006. http://dx.doi.org/10.1002/9780470987575.

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3

Glagov, Seymour, William P. Newman, and Sheldon A. Schaffer, eds. Pathobiology of the Human Atherosclerotic Plaque. Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3326-8.

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4

NATO Advanced Research Workshop on Progress, Problems, and Promises for an Effective Quantitative Evaluation of Atherosclerosis in Living and Autopsied Experimental Animals and Man (1990 Siena, Italy). Atherosclerotic plaques: Advances in imaging for sequential quantitative evaluation. Edited by Wissler Robert W. 1917- and North Atlantic Treaty Organization. Scientific Affairs Division. Plenum Press, 1991.

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5

Sinatra, Stephen T. Reverse heart disease now: Stop deadly cardiovascular plaque before it's too late. John Wiley & Sons, 2007.

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6

C, Merrell Woodson, and Thornton James 1952-, eds. The arginine solution: The first guide to America's new cardio-enhancing supplement. Warner Books, 1999.

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7

(Editor), Ron Waksman, Patrick W. Serruys (Editor), and Johannes Schaar (Editor), eds. The Vulnerable Plaque, Second Edition. 2nd ed. Informa Healthcare, 2007.

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8

Ramrakha, Punit, and Jonathan Hill, eds. Coronary artery disease. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199643219.003.0005.

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Atherosclerosis: pathophysiology 212Development of atherosclerotic plaques 214Epidemiology 216Assessment of atherosclerotic risk 218Risk factors for coronary artery disease 220Hypertension 226Treatment of high blood pressure 228Combining antihypertensive drugs 230Lipid management in atherosclerosis 232Lipid-lowering therapy 236When to treat lipids ...

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9

Fuster, Valentin, and William Insull. Assessing and Modifying the Vulnerable Atherosclerotic Plaque. Wiley & Sons, Incorporated, John, 2008.

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10

Valentin, Fuster, and Insull William, eds. Assessing and modifying the vulnerable atherosclerotic plaque. Futura Pub. Co., 2002.

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11

Biomechanics of Coronary Atherosclerotic Plaque. Elsevier, 2021. http://dx.doi.org/10.1016/c2017-0-03308-6.

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12

(Contributor), Pierre Amarenco, Mark Brezinski (Contributor), Allen Burke (Contributor), and Valentin Fuster (Editor), eds. Assessing and Modifying the Vulnerable Atherosclerotic Plaque (American Heart Association Monograph Series). Blackwell Publishing Limited, 2002.

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13

Seymour, Glagov, Newman William P, and Schaffer Sheldon A, eds. Pathobiology of the human atherosclerotic plaque. Springer-Verlag, 1990.

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14

1955-, Brown David L., ed. Cardiovascular plaque rupture. Marcel Dekker, 2002.

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15

Monaco, Claudia, and Giuseppina Caligiuri. Molecular mechanisms. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0014.

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The development of the atherosclerotic plaque relies on specific cognate interactions between ligands and receptors with the ability to regulate cell recruitment, inflammatory signalling, and the production of powerful inflammatory and bioactive lipid mediators. This chapter describes how signalling is engaged by cell-cell surface interactions when the endothelium interacts with platelets and leukocytes enhancing leukocyte recruitment during atherogenesis. It also exemplifies intracellular signalling pathways induced by the activation of innate immune receptors, the most potent activators of inflammation in physiology and disease. Differences are highlighted in innate signalling pathways in metabolic diseases such as atherosclerosis compared to canonical immunological responses. Finally, the key lipid mediators whose production can affect endothelial function, inflammation, and atherosclerosis development are summarized. This Chapter will take you through these fundamental steps in the development of the atherosclerotic plaque by summarizing very recent knowledge in the field and highlighting recent or ongoing clinical trials that may enrich our ability to target cardiovascular disease in the future.

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16

Narula, Jagat, Martin B. Leon, Renu Virmani, and James T. Willerson. Vulnerable Atherosclerotic Plaque: Strategies for Diagnosis and Management. Wiley & Sons, Incorporated, John, 2008.

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17

Valentin, Fuster, ed. The vulnerable atherosclerotic plaque: Understanding, identification, and modification. Futura Pub. Co., 1999.

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18

Fotiadis, Dimitrios I., Lambros S. Athanasiou, and Lampros K. Michalis. Atherosclerotic Plaque Characterization Methods Based on Coronary Imaging. Elsevier Science & Technology Books, 2017.

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19

Narula, Jagat, Martin B. Leon, Renu Virmani, and James T. Willerson. Vulnerable Atherosclerotic Plaque: Strategies for Diagnosis and Management. Wiley & Sons, Incorporated, John, 2008.

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20

Landmesser, Ulf, and Wolfgang Koenig. From risk factors to plaque development and plaque destabilization. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656653.003.0003.

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This chapter begins with a discussion of recent vascular research that has unveiled the complex interaction between exposure to risk factors and pathological changes at the vessel wall. Risk factors such as smoking or hyperlipidaemia first cause a pre-morbid phenotype with reversible dysfunction of flow-mediated vasodilation, known as endothelial dysfunction (ED). If exposure to risk factor(s) does not cease, ED develops into the first morphological vascular changes that finally lead to atherosclerosis. Cholesterol crystals have been shown to lead to pro-inflammatory activation of macrophages. Progression from stable coronary plaques to the plaque rupture that underlies the acute coronary syndrome is discussed in detail. The chapter provides a basic up-to-date concept of the development and progression of atherosclerosis and highlights the stages where preventive measures may still be effective.

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21

Willerson, James T., Martin Leon, and Jagat Narula. The Vulnerable Atherosclerotic Plaque Strategies for Diagnosis and Management. Blackwell Publishing Limited, 2006.

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22

Ohayon, Jacques, Roderic Pettigrew, and Gerard Finet. Biomechanics of Coronary Atherosclerotic Plaque: From Model to Patient. Elsevier Science & Technology Books, 2020.

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23

Ohayon, Jacques, Roderic Pettigrew, and Gerard Finet. Biomechanics of Coronary Atherosclerotic Plaque: From Model to Patient. Elsevier Science & Technology Books, 2020.

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24

Renu, Virmani, ed. The vulnerable atherosclerotic plaque: Strategies for diagnosis and management. Blackwell Futura, 2007.

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25

Fuster, Valentin. The Vulnerable Atherosclerotic Plaque: Understanding, Identifi- cation and Modification. Blackwell Publishing Limited, 1999.

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26

Ohayon, Jacques, Roderic Pettigrew, and Gerard Finet. Biomechanics of Coronary Atherosclerotic Plaque: From Model to Patient. Elsevier Science & Technology, 2020.

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27

Born, Gustav V. R. Factors in Formation and Regression of the Atherosclerotic Plaque. Springer, 2012.

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28

S, Suri Jasjit, and Laxminarayan Swamy, eds. Angiography and plaque imaging: Advanced segmentation techniques. CRC Press, 2003.

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29

Brown, David. Cardiovascular Plaque Rupture (Fundamental and Clinical Cardiology, 45). Informa Healthcare, 2002.

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30

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0040.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated monocytes differentiate into macrophages which acquire a specialized phenotypic polarization (protective or harmful), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoprotein via low-density lipoprotein receptor-related protein-1 receptors. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Both lipid-laden vascular smooth muscle cells and macrophages release the procoagulant tissue factor, contributing to thrombus propagation. Platelets also participate in progenitor cell recruitment and drive the inflammatory response mediating the atherosclerosis progression. Recent data attribute to microparticles a potential modulatory effect in the overall atherothrombotic process. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be modulated.

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31

Lutgens, Esther, Marie-Luce Bochaton-Piallat, and Christian Weber. Atherosclerosis: cellular mechanisms. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0013.

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Atherosclerosis is a lipid-driven, chronic inflammatory disease of the large and middle-sized arteries that affects every human being and slowly progresses with age. The disease is characterized by the presence of atherosclerotic plaques consisting of lipids, (immune) cells, and debris that form in the arterial intima. Plaques develop at predisposed regions characterized by disturbed blood flow dynamics, such as curvatures and branch points. In the past decades, experimental and patient studies have revealed the role of the different cell-types of the innate and adaptive immune system, and of non-immune cells such as platelets, endothelial, and vascular smooth muscle cells, in its pathogenesis. This chapter highlights the roles of these individual cell types in atherogenesis and explains their modes of communication using chemokines, cytokines, and co-stimulatory molecules.

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32

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_001.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.

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33

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_002.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.

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34

Horst, Robenek, and Severs Nicholas J, eds. Cell interactions in atherosclerosis. CRC, 1992.

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35

Khachigian, Levon Michael. High-Risk Atherosclerotic Plaques: Mechanisms, Imaging, Models, and Therapy. CRC, 2004.

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36

(Editor), Robert W. Wissler, M. Gene Bond (Editor), Michele Mercuri (Editor), Piero Tanganelli (Editor), and Giorgio Weber (Editor), eds. Atherosclerotic Plaques: Advances in Imaging for Sequential Quantitative Evaluation (Nato Science Series: A:). Springer, 1992.

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37

Zucker, Martin, Sinatra, and C. M. D. Roberts James. Reverse Heart Disease Now: Stop Deadly Cardiovascular Plaque Before It's Too Late. Wiley, 2006.

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38

Selected risk factors and carotid artery plaque in men with heart disease. 1987.

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39

Selected risk factors and carotid artery plaque in men with heart disease. 1985.

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40

Faioni, Elena M., Maddalena Lettino, and Marco Cattaneo. The role of thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656653.003.0004.

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This chapter is concerned with the sequence of events leading to thrombosis and its consequences. Acute thrombotic occlusions of arterial vessels, which may precipitate myocardial infarction and/or stroke, are often due to fissure of an atherosclerotic plaque, with consequent activation of haemostasis and clot formation. Arterial thrombosis also plays a crucial role in accelerating progression of atherosclerotic lesions. Chronic activation of endothelium, platelets, and leucocytes leads to plaque formation, while acute events, related to a flare-up of inflammation, precipitate plaque fissure and thereby promote thrombus formation on the plaque, partial or total vessel occlusion, and flow disturbance. Thrombus-derived proteins stimulate plaque growth and progression, and the thrombus itself is incorporated into the plaque, further restricting the vessel lumen. Detailed understanding of these various events is required if the success of primary and secondary prevention is to be improved.

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41

Michael, Khachigian Levon, ed. High-risk atherosclerotic plaques: Mechanisms, imaging, models, and therapy. CRC Press, 2005.

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42

Chong, Ji Y., and Michael P. Lerario. Arch Disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190495541.003.0014.

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Atherosclerosis of the ascending aorta and arch can potentially lead to high rates of embolic stroke. Evaluating plaque elements for complexity on transesophageal echocardiogram can help stratify this risk of stroke. Either antiplatelets or anticoagulants can be used for stroke prevention.

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43

Badimon, Lina, Felix C. Tanner, Giovanni G. Camici, and Gemma Vilahur. Pathophysiology of thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0018.

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Ischaemic heart disease and stroke are major causes of death and morbidity worldwide. Coronary and cerebrovascular events are mainly a consequence of a sudden thrombotic occlusion of the vessel lumen. Arterial thrombosis usually develops on top of a disrupted atherosclerotic plaque because of the exposure of thrombogenic material, such as collagen fibrils and tissue factor (TF), to the flowing blood. TF, either expressed by subendothelial cells, macrophage- and/or vascular smooth muscle-derived foam-cells in atherosclerotic plaques, is a key element in the initiation of thrombosis due to its ability to induce thrombin formation (a potent platelet agonist) and subsequent fibrin deposition at sites of vascular injury. Adhered platelets at the site of injury also play a crucial role in the pathophysiology of atherothrombosis. Platelet surface receptors (mainly glycoproteins) interact with vascular structures and/or Von Willebrand factor triggering platelet activation signalling events, including an increase in intracellular free Ca2+, exposure of a pro-coagulant surface, and secretion of platelet granule content. On top of this, interaction between soluble agonists and platelet G-coupled protein receptors further amplifies the platelet activation response favouring integrin alpha(IIb)beta(3) activation, an essential step for platelet aggregation. Blood-borne TF and microparticles have also been shown to contribute to thrombus formation and propagation. As thrombus evolves different circulating cells (red-blood cells and leukocytes, along with occasional undifferentiated cells) get recruited in a timely dependent manner to the growing thrombus and further entrapped by the formation of a fibrin mesh.

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44

Carton, James. Vascular pathology. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199591633.003.0003.

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Atherosclerosis 28Shock 30Hypertension 31Chronic lower limb ischaemia 32Acute lower limb ischaemia 33Aortic dissection 34Abdominal aortic aneurysm 35Varicose veins 36Deep vein thrombosis 37• An inflammatory disease of large- and medium-sized systemic arteries characterized by the formation of lipid-rich plaques in the vessel wall....

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45

Kisiel, Maria, and Alison Smith. Cardiac surgery. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642663.003.0026.

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Coronary heart disease is caused by the build-up of atherosclerotic plaques which, over time, narrow the lumen of the coronary arteries. Acute coronary syndrome describes a spectrum of conditions caused by coronary artery disease; these are unstable angina, ST-elevation myocardial infarction (STEMI), and non-ST-elevation myocardial infarction (NSTEMI). Coronary artery disease is the leading cause for cardiac surgical interventions, but other causes are hypertension, valve disease, arrhythmias, cardiomyopathies, infections, and congenital abnormalities. This chapter provides an overview of the signs and symptoms of these conditions, as well as the diagnosis and treatment options available.

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46

Reed, Ashley, and Tariq M. Malik. Chronic Abdominal Pain in the Elderly: Ischemic Pain. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190271787.003.0018.

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Elderly patients with chronic abdominal pain are commonly misdiagnosed, most likely due to atypical symptom presentations. Chronic mesenteric ischemia is a rare cause of chronic abdominal pain in the elderly. Symptoms are postprandial abdominal pain, weight loss, and an abdominal bruit. The disease results from atherosclerotic plaques that reduce the bowel’s ability to increase blood flow after meals. Patients often are malnourished. Diagnosis can be made with various imaging modalities, although a computed tomography angiogram is likely needed when the syndrome is suspected. The mainstay of therapy for chronic mesenteric ischemia is surgical intervention. Interventional pain techniques, such as celiac plexus neurolysis or spinal cord stimulation, are promising adjunct treatment options.

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47

The 30Day Heart TuneUp. Little, Brown & Company, 2014.

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48

Cheong, Adrian, Gabriel Steg, and Stefan K. James. ST-segment elevation myocardial infarction. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0043.

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Acute myocardial infarction with ST-segment elevation is a common and dramatic manifestation of coronary artery disease. It is caused by the rupture of an atherosclerotic plaque in a coronary artery, leading to its total thrombotic occlusion and resultant ischaemia and necrosis of downstream myocardium. The diagnosis of ST-segment elevation myocardial infarction is based on a syndrome of ischaemic chest pain symptoms, associated with typical ST-segment elevation on the electrocardiogram and an eventual rise in biomarkers of myocardial necrosis. The treatment of ST-segment elevation myocardial infarction is focused on re-establishing blood flow in the coronary artery involved, preferably by percutaneous coronary intervention, or by pharmacological thrombolysis in the case of expected lengthy time delays or lack of availability of facilities. Early mortality from ST-segment elevation myocardial infarction can be attributed to the sequelae or complications of myocardial ischaemia, or complications related to therapy. The former include arrhythmias (such as ventricular tachycardia or fibrillation), mechanical complications (such as ventricular free wall, septal, and mitral chordal rupture), and pump failure leading to cardiogenic shock. The latter includes haemorrhagic complications and coronary stent thrombosis. Given that myocardial necrosis is a critically time-dependent process, the organization of an ST-segment elevation myocardial infarction care system and adherence to the latest clinical trial evidence and guidelines are crucial to ensure that patients are treated in an optimal manner.

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49

Cheong, Adrian P., Gabriel Steg, and Stefan K. James. ST-segment elevation MI. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0043_update_001.

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Acute myocardial infarction with ST-segment elevation is a common and dramatic manifestation of coronary artery disease. It is caused by the rupture of an atherosclerotic plaque in a coronary artery, leading to its total thrombotic occlusion and resultant ischaemia and necrosis of downstream myocardium. The diagnosis of ST-segment elevation myocardial infarction is based on a syndrome of ischaemic chest pain symptoms, associated with typical ST-segment elevation on the electrocardiogram and an eventual rise in biomarkers of myocardial necrosis. The treatment of ST-segment elevation myocardial infarction is focused on re-establishing blood flow in the coronary artery involved, preferably by percutaneous coronary intervention, or by pharmacological thrombolysis in the case of expected lengthy time delays or lack of availability of facilities. Early mortality from ST-segment elevation myocardial infarction can be attributed to the sequelae or complications of myocardial ischaemia, or complications related to therapy. The former include arrhythmias (such as ventricular tachycardia or fibrillation), mechanical complications (such as ventricular free wall, septal, and mitral chordal rupture), and pump failure leading to cardiogenic shock. The latter includes haemorrhagic complications and coronary stent thrombosis. Given that myocardial necrosis is a critically time-dependent process, the organization of an ST-segment elevation myocardial infarction care system and adherence to the latest clinical trial evidence and guidelines are crucial to ensure that patients are treated in an optimal manner.

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50

Buechel, Ronny R., and Aju P. Pazhenkottil. Basic principles and technological state of the art: hybrid imaging. Edited by Philipp Kaufmann. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0121.

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The core principle of hybrid imaging is based on the fact that it provides information beyond that achievable with either data set alone. This is attained through the combination and fusion of two datasets by which both modalities synergistically contribute to image information. Hybrid imaging is, thus, more powerful than the sum of its parts, yielding improved sensitivity and specificity. While datasets for integration may be obtained by a variety of imaging modalities, its merits are intuitively best exploited when combining anatomical and functional imaging, particularly in the setting of evaluation of coronary artery disease (CAD) as this combination allows a comprehensive assessment with regard to presence or absence of coronary atherosclerosis, the extent and severity of coronary plaques, and the haemodynamic relevance of stenosis. In clinical practice, the combination of CT coronary angiography (CCTA) with myocardial perfusion studies obtained by single-photon emission computed tomography (SPECT) and by positron emission tomography (PET) has been well established. Recent literature also reports on the feasibility of combining CCTA with cardiac magnetic resonance imaging. Finally, recent advances in CCTA and SPECT imaging have led to a substantial reduction of radiation exposure, now allowing for comprehensive morphological and functional diagnostic work-up by cardiac hybrid SPECT/CCTA imaging at low radiation dose exposures ranging below 5 mSv.

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