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[[File:Atheroma.jpg|thumb|263x263px|Blood flow through an artery is partially occluded by the deposition of an [[atherosclerotic plaque]]. ]]'''Arterial occlusion''' is a condition involving partial or complete blockage of blood flow through an [[artery]]. Arteries are [[Blood vessel|blood vessels]] that carry oxygenated blood to body tissues<ref name=":1" /><ref>{{Cite book |last=Saladin |first=Kenneth S. |url=https://www.worldcat.org/oclc/927438903 |title=Human anatomy |date=2017 |others=Stephen J. Sullivan, Christina A. Gan |isbn=978-0-07-340370-0 |edition=Fifth |location=New York, NY |oclc=927438903}}</ref>. An occlusion of arteries disrupts oxygen and blood supply to tissues, leading to [[ischemia]].<ref name=":1" /> Depending on the extent of ischemia, symptoms of arterial occlusion range from simple soreness and pain that can be relieved with rest,<ref name=":10" /> to a lack of sensation or [[paralysis]] that could require [[amputation]].<ref name=":10" />
[[File:Atheroma.jpg|thumb|263x263px|Blood flow through an artery is partially occluded by the deposition of an [[atherosclerotic plaque]]. ]]'''Arterial occlusion''' is a condition involving partial or complete blockage of blood flow through an [[artery]]. Arteries are [[Blood vessel|blood vessels]] that carry oxygenated blood to body tissues<ref name=":1" /><ref>{{Cite book | vauthors = Saladin KS, Sullivan SJ, Gan CA |url=https://www.worldcat.org/oclc/927438903 |title=Human anatomy |date=2017 |isbn=978-0-07-340370-0 |edition=Fifth |location=New York, NY |oclc=927438903}}</ref>. An occlusion of arteries disrupts oxygen and blood supply to tissues, leading to [[ischemia]].<ref name=":1" /> Depending on the extent of ischemia, symptoms of arterial occlusion range from simple soreness and pain that can be relieved with rest,<ref name=":10" /> to a lack of sensation or [[paralysis]] that could require [[amputation]].<ref name=":10" />


Arterial occlusion can be classified into three types based on etiology: [[embolism]], [[thrombosis]], and [[atherosclerosis]]. These three types of occlusion underlie various common conditions, including [[coronary artery disease]],<ref name=":13">{{Cite web |date=2018-10-03 |title=Coronary heart disease |url=https://www.nhs.uk/conditions/coronary-heart-disease/ |access-date=2022-03-20 |website=nhs.uk |language=en}}</ref> [[peripheral artery disease]],<ref name=":8">{{Citation |last=Zemaitis |first=Michael R. |title=Peripheral Arterial Disease |date=2022 |url=http://www.ncbi.nlm.nih.gov/books/NBK430745/ |work=StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=28613496 |access-date=2022-03-29 |last2=Boll |first2=Julia M. |last3=Dreyer |first3=Mark A.}}</ref> and [[pulmonary embolism]],<ref name=":9" /> which may be prevented by lowering risk factors. With improper prevention or management, these diseases can progress into life-threatening complications of [[myocardial infarction]],<ref name=":14" /> [[gangrene]],<ref name=":5" /> [[Stroke|ischemic stroke]],<ref name=":2" /> and in severe cases, terminate in brain death or cardiac arrest.<ref name=":20">{{Citation |last=DeSai |first=Charisma |title=Cerebral Ischemia |date=2022 |url=http://www.ncbi.nlm.nih.gov/books/NBK560510/ |work=StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=32809345 |access-date=2022-04-14 |last2=Hays Shapshak |first2=Angela}}</ref><ref name=":0" />
Arterial occlusion can be classified into three types based on etiology: [[embolism]], [[thrombosis]], and [[atherosclerosis]]. These three types of occlusion underlie various common conditions, including [[coronary artery disease]],<ref name=":13">{{Cite web |date=2018-10-03 |title=Coronary heart disease |url=https://www.nhs.uk/conditions/coronary-heart-disease/ |access-date=2022-03-20 |website=nhs.uk |language=en}}</ref> [[peripheral artery disease]],<ref name=":8">{{cite book | vauthors = Zemaitis MR, Boll JM, Dreyer MA |chapter = Peripheral Arterial Disease |date=2022 | chapter-url=http://www.ncbi.nlm.nih.gov/books/NBK430745/ |title = StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=28613496 |access-date=2022-03-29 }}</ref> and [[pulmonary embolism]],<ref name=":9" /> which may be prevented by lowering risk factors. With improper prevention or management, these diseases can progress into life-threatening complications of [[myocardial infarction]],<ref name=":14" /> [[gangrene]],<ref name=":5" /> [[Stroke|ischemic stroke]],<ref name=":2" /> and in severe cases, terminate in brain death or cardiac arrest.<ref name=":20">{{cite book | vauthors = DeSai C, Shapshak HA | chapter = Cerebral Ischemia |date=2022 | chapter-url=http://www.ncbi.nlm.nih.gov/books/NBK560510/ | title = StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=32809345 |access-date=2022-04-14 }}</ref><ref name=":0" />


Arterial occlusion is diagnosed by exercise testing,<ref name=":10" /> [[Doppler ultrasonography|ultrasonic duplex testing]],<ref name=":10" /> and multi-detector coronary tomography [[angiography]].<ref name=":12" /> Meanwhile, treatment can vary from surgical interventions such as [[Bypass surgery|bypass]],<ref name=":16" /> [[endarterectomy]],<ref name=":17" /> and [[embolectomy]]<u>,</u><ref name=":18" /> to [[Anticoagulant|blood-thinning medication]]. <ref name=":15" />
Arterial occlusion is diagnosed by exercise testing,<ref name=":10" /> [[Doppler ultrasonography|ultrasonic duplex testing]],<ref name=":10" /> and multi-detector coronary tomography [[angiography]].<ref name=":12" /> Meanwhile, treatment can vary from surgical interventions such as [[Bypass surgery|bypass]],<ref name=":16" /> [[endarterectomy]],<ref name=":17" /> and [[embolectomy]]<u>,</u><ref name=":18" /> to [[Anticoagulant|blood-thinning medication]]. <ref name=":15" />
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Commonly observed types of arterial occlusion include thrombosis, atherosclerosis, and embolism.
Commonly observed types of arterial occlusion include thrombosis, atherosclerosis, and embolism.
=== Embolism ===
=== Embolism ===
An [[embolism]] involves the occlusion of blood vessels by an [[embolus]].<ref name=":1" /> Arterial occlusion by an embolus is termed ‘[[arterial embolism]]’. An embolus is an agent that blocks blood flow by physically obstructing blood vessels.<ref name=":1" /> This includes [[Air embolism|gas bubbles]],<ref>{{Cite journal |last=McCarthy |first=Colin |last2=Behravesh |first2=Sasan |last3=Naidu |first3=Sailendra |last4=Oklu |first4=Rahmi |date=2016-10-31 |title=Air Embolism: Practical Tips for Prevention and Treatment |url=http://www.mdpi.com/2077-0383/5/11/93 |journal=Journal of Clinical Medicine |language=en |volume=5 |issue=11 |pages=93 |doi=10.3390/jcm5110093 |issn=2077-0383 |pmc=PMC5126790 |pmid=27809224}}</ref> fatty deposits, [[Amniotic fluid embolism|amniotic fluid]],<ref>{{Cite journal |last=Metodiev |first=Y. |last2=Ramasamy |first2=P. |last3=Tuffnell |first3=D. |date=August 2018 |title=Amniotic fluid embolism |url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7808088/ |journal=BJA Education |volume=18 |issue=8 |pages=234–238 |doi=10.1016/j.bjae.2018.05.002 |issn=2058-5349 |pmc=7808088 |pmid=33456838}}</ref> blood clots, and foreign material. Arterial emboli occasionally detach from primary sites and travel via circulation to occlude secondary arteries, causing multiple ischemic sites.
An [[embolism]] involves the occlusion of blood vessels by an [[embolus]].<ref name=":1" /> Arterial occlusion by an embolus is termed ‘[[arterial embolism]]’. An embolus is an agent that blocks blood flow by physically obstructing blood vessels.<ref name=":1" /> This includes [[Air embolism|gas bubbles]],<ref>{{cite journal | vauthors = McCarthy CJ, Behravesh S, Naidu SG, Oklu R | title = Air Embolism: Practical Tips for Prevention and Treatment | journal = Journal of Clinical Medicine | volume = 5 | issue = 11 | pages = 93 | date = October 2016 | pmid = 27809224 | pmc = 5126790 | doi = 10.3390/jcm5110093 }}</ref> fatty deposits, [[Amniotic fluid embolism|amniotic fluid]],<ref>{{cite journal | vauthors = Metodiev Y, Ramasamy P, Tuffnell D | title = Amniotic fluid embolism | journal = BJA Education | volume = 18 | issue = 8 | pages = 234–238 | date = August 2018 | pmid = 33456838 | pmc = 7808088 | doi = 10.1016/j.bjae.2018.05.002 }}</ref> blood clots, and foreign material. Arterial emboli occasionally detach from primary sites and travel via circulation to occlude secondary arteries, causing multiple ischemic sites.


=== Thrombosis ===
=== Thrombosis ===
[[Thrombosis]] occurs when thrombi occlude vessels in the body.<ref name=":7" /> A [[thrombus]], or a blood clot, is a mobilized mass of blood cells that circulates within the body.<ref name=":19">{{Cite book |last=Hoffbrand |first=A. V. |url=https://www.worldcat.org/oclc/642278764 |title=Essential haematology |date=2011 |publisher=Wiley-Blackwell |others=P. A. H. Moss, J. E. Pettit |isbn=978-1-4051-9890-5 |edition=6th |location=Malden, Mass. |oclc=642278764}}</ref><ref>{{Cite journal |last=Oklu |first=Rahmi |date=December 2017 |title=Thrombosis |url=https://cdt.amegroups.com/article/view/17550 |journal=Cardiovascular Diagnosis and Therapy |language=en |volume=7 |issue=3 |pages=S131–S13S133 |issn=2223-3660}}</ref> Thrombi can occlude veins ([[venous thrombosis]]) or arteries (arterial thrombosis). The etiology of thrombosis is described by [[Virchow's triad|Virchow’s Triad]], which includes hemostasis, vascular wall damage, and [[hypercoagulability]].<ref name=":19" /> Arterial thromboses significantly narrow or completely block arterial blood flow and oxygen delivery to tissues.
[[Thrombosis]] occurs when thrombi occlude vessels in the body.<ref name=":7" /> A [[thrombus]], or a blood clot, is a mobilized mass of blood cells that circulates within the body.<ref name=":19">{{Cite book | vauthors = Hoffbrand AV, Moss PA, Pettit JE |url= https://www.worldcat.org/oclc/642278764 |title=Essential haematology |date=2011 |publisher=Wiley-Blackwell |isbn=978-1-4051-9890-5 |edition=6th |location=Malden, Mass. |oclc=642278764}}</ref><ref>{{Cite journal | vauthors = Oklu R |date=December 2017 |title=Thrombosis |url=https://cdt.amegroups.com/article/view/17550 |journal=Cardiovascular Diagnosis and Therapy |language=en |volume=7 |issue=3 |pages=S131–S13S133 |issn=2223-3660}}</ref> Thrombi can occlude veins ([[venous thrombosis]]) or arteries (arterial thrombosis). The etiology of thrombosis is described by [[Virchow's triad|Virchow’s Triad]], which includes hemostasis, vascular wall damage, and [[hypercoagulability]].<ref name=":19" /> Arterial thromboses significantly narrow or completely block arterial blood flow and oxygen delivery to tissues.


=== Atherosclerosis ===
=== Atherosclerosis ===
In [[atherosclerosis]], the inner [[Endothelium|endothelial]] layer of arteries<ref name=":21">{{Cite journal |last=Fan |first=Jianglin |last2=Watanabe |first2=Teruo |date=March 2022 |title=Atherosclerosis: Known and unknown |url=https://onlinelibrary.wiley.com/doi/10.1111/pin.13202 |journal=Pathology International |language=en |volume=72 |issue=3 |pages=151–160 |doi=10.1111/pin.13202 |issn=1320-5463}}</ref> is stiffened by the deposition of an [[Atheroma|atheromatous plaque]].<ref name=":1">{{Cite book |last=Widmaier |first=Eric P. |url=https://www.worldcat.org/oclc/820450614 |title=Vander's human physiology : the mechanisms of body function. |date=2014 |others=Hershel Raff, Kevin T. Strang, Arthur J. Vander |isbn=978-0-07-337830-5 |edition=13th |location=New York |oclc=820450614}}</ref><ref name=":0">{{Cite book |last=Waller |first=Derek |url=https://www.worldcat.org/oclc/1003529751 |title=Medical pharmacology & therapeutics |date=2018 |others=Anthony P. Sampson |isbn=978-0-7020-7193-5 |edition=5th |location=Edinburgh |oclc=1003529751}}</ref><ref>{{Cite web |title=Atherosclerosis |url=https://www.hopkinsmedicine.org/health/conditions-and-diseases/atherosclerosis |access-date=2022-03-29 |website=www.hopkinsmedicine.org |language=en}}</ref> Atheromatous plaques, also called atherosclerotic plaques, are made of fats and [[Foam cell|lipid-laden macrophages]].<ref name=":7">{{Cite journal |last=Mackman |first=Nigel |date=February 2008 |title=Triggers, targets and treatments for thrombosis |url=http://www.nature.com/articles/nature06797 |journal=Nature |language=en |volume=451 |issue=7181 |pages=914–918 |doi=10.1038/nature06797 |issn=0028-0836 |pmc=PMC2848509 |pmid=18288180}}</ref> Plaque deposition both physically narrows an artery and impairs the function of endothelial cells, potentiating their production of [[Vasoconstriction|vasoconstrictive]] chemicals to constrict the arterial lumen.<ref name=":0" /> This leads to turbulent blood flow in the arteries, affecting oxygen supply to tissues downstream.
In [[atherosclerosis]], the inner [[Endothelium|endothelial]] layer of arteries<ref name=":21">{{cite journal | vauthors = Fan J, Watanabe T | title = Atherosclerosis: Known and unknown | journal = Pathology International | volume = 72 | issue = 3 | pages = 151–160 | date = March 2022 | pmid = 35076127 | doi = 10.1111/pin.13202 }}</ref> is stiffened by the deposition of an [[Atheroma|atheromatous plaque]].<ref name=":1">{{Cite book | vauthors = Widmaier EP, Raff H, Strang KT, Vander AJ |url=https://www.worldcat.org/oclc/820450614 |title=Vander's human physiology : the mechanisms of body function. |date=2014 |isbn=978-0-07-337830-5 |edition=13th |location=New York |oclc=820450614}}</ref><ref name=":0">{{Cite book | vauthors = Waller D, Sampson AP |url=https://www.worldcat.org/oclc/1003529751 |title=Medical pharmacology & therapeutics |date=2018 |isbn=978-0-7020-7193-5 |edition=5th |location=Edinburgh |oclc=1003529751}}</ref><ref>{{Cite web |title=Atherosclerosis |url=https://www.hopkinsmedicine.org/health/conditions-and-diseases/atherosclerosis |access-date=2022-03-29 |website=www.hopkinsmedicine.org |language=en}}</ref> Atheromatous plaques, also called atherosclerotic plaques, are made of fats and [[Foam cell|lipid-laden macrophages]].<ref name=":7">{{cite journal | vauthors = Mackman N | title = Triggers, targets and treatments for thrombosis | journal = Nature | volume = 451 | issue = 7181 | pages = 914–918 | date = February 2008 | pmid = 18288180 | pmc = 2848509 | doi = 10.1038/nature06797 }}</ref> Plaque deposition both physically narrows an artery and impairs the function of endothelial cells, potentiating their production of [[Vasoconstriction|vasoconstrictive]] chemicals to constrict the arterial lumen.<ref name=":0" /> This leads to turbulent blood flow in the arteries, affecting oxygen supply to tissues downstream.


== Diseases of arterial occlusion ==
== Diseases of arterial occlusion ==
The pathophysiology of diseases of arterial occlusion depends on the type of occlusion, the severity of blockage, and the location of the occluded artery. Common diseases of arterial occlusion include Coronary Artery Disease, Peripheral Artery Disease, and Pulmonary Embolism.
The pathophysiology of diseases of arterial occlusion depends on the type of occlusion, the severity of blockage, and the location of the occluded artery. Common diseases of arterial occlusion include Coronary Artery Disease, Peripheral Artery Disease, and Pulmonary Embolism.
=== Coronary Artery Disease ===
=== Coronary Artery Disease ===
[[Coronary artery disease|Coronary Artery Disease]] (CAD) results from the [[stenosis]] of [[coronary arteries]] by an atherosclerotic plaque.<ref name=":13" /><ref name=":21" /> The coronary arteries perfuse the [[cardiomyocytes]] located within the myocardium. Cardiomyocytes require constant perfusion to aid the pumping of the heart.<ref>{{Cite journal |last=Woodcock |first=Elizabeth A. |last2=Matkovich |first2=Scot J. |date=September 2005 |title=Cardiomyocytes structure, function and associated pathologies |url=https://linkinghub.elsevier.com/retrieve/pii/S1357272505001342 |journal=The International Journal of Biochemistry & Cell Biology |language=en |volume=37 |issue=9 |pages=1746–1751 |doi=10.1016/j.biocel.2005.04.011}}</ref> In CAD, atheromatous plaque formation in a coronary artery limits oxygen supply to cardiomyocytes, impairing heart contractility.
[[Coronary artery disease|Coronary Artery Disease]] (CAD) results from the [[stenosis]] of [[coronary arteries]] by an atherosclerotic plaque.<ref name=":13" /><ref name=":21" /> The coronary arteries perfuse the [[cardiomyocytes]] located within the myocardium. Cardiomyocytes require constant perfusion to aid the pumping of the heart.<ref>{{cite journal | vauthors = Woodcock EA, Matkovich SJ | title = Cardiomyocytes structure, function and associated pathologies | journal = The International Journal of Biochemistry & Cell Biology | volume = 37 | issue = 9 | pages = 1746–1751 | date = September 2005 | pmid = 15950518 | doi = 10.1016/j.biocel.2005.04.011 }}</ref> In CAD, atheromatous plaque formation in a coronary artery limits oxygen supply to cardiomyocytes, impairing heart contractility.


CAD severity varies based on the extent of coronary artery occlusion. At 75% luminal narrowing, patients experience symptoms associated with limited perfusion of cardiomyocytes,<ref name=":0" /> especially under strenuous conditions.<ref name=":1" /> Under physical exertion, CAD induces chest pain, termed ‘[[Angina|stable angina]]’. Stable angina may deteriorate into [[unstable angina]], marking the initiation of [[Acute coronary syndrome|Acute Coronary Syndrome]], which may further deteriorate into a myocardial infarction.  
CAD severity varies based on the extent of coronary artery occlusion. At 75% luminal narrowing, patients experience symptoms associated with limited perfusion of cardiomyocytes,<ref name=":0" /> especially under strenuous conditions.<ref name=":1" /> Under physical exertion, CAD induces chest pain, termed ‘[[Angina|stable angina]]’. Stable angina may deteriorate into [[unstable angina]], marking the initiation of [[Acute coronary syndrome|Acute Coronary Syndrome]], which may further deteriorate into a myocardial infarction.  


Risk factors for CAD include smoking,<ref>{{Cite journal |last=Salehi |first=Nahid |last2=Janjani |first2=Parisa |last3=Tadbiri |first3=Hooman |last4=Rozbahani |first4=Mohammad |last5=Jalilian |first5=Milad |date=December 2021 |title=Effect of cigarette smoking on coronary arteries and pattern and severity of coronary artery disease: a review |url=http://journals.sagepub.com/doi/10.1177/03000605211059893 |journal=Journal of International Medical Research |language=en |volume=49 |issue=12 |pages=030006052110598 |doi=10.1177/03000605211059893 |issn=0300-0605 |pmc=PMC8647272 |pmid=34855538}}</ref> high cholesterol, obesity, and family history of CAD. Primarily, the accumulation of cholesterol in the bloodstream from high-fat diets lead to atherosclerotic occlusion and its clinical consequences. Therefore, preventative measures for CAD mainly involve diet changes. A diet low in saturated and trans fats with an abundance of vegetables, fruits, and grains may lower the incidence of CAD.<ref>{{Cite journal |last=Tuso |first=Phillip |date=2015 |title=A Plant-Based Diet, Atherogenesis, and Coronary Artery Disease Prevention |url=http://www.thepermanentejournal.org/issues/2015/winter/5781-pbd.html |journal=The Permanente Journal |volume=19 |issue=1 |doi=10.7812/TPP/14-036 |pmc=PMC4315380 |pmid=25431999}}</ref>
Risk factors for CAD include smoking,<ref>{{cite journal | vauthors = Salehi N, Janjani P, Tadbiri H, Rozbahani M, Jalilian M | title = Effect of cigarette smoking on coronary arteries and pattern and severity of coronary artery disease: a review | journal = The Journal of International Medical Research | volume = 49 | issue = 12 | pages = 3000605211059893 | date = December 2021 | pmid = 34855538 | pmc = 8647272 | doi = 10.1177/03000605211059893 }}</ref> high cholesterol, obesity, and family history of CAD. Primarily, the accumulation of cholesterol in the bloodstream from high-fat diets lead to atherosclerotic occlusion and its clinical consequences. Therefore, preventative measures for CAD mainly involve diet changes. A diet low in saturated and trans fats with an abundance of vegetables, fruits, and grains may lower the incidence of CAD.<ref>{{cite journal | vauthors = Tuso P, Stoll SR, Li WW | title = A plant-based diet, atherogenesis, and coronary artery disease prevention | journal = The Permanente Journal | volume = 19 | issue = 1 | pages = 62–67 | date = 2015 | pmid = 25431999 | pmc = 4315380 | doi = 10.7812/TPP/14-036 }}</ref>


=== Peripheral Artery Disease ===
=== Peripheral Artery Disease ===
[[Peripheral artery disease]] (PAD), or limb ischemia, affects the [[Femoral artery|femoral]], [[Popliteal artery|popliteal]], or [[Iliac artery|iliac arteries]].<ref name=":11">{{Citation |last=Smith |first=David A. |title=Acute Arterial Occlusion |date=2022 |url=http://www.ncbi.nlm.nih.gov/books/NBK441851/ |work=StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=28722881 |access-date=2022-03-29 |last2=Lilie |first2=Craig J.}}</ref> PAD is caused by atherosclerotic plaques that occlude blood flow to extremities.<ref name=":8" /> Once blood flow is impeded, ischemic [[Muscle cell|muscle cells]] switch from [[Aerobic respiration|aerobic]] to [[Anaerobic respiration|anaerobic metabolism]] to cope with oxygen scarcity. Anaerobic metabolism, however, is energy-inefficient, lowering the concentration of the intracellular energy molecule, [[Adenosine triphosphate|ATP]], within muscles. ATP depletion leads to a leakage of calcium into muscle cells, disrupting various muscular components and eventually causing muscle fiber [[necrosis]].<ref name=":11" />
[[Peripheral artery disease]] (PAD), or limb ischemia, affects the [[Femoral artery|femoral]], [[Popliteal artery|popliteal]], or [[Iliac artery|iliac arteries]].<ref name=":11">{{cite book | vauthors = Smith DA, Lilie CJ | chapter = Acute Arterial Occlusion |date=2022 | chapter-url = http://www.ncbi.nlm.nih.gov/books/NBK441851/ | title =StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=28722881 |access-date=2022-03-29 }}</ref> PAD is caused by atherosclerotic plaques that occlude blood flow to extremities.<ref name=":8" /> Once blood flow is impeded, ischemic [[Muscle cell|muscle cells]] switch from [[Aerobic respiration|aerobic]] to [[Anaerobic respiration|anaerobic metabolism]] to cope with oxygen scarcity. Anaerobic metabolism, however, is energy-inefficient, lowering the concentration of the intracellular energy molecule, [[Adenosine triphosphate|ATP]], within muscles. ATP depletion leads to a leakage of calcium into muscle cells, disrupting various muscular components and eventually causing muscle fiber [[necrosis]].<ref name=":11" />


Risk factors for PAD include old age,<ref>{{Cite journal |last=Song |first=Peige |last2=Rudan |first2=Diana |last3=Zhu |first3=Yajie |last4=Fowkes |first4=Freya J I |last5=Rahimi |first5=Kazem |last6=Fowkes |first6=F Gerald R |last7=Rudan |first7=Igor |date=2019-08-01 |title=Global, regional, and national prevalence and risk factors for peripheral artery disease in 2015: an updated systematic review and analysis |url=https://www.sciencedirect.com/science/article/pii/S2214109X19302554 |journal=The Lancet Global Health |language=en |volume=7 |issue=8 |pages=e1020–e1030 |doi=10.1016/S2214-109X(19)30255-4 |issn=2214-109X}}</ref> smoking, [[hypertension]], and high cholesterol, with smoking being the greatest contributing factor.<ref name=":8" /> This is because tobacco smoke contains potent chemicals that severely increase the occurrence of PAD. Thus, primary prevention of PAD is achieved with smoking cessation.<ref>{{Cite web |title=Prevention and Treatment of PAD |url=https://www.heart.org/en/health-topics/peripheral-artery-disease/prevention-and-treatment-of-pad |access-date=2022-04-11 |website=www.heart.org |language=en}}</ref>
Risk factors for PAD include old age,<ref>{{cite journal | vauthors = Song P, Rudan D, Zhu Y, Fowkes FJ, Rahimi K, Fowkes FG, Rudan I | title = Global, regional, and national prevalence and risk factors for peripheral artery disease in 2015: an updated systematic review and analysis | journal = The Lancet. Global Health | volume = 7 | issue = 8 | pages = e1020-e1030 | date = August 2019 | pmid = 31303293 | doi = 10.1016/S2214-109X(19)30255-4 }}</ref> smoking, [[hypertension]], and high cholesterol, with smoking being the greatest contributing factor.<ref name=":8" /> This is because tobacco smoke contains potent chemicals that severely increase the occurrence of PAD. Thus, primary prevention of PAD is achieved with smoking cessation.<ref>{{Cite web |title=Prevention and Treatment of PAD |url=https://www.heart.org/en/health-topics/peripheral-artery-disease/prevention-and-treatment-of-pad |access-date=2022-04-11 |website=www.heart.org |language=en}}</ref>


=== Pulmonary Embolism ===
=== Pulmonary Embolism ===
[[Pulmonary embolism]] (PE) involves occlusion of a [[pulmonary artery]] by an embolus, most often a thrombus, obstructing blood flow to the lungs.<ref name=":9" /> Impairment of [[pulmonary circulation]] leads to severe [[Ventilation/perfusion ratio|ventilation-perfusion]] mismatching of the lungs,<ref>{{Cite journal |last=Tapson |first=Victor F. |date=2008-03-06 |title=Acute Pulmonary Embolism |url=http://www.nejm.org/doi/abs/10.1056/NEJMra072753 |journal=New England Journal of Medicine |language=en |volume=358 |issue=10 |pages=1037–1052 |doi=10.1056/NEJMra072753 |issn=0028-4793}}</ref> terminating in [[hypoxemia]] and [[respiratory failure]]. Most PEs are sequelae of [[Deep vein thrombosis|Deep Vein Thrombosis]] (DVT), resulting from the breakage and propagation of a venous thrombus formed within the extremities to a pulmonary artery.<ref name=":9">{{Citation |last=Vyas |first=Vrinda |title=Acute Pulmonary Embolism |date=2022 |url=http://www.ncbi.nlm.nih.gov/books/NBK560551/ |work=StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=32809386 |access-date=2022-03-29 |last2=Goyal |first2=Amandeep}}</ref>
[[Pulmonary embolism]] (PE) involves occlusion of a [[pulmonary artery]] by an embolus, most often a thrombus, obstructing blood flow to the lungs.<ref name=":9" /> Impairment of [[pulmonary circulation]] leads to severe [[Ventilation/perfusion ratio|ventilation-perfusion]] mismatching of the lungs,<ref>{{cite journal | vauthors = Tapson VF | title = Acute pulmonary embolism | journal = The New England Journal of Medicine | volume = 358 | issue = 10 | pages = 1037–1052 | date = March 2008 | pmid = 18322285 | doi = 10.1056/NEJMra072753 }}</ref> terminating in [[hypoxemia]] and [[respiratory failure]]. Most PEs are sequelae of [[Deep vein thrombosis|Deep Vein Thrombosis]] (DVT), resulting from the breakage and propagation of a venous thrombus formed within the extremities to a pulmonary artery.<ref name=":9">{{cite book | vauthors = Vyas V, Goyal A | chapter = Acute Pulmonary Embolism |date=2022 | chapter-url=http://www.ncbi.nlm.nih.gov/books/NBK560551/ | title = StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=32809386 |access-date=2022-03-29 }}</ref>


As DVT commonly precedes PE, risk factors for PE overlap with risk factors for DVT. These include a sedentary lifestyle, prior surgery, trauma, history of DVT, and hypertension.<ref>{{Cite journal |last=Heit |first=John A. |last2=Spencer |first2=Frederick A. |last3=White |first3=Richard H. |date=2016 |title=The epidemiology of venous thromboembolism |url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4715842/ |journal=Journal of Thrombosis and Thrombolysis |volume=41 |pages=3–14 |doi=10.1007/s11239-015-1311-6 |issn=0929-5305 |pmc=4715842 |pmid=26780736}}</ref> A sedentary lifestyle and lack of movement are critical modifiable risk factors for PE.<ref>{{Citation |last=Jung |first=Jeenah |title=Surgical Management of Pulmonary Embolism |date=2018 |url=https://doi.org/10.1007/978-3-319-65226-9_31 |work=Current Management of Venous Diseases |pages=405–418 |editor-last=Chaar |editor-first=Cassius Iyad Ochoa |place=Cham |publisher=Springer International Publishing |language=en |doi=10.1007/978-3-319-65226-9_31 |isbn=978-3-319-65226-9 |access-date=2022-04-16 |last2=Bonde |first2=Pramod}}</ref> Immobility reduces the rate of leg muscle contraction, enhancing thrombus formation in vessels of the calves that may propagate to the lungs.<ref>{{Cite journal |last=Ro |first=Ayako |last2=Kageyama |first2=Norimasa |last3=Mukai |first3=Toshiji |date=2017-09-08 |title=Pathophysiology of Venous Thromboembolism with Respect to the Anatomical Features of the Deep Veins of Lower Limbs: A Review |url=http://dx.doi.org/10.7134/phlebol.17-14 |journal=The Japanese Journal of Phlebology |volume=28 |issue=3 |pages=309–316 |doi=10.7134/phlebol.17-14 |issn=0915-7395}}</ref> Thus, physical activity is essential in preventing PE.<ref name=":10" />
As DVT commonly precedes PE, risk factors for PE overlap with risk factors for DVT. These include a sedentary lifestyle, prior surgery, trauma, history of DVT, and hypertension.<ref>{{cite journal | vauthors = Heit JA, Spencer FA, White RH | title = The epidemiology of venous thromboembolism | journal = Journal of Thrombosis and Thrombolysis | volume = 41 | issue = 1 | pages = 3–14 | date = January 2016 | pmid = 26780736 | pmc = 4715842 | doi = 10.1007/s11239-015-1311-6 }}</ref> A sedentary lifestyle and lack of movement are critical modifiable risk factors for PE.<ref>{{cite book | vauthors = Jung J, Bonde P | chapter = Surgical Management of Pulmonary Embolism |date=2018 | title = Current Management of Venous Diseases |pages=405–418 | veditors = Chaar CI | place=Cham |publisher=Springer International Publishing |language=en |doi=10.1007/978-3-319-65226-9_31 |isbn=978-3-319-65226-9 }}</ref> Immobility reduces the rate of leg muscle contraction, enhancing thrombus formation in vessels of the calves that may propagate to the lungs.<ref>{{cite journal | vauthors = Ro A, Kageyama N, Mukai T | title = Pathophysiology of Venous Thromboembolism with Respect to the Anatomical Features of the Deep Veins of Lower Limbs: A Review | journal = Annals of Vascular Diseases | volume = 10 | issue = 2 | pages = 99–106 | date = June 2017 | pmid = 29034034 | doi = 10.7134/phlebol.17-14 }}</ref> Thus, physical activity is essential in preventing PE.<ref name=":10" />


== Complications ==
== Complications ==
Diseases of arterial occlusion may progress into life-threatening conditions with improper prevention or management. Myocardial infarction, gangrene, and ischemic stroke are among the complications of severe arterial occlusion.
Diseases of arterial occlusion may progress into life-threatening conditions with improper prevention or management. Myocardial infarction, gangrene, and ischemic stroke are among the complications of severe arterial occlusion.
[[File:Elevated ST Segments.png|thumb|311x311px|ECG traces recorded in a healthy heart (top) and in myocardial infarction (bottom). MIs cause an elevation of the ST segment on ECG traces.<ref name=":3" /> In MI, transmural ischemia impairs electrical potential within the heart, causing a great difference in voltage potential between uninjured and ischemic cardiomyocytes.<ref>{{Cite journal |last=de Bliek |first=Erwin Christian |date=2018-02-17 |title=ST elevation: Differential diagnosis and caveats. A comprehensive review to help distinguish ST elevation myocardial infarction from nonischemic etiologies of ST elevation |url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6009807/ |journal=Turkish Journal of Emergency Medicine |volume=18 |issue=1 |pages=1–10 |doi=10.1016/j.tjem.2018.01.008 |issn=2452-2473 |pmc=6009807 |pmid=29942875}}</ref> This difference is recorded by ECG leads and is presented as ST segment elevation in ECG traces.]]
[[File:Elevated ST Segments.png|thumb|311x311px|ECG traces recorded in a healthy heart (top) and in myocardial infarction (bottom). MIs cause an elevation of the ST segment on ECG traces.<ref name=":3" /> In MI, transmural ischemia impairs electrical potential within the heart, causing a great difference in voltage potential between uninjured and ischemic cardiomyocytes.<ref>{{cite journal | vauthors = de Bliek EC | title = ST elevation: Differential diagnosis and caveats. A comprehensive review to help distinguish ST elevation myocardial infarction from nonischemic etiologies of ST elevation | journal = Turkish Journal of Emergency Medicine | volume = 18 | issue = 1 | pages = 1–10 | date = March 2018 | pmid = 29942875 | pmc = 6009807 | doi = 10.1016/j.tjem.2018.01.008 }}</ref> This difference is recorded by ECG leads and is presented as ST segment elevation in ECG traces.]]


=== Myocardial Infarction ===
=== Myocardial Infarction ===
A [[myocardial infarction]] (MI), or heart attack, arises from complete occlusion of a coronary artery.<ref name=":2">{{Cite book |last=Seeley |first=Rod R. |url=https://www.worldcat.org/oclc/77271214 |title=Anatomy & physiology |date=2008 |publisher=McGraw-Hill |others=Philip Tate, Trent D. Stephens |isbn=978-0-07-296557-5 |edition=8th |location=Dubuque, IA |oclc=77271214}}</ref> The most frequent cause of MI is the rupturing of an atherosclerotic plaque formed in CAD. Plaque rupture exposes the subendothelial matrix beneath the plaque, initiating thrombus formation within the vasculature.<ref name=":14">{{Cite web |title=Myocardial Infarction—From Atherosclerosis to Thrombosis |url=https://www.ahajournals.org/doi/epub/10.1161/ATVBAHA.119.312578 |access-date=2022-03-29 |website=www.ahajournals.org |language=en |doi=10.1161/atvbaha.119.312578}}</ref> The thrombus deposits on the ruptured plaque to completely block the coronary artery, halting oxygen supply to cardiomyocytes. Under [[Hypoxia (medical)|hypoxia]], cardiomyocytes perform anaerobic respiration, producing more lactate.<ref name=":3">{{Cite journal |last=Vogel |first=Birgit |last2=Claessen |first2=Bimmer E. |last3=Arnold |first3=Suzanne V. |last4=Chan |first4=Danny |last5=Cohen |first5=David J. |last6=Giannitsis |first6=Evangelos |last7=Gibson |first7=C. Michael |last8=Goto |first8=Shinya |last9=Katus |first9=Hugo A. |last10=Kerneis |first10=Mathieu |last11=Kimura |first11=Takeshi |date=2019-06-06 |title=ST-segment elevation myocardial infarction |url=https://www.nature.com/articles/s41572-019-0090-3 |journal=Nature Reviews Disease Primers |language=en |volume=5 |issue=1 |pages=1–20 |doi=10.1038/s41572-019-0090-3 |issn=2056-676X}}</ref><ref name=":4">{{Cite journal |last=Wu |first=Alan H. B. |date=2017-09-01 |title=Release of cardiac troponin from healthy and damaged myocardium |url=https://www.sciencedirect.com/science/article/pii/S2542364917300997 |journal=Frontiers in Laboratory Medicine |language=en |volume=1 |issue=3 |pages=144–150 |doi=10.1016/j.flm.2017.09.003 |issn=2542-3649}}</ref> With blocked coronary circulation, lactate clearance from cardiomyocytes is also hindered.<ref name=":4" /> Lactate accumulation reduces contractility and eventually necroses cardiomyocytes, releasing their [[troponin]] storage into the bloodstream.<ref name=":3" /> Serum troponin elevation is a characteristic biomarker of MI.<ref name=":3" />
A [[myocardial infarction]] (MI), or heart attack, arises from complete occlusion of a coronary artery.<ref name=":2">{{Cite book | vauthors = Seeley RR, Tate P, Stephens TD |url=https://www.worldcat.org/oclc/77271214 |title=Anatomy & physiology |date=2008 |publisher=McGraw-Hill |isbn=978-0-07-296557-5 |edition=8th |location=Dubuque, IA |oclc=77271214}}</ref> The most frequent cause of MI is the rupturing of an atherosclerotic plaque formed in CAD. Plaque rupture exposes the subendothelial matrix beneath the plaque, initiating thrombus formation within the vasculature.<ref name=":14">{{Cite web |title=Myocardial Infarction—From Atherosclerosis to Thrombosis |url=https://www.ahajournals.org/doi/epub/10.1161/ATVBAHA.119.312578 |access-date=2022-03-29 |website=www.ahajournals.org |language=en |doi=10.1161/atvbaha.119.312578}}</ref> The thrombus deposits on the ruptured plaque to completely block the coronary artery, halting oxygen supply to cardiomyocytes. Under [[Hypoxia (medical)|hypoxia]], cardiomyocytes perform anaerobic respiration, producing more lactate.<ref name=":3">{{cite journal | vauthors = Vogel B, Claessen BE, Arnold SV, Chan D, Cohen DJ, Giannitsis E, Gibson CM, Goto S, Katus HA, Kerneis M, Kimura T, Kunadian V, Pinto DS, Shiomi H, Spertus JA, Steg PG, Mehran R | display-authors = 6 | title = ST-segment elevation myocardial infarction | journal = Nature Reviews. Disease Primers | volume = 5 | issue = 1 | pages = 39 | date = June 2019 | pmid = 31171787 | doi = 10.1038/s41572-019-0090-3 }}</ref><ref name=":4">{{Cite journal | vauthors = Wu AH |date=2017-09-01 |title=Release of cardiac troponin from healthy and damaged myocardium |journal=Frontiers in Laboratory Medicine |language=en |volume=1 |issue=3 |pages=144–150 |doi=10.1016/j.flm.2017.09.003 |issn=2542-3649}}</ref> With blocked coronary circulation, lactate clearance from cardiomyocytes is also hindered.<ref name=":4" /> Lactate accumulation reduces contractility and eventually necroses cardiomyocytes, releasing their [[troponin]] storage into the bloodstream.<ref name=":3" /> Serum troponin elevation is a characteristic biomarker of MI.<ref name=":3" />
Depending on the severity of ischemia, MIs are categorized as NSTEMI or STEMI. NSTEMI stands for ‘Non-ST Elevation Myocardial Infarction’,<ref name=":3" /> referencing the lack of [[ST elevation|ST-segment elevation]] in [[Electrocardiography|ECG]] traces. This is because in NSTEMI, only part of the myocardial wall is infarcted, which does not diagnostically present with ST-elevation.
Depending on the severity of ischemia, MIs are categorized as NSTEMI or STEMI. NSTEMI stands for ‘Non-ST Elevation Myocardial Infarction’,<ref name=":3" /> referencing the lack of [[ST elevation|ST-segment elevation]] in [[Electrocardiography|ECG]] traces. This is because in NSTEMI, only part of the myocardial wall is infarcted, which does not diagnostically present with ST-elevation.
Line 54: Line 54:


=== Gangrene ===
=== Gangrene ===
[[Gangrene]], specifically dry gangrene, is caused by an atherosclerotic or thromboembolic arterial occlusion.<ref name=":5">{{Citation |last=Buttolph |first=Amelia |title=Gangrene |date=2022 |url=http://www.ncbi.nlm.nih.gov/books/NBK560552/ |work=StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=32809387 |access-date=2022-03-29 |last2=Sapra |first2=Amit}}</ref> Gangrene is a complication of prolonged PAD, leading to shriveling, blackening, and infarction of peripheral tissue, commonly in the extremities.<ref name=":5" /> In severe cases, amputation of the affected limb is required.
[[Gangrene]], specifically dry gangrene, is caused by an atherosclerotic or thromboembolic arterial occlusion.<ref name=":5">{{cite book | vauthors = Buttolph A, Sapra A | chapter = Gangrene |date=2022 | chapter-url = http://www.ncbi.nlm.nih.gov/books/NBK560552/ | title = StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=32809387 |access-date=2022-03-29 }}</ref> Gangrene is a complication of prolonged PAD, leading to shriveling, blackening, and infarction of peripheral tissue, commonly in the extremities.<ref name=":5" /> In severe cases, amputation of the affected limb is required.


=== Ischemic Stroke ===
=== Ischemic Stroke ===
[[Stroke|Ischemic stroke]] is a thrombotic, or rarely, thromboembolic or atherosclerotic complication of arteries supplying the brain.<ref name=":2" /> Occlusion of brain arteries leads to rapid ischemic death of [[Neuron|neurons]], both at the infarct core and ischemic penumbra.<ref name=":20" /><ref name=":6">{{Cite journal |last=Tuo |first=Qing‐zhang |last2=Zhang |first2=Shu‐ting |last3=Lei |first3=Peng |date=2021-05-06 |title=Mechanisms of neuronal cell death in ischemic stroke and their therapeutic implications |url=https://onlinelibrary.wiley.com/doi/epdf/10.1002/med.21817 |journal=Medicinal Research Reviews |volume=42 |issue=1 |pages=259–305 |doi=10.1002/med.21817 |issn=0198-6325}}</ref> Similar to cardiomyocytes, neurons require constant perfusion for proper function. Any interruption of blood supply causes neurons to switch to anaerobic metabolism,<ref name=":6" /> exhausting intracellular ATP levels. ATP depletion causes an influx of calcium cations into neurons and efflux of excess [[Glutamate (neurotransmitter)|glutamate]], triggering the [[apoptosis]] and [[necroptosis]] of neurons.<ref name=":6" />
[[Stroke|Ischemic stroke]] is a thrombotic, or rarely, thromboembolic or atherosclerotic complication of arteries supplying the brain.<ref name=":2" /> Occlusion of brain arteries leads to rapid ischemic death of [[Neuron|neurons]], both at the infarct core and ischemic penumbra.<ref name=":20" /><ref name=":6">{{cite journal | vauthors = Tuo QZ, Zhang ST, Lei P | title = Mechanisms of neuronal cell death in ischemic stroke and their therapeutic implications | journal = Medicinal Research Reviews | volume = 42 | issue = 1 | pages = 259–305 | date = January 2022 | pmid = 33957000 | doi = 10.1002/med.21817 }}</ref> Similar to cardiomyocytes, neurons require constant perfusion for proper function. Any interruption of blood supply causes neurons to switch to anaerobic metabolism,<ref name=":6" /> exhausting intracellular ATP levels. ATP depletion causes an influx of calcium cations into neurons and efflux of excess [[Glutamate (neurotransmitter)|glutamate]], triggering the [[apoptosis]] and [[necroptosis]] of neurons.<ref name=":6" />


Neuronal necrosis precipitates irreversible brain damage. Cerebral areas most susceptible to ischemic damage include the [[Wernicke's area|speech]] and [[Broca's area|motor]] cortices, leading to contralateral paralysis, speech, and comprehension loss.<ref>{{Cite book |last=Guyton |first=Arthur C. |url=https://www.worldcat.org/oclc/56661571 |title=Textbook of medical physiology |date=2006 |publisher=Elsevier Saunders |others=John E. Hall |isbn=0-7216-0240-1 |edition=11th |location=Philadelphia |oclc=56661571}}</ref> Severe or prolonged strokes may terminate in coma or brain death.<ref name=":20" /> Therefore, the diagnosis and treatment of ischemic stroke are time-dependent.
Neuronal necrosis precipitates irreversible brain damage. Cerebral areas most susceptible to ischemic damage include the [[Wernicke's area|speech]] and [[Broca's area|motor]] cortices, leading to contralateral paralysis, speech, and comprehension loss.<ref>{{Cite book | vauthors = Guyton AC, Hall JE |url=https://www.worldcat.org/oclc/56661571 |title=Textbook of medical physiology |date=2006 |publisher=Elsevier Saunders |isbn=0-7216-0240-1 |edition=11th |location=Philadelphia |oclc=56661571}}</ref> Severe or prolonged strokes may terminate in coma or brain death.<ref name=":20" /> Therefore, the diagnosis and treatment of ischemic stroke are time-dependent.


== Diagnosis ==
== Diagnosis ==
Line 75: Line 75:
Traditionally, [[angiography]] is an invasive technique which involves inserting a flexible plastic [[catheter]] into the artery of interest.<ref>{{Cite web |last=Radiology (ACR) |first=Radiological Society of North America (RSNA) and American College of |title=Catheter Angiography |url=https://www.radiologyinfo.org/en/info/angiocath |access-date=2022-03-29 |website=Radiologyinfo.org |language=en}}</ref> A [[Radiocontrast agent|radioactive contrast dye]] is then injected through the catheter and viewed on an X-ray. This contrast material does not permanently discolor any organs, but simply interacts with X-rays to produce a more precise diagnosis.<ref>{{Cite web |last=Radiology (ACR) |first=Radiological Society of North America (RSNA) and American College of |title=Contrast Materials |url=https://www.radiologyinfo.org/en/info/safety-contrast |access-date=2022-03-29 |website=Radiologyinfo.org |language=en}}</ref>
Traditionally, [[angiography]] is an invasive technique which involves inserting a flexible plastic [[catheter]] into the artery of interest.<ref>{{Cite web |last=Radiology (ACR) |first=Radiological Society of North America (RSNA) and American College of |title=Catheter Angiography |url=https://www.radiologyinfo.org/en/info/angiocath |access-date=2022-03-29 |website=Radiologyinfo.org |language=en}}</ref> A [[Radiocontrast agent|radioactive contrast dye]] is then injected through the catheter and viewed on an X-ray. This contrast material does not permanently discolor any organs, but simply interacts with X-rays to produce a more precise diagnosis.<ref>{{Cite web |last=Radiology (ACR) |first=Radiological Society of North America (RSNA) and American College of |title=Contrast Materials |url=https://www.radiologyinfo.org/en/info/safety-contrast |access-date=2022-03-29 |website=Radiologyinfo.org |language=en}}</ref>


Due to technological advances, clinicians have begun to use a less invasive approach called Multi-Detector Coronary Tomography (MDCT) angiography. Rather than inserting a large catheter into the artery, this technique requires a small injection of contrast dye using a standard intravenous catheter inserted into the arm, much like a regular injection. MDCT scanners then locate the contrast dye to show blockages within the arteries.<ref name=":12" /> MDCT angiography is more sensitive in detecting blockage and subsequent diseases such as CAD compared to invasive X-ray angiography.<ref name=":12">{{Cite web |last=BrJCardiol |title=MDCT coronary angiography: does the benefit justify radiation burden? - The British Journal of Cardiology |url=https://bjcardio.co.uk/2010/09/mdct-coronary-angiography-does-the-benefit-justify-radiation-burden/ |access-date=2022-03-29 |website=bjcardio.co.uk |language=en-GB}}</ref>
Due to technological advances, clinicians have begun to use a less invasive approach called Multi-Detector Coronary Tomography (MDCT) angiography. Rather than inserting a large catheter into the artery, this technique requires a small injection of contrast dye using a standard intravenous catheter inserted into the arm, much like a regular injection. MDCT scanners then locate the contrast dye to show blockages within the arteries.<ref name=":12" /> MDCT angiography is more sensitive in detecting blockage and subsequent diseases such as CAD compared to invasive X-ray angiography.<ref name=":12">{{Cite journal | vauthors = Alfakih K, Budoff M | title = MDCT coronary angiography: does the benefit justify radiation burden? | journal = The British Journal of Cardiology | date = 2010 | volume = 17 | pages = 207-208 |url=https://bjcardio.co.uk/2010/09/mdct-coronary-angiography-does-the-benefit-justify-radiation-burden/ |access-date=2022-03-29 |language=en-GB}}</ref>


== Treatment ==
== Treatment ==
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=== Blood-thinning Medication ===
=== Blood-thinning Medication ===
[[Anticoagulant|Blood-thinning medications]] are beneficial short-term options in managing arterial occlusion. Anticoagulants such as [[warfarin]] and antiplatelets such as [[aspirin]] and [[clopidogrel]] reduce the risk of thrombosis by making blood flow easily through arteries.<ref name=":0" /><ref name=":19" /> Side effects include increased bleeding and heavier bruising.<ref name=":15">{{Cite web |date=2018-12-20 |title=Warfarin: a blood-thinning medicine to treat and prevent blood clots |url=https://www.nhs.uk/medicines/warfarin/ |access-date=2022-03-29 |website=nhs.uk |language=en}}</ref>
[[Anticoagulant|Blood-thinning medications]] are beneficial short-term options in managing arterial occlusion. Anticoagulants such as [[warfarin]] and antiplatelets such as [[aspirin]] and [[clopidogrel]] reduce the risk of thrombosis by making blood flow easily through arteries.<ref name=":0" /><ref name=":19" /> Side effects include increased bleeding and heavier bruising.<ref name=":15">{{Cite web |date=2018-12-20 |title=Warfarin: a blood-thinning medicine to treat and prevent blood clots |url=https://www.nhs.uk/medicines/warfarin/ |access-date=2022-03-29 |website=nhs.uk |language=en}}</ref>

== References ==
== References ==
{{Reflist}}

Revision as of 04:08, 9 June 2022

Blood flow through an artery is partially occluded by the deposition of an atherosclerotic plaque.

Arterial occlusion is a condition involving partial or complete blockage of blood flow through an artery. Arteries are blood vessels that carry oxygenated blood to body tissues[1][2]. An occlusion of arteries disrupts oxygen and blood supply to tissues, leading to ischemia.[1] Depending on the extent of ischemia, symptoms of arterial occlusion range from simple soreness and pain that can be relieved with rest,[3] to a lack of sensation or paralysis that could require amputation.[3]

Arterial occlusion can be classified into three types based on etiology: embolism, thrombosis, and atherosclerosis. These three types of occlusion underlie various common conditions, including coronary artery disease,[4] peripheral artery disease,[5] and pulmonary embolism,[6] which may be prevented by lowering risk factors. With improper prevention or management, these diseases can progress into life-threatening complications of myocardial infarction,[7] gangrene,[8] ischemic stroke,[9] and in severe cases, terminate in brain death or cardiac arrest.[10][11]

Arterial occlusion is diagnosed by exercise testing,[3] ultrasonic duplex testing,[3] and multi-detector coronary tomography angiography.[12] Meanwhile, treatment can vary from surgical interventions such as bypass,[13] endarterectomy,[14] and embolectomy,[15] to blood-thinning medication. [16]

Signs and symptoms

Signs and symptoms of arterial occlusion depend on several factors, including the location, extent, and onset of blockage. Normally, the blockage should affect approximately 70% of the artery for symptoms to become noticeable.[3] Symptoms can be less severe during gradual narrowing, as this allows time for the widening of existing vessels and the formation of new ones (collateral vessels), allowing blood to still reach the area. Symptoms in this case will simply be intermittent claudication.[3] Sudden narrowing leads to more severe consequences, given the lack of time for collateral vessels to grow. As such, coldness, numbness or even paralysis of the affected body parts may result.[3]

The commonest symptom of arterial occlusion is intermittent claudication, which consists of a painful, aching sensation in the affected muscle.[3] This is often provoked with physical activity and relieved with rest. Pain and muscle aching may build up with walking, and accelerate with light jogging or walking uphill. Often, pain is relieved after several minutes of rest.[3]  However, affected individuals are limited to short spurts of activity, impairing their quality of life.

For severe symptoms, the signs are usually visible and lead to ischemia. The clinical presentation of ischemia consists of the 6 Ps, including pallor, pain, paresthesia, paralysis, pulselessness, and poikilothermia.[17] Affected individuals initially notice a paleness of the affected region and feel severe pain. As the condition worsens, the region appears bluish and numb. In extreme cases, this will give way to paralysis and poikilothermia, possibly requiring amputation of the affected limb.[17]

Types of arterial occlusion

Commonly observed types of arterial occlusion include thrombosis, atherosclerosis, and embolism.

Embolism

An embolism involves the occlusion of blood vessels by an embolus.[1] Arterial occlusion by an embolus is termed ‘arterial embolism’. An embolus is an agent that blocks blood flow by physically obstructing blood vessels.[1] This includes gas bubbles,[18] fatty deposits, amniotic fluid,[19] blood clots, and foreign material. Arterial emboli occasionally detach from primary sites and travel via circulation to occlude secondary arteries, causing multiple ischemic sites.

Thrombosis

Thrombosis occurs when thrombi occlude vessels in the body.[20] A thrombus, or a blood clot, is a mobilized mass of blood cells that circulates within the body.[21][22] Thrombi can occlude veins (venous thrombosis) or arteries (arterial thrombosis). The etiology of thrombosis is described by Virchow’s Triad, which includes hemostasis, vascular wall damage, and hypercoagulability.[21] Arterial thromboses significantly narrow or completely block arterial blood flow and oxygen delivery to tissues.

Atherosclerosis

In atherosclerosis, the inner endothelial layer of arteries[23] is stiffened by the deposition of an atheromatous plaque.[1][11][24] Atheromatous plaques, also called atherosclerotic plaques, are made of fats and lipid-laden macrophages.[20] Plaque deposition both physically narrows an artery and impairs the function of endothelial cells, potentiating their production of vasoconstrictive chemicals to constrict the arterial lumen.[11] This leads to turbulent blood flow in the arteries, affecting oxygen supply to tissues downstream.

Diseases of arterial occlusion

The pathophysiology of diseases of arterial occlusion depends on the type of occlusion, the severity of blockage, and the location of the occluded artery. Common diseases of arterial occlusion include Coronary Artery Disease, Peripheral Artery Disease, and Pulmonary Embolism.

Coronary Artery Disease

Coronary Artery Disease (CAD) results from the stenosis of coronary arteries by an atherosclerotic plaque.[4][23] The coronary arteries perfuse the cardiomyocytes located within the myocardium. Cardiomyocytes require constant perfusion to aid the pumping of the heart.[25] In CAD, atheromatous plaque formation in a coronary artery limits oxygen supply to cardiomyocytes, impairing heart contractility.

CAD severity varies based on the extent of coronary artery occlusion. At 75% luminal narrowing, patients experience symptoms associated with limited perfusion of cardiomyocytes,[11] especially under strenuous conditions.[1] Under physical exertion, CAD induces chest pain, termed ‘stable angina’. Stable angina may deteriorate into unstable angina, marking the initiation of Acute Coronary Syndrome, which may further deteriorate into a myocardial infarction.  

Risk factors for CAD include smoking,[26] high cholesterol, obesity, and family history of CAD. Primarily, the accumulation of cholesterol in the bloodstream from high-fat diets lead to atherosclerotic occlusion and its clinical consequences. Therefore, preventative measures for CAD mainly involve diet changes. A diet low in saturated and trans fats with an abundance of vegetables, fruits, and grains may lower the incidence of CAD.[27]

Peripheral Artery Disease

Peripheral artery disease (PAD), or limb ischemia, affects the femoral, popliteal, or iliac arteries.[17] PAD is caused by atherosclerotic plaques that occlude blood flow to extremities.[5] Once blood flow is impeded, ischemic muscle cells switch from aerobic to anaerobic metabolism to cope with oxygen scarcity. Anaerobic metabolism, however, is energy-inefficient, lowering the concentration of the intracellular energy molecule, ATP, within muscles. ATP depletion leads to a leakage of calcium into muscle cells, disrupting various muscular components and eventually causing muscle fiber necrosis.[17]

Risk factors for PAD include old age,[28] smoking, hypertension, and high cholesterol, with smoking being the greatest contributing factor.[5] This is because tobacco smoke contains potent chemicals that severely increase the occurrence of PAD. Thus, primary prevention of PAD is achieved with smoking cessation.[29]

Pulmonary Embolism

Pulmonary embolism (PE) involves occlusion of a pulmonary artery by an embolus, most often a thrombus, obstructing blood flow to the lungs.[6] Impairment of pulmonary circulation leads to severe ventilation-perfusion mismatching of the lungs,[30] terminating in hypoxemia and respiratory failure. Most PEs are sequelae of Deep Vein Thrombosis (DVT), resulting from the breakage and propagation of a venous thrombus formed within the extremities to a pulmonary artery.[6]

As DVT commonly precedes PE, risk factors for PE overlap with risk factors for DVT. These include a sedentary lifestyle, prior surgery, trauma, history of DVT, and hypertension.[31] A sedentary lifestyle and lack of movement are critical modifiable risk factors for PE.[32] Immobility reduces the rate of leg muscle contraction, enhancing thrombus formation in vessels of the calves that may propagate to the lungs.[33] Thus, physical activity is essential in preventing PE.[3]

Complications

Diseases of arterial occlusion may progress into life-threatening conditions with improper prevention or management. Myocardial infarction, gangrene, and ischemic stroke are among the complications of severe arterial occlusion.

ECG traces recorded in a healthy heart (top) and in myocardial infarction (bottom). MIs cause an elevation of the ST segment on ECG traces.[34] In MI, transmural ischemia impairs electrical potential within the heart, causing a great difference in voltage potential between uninjured and ischemic cardiomyocytes.[35] This difference is recorded by ECG leads and is presented as ST segment elevation in ECG traces.

Myocardial Infarction

A myocardial infarction (MI), or heart attack, arises from complete occlusion of a coronary artery.[9] The most frequent cause of MI is the rupturing of an atherosclerotic plaque formed in CAD. Plaque rupture exposes the subendothelial matrix beneath the plaque, initiating thrombus formation within the vasculature.[7] The thrombus deposits on the ruptured plaque to completely block the coronary artery, halting oxygen supply to cardiomyocytes. Under hypoxia, cardiomyocytes perform anaerobic respiration, producing more lactate.[34][36] With blocked coronary circulation, lactate clearance from cardiomyocytes is also hindered.[36] Lactate accumulation reduces contractility and eventually necroses cardiomyocytes, releasing their troponin storage into the bloodstream.[34] Serum troponin elevation is a characteristic biomarker of MI.[34]

Depending on the severity of ischemia, MIs are categorized as NSTEMI or STEMI. NSTEMI stands for ‘Non-ST Elevation Myocardial Infarction’,[34] referencing the lack of ST-segment elevation in ECG traces. This is because in NSTEMI, only part of the myocardial wall is infarcted, which does not diagnostically present with ST-elevation.

NSTEMI becomes STEMI when the entire myocardial wall is infarcted. Diagnostically, STEMI displays prolonged ST-segment elevation in ECG traces,[34] and is thus named ‘ST-Elevation Myocardial Infarction’. Minutes after STEMI, fatal cardiac arrest could occur.[11] STEMI is life-threatening if immediate reperfusion therapy is not initiated.

Gangrene

Gangrene, specifically dry gangrene, is caused by an atherosclerotic or thromboembolic arterial occlusion.[8] Gangrene is a complication of prolonged PAD, leading to shriveling, blackening, and infarction of peripheral tissue, commonly in the extremities.[8] In severe cases, amputation of the affected limb is required.

Ischemic Stroke

Ischemic stroke is a thrombotic, or rarely, thromboembolic or atherosclerotic complication of arteries supplying the brain.[9] Occlusion of brain arteries leads to rapid ischemic death of neurons, both at the infarct core and ischemic penumbra.[10][37] Similar to cardiomyocytes, neurons require constant perfusion for proper function. Any interruption of blood supply causes neurons to switch to anaerobic metabolism,[37] exhausting intracellular ATP levels. ATP depletion causes an influx of calcium cations into neurons and efflux of excess glutamate, triggering the apoptosis and necroptosis of neurons.[37]

Neuronal necrosis precipitates irreversible brain damage. Cerebral areas most susceptible to ischemic damage include the speech and motor cortices, leading to contralateral paralysis, speech, and comprehension loss.[38] Severe or prolonged strokes may terminate in coma or brain death.[10] Therefore, the diagnosis and treatment of ischemic stroke are time-dependent.

Diagnosis

There are several methods of diagnosing arterial occlusion, ranging from straightforward setups like exercise testing, to advanced scanning equipment such as ultrasonic duplex scanning or Multi-Detector Coronary Tomography (MDCT) angiography.

Exercise Testing

Exercise testing is a simplistic, non-invasive method of diagnosing intermittent claudication. Blood pressure measurements at the suspected area can be taken before and after exercise, as some symptoms only appear during strenuous activity.[3] Commonly, a treadmill setting at 2 mph with a 12-degree slope is utilized. Subjects are asked to walk on the treadmill for a maximum of 5 minutes or until moderate pain is felt. The time to pain or maximal walking duration is recorded and compared with baselines.

Healthy individuals maintain systolic blood pressures at a normal range. Once exercise becomes more intense, there may be a temporary fall in systolic pressure, which quickly returns to normal with rest. However, those with intermittent claudication struggle to maintain standard values of systolic pressure, while recovery back to baseline is prolonged.[3]

Ultrasonic Duplex Testing

Ultrasonic duplex scanning was developed to primarily determine the extent of atherosclerosis in carotid arteries.[3] Since then, its application has widened to include arteries in the limbs. The technique utilizes high-frequency sound waves for visualization of flow direction and velocity within the arteries in an area of interest. The term duplex refers to 2 modes of ultrasound scanning being conducted. The B-mode transducer allows for an image of the vessel to be obtained, providing visual cues on the extent of occlusion. Meanwhile, the doppler probe is used to acquire data on velocity and direction of blood flow.[39]

Multi-Detector Coronary Tomography (MDCT) Angiography

Traditionally, angiography is an invasive technique which involves inserting a flexible plastic catheter into the artery of interest.[40] A radioactive contrast dye is then injected through the catheter and viewed on an X-ray. This contrast material does not permanently discolor any organs, but simply interacts with X-rays to produce a more precise diagnosis.[41]

Due to technological advances, clinicians have begun to use a less invasive approach called Multi-Detector Coronary Tomography (MDCT) angiography. Rather than inserting a large catheter into the artery, this technique requires a small injection of contrast dye using a standard intravenous catheter inserted into the arm, much like a regular injection. MDCT scanners then locate the contrast dye to show blockages within the arteries.[12] MDCT angiography is more sensitive in detecting blockage and subsequent diseases such as CAD compared to invasive X-ray angiography.[12]

Treatment

Treatment for arterial occlusion varies depending on the extent of blockage. In severe cases, surgical intervention is needed to remove the blockage from the affected artery. Currently, there are 3 types of surgical approaches, including surgical bypass, endarterectomy, and embolectomy. If surgery is not required, blood-thinning medication may be prescribed.

Surgical Bypass

A surgical bypass is a procedure performed to treat CAD. This procedure involves bypassing the blocked portion of the artery by replacing it with a healthy vessel from elsewhere in the body. The surgeon attaches one end of the new vessel right before the blockage, and the other end in the area after the affected portion.[13] This reestablishes proper blood flow toward the desired area.

Steps of performing an endarterectomy on the carotid artery, in which the accumulated atheroma is removed via surgery.

Endarterectomy

An endarterectomy is an intervention aiming to remove accumulated plaques directly from the affected artery.[14] This involves an incision on the side of the neck of the affected artery. The plaque is then exposed and removed accordingly, with the artery then stitched back together. With the plaque removed, blood can travel through the artery unimpeded.

Embolectomy

An embolectomy is a procedure conducted when a blockage moves from its original site to another place in the body, thus forming an embolus. There are two methods of performing embolectomy.[15] The first method is catheter embolectomy, which involves the insertion of a catheter into the affected artery and the subsequent removal of the embolus. This option is minimally invasive, and thus lowers risk and recovery time. The other option is a traditional surgical option, where the surgeon will expose the affected region, open the blood vessel and remove the embolus.

Blood-thinning Medication

Blood-thinning medications are beneficial short-term options in managing arterial occlusion. Anticoagulants such as warfarin and antiplatelets such as aspirin and clopidogrel reduce the risk of thrombosis by making blood flow easily through arteries.[11][21] Side effects include increased bleeding and heavier bruising.[16]

References

  1. ^ a b c d e f Widmaier EP, Raff H, Strang KT, Vander AJ (2014). Vander's human physiology : the mechanisms of body function (13th ed.). New York. ISBN 978-0-07-337830-5. OCLC 820450614.{{cite book}}: CS1 maint: location missing publisher (link)
  2. ^ Saladin KS, Sullivan SJ, Gan CA (2017). Human anatomy (Fifth ed.). New York, NY. ISBN 978-0-07-340370-0. OCLC 927438903.{{cite book}}: CS1 maint: location missing publisher (link)
  3. ^ a b c d e f g h i j k l m "Occlusive Peripheral Arterial Disease - Heart and Blood Vessel Disorders". MSD Manual Consumer Version. Retrieved 2022-03-24.
  4. ^ a b "Coronary heart disease". nhs.uk. 2018-10-03. Retrieved 2022-03-20.
  5. ^ a b c Zemaitis MR, Boll JM, Dreyer MA (2022). "Peripheral Arterial Disease". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID 28613496. Retrieved 2022-03-29.
  6. ^ a b c Vyas V, Goyal A (2022). "Acute Pulmonary Embolism". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID 32809386. Retrieved 2022-03-29.
  7. ^ a b "Myocardial Infarction—From Atherosclerosis to Thrombosis". www.ahajournals.org. doi:10.1161/atvbaha.119.312578. Retrieved 2022-03-29.
  8. ^ a b c Buttolph A, Sapra A (2022). "Gangrene". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID 32809387. Retrieved 2022-03-29.
  9. ^ a b c Seeley RR, Tate P, Stephens TD (2008). Anatomy & physiology (8th ed.). Dubuque, IA: McGraw-Hill. ISBN 978-0-07-296557-5. OCLC 77271214.
  10. ^ a b c DeSai C, Shapshak HA (2022). "Cerebral Ischemia". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID 32809345. Retrieved 2022-04-14.
  11. ^ a b c d e f Waller D, Sampson AP (2018). Medical pharmacology & therapeutics (5th ed.). Edinburgh. ISBN 978-0-7020-7193-5. OCLC 1003529751.{{cite book}}: CS1 maint: location missing publisher (link)
  12. ^ a b c Alfakih K, Budoff M (2010). "MDCT coronary angiography: does the benefit justify radiation burden?". The British Journal of Cardiology. 17: 207–208. Retrieved 2022-03-29.
  13. ^ a b "Coronary Artery Bypass Graft Surgery". www.hopkinsmedicine.org. Retrieved 2022-03-29.
  14. ^ a b "Carotid Endarterectomy". www.hopkinsmedicine.org. Retrieved 2022-03-29.
  15. ^ a b "Embolectomy - Brigham and Women's Hospital". www.brighamandwomens.org. Retrieved 2022-03-29.
  16. ^ a b "Warfarin: a blood-thinning medicine to treat and prevent blood clots". nhs.uk. 2018-12-20. Retrieved 2022-03-29.
  17. ^ a b c d Smith DA, Lilie CJ (2022). "Acute Arterial Occlusion". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID 28722881. Retrieved 2022-03-29.
  18. ^ McCarthy CJ, Behravesh S, Naidu SG, Oklu R (October 2016). "Air Embolism: Practical Tips for Prevention and Treatment". Journal of Clinical Medicine. 5 (11): 93. doi:10.3390/jcm5110093. PMC 5126790. PMID 27809224.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  19. ^ Metodiev Y, Ramasamy P, Tuffnell D (August 2018). "Amniotic fluid embolism". BJA Education. 18 (8): 234–238. doi:10.1016/j.bjae.2018.05.002. PMC 7808088. PMID 33456838.
  20. ^ a b Mackman N (February 2008). "Triggers, targets and treatments for thrombosis". Nature. 451 (7181): 914–918. doi:10.1038/nature06797. PMC 2848509. PMID 18288180.
  21. ^ a b c Hoffbrand AV, Moss PA, Pettit JE (2011). Essential haematology (6th ed.). Malden, Mass.: Wiley-Blackwell. ISBN 978-1-4051-9890-5. OCLC 642278764.
  22. ^ Oklu R (December 2017). "Thrombosis". Cardiovascular Diagnosis and Therapy. 7 (3): S131–S13S133. ISSN 2223-3660.
  23. ^ a b Fan J, Watanabe T (March 2022). "Atherosclerosis: Known and unknown". Pathology International. 72 (3): 151–160. doi:10.1111/pin.13202. PMID 35076127.
  24. ^ "Atherosclerosis". www.hopkinsmedicine.org. Retrieved 2022-03-29.
  25. ^ Woodcock EA, Matkovich SJ (September 2005). "Cardiomyocytes structure, function and associated pathologies". The International Journal of Biochemistry & Cell Biology. 37 (9): 1746–1751. doi:10.1016/j.biocel.2005.04.011. PMID 15950518.
  26. ^ Salehi N, Janjani P, Tadbiri H, Rozbahani M, Jalilian M (December 2021). "Effect of cigarette smoking on coronary arteries and pattern and severity of coronary artery disease: a review". The Journal of International Medical Research. 49 (12): 3000605211059893. doi:10.1177/03000605211059893. PMC 8647272. PMID 34855538.
  27. ^ Tuso P, Stoll SR, Li WW (2015). "A plant-based diet, atherogenesis, and coronary artery disease prevention". The Permanente Journal. 19 (1): 62–67. doi:10.7812/TPP/14-036. PMC 4315380. PMID 25431999.
  28. ^ Song P, Rudan D, Zhu Y, Fowkes FJ, Rahimi K, Fowkes FG, Rudan I (August 2019). "Global, regional, and national prevalence and risk factors for peripheral artery disease in 2015: an updated systematic review and analysis". The Lancet. Global Health. 7 (8): e1020–e1030. doi:10.1016/S2214-109X(19)30255-4. PMID 31303293.
  29. ^ "Prevention and Treatment of PAD". www.heart.org. Retrieved 2022-04-11.
  30. ^ Tapson VF (March 2008). "Acute pulmonary embolism". The New England Journal of Medicine. 358 (10): 1037–1052. doi:10.1056/NEJMra072753. PMID 18322285.
  31. ^ Heit JA, Spencer FA, White RH (January 2016). "The epidemiology of venous thromboembolism". Journal of Thrombosis and Thrombolysis. 41 (1): 3–14. doi:10.1007/s11239-015-1311-6. PMC 4715842. PMID 26780736.
  32. ^ Jung J, Bonde P (2018). "Surgical Management of Pulmonary Embolism". In Chaar CI (ed.). Current Management of Venous Diseases. Cham: Springer International Publishing. pp. 405–418. doi:10.1007/978-3-319-65226-9_31. ISBN 978-3-319-65226-9.
  33. ^ Ro A, Kageyama N, Mukai T (June 2017). "Pathophysiology of Venous Thromboembolism with Respect to the Anatomical Features of the Deep Veins of Lower Limbs: A Review". Annals of Vascular Diseases. 10 (2): 99–106. doi:10.7134/phlebol.17-14. PMID 29034034.
  34. ^ a b c d e f Vogel B, Claessen BE, Arnold SV, Chan D, Cohen DJ, Giannitsis E, et al. (June 2019). "ST-segment elevation myocardial infarction". Nature Reviews. Disease Primers. 5 (1): 39. doi:10.1038/s41572-019-0090-3. PMID 31171787.
  35. ^ de Bliek EC (March 2018). "ST elevation: Differential diagnosis and caveats. A comprehensive review to help distinguish ST elevation myocardial infarction from nonischemic etiologies of ST elevation". Turkish Journal of Emergency Medicine. 18 (1): 1–10. doi:10.1016/j.tjem.2018.01.008. PMC 6009807. PMID 29942875.
  36. ^ a b Wu AH (2017-09-01). "Release of cardiac troponin from healthy and damaged myocardium". Frontiers in Laboratory Medicine. 1 (3): 144–150. doi:10.1016/j.flm.2017.09.003. ISSN 2542-3649.
  37. ^ a b c Tuo QZ, Zhang ST, Lei P (January 2022). "Mechanisms of neuronal cell death in ischemic stroke and their therapeutic implications". Medicinal Research Reviews. 42 (1): 259–305. doi:10.1002/med.21817. PMID 33957000.
  38. ^ Guyton AC, Hall JE (2006). Textbook of medical physiology (11th ed.). Philadelphia: Elsevier Saunders. ISBN 0-7216-0240-1. OCLC 56661571.
  39. ^ "Duplex ultrasound". stanfordhealthcare.org. Retrieved 2022-03-29.
  40. ^ Radiology (ACR), Radiological Society of North America (RSNA) and American College of. "Catheter Angiography". Radiologyinfo.org. Retrieved 2022-03-29.
  41. ^ Radiology (ACR), Radiological Society of North America (RSNA) and American College of. "Contrast Materials". Radiologyinfo.org. Retrieved 2022-03-29.
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