Editing Cardiac arrest (section)

=== Cardiac causes ===

==== Coronary artery disease ====
[[File:Coronary Artery Disease.png|thumb|Normal vs blocked coronary artery]]
[[Coronary artery disease]] (CAD), also known as atherosclerotic cardiovascular disease, involves the deposition of cholesterol and subsequent inflammation-driven formation of [[Atherosclerosis|atherosclerotic plaques]] in the arteries. CAD involves the accumulation and remodeling of the [[Coronary circulation|coronary vessels]] along with other systemic blood vessels.<ref>{{cite book |title=StatPearls |vauthors=Pahwa R, Jialal I |date=2021 |publisher=StatPearls Publishing |place=Treasure Island (FL) |chapter=Atherosclerosis |pmid=29939576 |access-date=2021-11-05 |chapter-url=http://www.ncbi.nlm.nih.gov/books/NBK507799/}}</ref> When an atherosclerotic plaque dislodges, it can block the flow of blood and oxygen through small arteries, such as the coronary arteries, resulting in [[Ischemia|ischemic]] injury. In the heart, this results in myocardial tissue damage which can lead to structural and functional changes that disrupt normal conduction patterns and alter heart rate and contraction.<ref name="Saunders-2015" />

CAD underlies 68 percent of sudden cardiac deaths in the United States.<ref name="Zheng-2001">{{cite journal |vauthors=Zheng ZJ, Croft JB, Giles WH, Mensah GA |date=October 2001 |title=Sudden cardiac death in the United States, 1989 to 1998 |journal=Circulation |volume=104 |issue=18 |pages=2158–2163 |doi=10.1161/hc4301.098254 |pmid=11684624 |doi-access=free}}</ref> Indeed, postmortem examinations have shown that the most common finding in cases of sudden cardiac death is chronic, high-grade [[stenosis]] of at least one segment of a major [[Coronary arteries|coronary artery]].<ref>{{cite book | vauthors = Falk E, Shah PK | chapter = Pathogenesis of atherothrombosis. Role of vulnerable, ruptured, and eroded plaques | chapter-url= https://books.google.com/books?id=1WifwPEsKQMC&pg=PA460 |title=Atherothrombosis and Coronary Artery Disease | veditors = Fuster V, Topol EJ, Nabel EG |date=2005|publisher=Lippincott Williams & Wilkins|isbn=9780781735834|language=en|archive-url=https://web.archive.org/web/20160603002043/https://books.google.com/books?id=1WifwPEsKQMC&pg=PA460&lpg=PA460|archive-date=2016-06-03|url-status=live}}</ref>

While CAD is a leading contributing factor, this is an age-dependent factor, with CAD being a less common cause of sudden cardiac death in people under the age of 40.<ref name="CDC-2002">{{cite journal |author1=Centers for Disease Control Prevention (CDC) |date=February 2002 |title=State-specific mortality from sudden cardiac death--United States, 1999 |journal=MMWR. Morbidity and Mortality Weekly Report |volume=51 |issue=6 |pages=123–126 |pmid=11898927}}</ref>

==== Non-atherosclerotic coronary artery abnormalities ====

Abnormalities of the coronary arteries not related to atherosclerosis include inflammation (known as coronary [[arteritis]]), [[embolism]], [[vasospasm]], mechanical abnormalities related to connective tissue diseases or trauma, and congenital [[Coronary artery anomaly|coronary artery anomalies]] (most commonly anomalous origin of the left coronary artery from the pulmonary artery). These conditions account for 10-15% of cardiac arrest and sudden cardiac death.<ref name="Saunders-2015" />
* Coronary arteritis commonly results from a pediatric febrile inflammatory condition known as [[Kawasaki disease]]. Other types of [[vasculitis]] can also contribute to an increased risk of sudden cardiac death.
* Embolism, or clotting, of the coronary arteries most commonly occurs from septic emboli secondary to endocarditis with involvement of the aortic valve, tricuspid valve, or prosthetic valves.
* [[Coronary vasospasm]] may result in cardiac arrhythmias, altering the heart's electrical conduction with a risk of complete cardiac arrest from severe or prolonged rhythm changes.
* Mechanical abnormalities with an associated risk of cardiac arrest may arise from coronary artery dissection, which can be attributed to [[Marfan syndrome]] or trauma.<ref name="Saunders-2015" />

====Structural heart disease====
[[File:Heart left ventricular hypertrophy sa.jpg|thumb|Short axis view of the heart demonstrating wall thickening in left ventricular hypertrophy]]
Examples of structural heart diseases include: [[cardiomyopathy|cardiomyopathies]] ([[hypertrophic cardiomyopathy|hypertrophic]], [[dilated cardiomyopathy|dilated]], or [[Arrhythmogenic cardiomyopathy|arrhythmogenic]]), [[Cardiac arrhythmia|cardiac rhythm disturbances]], [[myocarditis]], and [[congestive heart failure]].<ref name="Kannel-1998">{{cite journal | vauthors = Kannel WB, Wilson PW, D'Agostino RB, Cobb J | title = Sudden coronary death in women | journal = American Heart Journal | volume = 136 | issue = 2 | pages = 205–212 | date = August 1998 | pmid = 9704680 | doi = 10.1053/hj.1998.v136.90226 }}</ref>
[[File:Left Ventricular Hypertrophy Unlabeled.jpg|thumb|EKG depiction of left ventricular hypertrophy]]
[[Left ventricular hypertrophy]] is a leading cause of sudden cardiac deaths in the adult population.<ref>{{cite journal | vauthors = Stevens SM, Reinier K, Chugh SS | title = Increased left ventricular mass as a predictor of sudden cardiac death: is it time to put it to the test? | journal = Circulation: Arrhythmia and Electrophysiology | volume = 6 | issue = 1 | pages = 212–217 | date = February 2013 | pmid = 23424223 | pmc = 3596001 | doi = 10.1161/CIRCEP.112.974931 }}</ref><ref name="Walls-2017" /> This is most commonly the result of longstanding [[Hypertension|high blood pressure]], or hypertension, which has led to maladaptive overgrowth of muscular tissue of the [[Ventricle (heart)|left ventricle]], the heart's main pumping chamber.<ref name="Katholi-2011">{{cite journal | vauthors = Katholi RE, Couri DM | title = Left ventricular hypertrophy: major risk factor in patients with hypertension: update and practical clinical applications | journal = International Journal of Hypertension | volume = 2011 | pages = 495349 | year = 2011 | pmid = 21755036 | pmc = 3132610 | doi = 10.4061/2011/495349 | doi-access = free }}</ref> This is because elevated blood pressure over the course of several years requires the heart to adapt to the requirement of pumping harder to adequately circulate blood throughout the body. If the heart does this for a prolonged period of time, the left ventricle can experience hypertrophy (grow larger) in a way that decreases the heart's effectiveness.<ref>{{cite book | vauthors = Bornstein AB, Rao SS, Marwaha K | chapter = Left Ventricular Hypertrophy |date=2021| chapter-url= http://www.ncbi.nlm.nih.gov/books/NBK557534/ | title = StatPearls|place=Treasure Island (FL) |publisher= StatPearls Publishing|pmid=32491466|access-date=2021-11-05 }}</ref> Left ventricular hypertrophy can be demonstrated on an [[Echocardiography|echocardiogram]] and [[Electrocardiography|electrocardiogram]] (EKG).<ref name="Katholi-2011" />

Abnormalities of the cardiac conduction system (notably the [[atrioventricular node]] and [[Purkinje fibers|His-Purkinje]] system) may predispose an individual to arrhythmias with a risk of progressing to sudden cardiac arrest, albeit this risk remains low. Many of these conduction blocks can be treated with internal cardiac defibrillators for those determined to be at high risk due to severity of fibrosis or severe electrophysiologic disturbances.<ref name="Saunders-2015" />

Structural heart diseases unrelated to coronary artery disease account for 10% of all sudden cardiac deaths.<ref name="Podrid-2016" /><ref name="Zheng-2001" /> A 1999 review of sudden cardiac deaths in the United States found that structural heart diseases accounted for over 30% of sudden cardiac arrests for those under 30 years.<ref name="CDC-2002" /><ref name="Zheng-2001" />

==== Inherited arrhythmia syndromes ====
Arrhythmias not due to structural heart disease account for 5 to 10% of sudden cardiac arrests.<ref>{{cite journal | vauthors = Chugh SS, Kelly KL, Titus JL | title = Sudden cardiac death with apparently normal heart | journal = Circulation | volume = 102 | issue = 6 | pages = 649–654 | date = August 2000 | pmid = 10931805 | doi = 10.1161/01.cir.102.6.649 | doi-access = free }}</ref><ref>{{cite journal | vauthors =  | title = Survivors of out-of-hospital cardiac arrest with apparently normal heart. Need for definition and standardized clinical evaluation. Consensus Statement of the Joint Steering Committees of the Unexplained Cardiac Arrest Registry of Europe and of the Idiopathic Ventricular Fibrillation Registry of the United States | journal = Circulation | volume = 95 | issue = 1 | pages = 265–272 | date = January 1997 | pmid = 8994445 | doi = 10.1161/01.cir.95.1.265 }}</ref><ref name="Drory-1991">{{cite journal | vauthors = Drory Y, Turetz Y, Hiss Y, Lev B, Fisman EZ, Pines A, Kramer MR | title = Sudden unexpected death in persons less than 40 years of age | journal = The American Journal of Cardiology | volume = 68 | issue = 13 | pages = 1388–1392 | date = November 1991 | pmid = 1951130 | doi = 10.1016/0002-9149(91)90251-f }}</ref> These are frequently caused by [[genetic disorder]]s.<ref name="Walls-2017" /> The genetic [[mutation]]s often affect specialized proteins known as [[ion channel]]s that conduct [[Ion|electrically charged particles]] across the [[cell membrane]], and this group of conditions is therefore often referred to as [[Channelopathy|channelopathies]]. Examples of these inherited arrhythmia syndromes include [[long QT syndrome]] (LQTS), [[Brugada syndrome]] (BrS), [[catecholaminergic polymorphic ventricular tachycardia]] (CPVT), and [[short QT syndrome]] (SQTS). Many are also associated with environmental or neurogenic triggers such as response to loud sounds that can initiate lethal arrhythmias.<ref name="Saunders-2015" />

LQTS, a condition often mentioned in young people's deaths, occurs in one of every 5000 to 7000 newborns and is estimated to be responsible for 3000 deaths annually compared to the approximately 300,000 cardiac arrests seen by emergency services.<ref name="American Heart Association">{{cite web | url = http://www.americanheart.org/presenter.jhtml?identifier=4741 | title = Sudden Cardiac Death | archive-url = https://web.archive.org/web/20100325174959/http://www.americanheart.org/presenter.jhtml?identifier=4741| archive-date=2010-03-25 | publisher = American Heart Association }}</ref> These conditions are a fraction of the overall deaths related to cardiac arrest but represent conditions that may be detected prior to arrest and may be treatable. The symptomatic expression of LQTS is quite broad and more often presents with [[Syncope (medicine)|syncope]] rather than cardiac arrest. The risk of cardiac arrest is still present, and people with family histories of sudden cardiac arrests should be screened for LQTS and other treatable causes of lethal arrhythmia. Higher levels of risk for cardiac arrest are associated with female sex, more significant QT prolongation, history of unexplained syncope (fainting spells), or premature sudden cardiac death.<ref name="Saunders-2015" /> Additionally, individuals with LQTS should avoid certain medications that carry the risk of increasing the severity of this conduction abnormality, such as certain anti-arrhythmics, anti-depressants, and [[Quinolone antibiotic|quinolone]] or [[macrolide]] antibiotics.<ref>{{cite journal | vauthors = Fazio G, Vernuccio F, Grutta G, Re GL | title = Drugs to be avoided in patients with long QT syndrome: Focus on the anaesthesiological management | journal = World Journal of Cardiology | volume = 5 | issue = 4 | pages = 87–93 | date = April 2013 | pmid = 23675554 | pmc = 3653016 | doi = 10.4330/wjc.v5.i4.87 | doi-access = free }}</ref>

Although it is not recognized as an inherited condition, [[Wolff–Parkinson–White syndrome]] in which an accessory conduction pathway bypassing the atrioventricular node is present and can cause abnormal conduction patterns leading to supraventricular tachycardia, pre-excited atrial fibrillation, and cardiac arrest.<ref name="Podrid-2016" />  [[Ebstein's anomaly]] has an increased risk of accessory pathways as well.