Editing Angina (section)

===Unstable angina===
{{main|Unstable angina}}
{{See also|Variant angina}}

[[Unstable angina]] (UA) (also "''crescendo angina''"; this is a form of [[acute coronary syndrome]]) is defined as angina pectoris that changes or worsens or begins suddenly at rest.<ref name="urlMerckMedicus : Dorlands Medical Dictionary">{{cite web |url=http://merckmedicus.com/pp/us/hcp/thcp_dorlands_content_split.jsp?pg=/ppdocs/us/common/dorlands/drlnd/one_04/000004949.htm#000004949 |title=MerckMedicus: Dorland's Medical Dictionary |access-date=2009-01-09}}</ref> Unstable angina is a medical emergency and requires urgent medical treatment from a doctor.<ref name=":0" />

It has at least one of these three features:<ref>{{Cite web |title=Unstable Angina |url=https://www.heart.org/en/health-topics/heart-attack/angina-chest-pain/unstable-angina |access-date=2023-10-23 |website=www.heart.org |language=en}}</ref>
# it occurs at rest (or with minimal exertion), usually lasting more than 10 minutes
# it is severe and of new-onset (i.e., within the prior 4–6 weeks)
# it occurs with a [[wikt:crescendo|crescendo]] pattern (i.e., distinctly more severe, prolonged, or frequent than before).

UA may occur often unpredictably and even at rest, which may be a serious indicator of an impending heart attack. The primary factor differentiating unstable angina from stable angina (other than symptoms) is the underlying [[pathophysiology]] of the [[atherosclerosis]]. The pathophysiology of unstable angina is the reduction of coronary blood flow due to transient [[platelet aggregation]] on apparently normal [[endothelium]], coronary artery spasms, or [[coronary thrombosis]].<ref>{{cite journal | vauthors = Hombach V, Höher M, Kochs M, Eggeling T, Schmidt A, Höpp HW, Hilger HH | title = Pathophysiology of unstable angina pectoris--correlations with coronary angioscopic imaging | journal = European Heart Journal | volume = 9 Suppl N | pages = 40–5 | date = December 1988 | pmid = 3246255 | doi = 10.1093/eurheartj/9.suppl_N.40 }}</ref><ref name="Simons2000">{{cite web| vauthors = Simons M |title=Pathophysiology of unstable angina |date=March 8, 2000 |url=http://cmbi.bjmu.edu.cn/uptodate/coronary%20heart%20disease/Pathophysiology/Pathophysiology%20of%20unstable%20angina.htm |access-date=April 28, 2010 |url-status = dead|archive-url=https://web.archive.org/web/20100330044046/http://cmbi.bjmu.edu.cn/uptodate/coronary%20heart%20disease/Pathophysiology/Pathophysiology%20of%20unstable%20angina.htm |archive-date=March 30, 2010 }}</ref>

The process starts with atherosclerosis, progresses through inflammation to yield an active unstable plaque, which undergoes thrombosis and results in acute myocardial ischemia, which, if not reversed, results in cell necrosis (infarction).<ref name="Simons2000" /> Studies show that 64% of all unstable anginas occur between 22:00 and 08:00 when patients are at rest.<ref name="Simons2000" /><ref name="nhlbi">{{cite web |publisher=National Heart Lung and Blood Institute |title=What Is Angina? |access-date=April 28, 2010 |url=http://www.nhlbi.nih.gov/health/dci/Diseases/Angina/Angina_SignsAndSymptoms.html}}</ref>

In stable angina, the developing [[atheroma]] (a fatty plaque) is protected with a [[fibrous cap]]. This cap may rupture in unstable angina, allowing [[blood clots]] to precipitate and further decrease the area of the coronary vessel's [[Lumen (anatomy)|lumen]]  or the interior open space within an artery. This explains why, in many cases, unstable angina develops independently of activity.<ref name="Simons2000" />