Acute coronary syndrome

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In medicine and cardiology, acute coronary syndrome (ACS) is a collection of signs and symptoms due to inadequate oxygenation of the heart muscle, the myocardium.[1] In common usage, ACS includes myocardial infarction ("heart attack") and angina.

Pain relief and proper oxygenation is the core of ACS treatment. When the root causie is angina, the temporary cause of ischemia should be reversed. For myocardial infarction, more vigorous interventions are appropriate if they can prevent damage to myocardium.

Etiology/causes

Atheroclerotic obstruction

ACS is usually caused by obstruction in an epicardial coronary artery.[2] The obstruction may be due to a thrombus at the site of a ruptured atherosclerotic plaque.[3]

Rupture seems more likely to occur during the morning hours.[4] Rupture may be precipited by inflammation from non-cardiac infections.[5] Rupture may be triggered by vigorous exercise among individuals who do not ordinarily do vigorous exercise.[6]

Coronary vasospasm

Approximately 15% of NSTEMI and 2% of STEMI patients have no obstruction of coronary vessels and in about half of these patients, spasm can be induced of a coronary artery.[2]

Emotional stress

The role of emotional stress was supported in a study of the incidence of coronary events in the Munich area during the 2006 FIFA World Cup Football (soccer) championship.[7] The incidence of coronary events was higher during the match, especially for people who had pre-existing coronary disease. Similar findings have been reported in Los Angeles, California during the American Super Bowl.[8] Stress, via increases in unhealthy behaviors, was also identified as more important than hypertension or C-reactive protein level in predicting coronary events.[9]

Stress-induced (takotsubo) cardiomyopathy

Stress-induced (takotsubo) cardiomyopathy may occur during acute medical illness or after intense emotional or physical stress.[10] It may be caused by catecholamines.

Classification

Classification of acute coronary syndrome[11]
  Electrocardiogram Serum biomarkers Typical appearance of culprit vessel at angioscopy[3]
Unstable angina "ST-segment depression or prominent T-wave inversion"[11] Normal Nonocclusive grayish-white thrombus
(platelet-rich)
Non-ST segment elevation myocardial infarction
(NSTEMI)
"ST-segment depression or prominent T-wave inversion"[11] Elevated Primary NSTEMI: Nonocclusive grayish-white thrombus
(platelet-rich)

Secondary NSTEMI: no thrombus

ST segment elevation myocardial infarction
(STEMI)
ST-segment elevation Elevated Occlusive reddish thrombus
(fibrin-rich)
Q-wave myocardial infarction Q-waves Elevated Occlusive reddish thrombus
(fibrin-rich)

Unstable angina

Unstable angina is defined as "precordial pain at rest, which may precede a myocardial infarction".[12]

Myocardial infarction

For more information, see: Myocardial infarction.

A myocardial infarction is defined as "gross necrosis of the myocardium, as a result of interruption of the blood supply to the area".[13] It is usually caused by occlusion of an epicardial coronary artery.[14]

Non-ST segment elevation myocardial infarction (NSTEMI)

NSTEMI is usually caused by a grayish-white thrombus that is platelet-rich.[3]

ST segment elevation myocardial infarction (STEMI)

STEMI is usually caused by a reddish thrombus that is fibrin-rich.[3]

Diagnosis

History and physical examination

A helpful finding is exact reproduction of chest pain upon palpating the chest.[15] In a patient whose other findings also suggest a non-cardiac course of their chest pain, this finding can help rule out coronary disease.[16]

Electrocardiogram

The electrocardiogram is a key part of decision making. For example, the presence of ST changes and Q-waves determines therapy.

A normal electrocardiogram has been reported not to exclude acute coronary syndrome, even when the electrocardiogram is taken during pain.[17] Although this study used defined unstable angina as either a coronary stenosis or positive stress test and so likely includes patients without true acute coronary syndrome as defined by the American Heart Association[11], the study was still not able to show that a normal electrocardiogram helped exclude a NSTEMI.

Isolated abnormalities of T-waves also confers worse prognosis.[18]

Laboratory tests

Clinical practice guidelines jointly written by multiple expert groups anchor the diagnosis on troponin blood assays obtained within 6 hours and again within 8-12 hours of a patient arriving for medical care.[11][19]

In NSTEMI, typical troponin I levels are less than 9 ng/ml with the median values 1.0 to 2.0 nl/ml.[20]

Clinical prediction rules

The Thrombolysis in Myocardial Infarction risk score for unstable angina or non-ST elevation myocardial infarction is a clinical prediction rule that may detect patients with chest pain who are at increased risk of acute coronary syndrome[21][22]

A second clinical prediction rule, the Acute Cardiac Ischemia Time-Insensitive Predictive Instrument (ACI-TIPI) can help diagnose patients with chest pain and has been shown to improve medical care in a randomized controlled trial.[23][24] The ACI-TIPI was studied up through 1993 before troponin assays were widely available and thus does not incorporate the troponin. However, the ACI-TIPI should retain its ability to use the medical history and the EKG to decide who should be observed for serial troponin levels. It is unclear why this role is not recognized by the ACC/AHA guidelines. One reason may be that the ACI-TIPI is patented.[25][26]

A third clinical prediction rule, also prior to availability of troponin tests, was created by Pozen.[27] The rule is available online through the New England Journal of Medicine website.

Treatment

Clinical practice guidelines address the treatment of unstable angina and non-ST-elevation myocardial infarction.[11][19]

In the absence of specific contraindications, aspirin may be of benefit, both in the prehospital and emergency department settings, for all forms of ACS. [28]

Patients without contraindication should receive anticoagulation with unfractionated heparin.[29] The risk of bleeding can be estimated with a clinical prediction rule (http://www.crusadebleedingscore.org/).

Unstable angina or NSTEMI

Adrenergic beta-antagonists

Adrenergic beta-antagonists (beta-blockers) are effective according to a systematic review[30]

Platelet ADP receptor blockers

Thienopyridine ADP blockers such as clopidogrel, ticlopidine, and the prodrug prasugrel may help especially for patients undergoing percutaneous coronary intervention (PCI). Ticagrelor may be better than clopidogrel for some patients.[31][32]

Glycoprotein IIb/IIIa inhibitors

Glycoprotein IIb/IIIa inhibitors such as eptifibatide should not be given until after percutaneous transluminal coronary angioplasty.[33]

Percutaneous transluminal coronary angioplasty

Among patients with unstable angina or NSTEMI and without ST-segment elevation (but may have other EKG evidence of ischemia such as ST-segment depression of ≥1 mm or transient ST-segment elevation or T-wave inversion of >3 mm) may benefit from early invasive management (percutaneous transluminal coronary angioplasty) if:

Urgent coronary catheterization may occur anytime within the first 24 hours.[37]

Myocardial infarction

For more information, see: Myocardial infarction.


Prognosis

Three clinical prediction rules can help prognosticate with similar ability:[38]

These rules can help estimate prognosis and guide decisions.

References

  1. Anonymous (2024), Acute coronary syndrome (English). Medical Subject Headings. U.S. National Library of Medicine.
  2. 2.0 2.1 Ong P, Athanasiadis A, Hill S, Vogelsberg H, Voehringer M, Sechtem U (August 2008). "Coronary artery spasm as a frequent cause of acute coronary syndrome: The CASPAR (Coronary Artery Spasm in Patients With Acute Coronary Syndrome) Study". J. Am. Coll. Cardiol. 52 (7): 523–7. DOI:10.1016/j.jacc.2008.04.050. PMID 18687244. Research Blogging.
  3. 3.0 3.1 3.2 3.3 Mizuno K, Satomura K, Miyamoto A, et al (January 1992). "Angioscopic evaluation of coronary-artery thrombi in acute coronary syndromes". N. Engl. J. Med. 326 (5): 287–91. PMID 1728732[e]
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  13. National Library of Medicine. Myocardial infarction. Retrieved on 2007-10-28.
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