Acute coronary syndrome

From Wikipedia, the free encyclopedia

Acute coronary syndrome

Blockage of a coronary artery

Classification and external resources

ICD-10

I24.9

eMedicine

emerg/31

Patient UK

Acute coronary syndrome

MeSH

D054058

Acute coronary syndrome (ACS) refers to a group of conditions due to decreased blood flow in
the coronary arteries such that part of the heart muscle is unable to function properly or dies. [1] The
most common symptom is chest pain, often radiating to the left arm or angle of the jaw, pressure-like
in character, and associated with nausea and sweating. Acute coronary syndrome usually occurs as
a result of one of three problems: ST elevation myocardial infarction (30%), non ST elevation
myocardial infarction (25%), or unstable angina (38%).[2]
These types are named according to the appearance of the electrocardiogram (ECG/EKG) as nonST segment elevation myocardial infarction (NSTEMI) and ST segment elevation myocardial
infarction (STEMI).[3] There can be some variation as to which forms of myocardial infarction (MI) are
classified under acute coronary syndrome.[4]
ACS should be distinguished from stable angina, which develops during exertion and resolves at
rest. In contrast with stable angina, unstable angina occurs suddenly, often at rest or with minimal

exertion, or at lesser degrees of exertion than the individual's previous angina ("crescendo angina").
New onset angina is also considered unstable angina, since it suggests a new problem in a coronary
artery.
Though ACS is usually associated with coronary thrombosis, it can also be associated
with cocaine use.[5] Cardiac chest pain can also be precipitated by anemia,bradycardias (excessively
slow heart rate) or tachycardias (excessively fast heart rate).
Contents
[hide]

1 Signs and symptoms

2 Diagnosis
o

2.1 Electrocardiogram

2.2 Imaging and blood tests

2.3 Prediction scores

3 Prevention

4 Treatment
o

4.1 STEMI

4.2 NSTEMI and NSTE-ACS

5 Prognosis
o

5.1 TIMI score

5.2 Biomarkers for diagnosis

5.3 Biomarkers for Risk Stratification

6 See also

7 References

8 External links

Signs and symptoms[edit]

The cardinal symptom of decreased blood flow to the heart is chest pain, experienced as tightness
around the chest and radiating to the left arm and the left angle of the jaw. This may be associated

with diaphoresis(sweating), nausea and vomiting, as well as shortness of breath. In many cases, the
sensation is "atypical", with pain experienced in different ways or even being completely absent
(which is more likely in female patients and those with diabetes). Some may report palpitations,
anxiety or a sense of impending doom (angor animi) and a feeling of being acutely ill.
The description of the chest discomfort as a pressure has little utility in aiding a diagnosis as it is
not specific for ACS.[6]

Diagnosis[edit]

Classification of acute coronary syndromes.[7]

Electrocardiogram[edit]
In the setting of acute chest pain, the electrocardiogram is the investigation that most reliably
distinguishes between various causes.[8] If this indicates acute heart damage (elevation in the ST
segment, new left bundle branch block), treatment for a heart attack in the form
of angioplasty or thrombolysis is indicated immediately (see below). In the absence of such changes,
it is not possible to immediately distinguish between unstable angina and NSTEMI.

Imaging and blood tests[edit]

As it is only one of the many potential causes of chest pain, the patient usually has a number of tests
in the emergency department, such as a chest X-ray, blood tests (including myocardial markers such
as troponin I or T, and H-FABP and/or a D-dimer if a pulmonary embolism is suspected), and
telemetry (monitoring of the heart rhythm).

Prediction scores[edit]
The ACI-TIPI score can be used to aid diagnosis; using seven variables from the admission record,
this score predicts crudely which patients are likely to have myocardial ischemia. [9] For example

according to a randomized controlled trial, males having chest pain with normal or non
diagnostic ECG are at higher risk for having acute coronary syndrome than women. [10] In this study,
the sensitivity was 65.2% and specificity was 44%. This particular study had an 8.4% prevalence of
acute coronary syndrome, which means the positive predictive value of being a male with chest pain
and having coronary syndrome is 9.6% and negative predictive value is 93.2% ( click here to adjust
these results for patients at higher or lower risk of acute coronary syndrome).
In a second cohort study, exercise electrocardiography was similarly found to be a poor predictor of
acute coronary syndrome at follow-up.[11] Of the patients who had a coronary event at 6 years of
follow up, 47% had a negative ECG at the start of the study. With an average follow up of 2.21 years
the receiver operating characteristic curves gave resting ECG a score of 0.72 and exercise ECG a
score of 0.74.
There are not only prediction scores for diagnosis of ACS, but also prognosis. Most notably, the
GRACE ACS Risk and Mortality score helps diagnose, and based upon that score predicts mortality
rate of a given patient. It takes into account both clinical (blood pressure, heart rate, EKG findings)
and medical history in its scoring system.[12]

Prevention[edit]
Acute coronary syndrome often reflects a degree of damage to the coronaries by atherosclerosis.
Primary prevention of atherosclerosis is controlling the risk factors: healthy eating, exercise,
treatment forhypertension and diabetes, avoiding smoking and controlling cholesterol levels; in
patients with significant risk factors, aspirin has been shown to reduce the risk of cardiovascular
events. Secondary prevention is discussed in myocardial infarction.
After a ban on smoking in all enclosed public places was introduced in Scotland in March 2006,
there was a 17% reduction in hospital admissions for acute coronary syndrome. 67% of the
decrease occurred in non-smokers.[13]

Treatment[edit]
Main article: Management of acute coronary syndrome
People with presumed ACS are typically treated with aspirin, clopidogrel or ticagrelor, nitroglycerin,
and if the chest discomfort persists morphine.[14] Other analgesics such as nitrous oxide are of
unknown benefit.[14]Angiography is recommended in those who have either new ST elevation or a
new left bundle branch block on their ECG.[1]

STEMI[edit]
If the ECG confirms changes suggestive of myocardial infarction (ST elevations in specific leads, a
new left bundle branch block or a true posterior MI pattern), thrombolytics may be administered
or primary coronary angioplasty may be performed. In the former, medication is injected that

stimulates fibrinolysis, destroying blood clots obstructing the coronary arteries. In the latter, a flexible
catheter is passed via the femoral or radial arteries and advanced to the heart to identify blockages
in the coronaries. When occlusions are found, they can be intervened upon mechanically
with angioplasty and usually stent deployment if a lesion, termed the culprit lesion, is thought to be
causing myocardial damage. Data suggest that rapid triage, transfer and treatment is essential.
[15]

The time frame for door-to-needle thrombolytic administration according toAmerican College of

Cardiology (ACC) guidelines should be within 30 minutes, whereas the door-to-balloon

Percutaneous Coronary Intervention (PCI) time should be less than 90 minutes. It was found
thatthrombolysis is more likely to be delivered within the established ACC guidelines among patients
with STEMI as compared to PCI according to a case control study .[16]

NSTEMI and NSTE-ACS[edit]

If the ECG does not show typical changes, the term "non-ST segment elevation ACS" is applied. The
patient may still have suffered a "non-ST elevation MI" (NSTEMI). The accepted management of
unstable angina and acute coronary syndrome is therefore empirical treatment with aspirin, a
second platelet inhibitor such as clopidogrel, prasugrel or ticagrelor, and heparin (usually a lowmolecular weight heparin such asenoxaparin), with intravenous glyceryl trinitrate and opioids if the
pain persists.
A blood test is generally performed for cardiac troponins twelve hours after onset of the pain. If this is
positive, coronary angiography is typically performed on an urgent basis, as this is highly predictive
of a heart attack in the near-future. If the troponin is negative, a treadmill exercise test or a thallium
scintigram may be requested.
If there is no evidence of ST segment elevation on the electrocardiogram, delaying
urgent angioplasty until the next morning is not inferior to doing so immediately.[17] Using statins in the
first 14 days after ACS reduces the risk of further ACS.[18]
In a cohort study comparing NSTEMI and STEMI, patients with NSTEMI had statistically
similar mortality at one year after PCI as compared to patients with STEMI (3.4% vs 4.4%).
[19]

However, NSTEMI had significantly more "major cardiac events" (death, myocardial infarction,

disabling stroke, or requiring revascularization) at one year (24.0% vs 16.6%).

Cocaine associated ACS should be managed in a manner similar to other patients with acute
coronary syndrome except beta blockers should not be used and benzodiazepines should be
administered early.[20]

Prognosis[edit]
TIMI score[edit]
The TIMI risk score can identify high risk patients[21] and has been independently validated.[22][23]

Biomarkers for diagnosis[edit]

The aim of diagnostic markers is to identify patients with ACS even when there is no evidence of
heart muscle damage.

Ischemia-Modified Albumin (IMA) - In cases of Ischemia - Albumin undergoes a

conformational change and loses its ability to bind transitional metals (copper or cobalt). IMA can
be used to assess the proportion of modified albumin in ischemia. Its use is limited to ruling out
ischemia rather than a diagnostic test for the occurrence of ischemia.

Myeloperoxidase (MPO) - The levels of circulating MPO, a leukocyte enzyme, elevate early
after ACS and can be used as an early marker for the condition.

Glycogen Phosphorylase Isoenzyme BB-(GPBB) is an early marker of cardiac ischemia and

is one of three isoenzyme of Glycogen Phosphorylase.

Troponin is a late cardiac marker of ACS

Biomarkers for Risk Stratification[edit]

The aim of prognostic markers is to reflect different components of pathophysiology of ACS. For
example:

Natriuretic peptide - Both B-type natriuretic peptide (BNP) and N-terminal Pro BNP can be
applied to predict the risk of death and heart failure following ACS.

Monocyte chemo attractive protein (MCP)-1 - has been shown in a number of studies to
identify patients with a higher risk of adverse outcomes after ACS.

See also[edit]

Copeptin

Troponin

Myocardial infarction

References[edit]
1.

^ Jump up to:a b Amsterdam, E. A.; Wenger, N. K.; Brindis, R. G.; Casey, D. E.; Ganiats, T. G.;
Holmes, D. R.; Jaffe, A. S.; Jneid, H.; Kelly, R. F.; Kontos, M. C.; Levine, G. N.; Liebson, P. R.;
Mukherjee, D.; Peterson, E. D.; Sabatine, M. S.; Smalling, R. W.; Zieman, S. J. (23 September 2014).
"2014 AHA/ACC Guideline for the Management of Patients With Non-ST-Elevation Acute Coronary
Syndromes: A Report of the American College of Cardiology/American Heart Association Task Force
on Practice Guidelines". Circulation 130 (25): e344
e426.doi:10.1161/CIR.0000000000000134. PMID 25249585.

2.

Jump up^ Torres M, Moayedi S (May 2007). "Evaluation of the acutely dyspneic elderly
patient". Clin. Geriatr. Med. 23(2): 30725, vi. doi:10.1016/j.cger.2007.01.007. PMID 17462519.

3.

Jump up^ Grech ED, Ramsdale DR (June 2003). "Acute coronary syndrome: unstable
angina and non-ST segment elevation myocardial infarction". BMJ 326 (7401): 1259
61. doi:10.1136/bmj.326.7401.1259.PMC 1126130. PMID 12791748.

4.

Jump up^ "Dorlands Medical Dictionary:acute coronary syndrome".

5.

Jump up^ Achar SA, Kundu S, Norcross WA (2005). "Diagnosis of acute coronary
syndrome". Am Fam Physician 72(1): 11926. PMID 16035692.

6.

Jump up^ Woo KM, Schneider JI (November 2009). "High-risk chief complaints I: chest pain-the big three". Emerg. Med. Clin. North Am. 27 (4): 685712,
x. doi:10.1016/j.emc.2009.07.007. PMID 19932401.

7.

Jump up^ Alpert JS, Thygesen K, Antman E, Bassand JP. (2000). "Myocardial infarction
redefined--a consensus document of The Joint European Society of Cardiology/American College of
Cardiology Committee for the redefinition of myocardial infarction". J Am Coll Cardiol 36 (3): 959
69. doi:10.1016/S0735-1097(00)00804-4.PMID 10987628.

8.

Jump up^ Chun AA, McGee SR (2004). "Bedside diagnosis of coronary artery disease: a
systematic review". Am. J. Med.117 (5): 33443. doi:10.1016/j.amjmed.2004.03.021. PMID 15336583.

9.

Jump up^ Selker HP, Griffith JL, D'Agostino RB (1991). "A tool for judging coronary care unit
admission appropriateness, valid for both real-time and retrospective use. A time-insensitive predictive
instrument (TIPI) for acute cardiac ischemia: a multicenter study". Medical care 29 (7): 610
27. doi:10.1097/00005650-199107000-00002.PMID 2072767.

10.

Jump up^ Goodacre, S; Pett, P; Arnold, J; Chawla, A; Hollingsworth, J; Roe, D; Crowder, S;

Mann, C; Pitcher, D; Brett, C (2009). "Clinical diagnosis of acute coronary syndrome in patients with
chest pain and a normal or non-diagnostic electrocardiogram.". Emergency medicine journal :
EMJ 26 (12): 86670.doi:10.1136/emj.2008.064428. PMID 19934131.

11.

Jump up^ Sekhri, N; Feder, GS; Junghans, C; Eldridge, S; Umaipalan, A; Madhu, R;

Hemingway, H; Timmis, AD (2008). "Incremental prognostic value of the exercise electrocardiogram in
the initial assessment of patients with suspected angina: cohort study.". BMJ(Clinical research
ed.) 337: a2240. doi:10.1136/bmj.a2240.PMC 2583389. PMID 19008264.

12.

Jump up^ Fox KA, Dabbous OH, Goldberg RJ, Pieper KS, Eagle KA, Van de Werf F, Avezum
A, Goodman SG, Flather MD, Anderson FA Jr, Granger CB. (2006). "Prediction of risk of death and
myocardial infarction in the six months after presentation with acute coronary syndrome: prospective
multinational observational study (GRACE).". BMJ 333 (7578):
1091. doi:10.1136/bmj.38985.646481.55. PMC 1661748.PMID 17032691.

13.

Jump up^ Pell JP, Haw S, Cobbe S et al. (2008). "Smoke-free Legislation and
Hospitalizations for Acute Coronary Syndrome". New England Journal of Medicine 359 (5): 482
91. doi:10.1056/NEJMsa0706740.PMID 18669427.

14.

^ Jump up to:a b O'Connor RE, Brady W, Brooks SC et al. (November 2010). "Part 10: acute
coronary syndromes: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation
and Emergency Cardiovascular Care". Circulation 122 (18 Suppl 3): S787
817. doi:10.1161/CIRCULATIONAHA.110.971028.PMID 20956226.

15.

Jump up^ Blankenship JC, Skelding KA (2008). "Rapid Triage, Transfer, and Treatment with
Percutaneous Coronary Intervention for Patients with ST-Segment Elevation Myocardial
Infarction". Acute Coronary Syndromes 9 (2): 5965.

16.

Jump up^ Janda, SP; Tan, N (2009). "Thrombolysis versus primary percutaneous coronary
intervention for ST elevation myocardial infarctions at Chilliwack General Hospital.". The Canadian
journal of cardiology 25 (11): e3824.doi:10.1016/S0828-282X(09)701655. PMC 2776568. PMID 19898701.

17.

Jump up^ Montalescot G, Cayla G, Collet JP, Elhadad S, Beygui F, Le Breton H et al. (2009).
"Immediate vs delayed intervention for acute coronary syndromes: a randomized clinical
trial.". JAMA 302 (9): 94754.doi:10.1001/jama.2009.1267. PMID 19724041.

18.

Jump up^ Vale, N; Nordmann, AJ; Schwartz, GG; de Lemos, J; Colivicchi, F; den Hartog, F;
Ostadal, P; Macin, SM; Liem, AH; Mills, EJ; Bhatnagar, N; Bucher, HC; Briel, M (Sep 1, 2014). "Statins
for acute coronary syndrome.".The Cochrane database of systematic reviews 9:
CD006870. doi:10.1002/14651858.CD006870.pub3.PMID 25178118.

19.

Jump up^ Cox, D. A.; Stone, G. W.; Grines, C. L.; Stuckey, T.; Zimetbaum, P. J.; Tcheng, J.
E.; Turco, M.; Garcia, E.; Guagliumi, G.; Iwaoka, R. S.; Mehran, R.; O'Neill, W. W.; Lansky, A. J.;
Griffin, J. J.; Cadillac, I. (2006). "Comparative Early and Late Outcomes After Primary Percutaneous
Coronary Intervention in ST-Segment Elevation and NonST-Segment Elevation Acute Myocardial
Infarction (from the CADILLAC Trial)". The American Journal of Cardiology 98 (3): 331
337. doi:10.1016/j.amjcard.2006.01.102. PMID 16860018. edit

20.

Jump up^ McCord J, Jneid H, Hollander JE et al. (April 2008). "Management of cocaineassociated chest pain and myocardial infarction: a scientific statement from the American Heart
Association Acute Cardiac Care Committee of the Council on Clinical
Cardiology". Circulation 117 (14): 1897
907.doi:10.1161/CIRCULATIONAHA.107.188950. PMID 18347214.

21.

Jump up^ Antman EM, Cohen M, Bernink PJ et al. (2000). "The TIMI risk score for unstable
angina/non-ST elevation MI: A method for prognostication and therapeutic decision
making". JAMA 284 (7): 83542.doi:10.1001/jama.284.7.835. PMID 10938172.

22.

Jump up^ Pollack CV, Sites FD, Shofer FS, Sease KL, Hollander JE (2006). "Application of
the TIMI risk score for unstable angina and non-ST elevation acute coronary syndrome to an
unselected emergency department chest pain population". Academic Emergency Medicine 13 (1): 13
8. doi:10.1197/j.aem.2005.06.031.PMID 16365321.

23.

Jump up^ Chase M, Robey JL, Zogby KE, Sease KL, Shofer FS, Hollander JE (2006).
"Prospective validation of the Thrombolysis in Myocardial Infarction Risk Score in the emergency
department chest pain population". Annals of Emergency Medicine 48 (3): 252
9. doi:10.1016/j.annemergmed.2006.01.032. PMID 16934646.

External links[edit]