Acute coronary syndromes

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Resident
Survival
Guide

Acute Coronary Syndrome Chapters

Heart Attack Patient Information

Unstable Angina Patient Information

Overview

Classification

Unstable Angina
Non-ST Elevation Myocardial Infarction
ST Elevation Myocardial Infarction

Symptoms

Pathophysiology

Risk Factors

Differential Diagnosis

Prevention

AHA/ACC Guidelines for Acute Coronary Syndrome

Guideline for Risk Stratification in ACS
Guideline for Pre-Hospital Evaluation and Care
Guidelines for Initial Management of ACS
Guidelines for Patients with Atrial Fibrillation Complicating ACS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]; Tarek Nafee, M.D. [3]; Sabawoon Mirwais, M.B.B.S, M.D.[4]

Synonyms and Keywords: ACS

Overview

Acute coronary syndrome (ACS) refers to any group of symptoms attributed to obstruction of the coronary arteries. The most common symptom prompting diagnosis of ACS 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%). These types are named according to the appearance of the electrocardiogram. There can be some variation as to which forms of myocardial infarction (MI) are classified under acute coronary syndrome.

ACS should be distinguished from stable angina, which is chest pain which develops during exertion and resolves at rest. New onset angina however should be considered as a part of acute coronary syndrome, 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. Cardiac chest pain can also be precipitated by anemia, bradycardias or tachycardias.

Classification

Acute coronary syndrome may be classified as follows:

Symptoms

The signs and symptoms of acute coronary syndrome include:

Pathophysiology

For more information on atherosclerotic plaque, click here.

The pathophysiology of acute coronary syndromes depends on coronary atherosclerotic plaque which includes:

Initiation and Progression of Coronary Atherosclerotic Plaque

Plaque Vulnerability

The plaque vulnerability depends on the following factors:[1]

Pathogenesis

The pathogenesis of acute coronary syndrome depends on:

Following plaque rupture or endothelial erosion, the subendothelial matrix is exposed to the circulating platelets, which get activated leading to thrombus formation. Two types of thrombi can form:

  • White clots: Platelet-rich clots which partially occludes the artery
  • Red clots: Fibrin rich clots superimposed on white clots and cause total occlusion of the artery

Risk Factors

Common risk factors in the development of acute coronary syndrome are:[2]

Diagnosis

High-sensitivity Cardiac Troponin (hs-cTn)

99th percentile of a healthy reference population
(recommended cut-off)
Turnaround time Name and manufacturer FDA Approval?
Troponin T
hs-cTnT
14 ng/L[3] 18 minutes[4] Elecsys
(Roche Diagnostics)
Troponin I
hs-cTnI
26.2 ng/L[3] ARCHITECTSTAT
(Abbott Laboratories)

Clinical Implications of High-sensitivity Cardiac Troponin Assays

Compared with standard cardiac troponin assays, high-sensitivity assays:
Have higher negative predictive value for acute MI.
Reduce the “troponin-blind” interval leading to earlier detection of acute MI.
Reduce the “troponin-blind” interval leading to earlier detection of acute MI.
Are associated with a 2-fold increase in the detection of type 2 MI.
Levels of high-sensitivity cardiac troponin should be interpreted as quantitative markers of cardiomyocyte damage

(i.e. the higher the level, the greater the likelihood of MI):

Elevations beyond 5-fold the upper reference limit have high (>90%) positive predictive value for acute type 1 MI.
Elevations up to 3-fold the upper reference limit have only limited (50–60%) positive predictive value for acute MI

and may be associated with a broad spectrum of conditions.

It is common to detect circulating levels of cardiac troponin in healthy individuals.
Rising and/or falling cardiac troponin levels differentiate acute from chronic cardiomyocyte damage

(the more pronounced the change, the higher the likelihood of acute MI).

Adapted from European Heart Journal (2016) 37, 267–315



Available high sensitivity troponin assays:

  • Troponin T: Elecsys by Roche Diagnostics
  • Troponin I: ARCHITECTSTAT by Abbott Laboratories

When both tests have sensitivity of > 99%, cTnT can exclude infarction in more patients with a sensitivity of 90% according to meta-analysis.

The agreement between hscTnT and hscTnI measurements is excellent (Cohen's kappa =0.9)[3].

High sensitivity troponin levels have reduced predictive value when prevalence is low.

Clinical Prediction Rules

Clinical prediction rules can help diagnose:

  • HEART risk score (History, EKG, Age, Risk factors, and troponin) is the only one of these three prediction rules designed for use prior to diagnosis
  • GRACE risk score incorporates 8 findings
  • TIMI risk score

Regarding the comparative performance of the prediction rules:

  • In the setting of acute chest pain, the HEART score may best predict complications according to a cohort study.
  • In the setting of NSTEMI, the GRACE risk score may best predict complications according to a cohort study. However, the HEART risk score was not assessed in this cohort.

Diagnostic Pathways

Clinical diagnostic pathways may help. The European Society of Cardiology recommends two pathways[5]:

The last American Health Association guidelines were prepared prior to approval of hs-cTn tests by the FDA.

More recent strategies include:

  • Single cTnT measurement, combined with a non-ischemic EKG, that reports troponin is below the limits of detection.
  • Single cTnI measurement, combined with low-risk clinical prediction rule[8]

Differential Diagnosis

Diagnosis of ACS is initiated by a clinical suspicion based on a thorough history of the patient's symptoms. Subsequently, confirmatory tests should be ordered to confirm the diagnosis, identify the specific cause of ACS, or to rule out other possible differentials. In some circumstances, utilizing a clinical prediction tool may be beneficial in guiding the clinician's diagnosis. View the page on diagnosis using the clinical prediction rule for ACS for more detail. Acute Coronary Syndrome (ACS) may be differentiated from other diseases as follows:

Organ System Diseases Presentation Diagnostic Tests Past Medical History Other Findings
Chest Pain GI Symptoms Pulmonary Neck
On Palpation On inspiration Radiating to Extremeties Radiating to Back With Movement Nausea or Vomitting Epigastric Pain Odynophagia or Dysphagia Shortness of Breath Jugular

Distention

Cardiac Biomarkers CBC Findings ESR D-Dimer EKG

Findings

CXR Findings DM Hyperlipidemia Obesity Trauma Inxn* Htn
Cardiovascular Acute Coronary Syndrome + + + + + + + + + + + Palpitations

Sweating

Aortic Dissection + + + - + + - + •Pain maximal upon onset •Pain difficult to treat with opiates

Weak pulse in one arm compared to other

Syncope

•Symptoms similar to stroke

Smoking

Brugada Syndrome No chest pain + Syncope

Cardiac arrest

ST-segment elevation

•F/H of sudden cardiac death

Takotsubo carditis Sudden onset of chest pain mimicking myocardial infarction + + + + + - •Extreme emotional or physical stresssyncope

•Women>men

ST segment elevation

Left ventricular apical ballooning on echo

Normal coronary arteries

Pericarditis + + + •Relieving factor: Sitting up and leaning forward

•Aggravating factor: Lying down and breathing deep

+ + + + + + + •Other causes:Malignancy, autoimmune disorders, chest trauma

Pericardial friction rub

Organ System Diseases Presentation Diagnostic Tests Past Medical History Other Findings
Chest Pain GI Symptoms Pulmonary Neck
On Palpation On inspiration Radiating to Extremeties Radiating to Back With Movement Nausea or Vomitting Epigastric Pain Odynophagia or Dysphagia Shortness of Breath Jugular

Distention

Cardiac Biomarkers CBC Findings ESR D-Dimer EKG

Findings

CXR Findings DM Hyperlipidemia Obesity Trauma Inxn* Htn
Pulmonary Pleuritis
(pleurisy)
+ + + + Aggravating factor: Deep breathing + + + + + + •Other causesPulmonary embolism, malignancy, autoimmune diseases
Pulmonary Embolism + •Aggravating factors: Deep breathing, coughing, eating, bending and stooping + + + •Other causes: Immobility, pregnancy, oral contraceptive pills
Pneumonia + + + + + + •Complications: Sepsis, ARDS, Lung abscess
Gastrointestinal GERD + + + •Other symptoms: Hoarseness, Dry cough at night, Sensation of lump in throat etc
Esophageal Spasms + + + + + + + • Risk factors: Anxiety or depression and drinking wine, very hot or cold foods
Esophagitis + + + + + + + • Causes: Hiatal hernia, infection, medications, radiation therapy
Gastritis + + + + + + + • Causes: H.pylori infection, bile reflux, alcohol use, alcohol use
Organ System Diseases Presentation Diagnostic Tests Past Medical History Other Findings
Chest Pain GI Symptoms Pulmonary Neck
On Palpation On inspiration Radiating to Extremeties Radiating to Back With Movement Nausea or Vomitting Epigastric Pain Odynophagia or Dysphagia Shortness of Breath Jugular

Distention

Cardiac Biomarkers CBC Findings ESR D-Dimer EKG

Findings

CXR Findings DM Hyperlipidemia Obesity Trauma Inxn* Htn
Musculoskeletal Muscle sprain/Spasm + + + + • Causes: Over use, dehydration, electrolyte abnormalities
Costochondritis + + + + + + + + + + + • Risk factors: Rheumatoid arthritis, ankylosing spondylitis, Reiter's syndrome
Rib fracture/Trauma + + + + + + + + + + • Complications: Pneumothorax, hemothorax, surgical emphysema
Psychiatry Anxiety (Panic Attack) Chest tightness + + • Other symptoms: Palpitations, trembling, sweating, choking, light headed, hot or cold flashes.


The following table summarizes the significant history, and diagnostic test findings that will help differentiate the acute coronary syndromes from one another, as well as from other coronary artery diseases:

Acute Coronary Syndromes History and Symptoms Pathology Diagnostic tests Treatment Complications Prognosis
Chest pain Duration of Chest pain Coronary Artery Plaque Cardiac Biomarkers
(e.g.CK-MB, Troponins)
EKG Findings Medical Therapy Reperfusion
(e.g. PCI, CABG, or Medical)
At Rest Exertion
Unstable Angina + + <30 minutes Partial occlusion Erosion

or

Rupture

(39%)

Normal •Normal EKG findings (some cases)


•Flipped or inverted T waves


•ST segment depression


•Non-specific ST-T changes

+ Arrhythmias

Congestive heart failure

Hypotension

New mitral regurgitation

MI

•Sudden death

•1 year mortality rate is 1.7%
NSTEMI + + >30 minutes Partial or complete occlusion Rupture

(56%)

or

Erosion

Elevated •No EKG findings (some cases)


•Flipped or inverted T waves


•ST segment depression


•Non-specific ST-T changes

New left bundle branch block

+ + Arrhythmias

Congestive heart failure

Hypotension

New mitral regurgitation

Ventricular aneurysms

•Sudden death

•1 year mortality rate is 24.4%

•30 day mortality rate is about 2%

STEMI + + >30 minutes Complete occlusion Rupture

(50%-75%) or

Erosion

Elevated •ST elevation in at least 2

contiguous leads in V2-V3


•ST depression in at least

two precordial leads V1-V4


•ST depression in several

leads plus ST elevation in

lead aVR (suggestive of occlusion of the left main or proximal LAD artery)


+ + Reinfarction

Arrhythmias

Left ventricular aneurysm

Pseudoaneurysm

rupture of papillary muscle,

interventricular septum and LV free wall

•Sudden death

•30 day mortality rate is

1.1% in <45 yrs and 20.4% in >75 yrs patients

Other Coronary Artery Diseases
Chronic stable angina - + ≤ 5 minutes Severely narrowed

coronary vessels

Stable plaque Normal •Normal EKG in 50% of cases

•Down sloping, up sloping or

horizontal ST segment depression

•T wave inversion

+ Heart failure •Estimated annual mortality rate is 0.9%-1.4%

•Annual incidence of non-fatal MI between 0.5%-2.6%

•1 year mortality rate is 1.3%

Prinzmetal's angina •Occur at rest

(Mid night to early morning)

•Not associated with exertion

5-30 minutes Coronary artery vasospasm - Normal •Transient ST segment elevation + Arrhythmias

MI

•5 year survival is excellent (90%-95%)


Differential Diagnoses of Acute Coronary Syndromes in the Setting of Chest Pain


Cardiac Pulmonary Vascular Gastrointestinal Orthopedic Other
Myopericarditis

Cardiomyopathiesa

Pulmonary embolism Aortic dissection Esophagitis, reflex or spasm Musculoskeletal disorders Anxiety disorders
Tachyarrhythmias (Tension)-Pneumothorax Symptomatic aortic aneurysm Peptic ulcer, gastritis Chest trauma Herpes zoster
Acute heart failure Bronchitis, pneumonia Stroke Pancreatitis Muscle injury/inflammation Anemia
Hypertensive emergencies Pleuritis Cholecystitis Costochondritis
Aortic valve stenosis Cervical spine pathologies
Tako-Tsubo cardiomyopathy
Coronary spasm
Cardiac trauma
Bold = Common and/or important differential diagnoses

aDilated, hypertrophic and restrictive cardiomyopathies may cause angina or chest discomfort

Treatment

Coronary Angiography

Coronary angiography within 12 hours likely benefits high risk (elevated cardiac biomarkers at baseline or diabetes or a GRACE score more than 140) patients.

Recommendations for Anti-ischemic Drugs in the Acute Phase of Non-ST-elevation Acute Coronary Syndromes

Recommendations Class

of Recommendations

Level

of Evidence

Early initiation of beta-blocker treatment is recommended

in patients with ongoing ischemic symptoms and without contraindications.

I B
It is recommended to continue chronic beta-blocker therapy,

unless the patient is in Killip class III or higher.

I B
Sublingual or i.v. nitrates are recommended to relieve angina;a intravenous treatment is recommended

in patients with recurrent angina, uncontrolled hypertension or signs of heart failure.

I C
In patients with suspected/confirmed vasospastic angina, calcium channel blockers and

nitrates should be considered and beta-blockers avoided.

IIa B
aShould not be administered in patients with recent intake of sildenafil or vardenafil (< 24 h) or tadalafil (< 48 h).

Prevention

Primary Prevention

The primary prevention strategies include:

  • Dietary modifications:
  • Physical exercise
  • 30 minutes of moderate exercise

Secondary Prevention

The secondary prevention strategies include:

References

  1. Sukhova GK, Schönbeck U, Rabkin E, Schoen FJ, Poole AR, Billinghurst RC; et al. (1999). "Evidence for increased collagenolysis by interstitial collagenases-1 and -3 in vulnerable human atheromatous plaques". Circulation. 99 (19): 2503–9. PMID 10330380.
  2. Fuster V, Badimon L, Cohen M, Ambrose JA, Badimon JJ, Chesebro J (1988). "Insights into the pathogenesis of acute ischemic syndromes". Circulation. 77 (6): 1213–20. PMID 3286036.
  3. 3.0 3.1 3.2 van der Linden N, Wildi K, Twerenbold R, Pickering JW, Than M, Cullen L; et al. (2018). "Combining High-Sensitivity Cardiac Troponin I and Cardiac Troponin T in the Early Diagnosis of Acute Myocardial Infarction". Circulation. 138 (10): 989–999. doi:10.1161/CIRCULATIONAHA.117.032003. PMID 29691270.
  4. Roffi M, Patrono C, Collet JP, Mueller C, Valgimigli M, Andreotti F; et al. (2016). "2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC)". Eur Heart J. 37 (3): 267–315. doi:10.1093/eurheartj/ehv320. PMID 26320110.
  5. Twerenbold R, Neumann JT, Sörensen NA, Ojeda F, Karakas M, Boeddinghaus J; et al. (2018). "Prospective Validation of the 0/1-h Algorithm for Early Diagnosis of Myocardial Infarction". J Am Coll Cardiol. 72 (6): 620–632. doi:10.1016/j.jacc.2018.05.040. PMID 30071991.
  6. Pickering JW, Greenslade JH, Cullen L, Flaws D, Parsonage W, Aldous S; et al. (2016). "Assessment of the European Society of Cardiology 0-Hour/1-Hour Algorithm to Rule-Out and Rule-In Acute Myocardial Infarction". Circulation. 134 (20): 1532–1541. doi:10.1161/CIRCULATIONAHA.116.022677. PMID 27754881.
  7. Reaney PDW, Elliott HI, Noman A, Cooper JG (2018). "Risk stratifying chest pain patients in the emergency department using HEART, GRACE and TIMI scores, with a single contemporary troponin result, to predict major adverse cardiac events". Emerg Med J. 35 (7): 420–427. doi:10.1136/emermed-2017-207172. PMID 29622596.

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