creation date: 2025-06-18 01:31
tags: Pathologies Incomplete
Acute Coronary Syndrome
Background
Definitions
ACS refers to a group of conditions that include:
- ST-elevation myocardial infarction (STEMI)
- Non-ST elevation myocardial infarction (NSTEMI)
- Unstable angina (UA)
Each condition is discussed in more depth in their respective pages.
These represent varying degree of manifestation of coronary heart disease (CHD).
Etiology & Pathogenesis
Acute coronary syndromes are a manifestation of CHD and is due to atherosclerosis of the coronary arteries.
Symptomatic manifestation typically due to plaque rupture and formation of thrombus or to vasospasm. This results in a reduction in blood flow to a part of the heart musculature resulting in ischemia and then infarction.
Clinical Presentation
Signs & Symptoms
Classical symptoms of ACS are:
- Substernal chest pain (crushing or pressure-like feeling)
- Radiating pain to the jaw and/or left arm
It should be noted that classic presentations are not always seen, especially with female, diabetic, or older patients. Other more subtle complaints include:
- Dyspnea
- Lightheadedness
- Isolated jaw/left arm pain
- Nausea
- Epigastric pain
- Diaphoresis
- Weakness
History & Physical Exam
Further history taking can aid in distinguishing ischemic chest pain from noncardiac causes.
Onset:
- Gradual and may wax and wane
- Angina often occurs in the morning due to diurnal increase in sympathetic tone and other cardiovascular parameters.
Provocation: - Pain increases with myocardial oxygen demand
- Does not change with respiration, position, or palpation
- Pain may or may not respond to nitroglycerin; response to pain does not necessarily mean cardiac cause though
Quality: - Commonly used words: squeezing, tightness, pressure, constriction, crushing, strangling, burning, fullness, weight on chest
- Not described as: sharp, fleeting, knife-like, stabbing
Radiation: - Radiation is common as the heart overlies afferent nerves and referred pain correspond to dermatomes from that segment of the spinal cord (C5-6 and T1-6)
- Pain radiating to upper extremities is highly suggestive of ischemic pain
- May also radiate to epigastrium, shoulders, wrist, fingers, neck/throat, lower jaw, teeth, back
Site/Severity: - Diffuse discomfort (not specific spot)
Time: - Chest pain from ACS may occur at rest and generally lasts longer than 30 minutes (contrasted to stable angina: 2-5 min, relieved by rest)
- Continuous pain that does not wax and wane for >24 hrs is unlikely ACS
A number of historical factors also increase the likelihood of ACS:
- Past history of ACS
- Past history of vascular disease (eg. stroke)
- Risk factors for cardiovascular disease
- Recent use of cocaine or other sympathominetic drugs
On examination, there may be subtle findings:
- Increased heart rate
- Elevated BP
- Skin findings (disaphoresis, cool, clammy, pale skin)
- Evidence of heart failure or systemic hypoperfusion
- New heart sounds (second heart sound may split, s3, or s4)
- New murmur (systolic murmur may signify papillary muscle dysfunction or ventricular septal defect)
Risk factors
For cardiovascular disease:
- Age
- Male sex
- Diabetes
- Hypertension
- Dyslipidemia
- Smoking
- Family history of premature cardiovascular disease
Other risk factors:
- Cocaine use
- Family history of early MI (<55 years of age)
Diagnosis
Criteria
Diagnosis of ACS is made with clinical findings (presence of symptoms), ECG findings, and cardiac biomarkers. Note that management should begin with reasonable suspicion of ACS.
STEMIs can manifest with new ST-segment elevation in two anatomically contiguous leads with the following thresholds:
- ≥0.1 mV in any leads except V2 or V3
- For V2 and V3:
- ≥0.2 mV in males ≥40 years old
- ≥0.25 mV in males <40 years old
- ≥0.15 mV in females
ECG findings with presence of symptoms is sufficient for diagnosis of STEMI.
NSTEMIs can manifest as one or both of the following in two anatomically contiguous leads:
- New horizontal or down-sloping ST depression ≥0.05 mV
- T wave inversion ≥0.1 mV with prominent R wave or R/S ratio >1
High-sensitivity troponin testing is used for evaluation of myocardial infarction. Acute myocardial injury is defined biochemically as:
- Troponin above the 99th percentile of upper reference limit (URL) of assay
- Observed rise and/or fall of troponin value - typically rises 2-3 hours after onset but late presentation may not see a changing pattern over short time frame between serial assays.
Myocardial infarction can be subdivided into 5 types of which both STEMI and NSTEMI can manifest
- Type 1 - spontaneous atherothrombotic MI
- Type 2 - supply-demand mismatch without acute atherothrombosis
- Type 3 - sudden cardiac death with presumed MI (diagnosis made postmortem)
- Type 4 - PCI or stent related thrombosis
- Type 5 - CABG related
Work-up
Diagnosis of ACS often cannot be made with an initial 12-lead ECG. A follow-up ECG should be done 15-30 minutes following initial ECG. Note, ACS can present with no ECG findings. If patient is at intermediate-to-high risk for ACS, serial ECGs should be done until pain resolves.
In addition, high-sensitivity troponin should be done. Serial testing should ideally be done at 0 hours, 3 hours, and 6 hours. A change of at least 20% is significant for ischemia.
Cardiac monitoring should be used. Note, some arrhythmias such as VTach and SVTs can exacerbate ischemia by increasing oxygen demand.
A chest radiograph should be obtained if possible to evaluate for alternative diagnoses and/or complications.
Differential
Red Flags / Complications
Missed ACS can result in an increase in short-term mortality. This was most often due to atypical presentation.
Management
Acute treatment
In cases of respiratory or cardiorespiratory arrest, resuscitation protocols should be followed.
Patient should be placed on cardiac monitoring and IV access obtained. Supplemental oxygen should be used if necessary to maintain adequate oxygen saturation. Aspirin 162-325mg should be given to chew and swallow.
Symptomatic management:
Administer nitroglycerin 0.3-0.4mg sublingual every 5 minutes for 3 doses. Consider nitroglycerin IV if pain does not decrease. Note that nitrates are contraindicated with:
- Severe aortic stenosis
- Hypertrophic cardiomyopathy
- Suspected right ventricular infarct
- Hypotension
- Marked brady- or tachycardia
- Recent use of phosphodiesterase-5 inhibitor
In cases of significant pain, administer morphine 2-4 mg IV, with increments of 2-8 mg IV, repeated at 5-15 minute intervals. This should not be routine.
ST-elevation MI:
The following therapies are used routinely:
- Aspirin and nitrates (as above)
- Cardioselective beta blocker PO (eg. metoprolol or atenolol); IV also possible in some cases
- Anticoagulation and antiplatelets/P2Y12 inhibitor (selection depends on reperfusion strategy)
- Statins (if not already taking)
With STEMIs, selection and implementation of reperfusion strategy is the highest priority. Selection is based on the availability of percutaneous coronary intervention (PCI) within 120 minutes of medical contact. If that is not possible, patient should be given thrombolytic therapy.
Non-ST elevation ACS:
For NSTEMIs and UAs, treatment is indicated following confirmation with elevated biomarkers.
Similarly to STEMIs, the following therapies are used routinely:
- Aspirin and nitrates
- Cardioselective beta blocker - note that evidence does not show clear benefit with NSTEACS, can defer if hemodynamic stability can be compromised
- Statins
Aspirin, a platelet P2Y12 receptor blocker, and anticoagulant is recommended following diagnosis.
Further management can either be early PCI, or conservative medical therapy. Thrombolytic therapy is not indicated for NSTEACS.
Follow-up management
Long-term management of ACS focuses on secondary prevention of recurrent events and reducing cardiovascular mortality. The ACC and AHA recommends:
- Dual antiplatelet therapy with aspirin 81-325 mg daily and P2Y12 inhibitor
- Lipid-lowering therapy
- ACE inhibitor (or ARB) and beta-blocker
- Risk factor modifications