Acute coronary syndrome

Primary etiologies	Secondary etiologies
Coronary artery spasm	Increased myocardial oxygen demand
Disruption or erosion of atherosclerotic plaques	Reduced myocardial blood flow
Platelet aggregation or thrombus formation at the site of an atherosclerotic lesion	Reduced myocardial oxygen delivery

Presentation

Classic presentation

General signs and symptoms:
- Substernal or left-sided chest discomfort (heaviness, pressure, tightness, or squeezing).
- Radiation to the arms, jaw, or neck.
- Nausea, vomiting.
- Diaphoresis.
- Dyspnea.
Stable angina:
- Transient, episodic chest pain.
- Exercise or stress may induce symptoms.
- Episodes usually last <10 minutes.
- Usually resolves with rest or glyceryl nitrate.
Unstable angina:
- Occurs with minimal exertion or at rest.
- Episodes usually last >20 minutes despite glyceryl trinitrate or cessation of activity.
Acute myocardial infarction:
- Prolonged, continuous, severe chest discomfort at rest.
- May not respond to immediate symptomatic management.

Critical presentation

Patients may present with cardiogenic shock:
- Hypotension
- Pallor
- Diaphoresis
- Cardiac arrhythmias (ventricular fibrillation [VF] or ventricular tachycardia [VT])
- Variations in systolic blood pressure
- Bradycardia or heart block
- New murmur secondary to papillary muscle rupture
- Pulmonary edema manifested by shortness of breath and rales on auscultation
Patients in extremis may also present in cardiac arrest.

Diagnosis and evaluation

There are four main elements in the diagnosis of ACS:

Clinical history
Physical examination

Electrocardiogram (ECG) findings:

In addition to interpretation of an initial ECG, it is imperative that any patient with a concerning story have a repeat ECG within 10–15 minutes to assess for evolution of ischemia or myocardial injury.
Myocardial distress is manifest in the ST segments of the ECG; ST segment depression indicates myocardial ischemia whereas ST segment elevation (STE) indicates acute myocardial infarction (>1 mm in two contiguous standard limb leads or >2 mm in two contiguous precordial leads).

ECG changes occur in patterns on the ECG and may be suggestive of the location of the culprit lesion (Table 20.2).

Table 20.2. ECG findings in ACS

Common infarct locations	Corresponding electrocardiographic ST changes	Suggested potential lesion location
Anterior wall	V3, V4	Left anterior descending artery (LAD)
Anteroseptal wall	V1–V4, aVR	LAD, STE in aVR suggests left main coronary
Anterolateral wall	V3–V6, I, aVL	LAD, left circumflex artery (LCX)
Lateral wall	V5, V6, I, aVL	LAD and branches including perforators and obtuse marginals
Inferior wall	II, III, aVF	Right coronary artery (RCA), LCX
Right ventricle (often associated with inferior MI)	V1, V2, II, III, aVF, V3R–V6R	Proximal RCA
Posterior wall	V7–V9 (with ST depression in V1–V3)	RCA, LCX

Cardiac biomarkers:
- Troponin:
  - Myocardial troponin I (TnI) and troponin T (TnT) are elevated as early as 3 hours, but may stay elevated for up to 7 days.
Creatine kinase (CK):
- CK-MB is myocardial specific, usually elevated as early as 3 hours and peaking within 24 hours; it normalizes 2–3 days after injury.
Myoglobin:
- Myocardial myoglobin is not distinguishable from skeletal muscle myoglobin and thus is not a useful marker in ACS.
- Initially rises 1–2 hours post event, peaks at 5–7 hours, and normalizes by 24 hours.

Critical management of STEMI

Any patient with STEMI (ST-segment elevation myocardial infarction) should undergo reperfusion with percutaneous coronary intervention (PCI) within 90 minutes of presentation.
Fibrinolytics should be used for patients unable to undergo PCI within the recommended timeframe.
- Initiation of therapy should occur as soon as possible after the diagnosis of STEMI is made.
- Alteplase, tenecteplase and reteplase are all possible therapies.
- Inclusion criteria:
  - Patients presenting with STEMI.
  - Survival benefit is greatest for patients presenting within 12 hours of symptoms.
  - ST segment elevations >1 mm in two contiguous standard limb leads or ST segment elevation >2 mm in two contiguous precordial leads.
Exclusion criteria:
- Absolute contraindications:
  - Prior intracranial hemorrhage or known arteriovenous malformation (AVM).
  - Known intracranial mass.
  - Ischemic stroke within 3 months of presentation.
  - Active internal bleeding from other source.
  - Suspected aortic dissection.
Relative contraindications:
- BP >180/100.
- Elevated INR.
- Trauma or major surgical procedure within the past 3 months.
- Pregnancy.
Other pharmacological agents include antiplatelets, antithrombins, beta-antagonists, nitrates, and morphine (see Table 20.3).
- Antiplatelets such as aspirin have been linked to improved outcomes and should be uniformly used. The number needed to treat (NNT) to save 1 life is approximately 42.
- Anticoagulants such as heparin should also be considered.
  - Either unfractionated (UF) or low–molecular weight (LMW) heparin can be used; no specific data supports one over the other.
- Beta-blockers reduce myocardial oxygen demand and decrease the potential of arrhythmia. It is not necessary to give them in the emergency department (ED).
  - Contraindications to beta-blockade include hypotension, cardiogenic shock, or congestive heart failure.
- Nitrates are used to decrease pain and increase myocardial blood flow.
  - They can be administered sublingually.
  - Intravenous (IV) infusions should be considered if the pain persists after repeated sublingual doses.
- In patients with a right ventricular infarction (a preload-dependent condition), the use of nitrates can cause severe hypotension and should be avoided.
Morphine can be used to decrease pain and anxiety.