Acute Coronary Syndrome

Acute coronary syndrome:
■ Unstable angina: ECG—no ST elevation; cardiac biomarkers ⊝.
■ NSTEMI: ECG—no ST elevation; cardiac biomarkers ⊕.
■ STEMI: ECG—ST elevation; cardiac biomarkers ⊕.

A spectrum of clinical syndromes caused by plaque disruption or vasospasm that leads to acute myocardial ischemia. – Acute Coronary syndrome.

UNSTABLE ANGINA/NON–ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION – Acute Coronary Syndrome

Chest pain that is (1) new onset, (2) accelerating (ie, occurs with less exertion, lasts longer, or is less responsive to medications), or (3) occurs at rest.
Patient history distinguishes unstable angina from stable angina pectoris. Both stable and unstable angina have no elevated cardiac biomarkers. It signals the presence of possible impending infarction based on plaque instability. In contrast, NSTEMI indicates myocardial necrosis marked by elevations in troponin I and creatine kinase–MB isoenzyme (CK-MB) without ST-segment elevations seen on ECG.

Diagnosis

  • Patients should be risk stratified according to the Thrombolysis in Myocardial Infarction (TIMI) study criteria (see Table 1).
  • ECG: Unstable angina and NSTEMI are not associated with ST elevation, but ST changes (eg, ST depression, T-wave inversion, nonspecific changes) may be seen on ECG.
  • Cardiac markers (CK-MB /troponin): Unstable angina is not associated with elevated cardiac markers. NSTEMI is associated with elevations in cardiac markers.
  • NSTEMI is diagnosed by serial cardiac enzymes and ECG.
Acute coronary syndrome
TIMI Risk Score for Unstable Angina/NSTEMI – Table 1

Treatment

Best initial treatment:

  • Admit to CCU, and monitor closely.
  • If SaO2 < 90% or breathless, administer O2.
  • Analgesia: IV morphine with IV metoclopramide.
  • Nitrates: IV, GTN, or sublingual.
  • Antiplatelet therapy: ASA (↓ mortality in ACS) in combination with a second agent (ie, clopidogrel, prasugrel, or ticagrelor), unless contraindicated.
  • Consider β-blockers as hemodynamics allow (if hypertensive/tachycardic/LV function < 40%).
  • Low-molecular-weight heparin (eg, enoxaparin) to prevent clot formation in the coronary arteries.

Interventions:

  • Assess mortality risk (eg, TIMI score, GRACE score).
  • Heparin is recommended for non-ST elevation MI. Thrombolytics are only recommended in STEMI if percutaneous coronary intervention (PCI) is not available within 2 hours.
  • Patients with chest pain refractory to medical therapy, a TIMI score of ≥ 3, a troponin elevation, or ST changes > 1 mm should be given GPIIb/ IIIa inhibitors (abciximab, tirofiban, eptifibatide) and scheduled for angiography and possible revascularization within 72 hours (percutaneous coronary intervention [PCI] or coronary artery bypass graft [CABG]).
  • Dual antiplatelet therapy with aspirin and prasugrel or ticagrelor (also P2Y12 inhibitors but superior to clopidogrel) should be considered for up to 12 months after angioplasty and stenting to prevent restenosis of stenting.
  • Ensure patient is on long-term β-blockers (if depressed LV function), ACEIs/ARBs, and statin.
  • Address modifiable risk factors (ie, smoking, hypertension, hyperlipidemia, diabetes).

ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION -Acute Coronary Syndrome

ST-segment elevations and cardiac enzyme release 2° to prolonged cardiac ischemia and necrosis. STEMI is a common medical emergency, and prompt treatment is absolutely necessary.

Chest Pain in ER Protocol

History/PE

  • Presentation: Acute-onset substernal chest pain (> 10–30 min), commonly described as a pressure, tightness, or heaviness that can radiate to the left arm, shoulders, neck, or jaw. May present without chest pain (“silent” infarct).
  • Associated symptoms: Diaphoresis, shortness of breath, lightheadedness, anxiety, nausea/vomiting, epigastric pain (more common in women), and syncope.
  • PE: May reveal arrhythmias, hypotension (cardiogenic shock), new S4, pansystolic murmur, and evidence of new CHF. Clear lung fields are seen in right ventricular MI (inferior MI). In a young, otherwise healthy person, consider cocaine use as the etiology.
  • The best predictor of survival is left ventricular EF.
  • Differential diagnosis: Angina, myocarditis, pericarditis, aortic dissection, pulmonary embolism, esophageal reflux/spasm.

Diagnosis

  • ECG: ST-segment elevations, hyperacute (tall) T waves, or new LBBB within hours. ST-segment depressions and dominant R waves in leads V1–V2 can also be reciprocal change indicating posterior wall infarct. T-wave inversion and pathologic Q waves develop within hours to days.
    • Sequence of ECG changes: Peaked T waves → ST-segment elevation → Q waves → T-wave inversion → ST-segment normalization → T-wave normalization over several hours to days.
Typical pattern of serum marker elevation after an acute myocardial
infarction. CK-MB, creatine kinase MB isoenzyme; cTnI, cardiac troponin I; cTnT, cardiac
troponin T; LD1, lactate dehydrogenase isoenzyme 1; MLC, myosin light chain. (Figure 1)
  • Cardiac enzymes:
    • Troponin (T and I) is the most sensitive and specific cardiac marker.
    • CK-MB and the CK-MB/total CK ratio (CK index) are also regularly checked.
    • Both troponin and CK-MB can take up to 3–12 hours to rise following the onset of chest pain. Troponin peaks at 24–48 hours, and CK-MB peaks within 24 hours (see Figure 1).
  • ST-segment abnormalities:
    • Inferior MI (involving the RCA/PDA): ST-segment elevation in leads II, III, and aVF (see Figure 2). Obtain a right-sided ECG to look for ST elevations in the right ventricle.
    • Anterior MI (involving LAD and diagonal branches): ST-segment elevation in leads V1–V4 (see Figure 3).
    • Lateral MI (involving LCA): ST-segment elevation in leads I, aVL, and V5–V6.
    • Posterior MI: ST-segment depression in leads V1–V2 (anterior leads) can be indicative. Obtain posterior ECG leads V7–V9 (15-lead) to assess for ST-segment elevations.
acute coronary syndrome
Inferior Wall MI (Figure 2 )
Anterior MI (Figure 3)
acute coronary syndrome
MI Location

Treatment

Best initial treatment:

  • First line: Antiplatelet therapy; ASA (↓ mortality in ACS). Add prasugrel or ticagrelor (both superior to clopidogrel), or clopidogrel as second antiplatelet agent with aspirin only for patients undergoing angioplasty or stenting.
  • Analgesia: IV morphine with IV metoclopramide.
  • Nitrates: IV, GTN, or sublingual.
  • If SaO2 < 95%, breathless, or in acute LVF, administer O2.
  • Consider β-blockers as hemodynamics allow (if hypertensive/tachycardic/ LV function < 40%).
  • If the patient is in heart failure or in cardiogenic shock, do not give β-blockers; instead, give ACEIs provided that the patient is not hypotensive.
  • In inferior wall MI (ie, right ventricular infarction), avoid nitrates and diuretics due to risk for severe hypotension (preload dependent).
acute coronary syndrome
Management of Acute STEMI

Interventions:

  • Emergent angiography and PCI should be performed if possible (superior to thrombolysis).
  • If PCI cannot be performed < 120 minutes (door-to-balloon time should ideally be < 90 minutes), and there are no contraindications to thrombolysis, and the patient presents within 3 hours of chest pain onset, thrombolysis with tPA, reteplase, or streptokinase should be performed instead of PCI.
  • Thrombolysis target time (door-to-needle time) is < 30 minutes and is contraindicated if > 24 hours. Thrombolytics can be used up to 12 hours from the onset of symptoms (mortality benefit extends to 12 hours).
  • Long-term management (for all patients) includes ASA, ACEIs, β-blockers, nitrates, and high-dose statins.
  • If PCI was performed, add clopidogrel, prasugrel, or ticagrelor (dual antiplatelet therapy).
  • Address modifiable risk factors (ie, smoking, hypertension, hyperlipidemia, diabetes).

Complications

Acute coronary syndrome
  • Arrhythmia: VF and VT are the most common complications and the most common causes of sudden death following acute MI. Sinus bradycardia and third-degree (complete) heart block are also very common.
  • Less common complications include reinfarction, left ventricular wall rupture, VSD, pericarditis, papillary muscle rupture (with mitral regurgitation), left ventricular aneurysm or pseudoaneurysm, and mural thrombi (with subsequent acute limb ischemia, TIA, or stroke).
  • A timeline of common post-MI complications:
    • First day: Heart failure.
    • 2–4 days: Arrhythmia, pericarditis.
    • 5–10 days: Left ventricular wall rupture (acute pericardial tamponade causing electrical alternans, pulseless electrical activity, and JVD), papillary muscle rupture (severe mitral regurgitation, pulmonary edema), septal rupture (lower left sternal border murmur, increase in O2 saturation in the right ventricle).
    • Weeks to months: Ventricular aneurysm (CHF, arrhythmia, persistent ST-segment elevation, mitral regurgitation, thrombus formation).
  • Dressler syndrome, an autoimmune process occurring 2–10 weeks post-MI, presents with fever, pericarditis, pleural effusion, leukocytosis, and ↑ ESR.
  • Right ventricular infarction: Caused by the occlusion of the RCA. Presents with hypotension, JVD, and clear lungs. Treat with high-volume fluid replacement (preload dependent), and avoid nitrates and diuretics.

Apurva Popat

Apurva Popat

Dr Apurva Popat has been teaching Medical science since he was in his medical school and has helped many students to master medical and spiritual knowledge.

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