I. ETIOPATHOGENESIS
Acute plaque rupture is central to the pathogenesis of STEMI
Occurs when coronary blood blow decreases abruptly after a thrombotic occlusion of a coronary artery previously affected by atherosclerosis
II. CLINICAL MANIFESTATIONS
Diagnosed similarly as NSTE-ACS (e.g., clinical features, increased cardiac biomarkers) but with ECG findings evolving in a temporal pattern (see ECG Reading in Chapter 1)
III. DIAGNOSIS AND RISK STRATIFICATION FOR STEMI A. Killip Scoring for STEMI
CLASS DESCRIPTION RISK OF MORTALITY
Class I
No rales or signs of pulmonary or venous congestion
Normal BP 0-5%
Class II
Moderate HF, bibasal rales
Normal BP
S3 gallop
Tachypnea or signs of right-sided CHF (venous or hepatic congestion)
10-20%
Severe HF
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Class
III
(+) mid-basal rales and pulmonary edema
(+) S3 and S4
Peripheral cyanosis
Mental confusion and oliguria
85-95%
B. TIMI Risk Score for STEMI
TIMI risk score for STEMI: predicts 30-day mortality
Designed for risk assessment early after patient presentation and thus does not incorporate noninvasive and invasive data
COMPONENTS POINTS INTERPRETATION
Historical
DM, Hypertension, Angina 1 point
Examination
Anterior ST elevation or LBBB on ECG 1 point
Time to Treatment > 4 hours 1 point
IV. MANAGEMENT OF STEMI
A. Pre-hospital Management of STEMI
Major components:
o Recognition of symptoms
o Rapid deployment of an emergency medical team capable of performing resuscitative maneuvers o Expeditious transportation
o Expeditious implementation of reperfusion therapy
Most out-of-hospital deaths from STEMI are due to sudden ventricular fibrillation
Majority of deaths occur within 24 hours of the onset of symptoms (over half occur in the 1st hour) B. Reperfusion Therapy: Primary Goal of Management
Reperfusion Therapy (fibrinolysis or PCI) should be administered to all eligible patients with STEMI with symptom onset within the last 12 hours
o Primary PCI: recommended method of reperfusion when it can be performed in a timely fashion o Fibrinolysis: administered at non-PCI-capable centers
FIBRINOLYSIS / THROMBOLYSIS INVASIVE STRATEGY (PCI) Generally preferred if:
Early presentation (< 3 hours of symptom onset)
Invasive strategy is not available:
Delay to invasive strategy:
o Prolonged transport
o Door-to-balloon minus door-to-needle time >1 hr
o Medical contact-to-balloon or door-to-balloon time >90 minutes
Generally preferred if:
Available PCI laboratory with surgical backup
o Medical contact-to-balloon or door-to-balloon
< 90 minutes
o Door-to-balloon minus door-to-needle < 1 hr
High risk STEMI (cardiogenic shock, Killip > 3)
Contraindications to fibrinolysis
Late presentation (symptom onset > 3 hours)
Diagnosis of STEMI is in doubt
Fibrinolytic agents:
o Streptokinase
o Tissue plasminogen activators
Adjunct anti-platelet therapy with fibrinolysis:
Aspirin continued indefinitely
Percutaneous coronary intervention (PCI) or percutaneous transluminal coronary angioplasty (PTCA): balloon angioplasty and stenting
Anti-platelet therapy during Primary PCI:
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Clopidogrel for at least 14 days up to 1 year
Adjunctive anticoagulant therapy with fibrinolysis: given for a minimum of 48 hours or until revascularization is performed (same dose as in NSTE-ACS)
o Unfractioned heparin (UFH) o Enoxaparin
o Fondaparinux
o Aspirin indefinitely after PCI
o One P2Y12-receptor inhibitor continued for 1 year for those who receive a stent:
Clopidogrel
Prasugrel (not used if + prior stroke/TIA)
Ticagrelor
Anticoagulant therapy during primary PCI:
o UFH o Bivalirudin
Fibrinolysis is still reasonable if symptom onset is within 12-24 hours as long as there is evidence of ongoing ischemia (although primary PCI is preferred for this population)
CONTRAINDICATIONS TO FIBRINOLYSIS
ABSOLUTE CONTRAINDICATIONS RELATIVE CONTRAINDICATIONS
Previous intracranial hemorrhage
Structural cerebral vascular lesion (e.g., AVM)
Malignant intracranial neoplasm
Ischemic stroke within 3 months except acute ischemic stroke within 4.5 hours
Suspected aortic dissection
Active bleeding / bleeding diathesis (except mense)
Closed-head or facial trauma within 3 months
Intracranial/intraspinal surgery within 2 months
Severe uncontrolled hypertension (unresponsive to emergency therapy)
For streptokinase, previous treatment within the previous 6 months
History of chronic, severe, poorly controlled HPN
Significant HPN at initial evaluation (SBP > 180 mmHg or DBP > 110 mmHg)
History of previous ischemia stroke > 3 months
Dementia
Intracranial pathology not covered in absolute contraindications
Traumatic or prolonged (>10 minutes) CPR
Major surgery (<3 weeks)
Recent (within 2-4 weeks) internal bleeding
Noncompressible vascular punctures
Pregnancy
Active peptic ulcer
Oral anticoagulant therapy
AVM: Arteriovenous malformation CPR: cardiopulmonary resuscitation C. Other Routine Medications for STEMI
THERAPY DESCRIPTION
Beta Blockers
Should be initiated in the first 24 hours, except if with signs of HF, low output state, increased risk for cardiogenic shock, or other contraindications (PR interval > 0.24, 2nd or 3rd degree AVB, active asthma, reactive airway disease)
RAAS Inhibitors
ACE-inhibitors should be initiated in the first 24 hours to all patients with anterior wall STEMI, HF or EF < 40% sitting in a chair
2nd and 3rd day: ambulation in the room with increasing duration and frequency to a goal of 185 cm (600 ft) at least 3x a day
2 weeks: resumption of work and sexual activity
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Nothing or only clear liquids (due to risk of emesis and aspiration) for the first 4-12 hours
Use of stool softener
Sedation Many require sedation during hospitalization to
withstand period of enforced inactivity E. Secondary Prevention and Long Term Management
THERAPY DESCRIPTION
Smoking Complete cessation
BP Control BP <140/90 or <130/80 if CKD or DM Lipid Management High dose statins
<7% of total calories as saturated fats and <200 mg/day total cholesterol Physical Activity 30 minutes of moderate intensity aerobic exercise, 3 to 4 days per week Weight
Management
BMI 18.5 – 24.9 kg/m2
Waist circumference: women <35 inches, men <40 inches DM Management HbA1c <7%
Anti-platelets Aspirin or P2Y12-receptor inhibitors
RAAS Blockers ACEI in stable high-risk patients (anterior MI, previous MI, Killip > II, EF <40%) Beta Blockers Continued indefinitely
IV. USUAL COMPLICATIONS OF STEMI
COMPLICATION FREQUENCY DESCRIPTION
Ventricular Septal Rupture (VSR)
1-3% in those who did not undergo reperfusion
Bimodal peak (within 24 hours & 3-5 days; can range from 1-14 days)
Presents with chest pain, SOB and hypotension
Holosystolic murmur, S3, accentuated 2nd heart sound, pulmonary edema, RV and LV failure, cardiogenic shock
Ventricular Free Wall Rupture
0.8-6.2%
Bimodal peal (within 24 hours & 3-5 days; can range from 1-14 days)
Presents with angina, pleuritic or pericardial chest pain, syncope, hypotension, arrhythmia, nausea, restlessness, hypotension and sudden death
JV distention (29%), pulsus paradoxus (47%), electromechanical dissociation and cardiogenic shock
Papillary Muscle Rupture
1% (posteromedial more frequently affected than anterolateral muscle)
Bimodal peak (within 24 hours & 3-5 days; can range from 1-14 days)
Abrupt onset of dyspnea, pulmonary edema, and hypotension
Soft murmur in most cases, no thrill, variable signs of RV overload, severe pulmonary edema, cardiogenic shock
Hypercontractile LV, torn papillary muscle or chordae tendinae, flail leaflet and severe MR on echo with color flow