ST-Elevation MI

Definition of STEMI:

· ECG criteria:

o ≥2 mm of ST segment elevation in 2 contiguous precordial leads in men (1.5 mm for women)

o ≥1mm in other leads (2 contiguous)

o An initial Q wave or abnormal R wave develops over a period of several hours to days.

· Within the first 1-2 weeks (or less), the ST segment gradually returns to the isoelectric baseline, the R wave amplitude becomes markedly reduced, and the Q wave deepens. In addition, the T wave becomes inverted.

· In addition to patients with ST elevation on the ECG, two other groups of patients with an acute coronary syndrome are considered to have an STEMI: those with new or presumably new left bundle branch block and those with a true posterior MI

· An elevation in the concentration of troponin or CK-MB is required for the diagnosis of acute MI

· Anterior STEMI: ST elevation in the precordial leads + I and aVL (LAD territory)

· Posterior STEMI: reciprocal ST depressions in V1-V3 (ST elevation in post leads), may have component of inferior ischemia as well (ST elevations in II, III and aVF) Often occurs w/ inferior MI (L Cx)

· Inferior STEMI: ST elevation in II. III and aVF (+ ST elevation in R-sided precordial leads), reciprocal changes in I and aVL (R coronary or L Cx)

Ddx for MI (STEMI or NSTEMI) without atherosclerosis:

arteritis (PAN, lupus, Takayasu’s, Kawasaki’s)
trauma (laceration, radiation, iatrogenic)
initimal proliferative diseases (amyloidosis, inimal hyperplasia from OCPs, coronary fibrosis etc)
spasm (prinzmetal’s, after nitro withdrawl)
dissection (aorta or coronaries)
emboli to coronary arteries (IE, cardiac myxoma, catheters/guidewires, paradoxical emboli)
congenital coronary artery anomalies
myocardial 02 demand-supply mismatch (AS, AI, takotsubo, prolonged hypotension, thyrotoxicosis)
hematologic (DIC, PV, TTP etc.)
drugs (cocaine, amphetamines)

Other cause of ST elevation (not MI):

Acute pericarditis
Myocarditis (may look like MI or pericarditis)
Massive pulmonary embolism (leads V1-V2 in occasional cases)
Brugada-type patterns (V1-V3 with right bundle branch block-appearing morphology)
Hyperkalemia (only leads V1 and V2)
Hypothermia (J wave/Osborn wave)
Hypercalcemia (rarely)
Post-DC cardioversion (rarely)

Acute Management of ACS, STEMI:

Initial ACS management:

• Assess and stabilize ABCx

• Provide oxygen, establish IV access, cardiac/02 monitor

• Treat any sustained arrhythmias according to ACLS protocols

• Give aspirin 325 mg (non-enteric coated), to be chewed and swallowed (unless aortic dissection is being considered). If oral administration not feasible, give as rectal suppository.

• Draw labs for cardiac biomarkers (troponin preferred), electrolytes, coags, hematocrit/hemoglobin

• Treat left heart failure: Give afterload reducing agent (eg, nitroglycerin sublingual tab and/or IV drip at 40 mcg/minute provided no phosphodiesterase inhibitors [eg, for erectile dysfunction]); titrate drip up based on response; give loop diuretic (eg, furosemide 80 mg IV).

• Give SL nitroglycerin tablets (0.4 mg) x3, one at a time, spaced 5 minutes apart, IF patient has persistent chest pain, hypertension, or signs of heart failure AND there is no sign of hemodynamic compromise (eg, RV infarct) and no recent use of phosphodiesterase inhibitors, add IV nitro for persistent symptoms

• Give beta blocker (eg, metoprolol 25 mg orally) IF no signs of heart failure (or high risk for heart failure), hemodynamic compromise, bradycardia, or severe reactive airway disease.

• Give morphine IV for persistent discomfort or anxiety

• Give 80mg of atorvastatin po as early as possible, and preferably before PCI, in patients not on statin

Acute STEMI management:

• Select reperfusion strategy: PCI strongly preferred, especially for patients with cardiogenic shock, heart failure, late presentation, or contraindications to fibrinolysis.

• For patients with symptoms of >12 hours, fibrinolytic therapy is not indicated, but emergent PCI may be considered, particularly for patients with evidence of ongoing ischemia or those at high risk.

• Treat with fibrinolysis if PCI unavailable within 90-120 minutes, symptoms <12 hours, and no contraindications

• Give antiplatelet therapy (in addition to aspirin): clopidogrel 600 mg (300mg if fibrinolysis or no PCI). Consider adding glycoprotein IIb/IIIa inhibitor if PCI is planned.

• Give anticoagulant therapy: Unfractionated heparin (UFH) for patients undergoing PCI (IV bolus of 50 to 70 units/kg). Bivalirudin is an acceptable alternative to heparin in patients undergoing primary PCI. Enoxaparin only for patients not managed with PCI and GFR>30.

McConnell’s sign: well-recognized pattern of RV wall motion seen in acute PE; characterized by normal RV apex contractility with akinesis of the RV free wall with 77% sensitivity, 94% specificity, 71% positive predictive value, and 96% negative predictive value for PE. Etiology is not well understood; one explanation is the visual illusion of preserved RV apex contractility might simply reflect tethering of the RV apex to a hyperdynamic LV in the presence of an acutely dilated RV.

(Victoria Kelly MD, 10/28/10)