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Differential Diagnosis of ST Segment Elevation. ST Elevation and Chest Pain. Two series evaluated ER patients who had ST elevation and chest pain. Jayes et al. found that 171 of 203 had eventual diagnosis other than myocardial infarction. Brady found 63 of 123 had another diagnosis.
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ST Elevation and Chest Pain • Two series evaluated ER patients who had ST elevation and chest pain. • Jayes et al. found that 171 of 203 had eventual diagnosis other than myocardial infarction. • Brady found 63 of 123 had another diagnosis. • Most common causes other than MI were LVH, LBBB, early repolarization, or LV aneurysm.
ST Elevation and Thrombolysis • Two studies of thrombolytic treatment showed that between 5.7 and 11% of patients did not have myocardial infarction. • Most common actual diagnoses were LVH, early repolarization , conduction defects, or LV aneurysm.
Causes of ST Segment Elevation 1. Normal ST elevation 2. Normal variants- a) Normal early repolarization b)Terminal T wave inversion type 3. Left ventricular hypertrophy 4. Left Bundle Branch Block 5. Acute Pericarditis or Myocarditis 6. Hyperkalemia 7. Brugada Syndrome or RV Arrhythmogenic cardiomyopathy 8. Pulmonary Embolus 9. Post DC cardioversion 10 .Prinzmetal’s Angina 11. Left ventricular aneurysm 12. Intracranial Hemmorhage 13. Hypothermia 14. Aortic Dissection `15. Acute Myocardial Infarction
Normal ST Elevation • Measure ST at end of the P-R segment-not the T-P segment. • A USAF study by Hiss et.al. in 1960 looked at 6014 healthy men between 16 and 58 years of age- 91% had ST elevation of 1 to 3 mm in one or more precordial leads. Most common and most marked in V2. • In 2002 Surawitz looked at 529 men. In men 17-24 years of age there was greater than 1 mm. ST elevation in one or more leads (V1-V4) in 93%. • Prevalence decline gradually with increasing age-30% in men >76 years.
In women prevalence was 20% and there was no change with aging. • This is a NORMAL finding –not a normal variant. • ST segment is CONCAVE and the deeper the S wave the more the ST elevation.
ST Variants of Normal • In some healthy young people- especially black men -the ST segment is elevated by 1-4 mm in the mid precordial leads. • ST elevation is most marked in V4 and there is a notch at the J point. • St segment is CONCAVE. • T waves are tall and not inverted • May have P-R segment depression (< than in pericarditis)
Some young black men have ST elevation in the mid precordial leads in combination with T wave inversions as a normal variant. • Differs from early repolarization because T waves are inverted and the ST segment tends to be COVED. • May suggest MI and an echo may be necessary to differentiate it. • QT tends to be short in the normal variant –not in MI
PROBLEM! • These ST elevations meet the criteria for thrombolysis by guidelines of the ACC-AHA--- “St elevation greater than 0.1 mv in two or more contiguous leads. • American College of Emergency Physicians suggests adding “ST elevations… that are not characteristic of early repolarization or pericarditis nor of a repolarization abnormality of LVH or bundle branch block. • Even this may not address normal ST elevation.
LVH • May have precordial ST elevation V1-V3 • May also have QS pattern in V1-V3 • The deeper the S wave, the higher the ST elevation. • LVH is one of the most common conditions mistaken for acute MI,however St is CONCAVE compared with CONVEX in acute concomitant MI.
LBBB • In LBBB diagnosis of MI may be difficult - ST can be elevated or depressed and may simulate or mask MI. • Secondary ST changes are shifted in the opposite direction from the major component of the QRS(discordant) • When ST changes are concordant they are specific for acute MI. • If ST segments in V1-V3 become CONVEX instead of concave they may indicate associated anteroseptal MI. • If ST elevations greater than 5 mm MI is suggested (not highly reliable)
Acute Pericarditis or Myocarditis • ST segments are diffusely elevated in the precordial leads as well as limb leads-indicating involvement of more than one vascular bed which rarely happens in acute MI. • PR segment is depressed. (Not diagnostic because also found in early repolarization or atrial infarction.) • ST segment is elevated in III and aVL, but more elevated in II than III. In contrast, in acute inferior MI, ST elevation in III is always associated with reciprocal ST depression in aVL and ST elevation is greater in III than II. • In pericarditis there is reciprocal ST depression aVR • ST elevation in pericarditis is rarely greater than 5 mm.,whereas it may be in acute infarction. PR segment is usually not depressed in acute MI. • Myocarditis can cause diffuse ST elevation and can simulate MI.
Hyperkalemia • May see marked ST elevation , but usually see associated additional changes of a)widening of the QRS b) tall, pointed and tented T waves c) low amplitude or absent P waves. • ST elevation often is downsloping as compared to MI which usually has a plateau or shoulder or is upsloping. • Echocardiogram may be helpful in discriminating these conditions. • Serum K+ may help evaluation.
Acute Myocardial Infarction • Marked St elevation which is greater than 5 mm. and is convex or coved. (tombstone appearance)
Acute MI in the presence of RBBB • In acute anteroseptal MI complicated by RBBB the downstroke of the R`wave and the beginning of the ST segment have a distinct transition, and the ST segment is horizontal or upsloping , not downsloping.
The Brugada Syndrome and Arrhythmogenic Right Ventricular Cardiomyopthy • 1992 Brugada and Brugada described 8 patients with cardiac arrest and EKG changes of RBBB and ST elevation if the right precordial leads in the absence of long QT intervals or any structural heart disease. • It accounts for 40-60% of all idiopathic ventricular fibrillation. (Chen et. al.) • Linked to mutations in the cardiac sodium channel gene. This leads to a transmural voltage gradient which causes ST elevation and ventricular fibrillation. • Diagnosis: a) Complete or incomplete RBBB but no wide S waves are seen in I, aVL, or V6 like RBBB.b) ST elevation is usually in V1-V2. It begins from the top of the R`wave and is downsloping and ends with an inverted T wave. • ST elevation may be continuous or intermittent. Flecainide, procainamide, or cocaine may unmask EKG pattern.
Pulmonary Embolus • T wave inversions in right precordial leads. • Simultaneous T wave inversion and ST elevation in anteroseptal and inferior leads. • S1Q3T3 pattern • Complete or incomplete RBBB • Sinus tachycardia • May mimic anterior MI
Post DC Cardioversion • 23 of 146 patients cardioverted with atrial fibrillation or flutter (16%) had ST elevation pf 5mm. or more. • Usually normalized within 1.5 minutes. No enzyme rise noted. • These patients had lower conversion rate and were less likely to remain in NSR.(Van Gelder et.al.) • Kok et al. observed transient ST elevation in 20 of 130 (15.4%) of patients who received DC cardioversion for ventricular tachyarrythmias during EP studies. None had evidence of an acute coronary event. Those with ST changes had lower EF than those without.(25% vs.35%). Mechanism is unclear.
Prinzmetals’s Angina • Transmural myocardial ischemia caused by coronary vasospasm. When spasm is relieved the ST segments return to baseline. • If spasm is prolonged ,MI can occur. • Indistinguishable from Acute MI during vasospasm.
LV Aneurysm • Persistent ST elevation lasting greater than six weeks post MI.