1. ECG Lecture
Scott Ewing, D.O.
April 19, 2006

2. 34-year-old male. What's going on here ?

3. Acute Anterior MI
Classic findings of acute anterior wall Q wave myocardial infarction
Reciprocal inferior ST depressions
Hyperacute T waves
Distribution of changes is consistent with a proximal LAD occlusion
Confirmed at cardiac catheterization and treated with PTCA and stenting
Premature atherosclerosis with multiple risk factors including hypertension, hyperlipidemia, family history and tobacco.

4. 68-year-old female. What's going on here ?

5. Acute Anterior MI Note Q waves and loss of R waves V1 - V4
ST elevation in V2 - V5/V6
Left anterior fascicular block is also present, but does not account for the loss of R wave progression
The patient had had a very recent anterior MI
Cardiac catheterization revealed 3-vessel disease with a 90% mid-LAD "culprit" lesion

6. 53-year-old female. What's going on here ?

7. Acute Lateral MI ST elevations in I and aVL
Probable reciprocal ST depressions inferiorly consistent with acute lateral MI
Remember: ST elevations like this are never reciprocal but indicate the primary region of ischemia (diagonal or circumflex lesion)
Confirmed left circumflex occlusion at catheterization

8. 52-year-old male. What's going on here ?

9. Non-Q Wave Myocardial Infarction
Note slight inferior ST elevation with T wave inversion
Minimal reciprocal ST depression in aVL
Relatively low limb lead voltage makes these findings more subtle

10. 36-year-old male. What's going on here ?

11. Acute Pericarditis
Always consider myocardial infarction first when you see ST elevations
But don't forget the differential diagnosis of ST elevations
Ischemic heart disease
Pericarditis
Left bundle branch block (LBBB)
Normal ("early repolarization") variant
Two features here point to pericarditis
First, diffuseness of the ST elevations (I, II, III, aVF, V3-V6)
Second, PR depression in II, aVF, V4-V6 and PR elevation seen in aVR (attributed to subepicardial atrial injury)

12. 49-year-old male. What's going on here ?

13. Acute Pericarditis Diffuse ST segment elevations (I, II, aVF, V2-V6)
Subtle PR segment deviations (elevated in aVR and depressed in the inferolateral leads)
ST elevations are due to a ventricular current of injury from the pericardial inflammation
PR changes are due to an associated atrial current of injury
Note that the PR and ST segment vectors point in opposite directions, i.e., PR up and ST down in aVR and PR down and ST up in inferolateral leads
Resting sinus tachycardia is noted. The patient had a fever but no pericardial effusion

14. Middle aged female. What's going on here ?

15. Acute Myocardial Infarction
Marked inferior and lateral ST segment elevation
ST segment depression in anterior leads V1-V4
ST elevations (“current of injury” pattern) indicate transmural ischemia of the infero-lateral wall
ST depression most consistent with reciprocal change from the ST elevation generated by the acute posterior and lateral ischemia
Remember, acute pericarditis causes diffuse ST segment elevation (e.g., leads I, II, III, aVL, aVF, and the precordial leads)
Reciprocal ST depressions of the type seen here (V1-V4), are never a feature of pericarditis alone
Cardiac catheterization revealed acute occlusion of a dominant left circumflex coronary artery (along with occlusion of a smaller RCA)

16. GISSI-1: Gruppo Italiano per lo Studio della Streptochinasi nell’Infarto Miocardico
Purpose
To determine whether streptokinase (SK) reduces mortality when given shortly after onset of acute MI, and whether benefit, if present, depends on interval from pain onset to SK treatment
Reference
Gruppo Italiano per lo Studio della Streptochinasi nell’Infarto Miocardico. Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Lancet 1986;i:397–402.

17. GISSI-1: Gruppo Italiano per lo Studio della Streptochinasi nell’Infarto Miocardico - TRIAL DESIGN -
Multicenter, randomized, open, parallel group
Patients
11,806 patients with onset of acute MI within previous 12 h
Follow up and primary endpoint
Primary endpoint: all-cause mortality. 14–21 days follow up
Treatment
Patients randomized to treatment group (IV SK, 1.5 million U over 60 min) or control (no infusion)

18. GISSI-1: Gruppo Italiano per lo Studio della Streptochinasi nell’Infarto Miocardico - RESULTS -
21-day mortality significantly reduced in SK group (relative risk 0.81, P=0.0002) compared with control
For SK given at <6 h, the shorter the interval between pain onset and treatment, the bigger the reduction in mortality
For SK given at >6 h, no significant difference between treatment and control
SK judged safe in view of low incidence of adverse effects (major bleeds in 0.3% of SK group, anaphylactic shock in 0.1%)

19. GISSI-1: Gruppo Italiano per lo Studio della Streptochinasi nell’Infarto Miocardico - RESULTS continued -
Mortality and causes of death
Control SK
Relative risk P
(n=5852)
(n=5860)
(95% CI)
Mortality %
13.0
10.7
0.81 (0.72–0.90)
0.0002
No.
758
628
Causes of death
Cardiovascular
696
588
Noncardiovascular 45 32
Undefined 17 8
GISSI. Lancet 1986; i:397–402.

20. GISSI-1: Gruppo Italiano per lo Studio della Streptochinasi nell’Infarto Miocardico - RESULTS continued -
Mortality and time before treatment
Hours from onset
Control, %
SK, %
Relative risk P
to treatment
(deaths/n)
(deaths/n)
(95% CI)
<3*
12.0
9.2
0.74 (0.63–0.87)
0.0005
(369/3078)
(278/3016)
>3 – 6
14.1
11.7
0.80 (0.66–0.98)
0.03
(254/1800)
(217/1849)
>6 – 9
14.1
12.6
0.87 (0.64 –1.19) NS
(93/659)
(87/693)
>9 – 12
13.6
15.8
1.19 (0.75–1.87) NS
(41/302)
(46/292)
*<1
15.4
8.2
0.49 (0.34–0.69)
0.0001
(99/642)
(52/635)
GISSI. Lancet 1986; i:397–402.

21. Given within 6 h of onset of pain in acute MI, intravenous SK:
GISSI-1: Gruppo Italiano per lo Studio della Streptochinasi nell’Infarto Miocardico - SUMMARY -
Given within 6 h of onset of pain in acute MI, intravenous SK:
Reduced mortality
Conferred greater benefit when administered earlier

22. GUSTO-I: Global Utilization of Streptokinase and t-PA for Occluded coronary arteries - I
Purpose
To compare an aggressive thrombolytic strategy using accelerated tissue plasminogen activator (t-PA) with standard thrombolytic strategies in the treatment of acute myocardial infarction
Reference
The GUSTO Investigators. An international randomized trial comparing four thrombolytic strategies for acute myocardial infarction. N Engl J Med 1993;329:

23. GUSTO-I: Global Utilization of Streptokinase and t-PA for Occluded coronary arteries - I - TRIAL DESIGN -
Design: Randomized, parallel group
Patients: 41,021 patients with AMI, <6h after onset of symptoms
Follow up and endpoint: Primary endpoint death at 30 days
Treatment: Four thrombolytic strategies compared:
Streptokinase (SK) (1.5 million U over 60 min) and SC heparin (12,500 U twice daily)
SK (1.5 million U over 60 min) and IV heparin (bolus 5000 U then 1000 U/h)
IV t-PA (1 mg/kg over 60 min, 10% bolus) and SK (1 million U over 60 min) and IV heparin (bolus 5000 U then 1000 U/h)
Accelerated t-PA (accelerated dose t-PA administered as bolus 15 mg, 0.75 mg/kg over 30 min (max 50 mg) and 0.5 mg/kg over 1h (max 35 mg)) and IV heparin (bolus 5000 U then U/h)

24. GUSTO-I: Global Utilization of Streptokinase and t-PA for Occluded coronary arteries - I - RESULTS -
Significant reduction in 30-day mortality with accelerated t-PA compared with the streptokinase (SK) and combination strategies
No significant difference between combination strategy and the two SK strategies (P=0.352), or between the two SK strategies (P=0.731)
Significant excess of hemorrhagic stroke for accelerated t-PA
(P=0.03) and combination strategy (P<0.001), compared with the two SK-only strategies
However, combined endpoint of death or disabling stroke significantly lower with accelerated t-PA than with SK-only strategies (6.9% versus 7.8%; P=0.006)
Do we need anything on subgroups (esp age?)

25. GUSTO-I: Global Utilization of Streptokinase and t-PA for Occluded coronary arteries - I - RESULTS continued -
Thirty-day mortality and stroke in the four treatment groups
Mortality (%) 8 6
SK + IV heparin 4
SK + SC heparin
t-PA + SK + 2
IV heparin
Accelerated t-PA 10 20 30
Days after randomization
The GUSTO Investigators.
N Engl J Med
1993;
329
:673 –
82.

26. GUSTO-I: Global Utilization of Streptokinase and t-PA for Occluded coronary arteries - I - RESULTS continued -
Thirty-day mortality and stroke in the four treatment groups
Mortality
(%)
Stroke
SK + IV heparin
SK + SC heparin
t-PA + SK +
IV heparin
Accelerated t-PA
0.54
0.49
0.94
0.72
7.4
7.2
7.0
6.3
Comparison with
accelerated t-PA* P
0.003
0.009
0.04
*P=0.001 for accelerated t-PA compared with both SK strategies
The GUSTO Investigators.
N Engl J Med
1993; –
329
:673
82.

27. GUSTO-I: Global Utilization of Streptokinase and t-PA for Occluded coronary arteries - I - SUMMARY -
Although there was an excess of hemorrhagic stroke with t-PA plus heparin, compared with the other regimens, the combined 30-day endpoint of death or disabling stroke was significantly lower with accelerated t-PA
An aggressive thrombolytic strategy using accelerated t-PA (over 1.5 hours instead of 3 hours) with heparin, to produce earlier and sustained reperfusion, improves survival significantly compared with standard thrombolytic regimens comprising SK plus heparin