Initial Reperfusion T-waves, Followed by Pseudonormalization. Diagnosis?

A middle-aged woman had intermittent angina for 48 hours, then onset of constant, crushing chest pain for 1.5 hours when she called 911.  Her prehospital ECG was identical to her first ED ECG, and the cath lab was activated:

There is massive ST elevation (greater than 15 mm) in V2 and V3, with ST elevation in I and aVL and reciprocal ST depression in II, III, aVF.  There are Q-waves already present.
This is diagnostic of large and VERY Acute (NOT subacute) Antero-lateral MI due to proximal LAD occlusion.

Q-waves appear in 50% of anterior MI within the first hour.  These do NOT indicate late, subacute MI.   The ST elevation is far too high for a subacute MI.
----Raitt MH, et al. Appearance of abnormal Q waves early in the course of acute myocardial infarction: implications for efficacy of thrombolytic therapy. J Am Coll Cardiol 1995; 25:1084-1088.

The "ST score" is > 40 mm, which is extremely high and correlates well with high mortality, as does the presence of Q-waves.  There is a body of literature from the thrombolytic era showing that high ST score correlates with high mortality (see annotated bibliography below, from my book The ECG in Acute MI).


Angiogram: 100% occlusion in the mid LAD after first septal perforator (S1) and at the bifurcation of the mid-LAD and first diagonal (D1), obstructing flow down both. TIMI flow is 0.  It was treated with and dual "kissing balloons" and drug eluting stents.  Door to balloon time was 51 minutes.

Here is the post stent ECG:

There is greater than 50% resolution of ST elevation (all but diagnostic of successful reperfusion) and Terminal T-wave inversion (also highly suggestive of successful reperfusion).

However, much ST elevation remains, and there is no re-constitution of R-waves.  Both of these are very suggestive of "No-Reflow," or poor microvascular reperfusion due to downstream embolization of microscopic platelet-fibrin aggregates.  This ECG finding is stronlgy associated with completion of the MI into a "Transmural MI", as if there had been no successful reperfusion.  

Contemporary Troponin I Profile

time zero:           1.28 ng/mL
time 1.5 hours:   0.75
time 4.5 hours:   56.1
time 7.5 hours:   61.0
time 10.5 hours: 53.9

Formal Echo 6 hours later:
1. Decreased LV function, EF 35-40%
2. Regional wall motion abnormality-distal septum, anterior, anterolateral and apex
3. LV Thrombus, 1.5 cm diameter in the apex

The presence of thrombus led the clinicians to state that this was a "late presentation STEMI."  It does take some time for thrombus to form, but the EKG and the troponin profile show that this was NOT a late presentation STEMI.  More likely, the patient had crescendo angina, with REVERSIBLE ischemia for 48 hours that only became potentially irreversible (STEMI) at that point in time. During the 48 hours of angina, such reversible ischemia often leads to myocardial stunning with akinesis of the myocardial wall that puts it at risk for thrombus.


The next morning, this ECG was recorded 8 hours after the first one:

This shows some increase in the ST elevation and, even more importantly, the T-waves have again become fully upright.  The terminal T-wave inversion that signifies reperfusion is gone.

This returning-to-upright of T-waves is called Pseudonormalization and has two etiologies:
1. Re-occlusion
2. Post-infarction Regional Pericarditis (PIRP)


PIRP happens when MI is transmural, all the way from subendocardium to subepicardium, thus leading to inflammation of the subepicardium (next to the pericardium).  PIRP is associated with a higher risk for myocardial rupture.

---This comes from chapter 28 of my book The ECG in Acute MI).
MYOCARDIAL RUPTURE AND POSTINFARCTION REGIONAL PERICARDITIS

KEY POINTS

·      Myocardial rupture occurs in 1 to 1.5% of AMI patients and is often preceded by postinfarction     regional pericarditis (PIRP). 

·      PIRP is indicated by persistently positive (upright) T-waves 48 hours after onset of AMI.

·      PIRP is very likely if there is premature reversal of inverted T-waves to positive deflections 

·      Any STEMI patient in shock may have tamponade, often due to myocardial rupture.

·      Bedside echocardiography can easily confirm myocardial rupture.     

Case continued:       

The patient had recurrent pain at this time, but it was pleuritic and positional, so she was believed to have PIRP.  This is a bit risky to make this diagnosis based on symptoms alone (not angiogram), as re-occlusion is deadly.  But the assessment was correct, as troponins continued to decline.


An ECG was recorded 16 hours after the first one:

This shows decreasing ST elevation.  T-waves remain upright.  You would see this with either PIRP or re-occlusion

This was recorded 30 hours after the first:

Still less ST elevation

Much less STE, a good sign.  Perhaps she will not develop an LV aneurysm.  That remains to be seen.

Myocardial Rupture and Postinfarction Pericarditis.

The ECG in myocardial rupture

94.       Oliva PB, Hammill SC, Edwards WD. Electrocardiographic diagnosis of postinfarction regional pericarditis: ancillary observations regarding the effect of reperfusion on the rapidity and amplitude of T wave inversion after acute myocardial infarction. Circulation 1993; 88:896-904.  

Methods:  Oliva et al. (94) studied 200 consecutive AMI patients and compared ECG evolution with development of PIRP as diagnosed by typical clinical signs and symptoms including pleuritic-positional chest, left shoulder, or scapular pain or friction rub, with no re-elevation of CK-MB.

Findings:  Of 200 patients, 43 (21.5%) developed PIRP, all of whom displayed one of two types of unusual T-wave evolution (100% sensitivity).  Type I consisted of persistently positive T-waves >/= 48 to 72 hours after infarction and occurred in 29 (67%) of cases of PIRP.  Specificity for PIRP was 100%.  Type II consisted of premature, gradual reversal of inverted T-waves to positive deflections >/= 48 to 72 hours after AMI onset in 12 (33%) cases of PIRP.  Patients who received CPR or experienced reinfarction or very small infarcts due to thrombolysis also displayed Type II T-wave evolution.  Specificity of Type II for PIRP was 77%.  Widespread ST elevation of diffuse pericarditis was seen in only 2 patients (5%) with PIRP.  The authors conclude that premature “re-concordance” of the T-wave after AMI is a sensitive, fairly specific, and easily recognizable sign of PIRP and that reperfusion is associated with accelerated T-wave evolution and deepening.

366.     Oliva PB, Hammill SC, Edwards WD. Cardiac rupture, a clinically predictable complication of acute myocardial infarction: report of 70 cases with clinicopathologic correlations. J Am Coll Cardiol 1993; 22:720-726.  

Methods:  Oliva et al. (366) compared the clinical and ECG features of 70 AMI patients with myocardial rupture to findings from 100 AMI patients without rupture. 

Findings:  Patients with rupture had a significantly greater incidence of PIRP and persistent vomiting, restlessness, and agitation; 80% had at least 2 symptoms vs. 3% of AMI patients without rupture.  Deviation from the normal pattern of T-wave evolution occurred in 94% of patients with rupture and in only 34% of patients without rupture.  Midlateral wall rupture secondary to infero-postero-lateral infarction from circumflex occlusion was most common (34%).

Comment:  Although reasonably specific for PIRP, this deviation from normal T-wave evolution does not have a high PPV because of the relatively low incidence of rupture.

ST Score

109.     Mauri F, Gasparini M, Barbonaglia L, et al. Prognostic significance of the extent of myocardial injury in acute myocardial infarction treated by streptokinase. (the GISSI trial). Am J Cardiol 1989; 63:1291-1295

Methods: Mauri et al. (109) classified ECG’s from 8731 GISSI-1 patients (randomized to SK or placebo, see Appendix) with ST elevation and no previous infarct into 4 groups: 1) small (ST elevation in 2 or 3 leads, 41% of patients); 2) modest (4 to 5 leads, 25%); 3) large (6 to 7 leads, 19%); and 4) extensive infarct (8 to 9 leads, 15%).  ST depression and height of ST segments were not addressed. 

Findings:  Of large or extensive infarcts, 100% were anterior or multiple site and of small infarcts, 93% were inferior.  Although infarct size, mortality, ultimate development of Q-wave or loss of R-wave, and benefit from SK correlated with location (anterior infarction was the worst), they correlated more strongly with number of leads involved.  Small AMI (</= 3 leads) did not correlate with significant mortality benefit from SK.

111.     Bar FW, Vermeer F, de Zwaan C, et al. Value of admission electrocardiogram in predicting outcome of thrombolytic therapy in acute myocardial infarction. Am J Cardiol 1987; 59:6-13.

Methods:  Bar et al. (111) analyzed data from 488 patients randomized to intracoronary SK or control.   

Findings:  Patients with anterior location, high ST score (>12 mm for anterior, > 6 mm for inferior), marked ST depression, or presence of Q-waves had the greatest limitation of infarct size as measured by radionuclide left ventriculography and CK.  For both anterior and inferior locations, in the absence of concomitant Q-waves, no significant limitation was seen in patients with low ST score, BUT confidence intervals were wide.

122.     Lee KL, Woodlief LH, Topol EJ, et al. Predictors of 30-day mortality in the era of reperfusion for acute myocardial infarction: results from an international trial of 41,021 patients. Circulation 1995; 91:1659-1668.

  

Methods: Lee et al. (122) analyzed GUSTO-1 data (see Appendix). 

Findings:  Mortality was 9.9% for all anterior AMI’s vs. 5.0% for all inferior AMI’s (all patients received thrombolytics).  

Comment:  This study does NOT reflect the heterogeneity of inferior MI; although low for simple inferior MI, mortality is high for inferoposterior, infero-RV, and inferolateral MI.

117.     Vermeer F, Simoons ML, Bar FW, et al. Which patients benefit most from early thrombolytic therapy with intracoronary streptokinase? Circulation 1999; 74:1379-1389.

Methods:  Vermeer et al. (117) analyzed ECG’s, radionuclide left ventriculography and enzyme-release data from 533 patients randomized to intracoronary SK vs. control (no SK). 

Findings:  Thrombolysis with SK resulted in the greatest limitation of infarct size in patients with electrocardiographically larger AMI’s (large new Q-waves, high ST elevation, reciprocal depression, and anterior AMI) or in those admitted within 2 hours of symptom onset.  Among all patients with an ST score < 12 mm, those who received SK > 2 hours from symptom onset demonstrated no beneficial effects on mortality, LV function as measured by radionuclide left ventriculography, or enzymatic infarct size, over those who did not receive thrombolytics.

123.     Gwechenberger M, Schreiber W, Kittler H, et al. Prediction of early complications in patients with acute myocardial infarction by calculation of the ST score. Ann Emerg Med 1911; 30:563-570.  

Methods:  Gwechenberger et al. (123) conducted an observational study of 243 patients who presented with anterior or inferior AMI and received thrombolytics.

Findings:  Increased ST score was associated with an increased rate of complications.  A cutoff of 9 mm for inferior AMI and 13 mm for anterior AMI predicted worse outcome.

112.     Peterson ED, Hathaway WR, Zabel KM, et al. Prognostic significance of precordial ST segment depression during inferior myocardial infarction in the thrombolytic era: results in 16,521 patients. J Am Coll Cardiol 1996; 28:305-312.

Methods:  Peterson et al. (112) analyzed clinical and angiographic outcomes of 16,521 patients with inferior AMI who received thrombolytics in the GUSTO-1 trial (see Appendix).

Findings:  Greater reciprocal ST depression correlated strongly with poor outcome. 

84.       Willems JL, Willems RJ, Willems GM, Arno AE, Van de Werf F, Verstraete M. Significance of initial ST segment elevation and depression for the management of thrombolytic therapy in acute myocardial infarction. Circulation 1990; 82:1147-1158. 

Methods:  Willems et al. (84) analyzed data on enzyme release, ventriculographic EF, and wall motion from 665 patients in the ECSG trial of tPA for treatment of AMI (see Appendix).

Findings:  In-hospital mortality was greater, but benefit from thrombolytics as measured by mortality and by limitation of infarct size was also greater, with a total sum of ST elevation (as measured 60 ms after the J-point) of > 20 mm.  The sum was significantly different when measured at the J-point or 60 msec after the J-point (mean, 16 +/- 9 mm vs. 23 +/- 11 mm).

116.     Hathaway WR, Peterson ED, Wagner GS, et al. Prognostic significance of the initial electrocardiogram in patients with acute myocardial infarction.  GUSTO-I Investigators.  Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries. JAMA 1998; 279:387-381.   

Methods: Hathaway et al. (116) analyzed clinical and ECG findings from GUSTO-1 (see Appendix). 

Findings:  The strongest independent overall predictors of 30-day mortality were age, systolic BP, and Killip class.  The strongest independent ECG predictors were increased absolute ST deviation (in precordial and limb leads), HR, QRS duration, AND ECG evidence of previous infarct.  The study does not comment on thrombolytic benefit in these instances.  Data from Nixdorff et al. (124) and Sugiura et al. (125) support these findings.