9 Hours of Chest Pain and Deep Q-waves: Is it too late for Thrombolytics? (Time Window for Reperfusion; Acuteness on the ECG)

A 50 year old hypertensive presented with 9 hours of central crushing chest pain.  BP was 250/120, and after placement on an IV nitroglycerine drip, BP declined to 170/90.  Here is the presenting ECG:

There is diagnostic ST elevation with large T-waves.  However, there are deep QS-waves.  
1. How do we know these QS-waves do not represent LV aneurysm?
2. Do these Q-waves imply that the STEMI is too far progressed for benefit from tPA?

Let's answer question 1: The T-waves are too tall for LV aneurysm!  You can use this LV Aneurysm Rule to Determine whether there is acute STEMI or ST elevation due to LV aneurysm.
Question 2 is answered extensively below.

Time window for thrombolytics: The GISSI and the LATE trial both established that late thrombolysis, up to 12 hours after onset of chest pain, is beneficial for STEMI.  The FTT collaborative group meta-analysis confirmed this, and the benefit at various time points after pain onset is best described in the paper by Boersma (see Table below).  There are many STEMI, however, which will benefit beyond 12 hours of chest pain: the time onset of chest pain is not necessarily the time of onset of irreversible ischemia.  Many MIs have dynamic occlusion and reperfusion of the infarct-related artery and the pain can go on for days without any significnat necrosis.

The best indicator of MI "Acuteness" is the ECG, with these as indicators of high acuteness:
1. Absence of Q-waves
2. High ST segments
3. Large size of T-waves
4. Absence of T-wave inversion all indicators of high acuity.
At the bottom, I have reprinted a section that I wrote on "Acuteness" that comes from a chapter on reperfusion thereapy that I wrote with Bill Brady.

In this case, the ST segments are high, the T-waves are large, and there is no T-wave inversion.  The Q-waves are the only indicator of prolonged ischemia.  Moreover, the chest pain is less than 12 hours.  Unless there are important contraindications to reperfusion (i.e., high bleeding risk), then either tPA or PCI are indicated.

Case Progression

The physician could not get the interventionalist to take the patient for PCI (I am not sure why).  

The emergency physician sent this case to me real time, wondering if the QS-waves (absence of any R-wave) were a contraindication to tPA.  Before I could answer that, "no" they are not a contraindication, he gave tPA.

Shortly after tPA, this ECG was recorded:

There is significantly lower ST elevation, T-waves are no longer acute (tall) and have begun to invert.  These are signs of reperfusion.

In addition, and importantly, the pain completely resolved with thrombolytics.

An echocardiogram showed akinesis of the mid-apical portion of the anterior septum and mid-apical portion of the inferior septum.  There was no thinning to suggest old MI (not LV aneurysm). This was consistent with acute anterior STEMI.

Subsequently, the interventionalist agreed to take the patient for rescue PCI (even though the thrombolytics had clearly lysed the thrombus).  Angiogram revealed a severely stenotic mid-LAD lesion with no more thrombus present and TIMI-3 flow (excellent).  Thus, the artery had opened.  It was stented.

How long after onset of chest pain are thrombolytics effective (how long is the time window)?

Table 33-1 (from my book: The ECG in Acute MI): Time to thrombolysis and mortality reduction.  From: Boersma et al., Early thrombolytic treatment in acute myocardial infarction: reappraisal of the golden hour. Lancet October 21, 1996, 348:771-775.  (This applies to all MI: anterior, inferior, lateral)

Time Window	Lives saved per 1000 patients treated (confidence intervals)
0-1 hour	65 (38-93)
1-2 hours	37 (20-55)
2-3 hours	26 (14-37)
3-6 hours	29 (19-40)
6-12 hours	18 (7-29)
12-24 hours	9 (-5-22) (not statistically significant)

What is the significance of pathologic Q-waves on the inital ECG?

Q-waves are often seen in the first hour after pain onset.  Raitt et al. found in a subgroup of 432 first MI patients whose ECG was recorded within the first hour after onset of chest pain that pathologic Q-waves were already present, and this was particularly true for anterior MI patients.  These patients had larger final infarct size, but equal benefit from thrombolytic therapy. 

More recently, Armstrong et al. showed that Q-waves on the baseline ECG are an independent marker of worse clinical outcome and, importantly, "after multivariable adjustment, baseline Q-wave but not time from symptom onset was significantly associated with a 78% relative increase in the hazard of 90-day mortality and a 90% relative increase in the hazard of death, shock, and CHF."  Thus, another study shows that the ECG is a better marker of "acuteness" of the ECG than is time of symptom onset.

Lastly, when is it too late for emergent PCI?  Never, if there is persistent chest pain.

How about if the chest pain is resolved, but there is still ST elevation?  That was assessed in this study by Schomig et al. (this is linked to full text; reference and abstract below). They randomized patients who had at least one chest pain episode of at least 20 minutes that occurred between 12 and 48 hours before presentation, and had no persistent symptoms (!), but had unequivocal ischemic ST elevation on the ECG.  Randomized to immediate angiogram with PCI vs. later unplanned invasive evaluation and treatment if they developed recurrent severe angina, hemodynamic and electrical instability, severe congestive heart failure and/or pulmonary edema, mechanical complications, new relevant electrocardiographic changes (new or reelevation of ST-segments of 0.2 mV in 2 contiguous precordial leads or 0.1 mV in 2 adjacent limb electrocardiographic leads), reelevation of creatine kinase or creatine kinase-MB by at least 50% above the trough level after documentation that the level was decreasing prior to this re-elevation, or signs of induced ischemia during exercise testing.

It is taken as a given that if there are persistent symptoms, emergent PCI is indicated!!

Mechanical Reperfusion in Patients With Acute Myocardial Infarction Presenting More Than 12 Hours From Symptom Onset: A Randomized Controlled Trial.  Schomig et al. JAMA. 2005;293:2865-2872
http://jama.jamanetwork.com/article.aspx?articleid=201080

Abstract

Context: No specifically designed studies have addressed the role of primary percutaneous coronary intervention in patients with acute ST-segment elevation myocardial infarction (STEMI) presenting more than 12 hours after symptom onset. Current guidelines do not recommend reperfusion treatment in these patients.
Objective: To assess whether an immediate invasive treatment strategy is associated with a reduction of infarct size in patients with acute STEMI, presenting between 12 and 48 hours after symptom onset, vs a conventional conservative strategy. Design, Setting, and Patients International, multicenter, open-label, randomized controlled trial conducted from May 23, 2001, to December 15, 2004, of 365 patients aged 18 to 80 years without persistent symptoms admitted with the diagnosis of acute STEMI between 12 and 48 hours after symptom onset.
Interventions: Random assignment to either an invasive strategy (n=182) based predominantly
on coronary stenting with abciximab or a conventional conservative treatment
strategy (n=183).
Main Outcome Measures: The primary end point was final left ventricular infarct size according to single-photon emission computed tomography study with technetium Tc 99m sestamibi performed between 5 and 10 days after randomization in 347 patients (95.1%). Secondary end points included composite of death, recurrent MI, or stroke at 30 days.
Results: The final left ventricular infarct size was significantly smaller in patients assigned to the invasive group (median, 8.0%; interquartile range [IQR], 2.0%-15.8%) vs those assigned to the conservative group (median, 13.0%; IQR, 3.0%-27.0%; P .001). The mean difference in final left ventricular infarct size between the invasive and conservative groups was −6.8% (95% confidence interval [CI], −10.2% to −3.5%). The secondary end points of death, recurrent MI, or stroke at 30 days occurred in 8 patients in the invasive group (4.4%) and 12 patients in the conservative group (6.6%) (relative risk, 0.67; 95% CI, 0.27-1.62; P=.37).
Conclusion: An invasive strategy based on coronary stenting with adjunctive use of
abciximab reduces infarct size in patients with acute STEMI without persistent symptoms
presenting 12 to 48 hours after symptom onset.


This is a section on "Acuteness" that I wrote in a Chapter on Reperfusion therapy that I wrote with Bill Brady in Critical Decisions in Emergency and Acute Care Electrocardiography.  I have updated it here.

Here are a couple posts that demonstrate the issue of acuteness.

Acuteness—when is it too late for reperfusion?  

In deciding on reperfusion, particularly on fibrinolytic therapy, it is important to assess the amount of viable injured myocardium at risk of infarction.  This is traditionally done by assessing time since pain onset, and randomized trials of fibrinolytics found no significant advantage if pain duration was greater than 12 hours.[12, 32, 49]  However, time since pain onset is a crude way of assessing amount of infarcted (irreversible), vs. ischemic (viable, salvageable), myocardium.  Often, occlusion is incomplete, or collateral circulation maintains the viability of ischemic myocardium, or there is ischemic preconditioning, and myocardium that is fully salvageable may have pain duration of days.  Fortunately, the ECG is a better indicator of salvageable myocardium than pain duration. 

            High ECG “acuteness” is associated with significant salvageable myocardium.   An ECG has a high acuteness score if it has tall T-waves, and lower acuteness if there are Q-waves or T-wave inversion is present.[50]  In 395 patients, this score was shown to add the most value in situations of data disagreement: 1) in acute anterior MI when the history indicates symptom onset of greater than 2 hours but the acuteness score is high, or 2) in acute inferior MI, if history indicates a time since symptom onset less than 2 hours but the acuteness score is low.[51]  More recently, a high acuteness score was found on SPECT scanning and Cardiac MRI to be associated with more salvageable myocardium, and to be superior to time since pain onset for determining myocardium at risk (but not yet infarcted).[52]  This corresponds to other data showing that tall T-waves are an independent marker of benefit from fibrinolytics.[53] and that, among those with positive T waves, mortality after thrombolytics is the same for those who have greater than 2 hours vs. less than 2 hours of symptoms.[54]  It is also important to know that QR-waves are present in 50% of anterior MI within the first hour, and represent ischemia of the conducting system, not infarction.[55]      

            There are no randomized fibrinolytic trials based on EKG characteristics of acuteness.  However, PCI is proven beneficial in a randomized trial of patients with persistent ST elevation at greater than 12 hours after onset, even though they were pain free.[56] 

            Finally, ischemic discomfort is far less predictive of on ongoing ischemia than is persistent STE and tall T-waves.  ECG acuteness should not be ignored because of resolution of symptoms.[57]

            In summary, tall T-waves indicate a large amount of viable, salvagable, myocardium.  Q-waves indicate lower acuteness, but may be present early in anterior MI; thus, in anterior MI, T-waves are more important.   Inverted T-waves signify either low acuteness or an open artery (see chapter 11 on reperfusion).

12.       LATE Study Group, Late assessment of thrombolytic efficacy (LATE) study with alteplase 6-24 hours after onset of acute myocardial infarction. Lancet, 1993. 342: p. 759-766.

32.       Fibrinolytic Therapy Trialists' (FTT) Collaborative Group, Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results from all randomised trials of more than 1000 patients. Lancet, 1994. 343: p. 311-322.

49.       EMERAS (Estudio Multicentro Estreptoquinsa Republicas de America del Sur), Randomised trial of late thrombolysis in patients with suspected acute myocardial infarction. Lancet, 1993. 342(8874): p. 767-772.

50.       Wilkins, M.L., et al., An electrocardiographic acuteness score for quantifying the timing of a myocardial infarction to guide decisions regarding reperfusion therapy. Am J Cardiol, 1995. 75(8): p. 617-620.

51.       Corey, K.E., et al., Combined historical and electrocardiographic timing of acute anterior and inferior myocardial infarcts for prediction of reperfusion achievable size limitation. Am J Cardiol, 1999. 83(6): p. 826-831.

52.       Engblom, H., et al.  The evaluation of an electrocardiographic myocardial ischemia acuteness score to predict the amount of myocardial salvage achieved by early percutaneous coronary intervention ^☆: Clinical validation with myocardial perfusion single photon emission computed tomography and cardiac magnetic resonance.  Journal of Electrocardiology 44(5):525-532; Sept-Oct 2011.

53.       Hochrein, J., et al., Higher T-wave amplitude associated with better prognosis in patients receiving thrombolytic therapy for acute myocardial infarction (a GUSTO-1 substudy).  Global Utilization of Streptokinase and Tissue plasminogen activator for Occluded Coronary Arteries. Am J Cardiol, 1998. 81(9): p. 1078-1084.

54.       Herz, I., et al., The prognostic implications of negative T-waves in the leads with ST segment elevation on admission in acute myocardial infarction. Cardiology, 1999. 92(2): p. 121-127.

55.       Raitt, M.H., 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(5): p. 1084-1088.

56.       Schomig, A., et al., Mechanical reperfusion in patients with acute myocardial infarction presenting more than 12 hours from symptom onset: a randomized controlled trial. Jama, 2005. 293(23): p. 2865-72.

57.       2007 Writing Group to Review New Evidence and Update the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction, 2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients with ST-Elevation Myocardial Infarction. J Am Coll Cardiol, 2008. 51(2).

Left Bundle with Convex ST Segment: Where is the J-point?

On July 26, I posted a similar problem, but in that case, the huge ST elevation was proportional.  

Here is another case in which it may be difficult to find the J-point if lead II was not there to help:

An elderly woman had a cardiac arrest, VT then PEA, and was resuscitated.  Here is her initial ECG:

There is SVT, probably sinus, at a rate of 149, with Left Bundle Branch Block.  There is no septal r-wave in V2 or V3.
Because of the convex morphology of the ST segment (which is highly suggesive of STEMI by itself), it is difficult to find the J-point in order to calculate the ST/S ratio (the ST segment is measured at the J-point, relative to the PQ junction).  However, the J-point is easy to find on lead II which runs across the bottom (see below)

(In our data, a convex ST Segment in LBBB was quite specific for anterior STEMI, but only 50% sensitive)

Here is the same ECG, annotated:

Here I found the J-point in lead II and draw a line up to find the J-points in V1-V3.  I have magnified this below:

V2 STE = 3 mm, divided by 10.5 mm S-wave: ratio = 0.285
V3 STE = 11 mm, divided by 24.5 mm S-wave: ratio = 0.45
Notice also the disproportional excessively discordant ST depression in V5: 3.5/10 = 0.35.

A single lead with proportionally excessively discordant ST elevation greater than 0.25 indicates STEMI
A single lead with proportionally excessively discordant ST depression greater than 0.30 indicates STEMI

However, we did not study patients with a heart rate greater than 130, as such tachycardia tends to exaggerate the ST deviation of LBBB.

Nevertheless, this is almost certainly STEMI, especially as the pretest probability (cardiac arrest) is very high.

Usually the heart rate comes down gradually after resuscitation (supportive care, diminished endogenous and exogenous epinephrine).  It would be helpful to repeat the ECG after 10-15 minutes, with a slower heart rate.  This was not done.

She went to the cath lab and was found to have severe 3 vessel disease, with thrombotic culprit lesions of 85% in both the LAD and circumflex.  It is quite likely that these were 100% at the time of the ECG.

This is 3 hours after the PCI:

The left bundle branch block is resolved.  There are Q-waves in anterior leads due to MI.

The patient did well.


Lesson:

Use lead II across the bottom to help you find the end of the QRS when it is difficult to find.

A Very Fast Regular Narrow Complex, Followed by an Equally Fast Regular Wide Complex

This case was sent to me by for analysis by Scott Flannagan in Australia.  I am by no means a rhythm master like Dr. K. Wang, but I think I was able to figure this one out.  If anyone has a better idea, let me know.  He will be able to get me the electrophysiology results in a few weeks, but I couldn't wait to post it now.

Case

A young woman in otherwise excellent health presented with one year history of intermittent palpitations.  She was alert but not well perfused: she had cool skin but she had no chest pain and was not diaphoretic.  Her BP was 110/90.

Here was her 12-lead:

There is a narrow complex, regular tachycardia that is very fast, at 259 BPM.   Computerized QRS duration in 94 ms. 

No matter what is causing this, the rate is extremely fast and suggests remarkably fast AV nodal conduction.  Children and infants can normally conduct this fast through the AV node, but not adults.

ECG Differential Diagnosis includes: 
Paroxysmal SVT 
        --AV nodal re-entrant tachycardia vs. 
        --Orthodromic re-entrant tachycardia through a bypass tract (accessory pathway)
        --If there are P-waves: Very fast Atrial Tachycardia with Very Fast AV conduction
Slow atrial flutter (rate 259) with 1:1 conduction through a fast conducting AV node

Every possibility includes very fast AV node conduction.

Pads were placed and the patient was given 6 mg of adenosine.  Here is the subsequent 12-lead ECG:

Now there is a wide complex rhythm with a rate of 257 (essentially the same rate).  Computerized QRS duration is 112 ms.  Lead V4 gives the suggestion that there is no wide complex, but rather a narrow complex that mimics a wide complex  because of ST depression (the link takes you to such a case).
But all other leads confirm that this is wide complex.

There were no atrial flutter waves uncovered during the pause induced by adenosine, so this is not atrial flutter.

Turns out the patient had asthma, and adenosine can trigger asthma. [An increase in intracellular cAMP in bronchial smoothe muscle cells relaxes them and improves asthma.  Adenosine decreases intracellular cyclic AMP; Xanthines such as theophylline increase intracellular cAMP]

She became distressed and SOB, and had a vigorous spasm of coughing, then converted!!

Here is her post conversion ECG:

Sinus tachycardia at a rate of about 130, with a very short PR interval.  Computerized QRS duration is 80 ms.

Her respiratory distress subsided and she did well.

Analysis

We knew there would be a short PR interval because, by the extremely fast rate of the narrow complex, we knew that the AV node must conduct fast.

What is the diagnosis here?  Here is what I wrote to Scott:

--So, there are two abnormalities here:
       1) Accelerated AV conduction
       2) An accessory pathway (WPW), in which the conduction down the AV node occurs before it can get to the accessory pathway (thus, no delta wave on baseline ECG).

--I believe that the first rhythm was a re-entrant rhythm that went down through that fast AV Node, then up through an accessory pathway (which is equally fast, as they often are).

--After adenosine, the re-entry reversed: it went down through the accessory pathway (Atrioventricular reciprocating tachycardia, or AVRT), with a wide QRS because the accessory pathway activates the ventricle first, and then up through the very fast AV node.  See Case 2 of this post for more on AVRT.

--Thus, both rhythms have identical rates, but are going in opposite directions.

--The problem with this explanation is that the beginning of the QRS in both tachycardias is fast.  If it were through an accessory pathway, then the beginning of the antidromic rhythm should be wider, and it does not appear to be so.

--The baseline ECG does NOT have any delta wave: the impulse travels down through the AV node too fast for it to make it down the accessory pathway.  This is often called "concealed conduction."  See this post for an explanation of Concealed Conduction.--the explanation starts halfway down the page.

--Since the wide complex rhythm has an LBBB configuration, the accessory pathway must be on the right side.

--Alternative explanations:
Dual AV nodal pathways (but why is one tachycardia wide?)
AV nodal pathway with "slow-fast" component (I don't see how this explains that the latter part of the QRS in the wide complex is slow)

The EP results are back, and:

1. Accelerated AV conduction
2. Left lateral accessary pathway

Does this single lead show a wide complex tachycardia?

A woman in her 50's had a v fib arrest and required defibrillation 10 times before resuscitation to an organized rhythm.

Here was the monitored rhythm:

ventricular tachycardia?

There are two clues that it is not:

1) The rhythm is irregularly irregular, which strongly suggests atrial fibrillation
2) There is a "shelf" on the upslope of the S-wave.  This suggests that it is ST segment, not part of the QRS.

Here is the 12-lead:

Here you can see in leads V4-V6 that the QRS is indeed narrow.  All of the apparent width is really ST segment depression, as well as ST elevation in aVR and V1.

Here I have placed lines to demonstrate the end of the QRS in all leads, using lead II across the bottom for orientation:

After resuscitation, her ECG normalized:

She was found to have an 80% LAD lesion, with open artery and good flow.  This was not definitely a culprit, and not definitely the etiology of arrest.

Lessons:

1. In the presence of ST deviation, the rhythm strip may deceive you into believing there is a wide complex.
2. ST depression is often seen immediately after resuscitation from cardiac arrest.  After a short period of stabilization, it will resolve if there is no underlying acute ischemia

Middle Aged Male with Burning Chest Pain -- Assess the Entire Clinical Scenario

A middle-aged male presented with “burning” mid chest pain, with radiation to bilateral shoulders (pain radiating to both shoulder is very specific for ischemia).  It started about 5 hours prior to arrival.  He obtained little relief from nitro x 3 by EMS.  There was a history of previous MI, with a stent in the 1st Obtuse Marginal.  He had taken his Plavix for 6 months, then discontinued and also stopped taking his antihypertensives and statin.  He continued to smoke about 1.5 pks per day.

Here is his ECG:

Junctional Bradycardia (this is sinus arrest with junctional escape, and is highly suggestive of ischemia).
  There is a pathologic Q-wave in lead III (old? new?).  
There is slight ST depression in leads I, II, and V3-V6 (fairly specific for ischemia). 
Down-Up T-wave in aVL: very specific for ischemia! 
There are slightly hyperacute T-waves in inferior leads (probable ischemia). 

These are subtle findings.  No single finding is diagnostic of ischemia but he has a very specific combination of factors:

1. typical pain
2. h/o coronary disease
3. pain radiating to both shoulders
4. junctional bradycardia
5. Q-waves
6. ST depression
7. Down-Up T-wave in aVL
7. Possible hyperacute T-waves 

All of these together, but none of them by themselves, diagnose acute MI.

One of my former residents diagnosed this as inferior MI and activated the cath lab.  I love it when my residents become better than I at reading ECGs!

There was a 100% acute occlusion of the RCA, with ischemia of the SA node causing sinus arrest.

Lesson:

1. When highly suggestive ECG signs of ischemia combine with a high pretest probability and refractory ischemic pain, activate the cath lab even if the ECG does not meet STEMI criteria.

A Very Wide Complex Tachycardia. What is the Rhythm? Use Lewis Leads!!

A patient with a history of severely reduced left ventricular function, renal insufficiency and atrial fibrillation presented with slight dyspnea, without chest pain or syncope.

He had this initial ECG:

There is a very wide, regular, QRS at 250 ms.  There are no P-waves apparent.   There are few isolated conditions which result in this.
What is one?

Here is the patient's previous ECG: 

There is a wide complex with a Left Bundle Branch Block morphology.  There are no P-waves here either, so it appears to be a junctional rhythm.  (The Differential Diagnosis would also include accelerated idioventricular rhythm originating in the right ventricle).  The QRS here also very wide, but not as wide as on the first ECG above.  Notice that the initial r-wave is wider than normal for LBBB.  

Also note that there is notching in the QRS (a "fragmented" QRS), which contributes to the wider-than-normal LBBB [this is Cabrera's sign (a notch on the ascending limb of the S-wave in V3-V5), a fairly reliable sign of previous MI, similar to a Q-wave].  Notice there is also a notch on the descending limb of the S-wave in all inferior leads II, III, aVF.  There is some T-wave Peaking, suggesting hyperkalemia.  

Overall impression of old ECG: Junctional rhythm and peaked T-waves and wide QRS.  This should make you think of hyperkalemia at the time of the old ECG (unfortunately, I don't know if that is the case).

Overall impression of QRS of new ECG: Even worse hyperkalemia superimposed on the conditions present on the old ECG above.  Indeed, the even wider QRS is due to a K of 7.8 mEq/L.  

How about the rhythm on that first ECG?

The patient was diagnosed with Ventricular Tachycardia and given both amiodarone and lidocaine.  I presume the hyperkalemia was treated as well, but do not have that information.  The rate slowed and became irregular, and the QRS narrowed significantly, but the rhythm still could not be discerned (it was still a wide complex).   This ECG is unavailable.

A consulting physician suspected that the underlying rhythm was atrial flutter, and so applied Lewis Leads.

1. Place the Right Arm electrode on the patient’s manubrium.
2. Place the Left Arm electrode on the 5th intercostal space, right sternal border.
3. Place the Left Leg electrode on the right lower costal margin.
4. Monitor Lead I.

Here is the resulting ECG (limb leads only): 

Perhaps it is better seen here:

Now slow flutter waves (with variable block) are apparent.  They are slow at least partly due to the amiodarone.  Note the axis is different than in the first ECG.  One might be tempted to say "Ahaa!  This different axis is proof that the first ECG was indeed VT!"  But, remember, the Lewis Leads change the axis.  All axis difference is due to lead placement.

The patient was put on hemofiltration to lower the K.  

Diagnosis:

1. Rhythm: Atrial Flutter with 2:1 block, only diagnosed with Lewis leads

2. QRS: Combination of LBBB, old MI and hyperkalemia, all leading to very wide QRS.

LBBB alone seldom has a QRS longer than 200 ms.  See this case of LBBB and hyperK.  

See this case for RBBB and very wide QRS due to hyperK.

Here is an even better case of use of the Lewis Leads

Poor Microvascular Reperfusion ("No Reflow"): Best Diagnosed by ECG

A previously healthy woman about 50 years old with no previous medical history or coronary risk factors presented 30 minutes after the sudden onset of severe substernal chest pain.  An ECG was recorded and interpreted within 13 minutes:

Sinus rhythm.  Intraventricular conduction delay with a QRS of 117 ms (really, incomplete LBBB)

There are hyperacute T-waves in V4-V6, I and aVL, with reciprocal ST depression and T-wave in version in III and aVF.  V4 shows a de Winter's T-wave, with some ST depression.

  This is diagnostic of proximal LAD occlusion, and I activated the cath lab the moment I saw this ECG. 

We gave clopidogrel 600 mg, aspirin, and a heparin bolus.  There was time to get another ECG, 13 minutes later, before going to the cath lab:

Now there is evolution to ST elevation in V2-V6.

Cath lab results

The patient went to the cath lab and had a door to balloon time of 50 minutes, for a total symptom onset to balloon time of 80 minutes (very fast).  There was complete occlusion of the proximal LAD which was opened and revealed a very large first diagonal (this explains the predominance of V4-V6 on the ECG).   After reperfusion, there was somewhat less "blush" (micovascular reperfusion as demonstrated by slight opacification, by contrast, of the affected myocardium).

There was now TIMI-3 flow, and the patient was pain free, but there was persistent ST elevation in lead V5 on the 6-lead monitor in the cath lab.   Therefore, in addition to thrombectomy, the interventionalist gave intra-coronary adenosine (a vasodilator) to try to improve distal microvascular flow.  As is routine, he also gave intracoronary nitro.  And, of course, he used an eptifibatide bolus and infusion to maximally inhibit platelets.  He did not see any distal "cut off" of vessels in the distribution of the large diagonal or the LAD, but he suspected, based on the persistent ST elevation, that the patient had a significant shower of debris down the diagonal distribution.  He states that "this probably occurred at the time of the acute vessel closure because we did not have any "no flow" or "slow flow" issues that developed acutely during the case."

Here was the post-cath ECG:

Sinus rhythm and a narrower QRS.
 There is persistent ST elevation, and persistently upright T-waves (absence of reperfusion T-waves) in V4-V6.  Though T-waves are inverted in aVL, they are not inverted in lead I, and there is persistent ST elevation in aVL.

After cath, the troponin I was already 107 ng/mL at 5 hours after presentation, and peaked at 178 ng/mL (very large MI).

The patient had a post cath ejection fraction of 36% and persistent chest pain for much of the day.  Due to high risk of cardiogenic shock and dysrhythmia, ICU admission was warranted (usually not necessary for completely successful reperfusion).  

Usually, a low ejection fraction in a patient with rapid restoration of TIMI-3 flow means that the patient has stunned myocardium that will recover.  However, the absence of resolution of ST elevation here is consistent with poor microvascular reperfusion, as is the very high troponin I, and thus recovery of function is not likely to be excellent.

The pain did eventually resolve, but significant damage was done.  For instance, the risk of sudden death from dysrhythmia is much higher than it would have been with good microvascular reperfusion, and she may need to go home on a temporary external automatic defibrillator.

2 days after presentation, here is the ECG:

There is still persistent ST elevation in lateral leads, though now there is T-wave inversion.  There is a new Q-wave in lead I.

No Reflow

This patient had remarkably fast symptom onset to balloon time, and optimal reperfusion therapy, and yet did not get good reperfusion because of poor microvascular reperfusion (thought to be due mostly to downstream microvascular obstruction and/or vasoconstriction).  About 2-5% of patients with successful PCI have no reflow.  Absence of resolution of ST elevation on the ECG is the best indicator of no reflow.   Suffice it to say that these patients have a much worse outcome than patients with good microvascular reperfusion. It's etiology is not uniform for every patient.  It is associated with, among other factors, clopidogrel resistance.  (We usually think of using Prasugrel or Ticagrelor to prevent re-occlusion; maybe we should be using these alternatives to clopidogrel to prevent "no reflow."    The therapy of "No reflow" is based on vasodilators such as adenosine, verapamil, and nitroprusside, as well as on triple antiplatelet therapy; no single mechanical or pharmacologic therapy has proven consistently effective.

Here is one review from 2010.

Here is another review from 2012.

Reperfusion on the ECG: Summary

I will leave the details for the below chapter from my book.

1. The ECG is the best predictor of reperfusion of the microvasculature, even better than angiographic assessment by TIMI flow.  Notice that the interventionalist relied on the ECG to diagnose "no reflow" in this patient.
2. TIMI myocardial perfusion grading (TMP) flows 1-3 grade the amount of microvascular reperfusion seen on angiogram, called "blush".  Absence of microvascular perfusion in the presence of good epicardial blood flow is called "no reflow."
3. "No reflow" is probably mostly caused by downstream showering emboli of platelet aggregates, and also by vasoconstriction.
4.  After reperfusion, the first ECG marker of microvascular reperfusion is T-wave inversion
5.  After reperfusion, the best ECG marker of microvascular reperfusion is resolution of ST segment elevation by at least 50% from maximum, and preferably, > 70% (or complete) resolution.
6.  The ECG is far more reliable at gauging microvascular reperfusion than is resolution of chest pain.

The ECG in REPERFUSION AND REOCCLUSION

This is Chapter 27 (Reperfusion and Reocclusion) from my book, The ECG in Acute MI.  It is long, and has a detailed annotated bibliography.  It comes from literature before 2002, but it is still accurate and almost everything you need to know (unless you are an interventionalist) about the ECG in Reperfusion and Reocclusion.  

Chapter 27:

GENERAL BACKGROUND

Arterial patency and microvascular circulation     

Reperfusion therapy is guided by the ongoing assessment of myocardial reperfusion.  This depends on two factors: 1) reperfusion of the epicardial infarct-related artery (IRA); and 2) reperfusion of the microvascular circulation, which may be damaged by ischemia and reperfusion (the “no-reflow” phenomenon) and result in impeded capillary flow. 

Hemodynamic status and age are the best clinical prognostic indicators for AMI outcome.  The best ECG indicator for AMI outcome is ST resolution or the lack thereof (318-322).  The best overall predictor of failed myocardial reperfusion is a finding of < 50% recovery of ST segments from maximal elevation.  However, the ECG cannot determine whether the cause of failed reperfusion is persistent arterial occlusion or microvascular damage.  Angiography is necessary to assess and grade IRA patency and microvascular circulation and to guide subsequent therapy.  Rescue PCI, which we define as PCI undertaken within 6 hours of the start of thrombolytic therapy, (323) should be strongly considered when clinicians have determined that thrombolytic reperfusion has failed and should be done immediately after transfer to a PCI facility if there is no ECG evidence of good reperfusion (324).  This is especially true for a large AMI, as indicated by anterior location, high ST elevation, or ST deviation in numerous leads.  A patent IRA with inadequate flow may be due to residual stenosis or abnormal microvascular circulation and may be treated with vasodilators, antiplatelet, and antithrombotic agents +/- PCI.

TIMI grading of IRA patency

IRA patency can only be definitively assessed by angiography.  Angiographic assessments are then systematized by TIMI grading, as follows (325): 

·       TIMI-0 = no flow

·       TIMI-1 = penetration of contrast without perfusion.  These patients have persistent ST elevation and a poor prognosis and must be identified for rescue PCI

·       TIMI-2 = partial reperfusion. These patients may have resolution of ST elevation and a prognosis intermediate between TIMI 0/1 and TIMI 3 flow.

·       TIMI-3 = complete reperfusion.  These patients usually (but not always) show ST resolution.  TIMI-3 flow after reperfusion is associated with lower mortality and lower incidence of CHF (326, 327), but its prognostic value may not be independent of resolution of ST elevation (318).

By outcome measures, a flow grade < TIMI-3 indicates failed reperfusion (26, 328).  After reperfusion therapy for AMI, TIMI-3 flow is associated with a 30-42 day mortality of 3.6%, in contrast to TIMI-2 flow (6.6% mortality) and TIMI-0/1 flow (9.5% mortality) (327).

TIMI Frame Count

The TIMI frame count (TFC) further systematizes TIMI flow categorization.  The TFC is the measure of the exact number of cineangiographic frames required for contrast to reach a defined distal segment of the IRA (see Background discussion under Angiographic Reperfusion Grades in the annotated bibliography of this chapter).

TIMI myocardial perfusion grading of microvasculature

TIMI flow and TFC are impacted by both the severity of the underlying stenosis and thrombus and by the microvasculature.  Intact microvasculature is most accurately assessed by the appearance on an angiogram of diffuse and faint highlighting of the myocardium by contrast, known as “myocardial blush.”  These assessments are systematized with TIMI myocardial perfusion grading (TMP), which is based on a scale from 0-3 as follows (319, 326, 329):

·       TMP grade 0 = no microvascular perfusion

·       TMP grade 1 = no clearance of contrast

·       TMP grade 2 = slow clearance of contrast

·       TMP grade 3 = normal clearance.

An open coronary artery may have brisk TIMI-3 flow but have a TMP grade of 0 or 1 (326); patients with these findings show persistent ST elevation (318, 319, 329).  TMP grade 3 is associated with a good prognosis, independent of TIMI flow. 

ECG DIAGNOSIS OF REPERFUSION

ST segments in reperfusion

With a reperfused IRA AND intact microcirculation, ST segments usually fall rapidly and are near baseline within 3 hours of reperfusion (see Case 27-1).  Approximately 80% of cases with IRA reperfusion manifest 50% ST recovery within 90 minutes.  Most of the remaining 20% likely have microvascular injury with resultant poor capillary flow; their prognosis is as poor as patients with poor flow in the IRA (318, 319, 329).  This contrasts with a non-reperfused IRA, in which ST segments fall gradually and plateau, with or without persistent elevation.  Plateauing occurs as early as 6 to 12 hours, due to myocardial cell death (330). 

ST resolution is an accurate predictor of reperfusion, especially in patients whose ECG’s show ST elevation > 4 mm (331).  During or shortly before reperfusion, ST segments often continue to rise before resolving, frequently with an increase in CP (156, 157, 332, 333, 334).  Some patients experience “cyclic reperfusion,” in which there is reperfusion and subsequent reocclusion.  This may occur with or without therapy.  Cyclic reperfusion occurs in 25-30% of AMI before reperfusion therapy and can be detected with ST segment monitoring (335).

T-waves in reperfusion

In reperfused AMI, terminal T-wave inversion often occurs rapidly (within 90 minutes) in the leads that manifested the greatest ST elevation on presentation, and before full ST resolution (156, 157).  This contrasts with non-reperfused AMI, 90% of which show gradual T-wave inversion (over 48 to 72 hours), with a depth < 3 mm (94) (Fig. 8-3).  If there is some myocardial injury, as measured by elevated troponin, expect terminal T-wave inversion to develop into deep and symmetric T-wave inversion over the first 48 hours after the onset of AMI (94) (see Case 27-2). Accordingly, early T-wave inversion (< 24 hours) is associated with greater IRA patency, better perfusion grade, and a more benign in-hospital course than later inversion (336). In some patients with very early reperfusion and very little or no myocardial cell death, as measured by troponin, there may be no T-wave inversion, very late inversion, or reversible inversion (94). 

      Q-wave and R-wave changes are not accurate markers of AMI reperfusion (337).

Reperfusion monitoring

            Monitoring for reperfusion may include observation of 5 elements, as follows: 1) ST resolution, or “recovery;” 2) terminal T-wave inversion; 3) resolution of CP; 4) reperfusion arrhythmias; and 5) biochemical markers. 

1.  ST resolution

ST segment resolution, or “recovery,” is the best marker for reperfusion (see Cases 27-1 and 27-2).  ST segments may be monitored continuously or with static ECG’s every 5 minutes from the time of thrombolytic administration.  If ST elevation is > 4 mm and there is NEITHER  >/= 50% recovery at 60 minutes NOR terminal T-wave inversion, TIMI-3 flow is unlikely.  Strongly consider rescue PCI.

Continuous ST segment monitoring is the best method for monitoring ST segment changes (156, 159, 338, 339) (see Case 27-3).  Commercial products are available.  Select one lead with the greatest ST elevation, plot the ST segment elevation continuously, and observe for peaks and troughs.  By convention, ST elevation is measured on continuous monitors at 80 ms after the J-point.  See Table 27-1.

·       ST recovery >/= 50% from MAXIMAL ST elevation (peak level attained) within 60 minutes and without re-elevation is a very good predictor of reperfusion.  These patients do not need early angiography or rescue PCI.  ST recovery  >/= 50% has a positive predictive value (PPV) for patency (TIMI-2 or -3 flow) of 87%.

·       ST recovery < 50%, consider rescue PCI.  The negative predictive value (NPV) for occlusion (lack of recovery) is 71%; i.e., 71 % of patients who do not show ST recovery >/= 50% have closed arteries and 29% have TIMI 2-3 flow.  These patients are candidates for rescue PCI.  Most importantly, ST recovery < 50% with no terminal T-wave inversion indicates a TIMI flow of 0-2 with a PPV of 86%.  TIMI-3 flow is true successful reperfusion.  Of patients with persistent ST elevation (< 50% recovery), 14% have TIMI-3 flow but presumably continue to have ST elevation due to microvascular injury.

·       The higher the maximal or initial ST elevation, the more accurate the patency prediction (331).

Although static ECG’s are inferior to continuous ST segment monitoring (339), if continuous monitoring is unavailable, recording static ECG’s every 5 minutes from the time of thrombolytic administration is a reasonable substitute (158).  Use the single lead with the highest ST elevation and measure resolution from the maximal height.  ST resolution > 50% at 60 minutes after treatment is a good indicator of reperfusion (158).  Complete ST resolution assures reperfusion but occurs infrequently by 60 minutes after treatment (339).

2.  Terminal T-wave inversion

(See also Chapter 8)

Terminal T-wave inversion within the first 90 minutes is a specific marker of reperfusion and is approximately 60% sensitive (156, 157, 158).  If leads with ST elevation develop terminal T-wave inversion within 60 minutes of thrombolysis, reperfusion is highly likely.  Because T-wave inversion usually indicates some myocardial injury, rapid ST resolution without any T-wave inversion may be evidence that reperfusion occurred before myocardial cell death; in such cases, biomarkers may not be elevated.  Terminal T-wave inversion usually occurs before full resolution of the ST segment.

Deep, symmetric T-wave inversion (> 3 mm) indicates reperfusion that is less recent than reperfusion indicated by terminal T-wave inversion (see Case 27-2).  Terminal T-wave inversion undergoes further development into symmetric T-wave inversion (94).  Deep, symmetric T-wave inversion need not be preceded by ST elevation, although there is usually no development of Q-waves without ST elevation.  Symmetric T-wave inversion is generally present after full resolution of the ST segment.

T-waves also eventually invert in persistently occluded vessels.  T-wave inversion in the presence of deep Q-waves, especially QS-waves, may be a manifestation either of reperfusion late in the course of AMI or of a well-developed, non-reperfused AMI (94, 340).  These inverted T-waves are usually < 3 mm, in contrast with inverted T-waves of reperfused AMI, which are > 3 mm (94).  Such T-wave inversion may be evident at presentation if the patient presents late after onset (see Case 33-3).

With posterior AMI, if the T-wave is upright before reperfusion and there is ST recovery, reperfusion usually results in precordial T-waves (especially V2) becoming fully upright and taller and wider than before AMI onset.  This is a reciprocal view of posterior inverted T-waves.  Reocclusion in this case is unlikely to result in T-wave inversion.  If the T-wave is asymmetrically inverted before reperfusion, reperfusion usually results in T-waves pseudonormalizing (turning upright) and becoming taller and wider than before the onset of AMI; reocclusion generally results in re-inversion of T-waves.  See Case 27-1.  (See also: Cases 16-10 and 13-4).

3.  Relief of Chest Pain

Two studies showed that complete relief of CP, often with an initial transient increase in pain, had a good PPV, with an 84% (339) to 96% (156) chance of reperfusion.  However, relief of CP with neither any recovery of ST segments nor terminal T-wave inversion is unlikely to represent reperfusion.  If CP resolves, record serial ECG’s; pursue rescue angioplasty if there is no ECG evidence of reperfusion.

With spontaneous relief of CP, do not abort reperfusion unless accompanied by some amount of ST recovery:

·       With increased, unchanged, or < 25% ST elevation resolution, continue reperfusion therapy.

·       With 25%-50% resolution, or terminal T-wave inversion, record serial ECG’s or continuous monitoring and look for >/= 50% ST resolution.

·       With 50%-100% resolution, reperfusion therapy may be suspended, pending further assessment, especially continuous ST monitoring.

Relief of CP has a poor NPV, in that persistent pain did not necessarily imply persistent occlusion (159, 339).

4.  Reperfusion arrhythmias

            Occurrence of early accelerated idioventricular rhythm (AIVR) indicates reperfusion with 97% specificity but only 45% sensitivity (335).  A sudden burst of ventricular tachycardia may also indicate reperfusion.

5.  Biochemical markers of reperfusion

Biochemical markers may also be useful in assessing reperfusion; see Chapter 29 for details.

See Cases 27-1 to 27-3 for examples of reperfusion.  (See also: Cases 6-4, 12-3, 16-10, 20-11, and 32-1).

. 

Management

A meta-analysis of randomized trials showed that rescue angioplasty performed in patients with failed reperfusion results in a decreased incidence of CHF, death, and recurrent MI, without significant adverse effects (324).  These trials were performed without the latest technology and with prolonged time intervals from thrombolysis to rescue.  In this age of abciximab and stenting, we highly recommend rapid rescue PCI for failed reperfusion as evidenced by the above-mentioned ECG indicators or by persistent clinical instability.  If TIMI-3 flow is present but TMP grade is low, treatment with vasodilators, antiplatelet, and antithrombotic agents is particularly important.

REOCCLUSION

Once reperfusion is achieved, monitor ST segments for reocclusion.  Symptoms are not reliable indicators of reocclusion and many recurrent AMI’s are asymptomatic (69, 89).  If continuous monitoring is unavailable, record frequent static ECG’s every 30 to 60 minutes until stability is assured.  At a minimum, record hourly ECG’s for several hours after reperfusion.

ECG manifestations of reocclusion

Each AMI has an “ischemic fingerprint,” such that reocclusion of the same vessel at the same location reproduces the same ECG findings (83, 190).  Thus, reocclusion manifests the reverse of reperfusion on the ECG, as follows:

·       Initial rapid “pseudonormalization” of T-waves, in which inverted T-waves turn upright.

·       Subsequent re-elevation of ST segments.

Caution: post-infarction regional pericarditis (PIRP) may mimic reocclusion (see Chapter 28) (94).  This is characterized by gradual pseudonormalization of T-waves or persistent upright T-waves in the leads that had the greatest ST elevation at presentation.  There is also gradual ST re-elevation, over 24-72 hours.  PIRP lacks the typical diffuse ST elevation of nonspecific pericarditis. 

See Case 27-3 of reocclusion.  (See also: Case 8-12, of pseudonormalization of symmetrically inverted T-waves; Case 13-4 of an inferoposterior AMI with reperfusion and reocclusion; and Case 3-3 of reocclusion a week after reperfusion).

Management

Reocclusion after thrombolysis mandates either repeat thrombolysis or, preferably, rescue angiography +/- PCI. 

ANNOTATED BIBLIOGRAPHY

Reperfusion: General background

Krucoff MW et al., Continuously updated 12-lead ST-segment recovery analysis for myocardial infarct artery patency assessment and its correlation with multiple simultaneous early angiographic observations, 1993.  

Methods:  Krucoff et al. (341) performed angiography and continuous ST segment monitoring in 22 AMI patients. 

Findings:  Forty-four episodes of arterial patency and multiple ST trend transitions in 11 of 22 patients after thrombolysis suggested cyclic changes in coronary flow before catheterization. 

Comment:  These authors and others (158, 159) have shown repeatedly that ST recovery must be measured from maximal ST elevation for accurate assessment of reperfusion.  Peak ST elevation may occur in the absence of or any time after thrombolytic therapy.  Static ECG’s are less effective than continuous monitoring because ST segments may rise from baseline before actual reperfusion and fall again (or vice versa) to nearly the same level without detection.

Angiographic reperfusion grades, persistent ST elevation, and prognosis

Background: TIMI flow grade is a measurement of reperfusion of a coronary vessel and TMP flow grade is a measurement of myocardial microvascular perfusion.  TFC is the measure of the exact number of cineangiographic frames required for contrast to reach a defined distal segment of the IRA. TFC is especially helpful to further categorize TIMI-2 and TIMI-3 flow.  Normal mean TFC’s are: 36.2 +/- 2.6 for the LAD, 20.4 +/- 3.0 for the RCA, and 22.2 +/- 4.1 for the circumflex artery (342).  To standardize TFC for all arteries, the TFC of the LAD is divided by 1.7 to give a “corrected” TFC (CTFC) (342).  At 90 minutes after thrombolysis for STEMI in all locations. a CTFC of 0-13 is above normal blood flow and is associated with mortality of 0%.  A CTFC of 14-40 is associated with mortality of 2.7%, and a CTFC > 40 is associated with mortality of 6.4% (343).  Of patients with TIMI-3 flow, CTFC </= 20 vs. > 20 is associated with complication rates of 7.9% vs. 15.5%, respectively (343).  

 

Van’t Hof et al., Clinical value of 12-lead electrocardiogram after successful reperfusion therapy for acute myocardial infarction, 1998. 

Methods:  Van ‘t Hof et al. (320) studied ST resolution in 403 AMI patients with TIMI-3 flow after primary angioplasty.

Findings:  ST segments normalized in 51% of patients (ST < 0.1 mV).  Partial normalization (30-70% of initial height) was associated with a relative risk (RR) of death of 3.6 (CI =  1.6-8.3) compared with full normalization(< 30% of initial height).  Absence of resolution or increased ST elevation was associated with a RR of death of 8.7 (range = 3.7-20.1).

Van’t Hof et al., Angiographic assessment of myocardial reperfusion in patients treated with primary angioplasty for acute myocardial infarction: myocardial blush grade, 1998.  

Methods:  Van ‘t Hof et al. (329) studied myocardial blush during primary angioplasty in 777 AMI patients. 

Findings:  Angioplasty resulted in TIMI-3 flow in 89% of patients and in TIMI-0, -1, or -2 flow in 11%.  Patients with TMP grades 3, 2, and 0/1 had:  1) CK infarct sizes of 757 IU/L, 1143 IU/L, and 1623 IU/L; 2) EF’s of 50%, 46%, and 39%; and 3) mortality (after a mean follow-up of 1.9 +/- 1.7 years) of 3%, 6%, and 23%, respectively.  TMP grade predicted mortality independently of Killip class, TIMI grade flow, EF, and other clinical variables.  TMP grade was the best predictor of 3-year mortality, with rates of 3%, 15%, and 37% for patients with grades 3 (19% of patients), 2, and 0/1, respectively.  Among TMP grade 3 patients, ST elevation normalized in 65% and ST elevation decreased in an additional 28%.

Gibson CM et al., Relationship of TIMI myocardial perfusion grade to mortality after administration of thrombolytic drugs, 2000. 

Methods:  Gibson et al. (326) studied 762 patients in the TIMI-10B trial, in which 854 patients with AMI were randomized to TNK-tPA or standard alteplase and underwent angiography at 90 minutes post-thrombolytic administration.

Findings:  TMP grade 3 myocardial perfusion was independently associated with low 30-day mortality of 2.0%, as compared to 3.5% for patients with TIMI-3 flow.  The decreased risk was additive to the low risk of TIMI-3 flow, such that mortality was a mere 0.73% (1 of 137) for patients with TIMI-3 flow and TMP grade 3 perfusion compared to a 10.9% mortality (14 of 129) for those with both TIMI 0-2 and TMP 0/1 grading.   Mortality was approximately the same for patients with: (1) both TIMI 0-2 flow and TMP grade 3 perfusion, presumably through collaterals; and (2) both TIMI-3 flow and TMP 0/1 perfusion.

ST recovery and prognosis

ST recovery can be a good prognostic indicator, even in the presence of an occluded vessel.  Lack of ST recovery portends a poor prognosis, even with an open artery.

Claeys MJ, Determinants and prognostic implications of persistent ST-segment elevation after primary angioplasty for acute myocardial infarction: importance of microvascular reperfusion injury on clinical outcome, 1999. 

Methods:  Claeys et al. (319) studied 91 AMI patients with reperfusion after angioplasty. 

Findings:   Of 91 patients, 75 had TIMI-3 and 16 had TIMI-2 flow.  Persistent ST elevation, defined as ST >/= 50% of the initial height, was observed in 33 (36%) patients and was associated with high one-year mortality (15% vs. 2%) and high total major adverse cardiac event rate (45% vs. 15%).  Persistent ST elevation was the most important independent determinant of major adverse cardiac event rate, with an adjusted RR of 3.4, and both were attributed to impaired microvascular circulation.

Shah A et al., Prognostic implications of TIMI flow grade in the infarct related artery compared with continuous 12-lead ST-segment resolution analysis.  Reexamining the "gold standard” for myocardial reperfusion treatment, 2000. 

Methods:  Shah et al. (318) identified 258 AMI patients who underwent thrombolysis and then angiography in the TIMI-7 and GUSTO-1 trials (see Appendix).  Patients were stratified according to TIMI 0-3 reperfusion and by ST resolution >/= 50% vs. < 50%. 

Findings:  ST resolution WAS an independent predictor of the combined clinical outcome of death or CHF but TIMI flow grade was NOT.  ST resolution among patients with TIMI grade 0-1 flow identified a group with a relatively benign clinical course.

Dissman R et al., Early assessment of outcome by ST segment analysis after thrombolytic therapy in acute myocardial infarction, 1994. 

Methods:  Dissman et al. (321) studied CK levels and EF’s in 77 AMI patients to correlate ST resolution and infarct size. 

Findings:  The enzyme-determined infarct size and the resulting EF correlated closely with complete (>70%), partial (30-70%), or no ST (<30 3="" 43="" 53="" 58="" and="" at="" complete="" ef="" for="" hours="" nbsp="" no="" o:p="" or="" partial="" patients="" post-thrombolysis.="" resolution="" respectively.="" s="" were="" with="">

Schroder R et al., Extent of early ST segment elevation resolution: a strong predictor of outcome in patients with acute myocardial infarction and a sensitive measure to compare thrombolytic regimens, 1995.  

Methods:  Schroder et al. (322) analyzed ECG’s, CK levels, and mortality data of 1909 AMI patients randomized to reteplase or SK. 

Findings:  In 1398 patients who presented </= 6 hours from AMI onset, 35-day mortality rates for complete (>/= 70%), partial (30-70 %), or no (< 30%) ST resolution by 3 hours post-thrombolytic administration were 2.5%, 4.3%, and 17.5%, respectively.

Saran RK et al., Reduction in ST segment elevation after thrombolysis predicts either coronary reperfusion or preservation of left ventricular function, 1990. 

Methods:  Saran et al. (344) studied ST segment changes and angiographic findings in 45 patients (see more detailed annotation below).

Findings:  LV function was well-preserved if the ST segment had fallen by >/= 25% at 3 hours.

Continuous ECG monitoring for prediction of reperfusion

Note:  It is important to remember when evaluating the following studies that 15% of IRA’s are open without treatment by 6-8 hours post-coronary occlusion (345).

Krucoff MW et al., Continuous 12-lead ST-segment recovery analysis in the TAMI 7 study.  Performance of a non-invasive method for real-time detection of failed myocardial reperfusion, 1993. 

Methods:  Krucoff et al. (159) tested a method of 12-lead continuous ST segment recovery in a blinded, prospective, and angiographically correlated study of 144 TAMI-7 patients who received thrombolytics in early MI.  Summated ST elevation was plotted against time by PC-based software and read by experienced cardiologists.  The ST segment was plotted and assessed for peaks, troughs, and general trend.  The ST score at the moment of angiography was compared to the peak elevation attained.  Patency was predicted based on ST recovery, defined as a 50% drop from the maximum summated ST elevation, and continued downward trend.   Occlusion was predicted by (1) persistent ST elevation, (2) re-elevation after recovery or a downward trend, or (3) increased ST elevation.  The study was considered indeterminate if no definite peaks or troughs and corresponding trends could be discerned. 

Findings:  There were 144 ST segment analyses.  Of 35 angiograms performed during definite (re-) elevation periods (indicating occlusion), 25 IRA’s were angiographically occluded.  Of 91 angiograms during definite recovery periods (indicating reperfusion), 81 IRA’s were angiographically patent.  Of 18 indeterminate analyses, 14 were angiographically patent.  If the indeterminate group is considered to be “probably not occluded,” then the IRA was patent in 95 of 109 cases (87%) so predicted and occluded in 25 of 35 cases (71%) so predicted.  Of 35 patients whose ST recovery analysis determined IRA’s to be “occluded” (based on persistent or recurrent ST elevation), only 5 had TIMI-3 flow.  In 109 patients, analysis determined “probably not occluded,” (“indeterminate” or “patent”) and 73 of these had TIMI-3 flow, 22 had TIMI-2 flow, and 14 had TIMI-0 or 1 flow.  Thus, “occluded” had a PPV for TIMI 0-2 flow of 86% and “probably not occluded” had a sensitivity of 94% and a PPV of 67% for TIMI-3 flow and of 87% for TIMI-2 or -3 flow.  

Comment:  Post-thrombolytic TIMI-3 flow is associated with a much better outcome than even TIMI-2 flow (26, 328).  Therefore, the ability to distinguish TIMI-3 flow from TIMI-0 to -2 flow on the ECG is important.

Klootwijk P et al., Non-invasive prediction of reperfusion and coronary artery patency by continuous ST segment monitoring in the GUSTO-I trial, 1996. 

Methods:  Klootwijk et al. (331) studied ECG’s of 373 GUSTO-1 patients (see Appendix) using continuous 12-lead ST segment recovery analysis.

 Findings:  The predictive values for reperfusion or persistent occlusion were not as good as in the study of Krucoff et al. described above (159).  Angiograms were performed significantly later (between 90-180 minutes) in this study.  Thus, the predictive accuracy would be expected to be lower because ST segments in areas of persistent infarction decline over time, due to myocardial cell death.  A decrease of >/= 50% from peak and no persistent re-elevation before angiography was used as a prediction of “patent.” Accuracy was very high (79-100%) in patients with high ST elevation (> 4 mm).  In 116 patients with a peak ST elevation >/= 4 mm, a prediction of “patent” had a PPV of 79% and NPV of 75%.

Doevendans PA et al., Electrocardiographic diagnosis of reperfusion during thrombolytic therapy in acute myocardial infarction, 1995. 

Methods:  Doevendans et al. (156) performed continuous ST segment monitoring of 61 AMI patients for 60 minutes after thrombolytic therapy. 

Findings:  Reperfusion was associated with rapid ST resolution, often after a transient elevation.  Of 44 patients with reperfusion, 42 showed >/= 25% decrease in ST elevation from maximal height (sensitivity 95%), but only one of 17 patients without reperfusion showed this amount of normalization (specificity 94%).  Using a 50% decrease in ST elevation as a cutoff, sensitivity was 85% (38 of 44 patients) and specificity was, again, 94%.  Relief of CP was also a very sensitive sign of reperfusion; 25 of 26 patients with reperfusion had relief within 1 hour.  Eighteen patients experienced relief after a transient, often marked, increase in pain.  Terminal T-wave inversion was very specific for reperfusion; 28 of 44 patients with reperfusion had terminal T-wave inversion, whereas only 1 of 17 without reperfusion had terminal T-wave inversion.  AIVR was a specific but insensitive marker of reperfusion; 16 of 42 in the reperfused group demonstrated AIVR vs. one of 17 in the nonreperfused group.  Other “reperfusion arrhythmias” were uncommon and of little prognostic utility.  CK-MB peaked earlier in the reperfused group.

Veldkamp RF et al., Comparison of continuous ST-segment recovery analysis with methods using static electrocardiograms for noninvasive patency assessment during acute myocardial infarction, 1994. 

Methods:  Veldkamp et al. (346) analyzed ECG’s and clinical data from 82 patients in the above study by Krucoff et al. (159) to compare continuous ST recovery analysis with 5 static methods. 

Findings:  Static methods such as those used by Saran et al. (344), Hackworthy et al. (347), and Clemmensen et al. (348) had comparable accuracies to continuous ST recovery analysis; see section below on static ECG’s.

Hohnloser SH et al., Assessment of coronary artery patency after thrombolytic therapy: accurate prediction using the combined analysis of three noninvasive markers, 1991.

Methods:  Hohnloser et al. (338) used Holter monitoring and angiography in a prospective study of 82 patients undergoing thrombolysis for first MI. 

Findings:  Of 82 patients, 63 had TIMI-2 or -3 reperfusion.  A 50% reduction in ST elevation measured 60 to 90 minutes after thrombolysis had a PPV of 97% and an NPV of 43% for reperfusion.  CK peak < 12 hours was an accurate marker of reperfusion.

Frequent static ECG’s

Shah PK et al., Angiographic validation of bedside markers of reperfusion, 1993. 

Methods:  Shah et al. (158) obtained static ECG’s every 5-10 minutes after thrombolytic therapy in 82 AMI patients, for up to 3 hours, until angiography. 

Findings:  Their findings were very similar to those of Doevendans et al. (156) described above.  Angiography demonstrated that 69 of 82 patients had a patent IRA with TIMI-3 flow and that these patients consistently manifested a rapid, progressive decrease in both CP and ST elevation.  Pain resolved in 24 +/- 23 minutes (maximum 50 minutes) and decreased ST elevation >/= 50% occurred within 16 +/- 14 minutes (maximum 41 minutes) after restoration of TIMI-3 flow.  Terminal T-wave inversion and AIVR were also specific but insensitive markers of reperfusion.  This study demonstrates the importance of frequent static ECG’s and the insensitivity of using only 2 static ECG’s to detect reperfusion.  In 58% of patients, ST segments were unstable, rising and falling, before final resolution.

Infrequent static ECG’s

Califf RM et al., Failure of simple clinical measurements to predict perfusion status after intravenous thrombolysis, 1988. 

Methods:  Califf et al. (339) performed angiography on 386 TAMI patients at 60 and 90 minutes post-administration of tissue plasminogen activator (tPA).  They recorded a baseline ECG and another at 90 minutes post-tPA, before the 90-minute coronary injection. 

Findings:  They found no sensitive AND specific marker of reperfusion using infrequent static ECG’s.  Complete resolution of ST segment and T-wave changes was associated with a 96% IRA patency rate at 90 minutes post-tPA, but this occurred in only 6% of patients.  Only 38% of patients had “partial resolution” of ST segments, 84% of whom showed reperfusion.  Complete resolution of CP occurred in 29%, of whom 84% had reperfusion of the IRA.  Unchanged or worsened CP occurred in 20%, of whom 60% showed reperfusion.  Patent IRA’s were demonstrated in 56% of patients with neither symptom nor ST resolution and 63% of patients with no change in ST segments showed reperfusion.  Although arrhythmias occurred frequently during the first 90 minutes of therapy, none were associated with a higher patency rate.

Saran RK et al., Reduction in ST segment elevation after thrombolysis predicts either coronary reperfusion or preservation of left ventricular function, 1990. 

Methods:  Saran et al. (344) performed angiography on 45 AMI patients by 3 hours post-administration of anistreplase.

 Findings:  Using the lead with the greatest ST elevation on static ECG’s, ST recovery  >/= 25% at 3 hours was nonspecific.  ST segments had fallen by >/= 25% in 30 of 31 patients with TIMI-2 or -3 reperfusion, but also in 8 of 14 patients who had only TIMI-0 or -1 flow.  Thus, if the ST segment fell by >/= 25%, the specificity was only 43%; that is, many IRA’s remained occluded.  Three hours post-thrombolytic therapy is too late for ST recovery to be a meaningful indication of reperfusion because ST segments fall gradually, even in persistently infarcted myocardium.  It is also too late to make a decision for rescue PCI.  If the ST segment fell by < 25%, persistent occlusion was likely, with a PPV of 86%.  Importantly, the global EF was well maintained in patients whose ST segments fell > 25% and whose arteries were occluded.  Saran et al. concluded that a reduction in ST elevation of > 25% within 3 hours of thrombolysis indicates either a patent IRA or preservation of LV function. 

Clemmensen P et al., Changes in standard electrocardiographic ST-segment elevation predictive of successful reperfusion in acute myocardial infarction, 1990. 

Methods:  Clemmensen et al. (348) studied 53 patients up to 8 hours post-SK administration.  They calculated the ST score as the sum of ST elevation in 11 leads, based on static ECG’s obtained within 5 minutes of angiography. 

Findings:  Angiography demonstrated reperfusion (TIMI-2 or -3 flow) in 33 of 53 patients.  A decrease of >/= 20% in ST elevation was 88% sensitive and 80% specific for reperfusion, with a PPV of 88% and an NPV of 80%.  Clemmensen et al. concluded that a decrease of only 20% in the ST score following thrombolytic therapy is a useful and noninvasive predictor of reperfusion status in patients with evolving AMI. 

Comment:  The use of angiographic patency assessment up to 8 hours post-treatment diminishes the value of this data.  

 

T-wave inversion and prognosis

See also Doevendans et al. (156) above.

Oliva PB et al., 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, 1993. 

Methods:  Oliva et al. (94) studied 200 AMI patients to assess serial T-wave changes as prognostic indicators. 

Findings:  Ninety percent of patients with reperfusion demonstrated a maximum T-wave negativity of >/= 3 mm in the lead that initially showed the greatest ST elevation within 48 hours of CP onset.  Seventy-six percent of patients with no reperfusion demonstrated a maximum T-wave negativity of </= 2 mm within 72 hours.  Oliva et al. conclude that rapid evolution and deepening of the T-wave may be useful noninvasive markers of reperfusion.

Matetzky S et al., Early T wave inversion after thrombolytic therapy predicts better coronary perfusion: clinical and angiographic study, 1994. 

Methods:  Matetzky (336) et al. performed admission and pre-discharge angiography and radionuclide ventriculography on 94 consecutive AMI patients who received tPA.

Findings:  Early T-wave inversion (< 24 hours) was associated with greater IRA patency, better perfusion grade, and a more benign in-hospital course.  Additionally, although the number of patients with normal EF’s (>55%) at presentation was similar, 71% of patients with early T-wave inversion had a normal EF at discharge, vs. 44% of patients without early T-wave inversion.

Increased pain and ST elevation post-thrombolytic therapy

Dissman R et al., Sudden increase of the ST segment elevation at a time of reperfusion predicts extensive infarcts in patients with intravenous thrombolysis, 1993. 

Methods:  Dissman et al. (332) measured ST elevation and CK every 15 minutes after thrombolytic administration in 61 AMI patients. 

Findings:  Eight patients showed increased ST elevation immediately after reperfusion.  This was associated with an enzymatically very large AMI, a very early enzyme peak, and much worse LV EF (39% +/- 14 vs. 58% +/- 11, p < 0.0005).  Six patients also experienced very clearly intensified CP at the time of the ST elevation.  The study by Doevendans et al. (156) described above and a study by Wehrens et al. (157) both found a similar increase in CP after treatment and before ECG evidence of reperfusion.

Reciprocal depression and reperfusion

Shah A et al., Comparative prognostic significance of simultaneous versus independent resolution of ST segment depression relative to ST segment elevation during acute myocardial infarction, 1997. 

Methods:  Shah et al. (143) performed continuous ST segment monitoring of 413 AMI patients who received thrombolytics; 261 patients met technical criteria for blinded analysis of ST depression resolution patterns.  

Findings:  In-hospital mortality was 13% among patients whose reciprocal ST depression persisted after resolution of ST elevation vs. 1% mortality for patients whose ST elevation and ST depression resolved simultaneously.

Reperfusion arrhythmias

Although there is little literature to support malignant reperfusion ventricular arrhythmias, many interventionalists and clinicians who treat AMI are certain that runs of ventricular tachycardia are directly related to opening the IRA, especially in large infarcts that are reperfused very early. 

Gorgels AP et al., Usefulness of the accelerated idioventricular rhythm as a marker for myocardial necrosis and reperfusion during thrombolytic therapy in acute myocardial infarction, 1988 and Goldberg S et al., Limitation of infarct size with thrombolytic agents: electrocardiographic indexes, 1983 and Miller FC et al., Ventricular arrhythmias during reperfusion, 1986.  

Methods:  Gorgels et al. (349) and Goldberg et al. (350) were among the first to describe “reperfusion arrhythmias.” Gorgels et al. prospectively studied 87 patients admitted with ischemic CP and Goldberg et al. studied 44 AMI patients who underwent angiography.  Miller et al. (351) conducted Holter monitoring of 52 patients.

Findings:  Gorgels et al. found AIVR in 27 of 70 AMI patients with reperfusion.  Goldberg et al. found some type of reperfusion arrhythmia, most commonly AIVR, in 20 of 27 AMI patients with reperfusion.  Miller et al. found no significant relationship of either AIVR or ventricular tachycardia with reperfusion or persistent occlusion.

Hohnloser SH et al., Assessment of coronary artery patency after thrombolytic therapy: accurate prediction using the combined analysis of three noninvasive markers, 1991.

Methods:  Hohnloser et al. (338) prospectively studied 82 first AMI patients treated with thrombolytics.  

Findings:  AIVR was associated with reperfusion only in inferior AMI.

Shah PK et al., Angiographic validation of bedside markers of reperfusion, 1993.  

Findings:  Shah et al. (158) (described above) found that 49% of patients with reperfusion developed AIVR.

Gore JM et al., Arrhythmias in the assessment of coronary artery reperfusion following thrombolytic therapy, 1988.  

Methods:  Gore et al. (352) performed angiography within 8 hours of symptom onset in 67 AMI patients treated with thrombolytics. 

Findings:   Fifty-six patients had total IRA occlusion, 25 of whom reperfused within 90 minutes of treatment.  Arrhythmias (including AIVR) were not significantly associated with reperfusion.

Gressin V et al., Holter recording of ventricular arrhythmias during intravenous thrombolysis for acute myocardial infarction, 1992. 

Methods:  Gressin et al. (353) performed 24-hour Holter monitoring of 40 AMI patients treated with thrombolytics. 

Findings:  Increased incidence of AIVR was associated with IRA patency.

Clements IP, The electrocardiogram in acute myocardial infarction, 1998. 

Findings:  Clements (335) cites a thesis by Veldkamp, who combined analysis from 6 studies (317 patients) and found that early AIVR predicted patency with a specificity of 97% but a sensitivity of only 45%.

Vectorcardiography

Dellborg M et al., Dynamic QRS complex and ST segment vectorcardiographic monitoring can identify vessel patency in patients with acute myocardial infarction treated with reperfusion therapy, 1991. 

Findings:  Dellborg et al. (354) identified 15 of 16 patients with reperfusion and 5 of 6 with persistent occlusion using vectorcardiographic analysis of ST vectors.  Further detail is beyond the scope of this book.  See Clements (335) for an excellent discussion of alternative electrocardiographic methods such as vectorcardiography and precordial mapping.  See also von Essen et al. (355) and Badir et al. (356) for vectorcardiographic analyses of reperfusion. 

Rescue PCI

Ross AM et al., Rescue angioplasty after failed thrombolysis: technical and clinical outcomes in a large thrombolysis trial, 1998.  

Methods:  Ross et al. (323) analyzed GUSTO-1 (see Appendix) data on rescue angioplasty, defined as angioplasty undertaken within 6 hours of the start of thrombolytic therapy.  They compared 198 patients selected non-randomly for rescue angioplasty, 226 patients with failed thrombolysis who were managed conservatively, and 1058 patients with successful thrombolysis. 

Findings:  Patients with rescue angioplasty had more impaired LV function prior to intervention.  Rescue was successful in 88.4% of occluded arteries, resulting in TIMI-3 flow in 68%.  Successful rescue angioplasty was associated with better LV function and lower mortality than conservative management of occluded arteries.  Neither bleeding complications (8.6% vs. 6.8%) nor the need for CABG (1.0% vs. 0.4%) differed significantly between the 2 groups.

Ellis SG et al., Randomized comparison of rescue angioplasty with conservative management of patients with early failure of thrombolysis for acute anterior myocardial infarction, 1994.

Methods:  Ellis et al. (357) randomized 151 patients with first anterior AMI and failed thrombolysis, as determined by angiography done within 8 hours after treatment, to angioplasty or to conservative management. 

Findings:  Angioplasty performed at a mean of 4.5 +/- 1.9 hours after thrombolytic therapy was successful in 72 of 78 (92%) patients.  Outcomes in the angioplasty vs. conservatively managed groups, respectively, were death in 5% vs. 10% (P = 0.18), severe heart failure in 1% vs. 7% (P = 0.11), and either death or severe heart failure in 6% vs. 17% (P = 0.05).  LV function at rest did not differ. 

McKendall GR et al., Value of rescue percutaneous transluminal coronary angioplasty following unsuccessful thrombolytic therapy in patients with acute myocardial infarction, 1995. 

Methods:  McKendall et al. (358) studied 133 patients enrolled in TIMI Phase I Open Label and Phase II trials; 100 had received no rescue angioplasty and 33 patients had undergone rescue angioplasty by protocol (not by physician choice) if the 90-minute angiogram revealed persistent IRA occlusion. 

Findings:  Time to angioplasty from symptom onset or from thrombolytic treatment is not stated, but appears to be 90 to 120 minutes.  The two groups had similar baseline features.  Rescue was technically successful in 26 of 33 patients (82%).  Mortality at 21 days was 12% in the rescue group and 7% in the no-rescue group (p=NS).  Failed rescue was associated with a mortality of 33%.  Mean LV EF was the same in both groups.

CORAMI Study Group, Outcome of attempted rescue coronary angioplasty after failed thrombolysis for acute myocardial infarction, 1994. 

Methods:  The CORAMI Study Group (359) evaluated short and mid-term outcomes of 299 consecutive AMI patients who received thrombolytics < 6 hours after symptom onset and underwent angiography at 90 minutes post-thrombolytics. 

Findings:  Of 299 patients, 87 (29%) had failed thrombolysis (TIMI-0 to -1 flow), of whom 72 underwent rescue angioplasty within 8 hours of symptom onset.  Seven patients (10%) were in cardiogenic shock at the time of angiography.  Technical success (TIMI-3 flow) was achieved in 65 patients (90%) at a mean of 300 +/- 101 minutes after thrombolytic therapy.    Nine patients (12%) had access site hematoma.  Three patients (4%) died, 2 of 65 successful rescues and 1 of 7 failed rescues.

Gibson C et al., Rescue angioplasty in the Thrombolysis in Myocardial Infarction (TIMI) 4 trial, 1997. 

Methods:  Gibson et al. (360) studied 95 AMI patients with failed thrombolysis (TIMI 0-1 flow) in the TIMI-4 trial. 

Findings:  Fifty-eight patients underwent rescue angioplasty 120 minutes post-thrombolytic therapy and 37 had no rescue angioplasty.  Rescue and non-rescue groups had similar baseline characteristics.  Fifty-two of 58 procedures were successful.  In-hospital adverse outcomes, including death, recurrent AMI, severe CHF, cardiogenic shock, and EF < 40%, occurred in 35% of rescue cases (29% of successful rescues and 83% of failed rescues, p = 0.01), and also in 35% of non-rescue cases (p = NS).

Miller JM et al., Effectiveness of early coronary angioplasty and abciximab for failed thrombolysis (reteplase or alteplase) during acute myocardial infarction (results from the GUSTO-III trial), 1999. 

Methods:  Miller et al (361) prospectively studied 392 patients entered into the GUSTO-III trial (reteplase vs. tPA for STEMI) (362) who underwent rescue angioplasty in a nonrandomized fashion; 83 patients received abciximab and 309 did not.

Findings:  When adjusted for baseline differences, patients who received abciximab had significantly lower mortality.  Incidence of severe bleeding (without ICH), with vs. without the use of abciximab during angioplasty was 3.5% vs. 1.0% (p = 0.08).

Ellis SG et al., Review of immediate angioplasty after fibrinolytic therapy for acute myocardial infarction, 2000. 

Methods: Ellis et al. (324) performed a meta-analysis of 9 heterogeneous randomized trials of rescue angioplasty (1456 patients).  

Findings:  Rescue angioplasty decreased the incidence of CHF, death, and recurrent MI.

In summary, although the value of rescue PCI makes intuitive and scientific sense, the available studies are too small and the methodology inadequate for definite conclusions.  All of the studies had a minimum delay of 2 hours and a mean delay of 4-5 hours between thrombolytic therapy and balloon inflation.  None used up-to-date technique including stents, abciximab, and/or clopidogrel.  We recommend rescue PCI for large infarctions with no ECG evidence of reperfusion at one hour post-thrombolytic therapy unless and until there are studies that take these factors into account and demonstrate lack of efficacy.

 

Reocclusion

Langer A et al., Prognostic significance of ST segment shift early after resolution of ST elevation in patients with myocardial infarction treated with thrombolytic therapy: the GUSTO-I ST Segment Monitoring Substudy, 1998. 

Methods:  Langer et al. (363) performed ST segment monitoring within 30 minutes of thrombolytic therapy in 734 AMI patients.

Findings:  “ST segment shift,” defined as elevation of >/= 1 mm in the 6-24 hours after reperfusion, was correlated with 7.8% mortality at 30 days and 10.3% mortality at 1 year vs. 2.3% and 5.7% mortality respectively for patients without ST shift.

Ohman EM et al., Consequences of reocclusion after successful reperfusion therapy in acute myocardial infarction, 1991. 

Methods:  Ohman et al. (89) studied 810 AMI patients who had angiography performed 90 minutes post-thrombolytic therapy. 

Findings:  Reperfusion occurred acutely in 735 patients, 645 of whom (88%) underwent angiography 7 days later.  IRA REocclusion occurred in 91 patients (14%) and was symptomatic in 53.  Reocclusion was associated with greater in-hospital mortality (11% vs. 4.5%), a more complicated hospital course, and initial angiographic findings including RCA stenosis, a greater degree of stenosis, and lower TIMI flow grade.

Dissman R et al., Early recurrence of ST-segment elevation in patients with initial reperfusion during thrombolytic therapy: impact on in-hospital reinfarction and long-term vessel patency, 1994. 

Methods:  Dissman et al. (364) performed 24-hour Holter monitoring on 81 AMI patients.

Findings:  ST resolution within the first 4 hours occurred in 67 patients (83%), 31 of whom (46%, Group 1a) did have subsequent ST re-elevations and 36 of whom (54%, Group 1b) did not.  Group 1a had a much greater incidence of CK-MB-confirmed re-infarction (26% vs. 6%) and angiographic occlusion at follow-up (40% vs. 17%) than Group 1b.

Veldkamp RF et al., Performance of an automated real-time ST segment analysis program to detect coronary occlusion and reperfusion, 1996. 

Methods:  Veldkamp et al. (212) used an automated real-time ST segment analysis program to detect reocclusion during 78 balloon occlusions in 31 patients. 

Findings:  The program detected balloon reocclusion and reperfusion within seconds of all occlusions that caused a peak ST elevation >/= 0.2 mV.

Krucoff MW et al., Stability of multilead ST-segment "fingerprints" over time after percutaneous transluminal coronary angioplasty and its usefulness in detecting reocclusion, 1988. 

Methods:  Krucoff et al. (190) analyzed multi-lead ST segment recordings performed during angioplasty in 39 patients. 

Findings:  Similar to Bush et al. (83) described above, within one hour, balloon occlusion during repeat angioplasty resulted in an identical “ischemic fingerprint” 90% of the time.  AMI of the same vessel within 24 hours of the balloon inflation resulted in this ischemic fingerprint 87% of the time.  Thus, reocclusion reliably produces the initial ECG pattern of infarction.  Monitoring for reocclusion can be done using continuous ST segment monitoring.

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