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?

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)


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.