July 7th, 2012
New Algorithm for Patients with LBBB and Suspected MI
CardioExchange editor John Ryan interviews John W. McEvoy, cardiology fellow at Johns Hopkins, about an algorithm — newly proposed by Ian Neeland and colleagues in JACC — for selecting patients with left bundle-branch block and suspected MI for primary PCI. Neeland and coauthor James de Lemos respond to each of McEvoy’s comments.
In their JACC Viewpoint article, Neeland and his colleagues highlight that ACCF/AHA guidelines, which recommend patients with new or presumed-new LBBB undergo early reperfusion therapy (fibrinolysis or PCI), are based on studies from more than 20 years ago. Citing newer research, the authors observe that a substantial proportion of patients who present with LBBB are not actually experiencing a STEMI-equivalent MI: For example, in 2007 Larson and colleagues reported that among patients with LBBB at presentation, the rate of false activation of the catheterization laboratory was 44%, compared with a baseline of 14%. For patients with presumed-new LBBB and suspected MI, Neeland and coauthors propose a new algorithm involving Sgarbossa criteria on ECG, bedside echocardiography, and serial echocardiogram, as shown here.
Ryan: Do you often get called by the ED or house staff about a “new” LBBB?
McEvoy: Yes, this is a fairly common clinical dilemma at our institution. Previous registry studies would suggest that only about 2% of acute coronary syndrome patients present with LBBB. However, such studies did not include patients who were catheterized for LBBB but did not actually have ACS. Indeed, up to 40% of patients who undergo cardiac catheterization for LBBB are not found to have occlusive coronary artery disease. This has been my personal experience as well. Therefore, some catheterization-lab activations may be unnecessarily triggered by new LBBB and “concern for ACS.” Anecdotally, at least as many of these calls come from our general inpatient floors as from our ED. That’s presumably because such patients are often transferred from outside hospitals or directly admitted without prior EKGs recorded in our electronic medical record.
Neeland & de Lemos:We agree with Dr. McEvoy. Only a small minority of patients presenting with a suspected ACS have LBBB, but this group is over-represented among patients who prompt a false activation of the catheterization lab. In a recent study by McCabe et al., of the 146 patients with false STEMI lab activations, over 10% had LBBB. Notably, these figures reflect only patients who make it all the way to cardiac catheterization. In our institution and probably many others, it’s not uncommon to “deactivate” for a patient with LBBB whose clinical scenario is not consistent with STEMI.
Ryan: What do you normally do? And how has your practice evolved from when you were a resident, to junior fellow, and now a more-senior fellow at Hopkins?
McEvoy: My threshold to act on any suspicion for ACS has been—and remains—very low. However, my approach has become more nuanced. As a resident, I learned that although “time is muscle,” one needs to “treat the patient and not the EKG.” Of course, the EKG is more than enough to proceed to catheterization if the patient is unstable or has elevated cardiac enzymes. However, we are not currently considering such a straightforward scenario.
In cases (not uncommon) where the story is atypical, the vital signs and exam are stable, and the enzymes are initially negative, my approach has changed. I have found it helpful to get aggressive about chasing down old ECG reports in such cases. Primary care providers and outside hospital records can often establish that the LBBB is old, even when the actual ECGs are not obtained. If the LBBB is old, the management can change drastically. Similarly, if the LBBB is definitively new, I think the threshold to perform cardiac catheterization should be extremely low. However, a management dilemma often arises when the LBBB is not proven to be old or new in this type of intermediate-risk patient. I have come to see in these cases that the ECG, on its own, is not a helpful bedside triage test.
Thankfully, these are the very cases when you may have some time to consider everything before activating the catheterization lab. Of course, such a strategy may jeopardize the door-to-needle or door-to-balloon time if the presentation is, in fact, a real ACS. If such a patient presents very early, it is often interesting to obtain a STAT myoglobin level (although I suspect such a maneuver will be superseded by highly sensitive troponin assays and circulation endothelial cells). However, my usual strategy is to bring an echocardiography machine directly to the bedside. We know that ACS-induced LBBB is caused by a large anterior infarct. Therefore, a normal echocardiogram would reassure me in the right clinical scenario.
As a fellow, I also like to discuss all intermediate-risk patients who present with possible-new LBBB with the on-call interventionalist. It is important to acquire as much information as possible (including echocardiographic data) within the required time window, to facilitate a complete discussion of the case with interventionalist colleagues.
Neeland & de Lemos: We agree that the decision threshold to activate the catheterization lab should be low, given the clear benefits of timely PCI and the relatively less important consequences of false cath-lab activation versus lytic administration. It may also differ a bit depending on whether the cath-lab personnel are present or must be called in from home.
At our institution, we’ve created a rapid fellow/faculty consult pathway for ED cases where STEMI is ambiguous or the indications for emergent cath are not clear. This represents a “stop and take a breath” approach for cases where primary PCI is not obviously indicated. LBBB patients make up a sizable proportion of this pathway. Bedside echocardiography, a class IIa indication in this setting, can be very helpful to differentiate an acute ischemic syndrome from chronic disease in a patient with LBBB.
We think it’s important to emphasize that even “new” LBBB may not necessarily translate to an occluded coronary artery/STEMI equivalent. In our experience, truly new LBBB from complete coronary artery occlusion is very rare, given the size and extent of infarcted myocardium necessary to cause a new LBBB; so most of the cases of even new LBBB are not concordant with an occluded coronary artery. In fact, from 4 contemporary angiographic studies of patients presenting with ACS and LBBB, the prevalence of a STEMI-equivalent MI ranged only from 7% to 61% among those with a new LBBB. In Dr. de Lemos’s experience, the prevalence is much closer to 7% than 61%! We’ve seen very few true acute LBBB “STEMI equivalents” in our entire careers. We’d be very interested to hear from other experienced cardiologists about how often they see “the big one” in the LBBB population in contemporary practice.
Ryan: Some people argue that it’s better to err on the side of caution by taking the “new” LBBB to the lab. Do you agree?
McEvoy: We should never allow a truly ischemic LBBB to go without rapid revascularization. Again, I have a very high threshold to not catheterize a proven-new LBBB. So I tend to agree with the above sentiment. However, such a strategy may be somewhat outdated in the modern era, particularly in those “grey zone” cases when the previous EKG is not available and the LBBB cannot be proven as either old or new. Specifically, we now have additional diagnostic tests, complementary to the EKG, which can be brought to bear in a timely manner. Echocardiography can be rapidly performed in most institutions (usually on a 24-hour basis). Whether CT coronary angiography will also find a role in the work-up of such cases is another interesting research question. I do realize that this may not be realistic in all medical facilities. However, any such patient presenting to a facility with limited resources must be transferred to a facility with a catheterization lab. Those facilities also have the ability to do an echocardiogram on arrival.
Neeland & de Lemos: It’s easy for those of us who don’t take interventional calls to say we should have a very low threshold! However, these false activations do put patients at some risk — and are demoralizing for the interventionalists and cath lab staff. That said, we agree that the downside risks of delayed reperfusion and missed diagnoses may matter even more. The challenge is to weigh these opposing risks and make the right decision for the patient. Additional information — ECG, biomarker, or echo-based — can be helpful in these situations, which is where our proposed algorithm should be applied.
Ryan: Neeland and colleagues suggest that because patients with LBBB have an overall higher risk for bleeding, they should, if possible, be preferentially transferred for primary PCI. In areas without cath lab access, what are your thoughts on fibrinolysis in patients with presumed new LBBB? And what was your approach to this issue in Ireland, where you worked as a cardiology registrar/fellow before coming to the U.S.?
McEvoy: For me, the fundamental question is not one of geography, but simply whether a patient presenting with LBBB needs to be rapidly considered for revascularization or not. Again, if the patient presents with clearly new LBBB, a good ACS story, or positive enzymes, revascularization must be prompt. However, if the LBBB duration is unknown, the story is atypical, and the enzymes are negative, a decision about the benefit of rapid triage for revascularization still needs to be made. If such a patient is deemed likely to benefit from revascularization (possibly with echocardiographic guidance) and the door-in/door-out (DIDO) time prior to transfer is <30 minutes (or the difference in door-to-needle time versus door-to-balloon time is <60minutes), the patient should be transferred for primary PCI. In addition to the bleeding risk with thrombolysis in LBBB, I would also suspect that the anterior and massive distribution of ischemia required to cause LBBB inherently means that the patient would derive probabilistic benefit from PCI. Unfortunately, in Ireland these temporal targets were often not realistic and thrombolysis would need to be performed.
Neeland & de Lemos: Given that the risks of bleeding are higher in patients with LBBB (because of a greater likelihood of comorbidities) and the chance of an occluded artery is lower, fibrinolysis is a riskier endeavor in these situations. Data from Pinto et al. suggest that longer PCI-related delay (up to about 2 hours) may still have a favorable risk/benefit ratio than fibrinolytic therapy. In older patients, such as those who present with LBBB, the risk/benefit tradeoff may occur even later. We feel that LBBB patients should be preferentially transferred to centers capable of primary PCI for these reasons and that fibrinolysis should be discouraged unless PCI really cannot be performed within a reasonable time frame. Another issue is that positive enzymes in the absence of a suggestive clinical history, even in the setting of a new LBBB, should not automatically be considered an ACS. Chronic elevations in troponin are common in these patients, related to concomitant structural heart and renal disease, and the trend of the enzymes can be very helpful to differentiate ACS from non-ACS causes of elevations.
Ryan: What do you think of this new proposed algorithm?
McEvoy: My biggest concern about this well-thought-out algorithm is the complete exclusion of the clinical history. I think a convincing and concerning history for ACS in the setting of LBBB should prompt rapid consideration for revascularization. I worry that not including the history and also the pretest probability for ACS (Diamond and Forrester, Duke clinical score, Genders score, etc.) in the algorithm may potentially lead to delays in unstable patients while echocardiography or serial enzymes are being performed. Multiple studies have also now demonstrated the value of CT coronary angiography in triaging patients presenting to the ED with intermediate probability of ACS. Interestingly, recent research also suggests that coronary artery calcium testing (with noncontrast CT) may also be useful in this situation. I would suggest that such tests could also be effectively incorporated into this algorithm in many cases.
Neeland & de Lemos: We completely agree with Dr. McEvoy’s point that the clinical history is a cornerstone of correct diagnosis and management. The first box of our proposed algorithm begins with LBBB and a clinical scenario consistent with ACS (“suspected ACS”), and it should not be extrapolated to situations where the pretest probability of ACS is low. The points about CT angiography are interesting, but it may be challenging to use in patients with LBBB, given their usually older age and greater probability of coronary calcification (which can create technical challenges), as well as a higher likelihood of diffuse coronary disease. We hope that our Viewpoint article will prompt more research into new approaches for rapid differential diagnosis of the patient with LBBB and possible ACS, because we are not satisfied with our current diagnostic and management approach.
Share your views on the new algorithm proposed by Neeland and colleagues.