Category: Cardiology

Patients With Brugada May Have Normal EKGs …and Then Drop Dead

The sodium-channelopathy that went many years before being described, now increasingly well-known.  More interestingly, the phenotype is apparently autosomal dominant in inheritance.  These investigators use this inheritance to retroactively diagnose deceased family members with a Brugada cause to their sudden cardiac death.

They found, unfortunately, that not only were most individuals who died of Brugada young, most were asymptomatic – and of the five patients for whom they could find an antemortem EKG, only one of them had a typical Type I Brugada pattern, and one had a single lead with a Type III pattern.

I think my take-home point from this article is that, in the young patients presenting with syncope, it’s important not just to do the EKG, but also to enquire regarding family history of sudden cardiac death – and then hope whatever cardiologist you refer them to is insightful enough to order a amajaline provocation test if needed.

http://www.ncbi.nlm.nih.gov/pubmed/21636035

The Single Troponin After 8 Hours of Symptoms

The ACEP guidelines still have, as level B recommendations, that a single cardiac biomaker “8 to 12 hours” after symptom onset is adequate to exclude the diagnosis of NSTEMI.

This study looked at all of Highland’s patients that received more than one troponin measurement in their ED.  Then, they looked at all the patients with initially negative troponins, and subsequently positive ones.  And, finally, they tried to see how many of those had symptoms >8 hours.  Their definitions are that troponins <0.06 ng/mL are negative, between 0.06 and 0.6 are indeterminate, and >0.6 are positive.

After starting with 5,596 patients, they had 125 that were negative initially, and then positive.  And, for symptoms greater than 8 hours, a grand total of seven troponins ≤0.06 ng/mL and then subsequently positive, and 18 others that were indeterminate and then subsequently positive.  They then say only two had a diagnosis of ACS.

Regardless, despite the size of the study, when you start talking about these sorts of tiny numbers and getting into splitting hairs on the diagnosis, you’re basically working on anecdotal evidence.  So, take it with a grain of salt – you’re usually safe in a patient with that symptom duration, but you’re working off mostly consensus opinion as opposed to great evidence.

More interesting, really, would be some kind of follow-up on the 1,086 patients that were discharged after a single negative troponin (many of which probably fulfilled the >8 hour criterion) – but there’s no way to actually make that sort of follow happen realistically.

http://www.hindawi.com/isrn/cardiology/2011/364728/

Bypassing The ER With STEMI

This is a paper cited in the most recent ACEP Weekend review that tries to draw more profound conclusions than it probably should.

It’s another piece of the growing body of literature that says “Hurry!  Prehospital activation is all we need in STEMI!”  From Israel, it’s a retrospective review of performance variables and patient outcomes between a cohort that was assessed in the ER and a cohort that went straight to the lab.  They draw a few conclusions, some of which are valid.

First, time.  One of the two “primary” outcome variables is door-to-balloon time.  No argument that skipping steps along the way will save you time.  No study is needed to prove that.

The second “primary” outcome variable is MACE within 30 days – another combined endpoint kludge of death, CHF, reinfarction, CVA, TIA, and urgent revascularization.  This one favored the direct-to-ICCU group, 22% to 30%.  How is 30-day CVA/TIA directly related to the effectiveness of PCI?  Looking at their secondary outcomes – death was not significantly different – but CHF was 8% different, which therefore accounts for essentially the entire difference between groups in this primary outcome.

And the problem?  Well, they also show in a secondary outcome that LVEF >30% was 7% greater in the direct-to-ICCU group…from which it follows there would obviously be less heart failure in that group.  But, in their demographic information, they don’t know the pre-intervention LVEF for their patients – only the Killip class on presentation, which is a measure of the heart failure associated with the acute cardiac event, not their pre-existing LVEF.

So, the only thing they’ve effectively proven in this study is that skipping steps saves time.  And, they don’t comment on the number of false positives in each group, either.

http://www.ima.org.il/imaj/ar11apr-07.pdf

NSAIDS Kill – Especially Diclofenac

While the protections for individuality make America the colorful place it is today, it sure is easy to run massive cohort studies in European countries where they sacrifice a little bit of anonymity for the common good.

Everyone in Denmark has a number, and they tracked every patient in Denmark with a history of MI to see if they had any adverse events after receiving a prescription for NSAIDs.  There were a few significant differences in the populations receiving each different kind of NSAID – rofecoxib and celecoxib tended to be given to older, female populations, and there were some differences throughout their groups regarding the prevalence of other co-administered cardiac medications.

This article really annoys me because the page with which they present their incidence of death by week has six charts that lend themselves immediately to visual comparison – but their chart scales are grossly different.  Ibuprofen looks terrible at first glance, but then you realize it has the smallest y-axis scale, and actually performs quite well.  In the end, they all demonstrated worsening of outcomes regarding death/MI compared to the total study population rate of death/MI not proximate to NSAID use.

In the end, ibuprofen and naproxen had the least effect on the OR for death; it is fair to avoid rofecoxib, celecoxib, and diclofenac in your routine prescribing without specific indications.

http://www.ncbi.nlm.nih.gov/pubmed/21555710

Erythropoietin is of No Benefit in STEMI

I have to say, the outcomes of this study both surprised and did not surprise me.  A couple years ago, I read a few articles regarding erythropoietin administration in animal models of myocardial ischemia, and they actually tended towards cardioprotective effects.  However, there have been some other retrospective reviews looking at erythropoietin levels in humans that have not been quite as conclusive.

The efficacy cohort rather favored the intervention group – the most important significant difference was primary vs. rescue PCI, and significantly more EPO group patients received primary PCI.  But, then, their results section is mostly a long list of non-significant differences, and some secondary outcomes favoring placebo.  Adverse events also favored placebo.  So, I don’t think we’ll be seeing EPO on the code STEMI order sheet anytime soon.

As another aside, and sort of a follow-up to the Annals of Internal Medicine article a month ago regarding conflicts of interest in the new ACC Guidelines – the disclosure list for this article is massive.  It is clearly the standard of care in Cardiology to be on the payroll of multiple pharmaceutical companies in one fashion or another.

http://www.ncbi.nlm.nih.gov/pubmed/21558517

…and Here is Why the Elderly Are Falling

Orthostatic intolerance.

Not much more to say.

An entire quarter of their convenience sample of elderly (mostly female) volunteers had a 60 point drop in their blood pressure upon standing, with only a modicum of recovery within 2 minutes.

Antihypertensive polypharmacy was weakly associated with orthostatic intolerance, and the presence of orthostatic intolerance was weakly associated with an increased number of falls.

So, if the disease (hypertension) doesn’t harm you, the treatment will.

http://www.ncbi.nlm.nih.gov/pubmed/21438868

Chest Pain and Recent Negative Stress Test

If your hospital is anything like our hospital, you have tons of low- and intermediate-risk chest pain.  Every one is stressful, but hopefully you have a friendly hospitalist, or better yet, an ED-run chest-pain unit that gives you a place for observation admissions.  They go there, get their rule-out, and get some sort of provocative test, as discussed in the most recent AHA guidelines.  The test is negative, they go home.

…and then they come back a week later with the same symptoms.

This is a great paper to have in your pocket when you need to justify why this patient still needs to be ruled out; I heard about it when it was mentioned on the April EM:RAP during the low-risk chest pain discussion.  Patients with negative stress tests may still be diagnosed with CAD on angiography – 20.7% incidence of CAD in their cohort which had negative or non-diagnostic stress within 3 years – and 7.8% were diagnosed with AMI.

When you add negative troponins and the negative stress from the previous visit, you’ve met the guidelines and standard of care to say they did not have acute myocardial ischemia and you cannot induce ischemia on provocative testing, and they are risk-stratified into a group of patients very unlikely to have ACS in the next 30 days/60 days/6 months.  However, you get that high NPV because you’re performing these tests on a low-risk population, not because the sensitivity of those tests, particularly stress testing, is good enough.  While this patient likely does not need another provocative test – although, depending on individual factors, they may be candidates for angiography of some sort – if their story is concerning for cardiac etiology, they still need enzymatic rule-out.

http://www.ncbi.nlm.nih.gov/pubmed/21079714

Prehospital STEMI Diversion to PCI

Time is muscle and the earlier you get to PCI the more muscle you can save.  So, we should just drive by all the critical access hospitals and go straight to PCI-capable centers?  The Dutch, in this retrospective study, think we should.  Everything in their protocol hinges on EMS reading a computer interpretation of the EKG, and, if it says STEMI, they go to the PCI center.  At the end of the day, everyone who went to the PCI capable center first rather than the spoke hospital first had a mortality benefit between 2% and 2.6% at one year.  


What they really don’t discuss much are the outcomes of the 5.7% of their intention-to-treat analysis that had false positives.  False positives, at least, are typically not harmful to the patient – the alternative diagnoses for chest pain that would benefit from immediate treatment at one of their non-PCI “spoke” hospitals are probably not that frequent – aortic dissections and submassive PEs tend to be the sorts of things that would benefit.  But, even if they did a true intention-to-treat analysis, they’d probably still have a mortality benefit.  The other problem with false positives is the financial costs associated with unneeded cath lab activation and the costs to the system associated with taking EMS out of service.  It’s obvious that treating patients for their disease in the most timely fashion for certain diseases improves outcomes – but we must always beware of the unintended consequences.


http://www.ncbi.nlm.nih.gov/pubmed/21315209


This is actually a big deal sort of topic in EM right now as it relates to the regionalization of care, which is something that the Academic Emergency Medicine consensus conference is dealing with right now.  Attempting to mirror what’s happened with trauma networks, they’re trying to extend the benefits to other acute conditions that otherwise benefit from transfer to higher levels of care.  Clearly, a myriad of life-threatening conditions benefit from the resources of tertiary referral centers – but the logistics and political issues associated with centralizing care for different conditions remains a significant barrier.


http://www.ncbi.nlm.nih.gov/pubmed/21122020

Sodium Nitroprusside with CPR

Here’s another interesting piece of animal literature to fight with your IRB about for performing studies on human subjects in your ED.  The article itself is a little hard to follow because of the terminology used – eCPR, SNPeCPR, and S-CPR, but, essentially, they have regular CPR, then they have their enhanced CPR which consists of an impedance device and compressive trousers, and then they have enhanced CPR plus sodium nitroprusside.  Additionally confounding, on top of different CPR methods, they only gave standard CPR epinephrine, while the other two methods received no epinephrine.  Sodium nitroprusside pigs did much better than the other two methods and medications.
So, with n = 8, in pigs, there’s only a couple statistical conclusions we can make.  Their pigs that received their no-drugs enhanced-CPR did no differently than standard CPR with epinephrine.  Then, their pigs that received sodium nitroprusside plus enhanced-CPR do way better than their no-drugs enhanced-CPR.  So, sodium nitroprusside is doing something.  As far as external validity, 1) it’s pigs and 2) it’s probably financially and logistically infeasible for our ACLS-equipped paramedics to go through the additional steps of enhanced-CPR.  I’d really like to see what would have happened in a blinded, three-arm, nitroprusside vs. epinephrine vs. placebo where each group had the same CPR.
That being said, if you can get your IRB to approve a prospective study in human subjects – more power to you.  All the literature shows our current ACLS is mostly useless – and the definition of insanity is doing the same thing over and over again and expecting different results – so I’m all for looking at new agents in cardiac arrest.

http://www.ncbi.nlm.nih.gov/pubmed/21358401

Mandatory EKG Screening for Athletes

Discussion today in the public forum about this article:

Has been going around the internet.  I only have access to the abstract, however, so I can only base my discussion on what data I see there.  This is one of those articles that reviewed the rate of death in NCAA athletes for the last few years, and, essentially, they found that the incidence of sudden cardiac death was 2.28 event per 100,000 participant years.  The commentary in the media: if only we had better screening!
Well, they tried that in Israel.  Mandatory EKG screening was instituted in 1997 in an attempt to curtain SCD in athletes.  The death rate before screening was 2.54 events per 100,000 participant years.  Afterwards, 2.66 events per 100,000. 
So, yes, if only we had better screening – because EKG alone doesn’t cut it.  EKG + echocardiography?  EP study?  At some point, you have to take a rational look at the costs of something and realize it’s not taken out of an infinite pool of money – money that almost certainly could be put towards a much higher yield public health effort.  Reactionary calls for more screening at this time are simply increased costs without proven benefit.