Cardiology – Page 16 – Emergency Medicine Literature of Note

If You Don’t Reperfuse STEMI, That’s Bad

I’m not sure why this is earthshaking news – other than some good statisticians had access to some good data. Of course, that’s pretty much what research is about – have data, will travel.

This JAMA article looks at door-in-door-out time for STEMI at transferring hospitals – and they suggest an association between between quicker transfer times and unadjusted mortality. There is still some debate regarding how much time to primary PCI matters, but, if you say this in-and-out time is a surrogate marker for time to primary PCI, you could presumably support the hypothesis of rapid PCI mattering.

There are a few interesting nuggets of information in the article – particularly looking at patients for whom the transfer time was exceptionally prolonged. Essentially, left bundle and patients with ambiguous or non-obvious STEMI were delayed. I.e., when the diagnosis is hard, it’s hard to make the diagnosis.

As usual, time matters to the individual, but system factors affect many patients. Mortality for STEMI is improved by faster transport, but you still need to consider the consequences of faster transport. Reckless abandon towards shoving a semi-stable patient out the door won’t always lead to better outcomes, but, then again, I have worked in some of those hospitals….

“Association of Door-In to Door-Out Time With Reperfusion Delays and Outcomes Among Patients Transferred for Primary Percutaneous Coronary Intervention.”
http://www.ncbi.nlm.nih.gov/pubmed/21693742

CCTA Only Predicts Revascularizations

This is an interesting systematic review of coronary computer tomography angiography that, I think, shows mostly that the endpoints for cardiology studies need to be re-evaluated. The conclusion that circulates in the new has been that positive CCTA was highly predictive of coronary events – patients with >1 segment of >50% stenosis on CCTA had an 11.9% annualized rate of coronary “events” when compared to the 1.1% annualized rate of patients without any >50% stenosis. This generates the 10.74 hazard ratio that has been circulating through the press releases trumpeting the predictive value of CCTA.

Unfortunately, this predictive value is a self-fulfilling prophecy because 62% of their “events” were revascularizations. If you subtract out the portion that went for revascularization, the remaining all-cause mortality, cardiovascular death, nonfatal MI, UA requiring hospitalization, that’s 5% annualized rate. Still higher than folks without any coronary stenoses at all, but you have to wonder – could we have predicted the population with a 5% cardiovascular morbidity risk without a CCTA? Does the management decision to perform revascularization confer upon this population a cardiovascular morbidity/mortality benefit? We are seeing a lot more in the literature showing that medical management is as advantageous as stenting, so, again, I’m not sure what the role of CCTA is – particularly from the Emergency Department.

“Meta-analysis and systematic review of the long-term predictive value of assessment of coronary atherosclerosis by contrast-enhanced coronary computed tomography angiography.”
http://www.ncbi.nlm.nih.gov/pubmed/21658564

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