Notes from Dr. RW

Novel H1N1 influenza in hospitalized patients

2009-11-23T13:46:00.000-06:00

JAMA has a recent issue devoted to this topic. Here’s what stands out:

In a series from California admitted patients tended to be younger (27) but of those admitted, those over 50 had the highest mortality (11% overall, 18-20% for those over 50). 66% of chest xrays showed infiltrates and 31% of patients required ICU. Viral pneumonia and ARDS were the most common causes of death. Secondary bacterial infection was only found in 4%.

A Canadian series looked at critically ill patients. Mean age was 32 and 28 day mortality was 14%. Patients’ illnesses progressed rapidly with a mean of 1 day from hospital admission to ICU transfer. Shock and nonpulmonary organ failure were common. Hypoxemia tended to be severe with the mean PO2/FiO2 of 147. 81% got mechanical ventilation with a mean duration of 12 days. Lung rescue therapies were commonly used.

A series from Mexico reported similar outcomes with additional findings of note: 31% were obese and antiviral treatment (adjusting for those with no opportunity for treatment due to early death) improved survival.

Investigators from Australia and New Zealand reported on a series of patients referred for ECMO. Those patients had a 21% mortality by study end. Patients transitioning to ECMO had a median PO2/FiO2 of 56 on a median of 18cm PEEP.

An editorial, commenting on a trial published in the same issue showing non-inferiority of surgical masks compared with N-95s noted that we still don’t have enough evidence on this issue and the controversy will continue.

Recognition of focused practice in HM

2009-11-23T08:21:00.001-06:00

Here's more info from The Hospitalist. When I posted about this a couple of months ago I wondered when we would see some resources to help with preparation. In article Scott Flanders said:

“SHM has to help develop the tools and resources hospitalists will need to successfully prepare for and pass this test,” he says. He expects educational resources and self-assessment modules will be available on SHM’s Web site (www.hospitalmedicine.org) and at HM10, April 8-11 in Washington, D.C.

Most hospitalists will work through the RFP process as part of their 10 year recert. What about those who are grandfathered in with lifetime certification? They don't have to take the test but they can. Details on how that will work are unclear.

AHA 2009: chronic pacemaker mediated cardiomyopathy?

2009-11-23T06:00:00.000-06:00

We've long known that right ventricular pacing is not physiologic. PACE study investigators, presenting at AHA 2009, looked at the difference between RV and BiV pacing in terms of EF after one year in patients with normal or nearly normal systolic function at baseline.

By one year there was no difference in 6 minute walk performance or quality of life indicators, but patients in the RV pacing group dropped their EF (by 7%) whereas those in the BiV group did not. For a patient starting with a normal EF, a 7% drop may not seem like much, but consider the impact of a few % per year!

RV pacing leads to cardiac remodeling. BiV pacing prevents it. Based on these findings, chronic RV pacing is a bit like depriving some patients of ACE inhibitors.

If you've taken care of many patients with pacemakers you've probably seen pacemaker mediated cardiomyopathy. The hypothesis needs further study before we implant BiV pacers in all patients, but for now there is an important take home message---minimize RV pacing via rate and AV interval programming and be aware that patients in whom this is not possible, because they are RV pacer dependent, may be at special risk to develop dilated cardiomyopathy.

For details on this fascinating study:

Presentation slides.

Discussant slides.

Presentation audio.

Discussant audio.

Summary slide.

Homeopathy is woo. Green Journal.

2009-11-22T21:57:00.004-06:00

I love the courage of the Green Journal in calling out quackery. You wouldn't find an article like this in JAMA or the Annals. Of note, one of the authors is identified with a department of complementary medicine. All the same, he knows things that go quack.

Patient safety 10 years after “To Err is Human”

2009-11-22T14:21:00.003-06:00

Commentary from key leaders in the latest issue of The Hospitalist reflects on where we've come in the decade since the Institute of Medicine released its patient safety report. Though the article is mainly congratulatory there has been spirited debate about the success (or lack thereof) of the patient safety movement. A recent report by the Consumers Union declared the movement a failure. Although the report lacked data on safety breaches and was based on a faulty premise (equating the continued high rate of hospital associated infections to unsafe practice) it correctly pointed out that we have done little to implement the IOM's recommendations.

Why haven't we done more? Maybe because the IOM's recommendations were predicated on a culture of transparency while over the past decade we have devolved into a culture of blame. These are mutually exclusive outcomes. I pointed that out here and in other posts as my own reason for giving the movement a failing grade.

Meanwhile Bob Wachter gives the patient safety movement less than glowing reviews but apparently for the opposite reason. He seems to believe we have achieved a no blame culture and not only that, it has gone too far. He opened his September 30 blog post with:

In this week’s New England Journal, Peter Pronovost and I make the case for striking a new balance between “no blame” and accountability. Come on folks, it’s time.

Why the seemingly divergent conclusions? Because we've conflated the ideas of accountability and blame. Blame is finger pointing when something goes wrong. The ad below reflects our culture of blame. Note the implied finger pointing: if the patient gets VAP it's someone else's fault.

That's the attitude that pervades medicine today and it's so counterproductive! But it's not the accountability Bob's talking about. If we make careful distinctions between accountability and blame Bob and I are not that far apart. He believes there should be consequences for stubborn, deliberate violation of known safety measures such as hand washing and time outs. I couldn't agree more. It's a form of disruptive behavior, for which Joint Commission already requires “zero tolerance”.

Low blame and high accountability are not conflicting goals. What we have now is too much blame and not enough accountability! In its report the IOM noted that transparency would be essential to effective process improvements for patient safety. The report also stated that such transparency would require movement toward a blame free culture. But, due to misinterpretation of research data and a blunder in the use of language the IOM report had the opposite effect! I explained here:

Ironically, the IOM, with the issuance of its report, undermined its own aspirations for a culture of transparency right out of the gate! They did this by indiscriminately referring to a broad spectrum of adverse patient outcomes as “errors.” This unfortunate attribution, based on faulty analysis of a landmark study on adverse hospital events, I have argued, did much to sabotage the cause of patient safety in the decade that followed. (For the original investigator’s own criticism of the IOM’s interpretation see this editorial). Instead of an era of transparency we entered a heightened culture of blame and finger pointing. The most vivid example of this, of course, is Medicare’s never events policy, of which we are just beginning to realize the adverse consequences.

Now we have a domino effect of more and more unintended consequences. Already in the works is a new legal standard which shifts the burden of proof to hospitals in certain malpractice cases. So much for transparency!

At a recent UWGrand Rounds presentation Bob described what he called a “masterful bit of spin” by the IOM in equating the rate of adverse events in health care to one commercial air crash per day. But the IOM did worse than spin data. They spun assumptions based on faulty interpretation of data. Masterful but unfortunate.

Mitosis

2009-11-22T11:41:00.001-06:00

I was taught to remember the acronym IPMAT.

(There’s also preprophase and prometaphase).

Many school kids in the 1960s learned about it from The Thread of Life, one of the Bell Laboratories science films. Clip below.

Novel H1N1 vaccine safety

2009-11-21T18:09:00.000-06:00

Monitoring has been intense but there have been no unusual concerns to date according to two reports.

Has public reporting impacted health care at all?

2009-11-20T19:52:00.001-06:00

Public reporting of health care performance measures has been a hot topic for several years. It already had a good head of steam in 2005, my first year of blogging, when policy mavens hoped it would be transformative. Last year Bob Wachter even wondered if we were entering a golden age of transparency.

But how was it supposed to work? The conventional wisdom was that it would work by influencing consumers' choices. That never came to pass, though, and Bob suggested another effect:

Shockingly, in the past five years, these mantras have proven to be way off the mark. Instead,

1.Some rudimentary quality data has been placed on the Web
2.Few people are looking at these data, and virtually no real patients are making their healthcare purchasing decisions based on them.
3.And yet… hospitals are doing organizational cartwheels trying to improve their performance on the publicly reported indicators.

Although #2 is surprising, #3 is truly flabbergasting -- it demonstrates the power of shame and embarrassment as motivating forces.

So, shame and embarrassment are motivating hospitals! Yes, it's true, but is it a good thing? In my view such motivation amounts to little more than a form of institutional narcissism---it's all about us (the institution) and our report cards, and has little to do with patients. (As regular readers know I believe that, with few exceptions, performance measures are weak, sometimes non-evidence based and occasionally even harmful).

OK, all cynicism aside: has this transparency movement had any meaningful impact at all? Up to now we've had no evidence one way or the other. That brings me to the EFFECT study, presented at AHA 2009 and published on line in JAMA. The conclusion in the published abstract doesn't give you the real flavor of the study but here's what it said:

Results The publication of the early feedback hospital report card did not result in a significant systemwide improvement in the early feedback group in either the composite AMI process-of-care indicator (absolute change, 1.5%; 95% confidence interval [CI], –2.2% to 5.1%; P=.43) or the composite CHF process-of-care indicator (absolute change, 0.6%; 95% CI, –4.5% to 5.7%; P=.81). During the follow-up period, the mean 30-day AMI mortality rates were 2.5% lower (95% CI, 0.1% to 4.9%; P=.045) in the early feedback group compared with the delayed feedback group. The hospital mortality rates for CHF were not significantly different.

Conclusion Public release of hospital-specific quality indicators did not significantly improve composite process-of-care indicators for AMI or CHF.

So, all in all, public reporting had little impact. I'll get back to that barely statistically significant improvement in MI mortality in a moment.

This study had a somewhat roundabout design. Both comparison groups of hospitals were subject to public reporting. The difference was, in the “intervention group” the reporting was early and accompanied by a media blitz. In the comparison group the reporting was later and there was no media blitz. According to post reporting surveys the intervention hospitals did scramble to enhance their performance, but in a heterogeneous and disorganized manner, accounting for the lack of measured difference in overall adherence to indicators between the comparison groups.

Now what about that improvement in MI mortality? It turns out that it was largely attributable to an improvement in STEMI mortality. Although the percentage of hospitals achieving time-to-reperfusion benchmarks didn't differ between the two groups the findings suggested that in the intervention group there may have been a shorter time to reperfusion. If so it appears to have been driven entirely by time to administration of thrombolytic agents (PCI was used infrequently, but, hey, this was Canada). The only difference in process indicators attributable to the intervention was the frequency of thrombolytics administered in the ER, before transfer to intensive care. Of note, the survey indicated that ten hospitals in the intervention group decided, after the reporting, to allow ER physicians to administer thrombolytics without specialty consultation.

Although I believe performance measures tend to be weak, time to reperfusion is a notable exception. The process change by which hospitals gave ER docs autonomy in the administration of thrombolytics may have made a difference.

So, after all these years and all this momentum, evidence for an impact of public reporting is slim. Institutional narcissism, up to now, has been largely ineffective, being driven by weak and perfunctory process measures. The quality movement needs to adopt a more thoughtful and nuanced approach to improvement.

AHA 09: the POPE study

2009-11-20T08:50:00.000-06:00

Hospitalists involved in the care of CABG patients will find this study of interest. Pericardial irritation occurs post CABG. Pericarditis can cause arrhythmias as well as lead to effusion progressing to tampanade. Frequently NSAIDs are given to reduce these complications. Evidence to support this strategy has been lacking. The POPE study, presented at AHA 09, looked at the use of diclofenac to reduce the volume of pericardial effusion. The findings, from the press release:

A non-steroidal anti-inflammatory drug, diclofenac, failed to reduce fluid accumulation around the heart after cardiac surgery.

The NSAID after heart surgery also did not reduce the serious problem of cardiac tamponade, compression of the heart by fluid.

Only patients with pericardial effusion at baseline were enrolled. The investigators concluded:

The use of NSAIDs in post-cardiac surgery patients is useless in this setting.

As pointed out in the presentation slides NSAID use post CABG has been common even though not supported by good evidence, and in spite of known adverse effects including increased renal failure, heart failure and myocardial infarction.

Amyloid cardiomyopathy

2009-11-20T07:46:00.000-06:00

This Clinical Perspective piece in Circulation stresses the little appreciated fact that there are actually three types of cardiac amyloidosis: the AL type that we’re used to thinking of as well as two types of transthyretin related disease, the mutant type (of which there are over 100 mutations) and the wild type seen almost exclusively in older men. The three types differ in clinical features and prognosis.

EMRs don't improve health care---yet

2009-11-19T12:41:00.002-06:00

Claims made over the last several years that EMRs lead to better quality of care have been devoid of supporting evidence. Now we have evidence from a large study that EMRs in fact don't improve quality. I apologize for not having a better source for this than a New York Times article, which reports that the findings were to have been reported at a conference in Boston. Unfortunately, the article didn't provide a link to the conference proceedings and didn't name the conference. Maybe I'll find the primary source later. In the mean time the article reports:

But a new study comparing 3,000 hospitals at various stages in the adoption of computerized health records has found little difference in the cost and quality of care.

“The way electronic medical records are used now has not yet had a real impact on the quality or cost of health care,” said Dr. Ashish K. Jha, an assistant professor at the Harvard School of Public Health, who led the research project.

Unfortunately the study looked at performance measures, and performance measures do not equal quality. But the study still makes a strong statement because performance measures represent the bare minimum standards, the lowest of the low hanging fruit. So if EMRs didn't improve performance measures you can be darn sure they had little or no impact on real quality.

I agree with the comments of the interviewees in the article, that we have years to go before we utilize EMRs effectively, in a way that will improve patient care.

Autoimmune polyendocrine syndromes

2009-11-19T06:15:00.000-06:00

Reviewed here (Expert Review of Endocrinology and Metabolism).

Colchicine toxicity

2009-11-19T06:00:00.000-06:00

Brief review and lessons from the courtroom.

AHA 09: the FOCUS study

2009-11-19T05:28:00.001-06:00

This study addressed an issue that often plagues hospitalists who are involved in co-management of patients undergoing hip fracture repair: when the patient's hemoglobin and hematocrit drop following surgery, what is the appropriate transfusion target in patients with cardiovascular disease or risk factors for CVD? While a H/H target of 8/24 has been validated for patients across the board, conventional wisdom has it that 10/30 is a more appropriate target for patients with cardiovascular disease. FOCUS compared strategies utilizing these two targets and found no advantage of the more aggressive transfusion strategy in terms of death or cardiac event rate. Results concerning the effect on functional outcomes have yet to be announced.

From AHA 09 scientific sessions: CT-STAT

2009-11-18T18:51:00.001-06:00

It's always fun, after national meetings, to observe how the popular press botches the reporting of important findings that were presented. CT-STAT compared two diagnostic strategies for ER evaluation of chest pain in low and intermediate risk patients: initial cardiac markers and electrocardiograms followed by either traditional stress imaging or CT coronary angiography. Here's an Associated Press report on the findings. Nowhere in the report is there a link to the primary source (other than a link to the AHA website) and nowhere is the name of the study mentioned. Moreover, the article failes to inform readers of which of the several types of CT scans was used (it was CT coronary angiography). The article gets it wrong right out of the gate:

A CT scan — a kind of super X-ray — provides a faster, cheaper way to diagnose a heart attack when someone goes to the emergency room with chest pains, a new study suggests.

On the whole CT scanning was indeed cheaper and resulted in faster determination of disposition. And, it was just as good as traditional work up in terms of freedom from events, short term and at 6 months. What's wrong with the statement is the notion that CT diagnosed heart attacks. Wrong, wrong, wrong. Patients enrolled in CT-STAT had already ruled out for MI via cardiac biomarkers and electrocardiograms. CTA is a rule out, not a rule in, test. Over two thirds of patients undergoing CTA had normal or near normal coronary arteries. Of the remaining patients it was not always possible to determine whether visualized disease was significant or “culprit” in nature, and this led to further evaluation.

An important caveat is that the CT strategy is not applicable to higher risk patients, in whom the negative predictive power is not as good. For those patients who rule in subsequent evaluation may be complicated. First, a cardiac catheterization would expose the patient to a second dye load and increased risk of renal failure. This might necessitate waiting an extra day with hydration before proceeding to cath. Second, after visualization of disease on CTA functional testing may then be necessary to establish the physiologic significance of the lesion(s). In other words, some patients, after CTA, may end up getting a stress nuc anyway. For patients who don't rule out with CTA the subsequent diagnostic strategies may in fact be slower and more expensive. We really don't know because the study was not designed to answer that question. Based on these study results, though, the CT strategy is cheaper and faster over all when used in low risk patients because the cost and time savings in the patients who rule out outweigh any increase in cost for the other patients, who are in the minority.

Additional resources about this study, direct from AHA, can be found here, here and here.

ARBITER 6–HALTS---what does it really mean?

2009-11-18T16:11:00.001-06:00

This is somewhat old news by now, but its results have been widely distorted in popular media. With this post I hope to put the issue in perspective.

From the NEJM abstract (italicized comments mine):

Methods We enrolled patients who had coronary heart disease or a coronary heart disease risk equivalent, who were receiving long-term statin therapy, and in whom an LDL cholesterol level under 100 mg per deciliter (2.6 mmol per liter) and an HDL cholesterol level under 50 mg per deciliter for men or 55 mg per deciliter for women (1.3 or 1.4 mmol per liter, respectively) had been achieved. (Since when is an HDL cholesterol below a certain target an achievement?). The patients were randomly assigned to receive extended-release niacin (target dose, 2000 mg per day) or ezetimibe (10 mg per day). (Added to statin therapy). The primary end point was the between-group difference in the change from baseline in the mean common carotid intima–media thickness after 14 months....

Results The mean HDL cholesterol level in the niacin group increased by 18.4% over the 14-month study period, to 50 mg per deciliter (P less than 0.001), and the mean LDL cholesterol level in the ezetimibe group decreased by 19.2%, to 66 mg per deciliter (1.7 mmol per liter) (P less than 0.001). Niacin therapy significantly reduced LDL cholesterol and triglyceride levels; ezetimibe reduced the HDL cholesterol and triglyceride levels. As compared with ezetimibe, niacin had greater efficacy regarding the change in mean carotid intima–media thickness over 14 months (P=0.003), leading to significant reduction of both mean (P=0.001) and maximal carotid intima–media thickness (P less than 0.001 for all comparisons). Paradoxically, greater reductions in the LDL cholesterol level in association with ezetimibe were significantly associated with an increase in the carotid intima–media thickness (R=–0.31, P less than 0.001). The incidence of major cardiovascular events was lower in the niacin group than in the ezetimibe group (1% vs. 5%, P=0.04 by the chi-square test).

From the conclusion:

...extended-release niacin causes a significant regression of carotid intima–media thickness when combined with a statin and that niacin is superior to ezetimibe.

Here are the take home points:

This trial does not refute the LDL hypothesis. For decades diet and drug trials have shown that the more LDL is lowered the fewer the events. The evidence to support this relationship is reproducible over time and is overwhelming.

It makes intuitive sense that lowering of cholesterol by an absorption blocker would be beneficial. An older class of absorption blockers, the bile acid resin binding agents, such as cholestyramine, has been shown to reduce cardiovascular events. Their mechanism, however, inhibition of reabsorption of bile acids thereby consuming cholesterol to make more bile acids, differs from that of ezetimibe. Ezetimibe directly inhibits cholesterol absorption by a novel mechanism as explained here in the product labeling:

The molecular target of ezetimibe has been shown to be the sterol transporter, Niemann-Pick C1-Like 1 (NPC1L1), which is involved in the intestinal uptake of cholesterol and phytosterols.

Evidently, though, ezetimibe does more, and that was the new finding in this study: it lowered HDL cholesterol. HDLC, contrary to popular distortion, is not “good cholesterol” that protects against atherosclerosis. Instead, the concentration of HDLC is a marker of the efficiency of reverse cholesterol transport. Ezetimibe is absorbed systemically and who knows what it's doing outside the intestinal brush border. So, if the finding of this study is real, that ezetimibe really does lower HDLC, that means it may be doing something to impede reverse cholesterol transport. That would be bad indeed. Niacin, on the other hand, has been known for years to improve reverse cholesterol transport, thereby raising HDLC.

The finding that ezetimibe was associated with a lowering of HDLC is indeed surprising. The final study conclusions, though, are not surprising for this reason: it has been well understood for decades that, despite the clinical efficacy of lowering LDL, it's not enough in many patients. Consider all those statin trials that show relative risk reductions on the order of 30%. Laudable as that is it's far from 100%! Thus was born the notion of residual risk after statin therapy. Once LDLC is lowered to goal, via statin therapy or other means, many patients remain at risk. Niacin addresses that residual risk. Further LDLC reduction does not. Why?

The residual risk is composed of a mixed bag of metabolic disturbances, most of them attributable to the metabolic syndrome which includes impaired reverse cholesterol transport, insulin resistance, elevation of triglyceride-rich atherogenic particles and small LDL particle diameter. Niacin reverses these disturbances. For an in depth explanation of these risk factors check these references: [1] [2] [3].

One finding was reassuring. Combo therapy with niacin and a statin was safe. Although it was a small study there were apparently no issues with increased myositis or hepatotoxicity risk attributable to the combination as is seen with statin-fibrate combinations.

How should hospitalists be cultivated?

2009-11-18T06:00:00.000-06:00

Here are the two competing models: 1) as clinicians at the top of their game and 2) as stage performers. I’ve been in the field since its beginnings and over the years I’ve seen it devolve from model number 1 towards model number 2. If the practice management track at SHM 2009 is any indication, model 2 is winning. Not a good thing, in my opinion.

The title of hospitalist leader Mary Jo Gorman’s talk about running a program is a dead giveaway: “Performance Reviews: Dealing with the Problem Performer.” I don’t run a hospitalist program but if I did I’d be more interested in how my hospitalists functioned as clinicians than how they performed. Anyway, the focus of the talk was on behavior and conformity. Clinical skills were mentioned only in passing.

There were some good points in the talk. Most importantly, don’t expect the hospitalists on your team to read minds. Be clear in your expectations. Good, explicit communication (not just abstract goals like “be a team player”) solves a lot of problems. And yes, rules are important, but tools---tools that help the hospitalist function optimally as a clinician---are even better.

Monitoring patients for HIT

2009-11-17T06:15:00.000-06:00

Guidelines exist for monitoring hospitalized patients for the development of HIT and for evaluation of patients who develop thrombocytopenia. How well are they followed? Not very well at one academic medical center in the Netherlands:

The frequency of compliance with platelet count monitoring recommendations was 26.3% for all patients receiving dalteparin, 35.6% for all patients receiving nadroparin, 23.0% for surgical patients receiving prophylactic dosing of either dalteparin or nadroparin, and 41.5% for patients exposed to UFH within 100 days before the start of either dalteparin or nadroparin treatment. Regular platelet count monitoring was strongly positively associated with medical patients (relative risk [RR] 2.33), surgical patients (RR 2.03), critically ill patients (RR 2.80), and those with recent exposure to UFH (RR 2.19). The frequency of testing for HPF4-Ab was 5.4% and the initiation of alternative anticoagulation with danaparoid in patients with a 50% drop in platelet count was 0%.

Proper diet and exercise may stem cognitive decline

2009-11-17T06:00:00.000-06:00

Via Internal Medicine News.

Another review of autoimmune pancreatitis

2009-11-16T11:21:00.001-06:00

Via Expert Review of Gastroenterology and Hepatology.

Key points:

This is a newly appreciated clinical entity.

It is a mimic of pancreatic carcinoma.

It is very responsive to corticosteroids.

Elevated IgG4 is characteristic.

Mechanical ventilation 101---understanding the modes

2009-11-16T10:16:00.001-06:00

This review in CCJM can be considered a companion paper to an earlier one I linked here, explaining the terminology of modes of mechanical ventilation. The CCJM review bridges the gap between theory and practice, focusing more on clinical application. It briefly covers basic terminology and focuses on newer (“alternative”) modes:

We call these innovations “alternative” modes to differentiate them from the plain volume-control and pressure-control modes. Some clinicians rarely use these new modes, but in some medical centers they have become the most common ones used, or are being used unknowingly (the operator misunderstands the mode name).

Say, for example, your hospital uses Dräger ventilators. You order CMV, and dial in a tidal volume. Think your patient's getting simple volume controlled ventilation? Think again.

Methadone and Torsades

2009-11-14T21:00:00.000-06:00

This review contains a summary of the literature and recommendations for safety monitoring.

The ECG that screams for bicarb

2009-11-14T20:57:00.000-06:00

When AVR points toward heaven in the appropriate clinical setting your patient may be headed there before her appointed time without prompt action on your part. In another of his entertaining and fascinating discussions on telltale ECG patterns which guide emergency decision making Dr. James Roberts discusses the electrocardiographic toxidrome of tricyclic antidepressant poisoning.

ECG changes in STEMI

2009-11-13T10:09:00.001-06:00

This review in the American Journal of Emergency Medicine describes in detail the sequence of electrocardiographic changes over time in STEMI.

Stress testing in low risk chest pain patients---is it always necessary?

2009-11-13T08:02:00.001-06:00

Stress testing for patients presenting to the hospital with chest pain, particularly in this era of order sets and templates, has become knee-jerk. For low risk patients under 40 it may not be necessary according to this study:

In our study, a combination of age younger than 40 years, nondiagnostic ECG result, and 2 sets of negative cardiac biomarker results at least 6 hours apart identified a patient group with a very low rate of true-positive provocative testing. Routine stress testing added little to the diagnostic evaluation of this patient group and was falsely positive in all patients who consented to diagnostic coronary angiography (4 of 6 cases).

If nothing else, maybe stress testing could be deferred to out patient testing in some low risk patients who “rule out”, resulting in considerable cost savings to the hospital.

H/T to The Hospitalist.