Electrocardiographic findings in pulmonary embolism and acute coronary syndrome

Due to overlapping clinical presentations acute coronary syndrome (ACS) and pulmonary embolism (PE) can be confused. Moreover, both can be associated with electrocardiographic manifestations (T wave abnormality), elevated troponin levels (present in 42% of patients with PE in this study), and elevated d-dimer levels.

This case report (free full text after registration) illustrates disastrous consequences of massive PE mistaken for ACS. The electrocardiogram shown in the case report displayed findings which could be attributed to either ACS or PE. And while the tracing had a few previously described “red flags” for PE the elecrocardiographic distinction between ACS and PE had not been systematically studied as far as I am aware.

That’s why this paper from the March 15 issue of the American Journal of Cardiology is important. The authors studied patients with either ACS or PE who had T wave inversion on consecutive precordial leads. Among the findings: “In patients with APE, negative T waves were commonly present in leads II, III, aVF, V1, and V2, but were less frequent in leads I, aVL, and V3 to V6” and “Negative T waves in leads III and V1 were observed in only 1% of patients with ACS compared with 88% of patients with APE”. The sensitivity for PE in patients showing negative T waves in both III and V1 must be interpreted with caution, since the study population consisted only of patients with precordial lead T wave inversion. The sensitivity of the finding among PE patients in general is low. A normal electrocardiogram does not rule out PE. Nevertheless the findings of this paper should prove useful in distinguishing between ACS and PE in patients who have precordial T wave abnormality.

Viral glomerulopathy

Hepatitis B, Hepatitis C, HIV and the kidney. Via CCJM.

Central venous catheterization

Nice review in Critical Care Medicine.

Details unfold about Flea’s day in court

The New York Personal Injury Law Blog, to which I linked earlier today, wrote a follow up post in which he reported that the hard copy of the Boston Globe story is on the front page above the fold for all of Flea’s friends, family and patients to see. A big list of links can be found there.

He provided information on two other questions: What was the timing of the take down of Flea’s blog in relation to the events at trial? Who is the guy pictured at the upper left of Flea’s blog?

Finally, he provided a little reminder. Don’t think your risk is eliminated when you take down your blog. An update of his original post has this link to Google’s cache of Flea’s site.

Bacdground:

Kevin updated his post here.

The other Flea.

An attorney weighs in on Flea’s malpractice settlement

As Kevin reported earlier this morning, pediatrician blogger Flea settled his medical malpractice case the morning after his blog was revealed in trial. A New York attorney reflects on what it means:

The issues I raised, in the event plaintiffs' counsel discovered his blog, ran to the risks of losing his attorney-client privilege for all such communications. If this happened, he could be cross-examined on how he was coached by his defense team to act in front of the jury and the advice they gave him. He also ran the risk of his own insurance carrier trying to disclaim coverage if it thought he was hindering the defense.

Chilling indeed.

Colchicine for acute pericarditis

It’s old and off label, but is emerging as the best treatment.

CCJM review.

CCJM editorial outlining precautions against adverse effects.

The COPE trial.

What would you do if you encountered a patient with avian influenza?

I’ve referenced many reviews on this topic, but this one is the first to cover practical aspects of management and infection control.

A clinician needs to be a good observer

So test your powers of observation with this quiz.

Journalistic malpractice?

From the Wall Street Journal:

The behavior of the New England Journal of Medicine (NEJM) is a case in point, when it rushed onto its Web site a limited and flawed analysis of safety concerns around the diabetes drug ...

Via Kevin M.D.

Some ER docs are gonna be hopping mad

….about this New York Times article on tPA for stroke. It’s full of distortions and misstatements although it makes one interesting (and controversial) assertion, which is that defensive medicine is a significant reason for under treatment of patients:

Dr. Richard Burgess, a member of Dr. Warach’s stroke team, explained the situation: There is no particular penalty for not giving tPA. Doctors are unlikely to be sued if the patient dies or is left with brain damage that could have been avoided. But there is a penalty for giving tPA to someone who is not having a stroke. If that patient bleeds into the brain, the drug not only caused a tragic outcome but the doctor could also be sued. Few emergency room doctors want to take that chance.

Through several dramatic stroke anecdotes the piece, with little apparent regard for perspective or accuracy, paints tPA as some sort of miracle drug. Here are some of the distortions.

Doctors are therefore reluctant to give the only drug shown to make a real difference, tPA, or tissue plasminogen activator. The only drug shown to make a real difference? Wrong. Aspirin is associated with improved outcomes and reduced mortality in the first few weeks. This, in fact, is more than can be said for tPA, which does not reduce mortality.


Although tPA was shown in 1996 to save lives and prevent brain damage… Since the article contains no citations to back up its assertions I can only guess that this statement refers to the NINDS study, even though that study was published in 1995, not 1996. The study, the only large randomized trial to show benefit from tPA, showed no statistically significant reduction in mortality. The title of the NYT piece, Lost Chances for Survival, Before and After Stroke, also deceptively implies that tPA is life saving.

Concerning the evaluation of patients for tPA treatment, the article says Many hospitals say they cannot afford to have neurologists on call to diagnose strokes, and cannot afford to have M.R.I. scanners, the most accurate way to diagnose strokes, for the emergency room. Nonsense. The widely accepted guidelines for the use of tPA, which are based on clinical assessment and CT imaging, mention no role for MRI scans.

There’s more. Although the New York Times is widely regarded as a reputable source of medical news this particular NYT piece is yet another example of how scientific issues are distorted when discussed in popular media.

Grand Rounds 3.36

…is up at From Medskool.

Greedy Trial Lawyer distorts my comments on Avandia controversy

Today the Greedy Trial Lawyer referenced my discussion on the Avandia hype and built, then easily ridiculed, this straw man:

Dr. RW has a valid point. I am sick and tired of all this gibberish about medicine clogging up the media. What this country needs is a separation of scientific discourse (including medicine) from the public. What possible good comes from public awareness and discussion of scientific matters? We should ban any scientific thought and discourse by anyone without a Dr. before his name.

Heck, I don’t care whether you have Dr. before your name if you want to discuss science. The real points of my argument, which Greedy Trial Lawyer didn’t address, were these:

Scientific discussion was hijacked by CNN, the New York Times, activists and trial lawyers. (Do I really have to explain what’s so wrong with that?).

The “jury verdict” on Avandia was in within hours of the release of the scientifically flawed NEJM meta-analysis.

The irresponsible media hype surrounding Avandia jeopardized not only reasoned scientific discussion but also an important and much needed clinical trial whose future is now in question.

Public Citizen on Avandia: We told you so

The Public Citizen Health Research Group took advantage of the Avandia controversy for a little self congratulation, saying in effect “We told you so”. But that may be a little deceptive. What they actually told us about was stuff we already knew and had addressed, principally related to the problem of fluid retention which can exacerbate heart failure, and which in no way anticipated the concerns raised by the NEJM meta-analysis.

Worse, they come just short of advising patients to unilaterally discontinue Avandia with this statement: We strongly urge patients - as we have for almost two and a half years - not to use this drug. Wouldn't it suffice to say "ask your doctor"?

Tabloid based medicine trumps evidence based medicine

Mere moments following NEJM’s release of the Avandia meta-analysis and editorial there were millions of Google search queries for Avandia according to a recent post from Clinical Cases and Images. Malpractice attorney ads began appearing only hours later. Hype spreads more rapidly than nuanced critical analysis. So, long before defects in the paper had a chance to be exposed, the popular media, consumer activists and the trial lawyers had taken over the debate. Within hours Avandia was the new Vioxx. More recently we have learned that the ongoing prospective RECORD trial, designed to look at macrovascular outcomes in patients taking Avandia, is in jeopardy (hat tip to Kevin M.D.) due to patients dropping out as a result of the publicity. Something’s terribly wrong with this picture.

Some are accusing NEJM as being like a tabloid and PharmaGossip proposes a new cover style. Is NEJM deserving of the tabloid label? In my considered opinion, yes, for two reasons. First, the journal could have published a more critical, less inflammatory editorial. Even worse was the journal’s decision for early open access release of the paper and editorial. Such a tactic might be appropriate for a public health emergency such as the SARS outbreak. This is not SARS. This is not a public health emergency.

Clearly tabloid based medicine has trumped evidence based medicine and done much harm. I have repeatedly argued that discussions of science are corrupted when played out in the arena of public debate. The Avandia controversy is a case in point.

Is low molecular weight heparin better than unfractionated heparin for VTE prophylaxis?

The best regimen for VTE prophylaxis is controversial. Some recent research helps clarify but does not completely settle the controversy. This study in Thrombosis Journal evaluated outcomes in patients with a variety of medical conditions who received VTE prophylaxis with either the low molecular weight heparin (LMWH) enoxaparin versus unfractionated heparin (UH). There was a markedly reduced incidence of VTE in the enoxaparin group with no difference in adverse effects. The study received support from Aventis Pharmaceuticals, makers of enoxaparin. A potential weakness in this retrospective study is the lack of control over the doses of UH and LMWH. On the other hand it reflects real world use of the agents.

Then there was this prospective randomized open label study of enoxaparin versus UH for VTE prophylaxis in post-stroke patients presented at the American Stroke Association last February, showing a lower rate of VTE with enoxaparin and no difference in bleeding rates. This study, entitled Prevention of VTE After Acute Ischemic Stroke with Low-Molecular-Weight-Heparin Enoxaparin (PREVAIL), was also sponsored by Aventis. One weakness of this study, some might argue, is that it set up a straw man by testing enoxaparin against what some experts assume to be a less than optimal dose of UH (5000 units bid). However, this recent meta-analysis in Chest questions that assumption in that, in medical patients, the higher dose of UF, 5000 units tid, was no better than bid despite a higher bleeding rate.

Although the issue remains controversial, recent data suggest superiority of LMWH over UH for VTE prophylaxis in a variety of settings.

Anaphylaxis

Atypical presentations. Southern Medical Journal.

The Avandia meta-analysis: critical appraisal versus hype

Musings of a Distractible Mind shared some Thoughts on Avandia today (via Kevin M.D.) and is rightfully concerned that irresponsible popular media coverage seems to be guiding scientific discussion. In discussing some of the flaws of the meta-analysis he notes this:

We had an endocrinologist in our office a few days ago (not representing GSK) and we discussed this issue, and his comment was that Dr. Nissen is “the Michael Moore of the medical industry.” Strong words. Mr. Moore is a crusader against the big and rich for the protection of the little guy (in his opinion). The problem is (in my opinion) that Mr. Moore does not always come to conclusions based on evidence, but starts with a conclusion and finds evidence to support this. This is precisely the danger of a meta-analysis of the sort that was done in this case.

But the Medscape piece he cites seems to portray the writers of the related NEJM editorial, Psaty and Furberg, as the real crusaiders:

Dr Steven Haffner (University of Texas Health Science Center, San Antonio), who was involved in the ADOPT study of rosiglitazone, said the paper needed to be published, but it should have undergone a more extensive review, and there should have been a different editorial with more emphasis on the flaws of the study. “The NEJM was irresponsible to go to [Drs Bruce] Psaty and [Curt] Furberg for the editorial--they were always going to emphasize concerns about drug safety; that’s what they do," he commented.

Dr. Robert Califf of Duke University commented on the harmful effect of scientific discussions being played out in popular media:

“It would be better if we had a system of postmarketing signal detection in which signals were vetted scientifically rather than splashed over TV and newspapers. I can't help but wonder if the NEJM is functioning more like the mainstream press than a scientific journal at this point, since many potential peer reviewers seem to feel that Dr Nissen's analyses are missing key elements that could have been added."

Points I’ve made many times in these pages.

Clinical pharmacists as members of the health care team

The latest MedGenMed video editorial reminds us of the importance of the clinical pharmacist. It’s worth viewing and makes valid points. I’m wondering, though, if it’s part of a promotional campaign. It’s the third MedGenMed video editorial in just over a month telling us not to forget the clinical pharmacist. I think I get the message.

Stinging rebuke of the Avandia meta-analysis

In my humble opinion a bad meta-analysis belongs at the bottom of the evidence based medicine hierarchy. The Avandia meta-analysis has been accepted uncritically by the media but how good is it, really? The Angry Pharmacist has some questions. The entire post is compelling reading, but I was most interested in the part about the conflict of interest disclosure, a point the popular media missed entirely: Dr. Nissen reports receiving research support to perform clinical trials through the Cleveland Clinic Cardiovascular Coordinating Center from Pfizer, AstraZeneca, Daiichi Sankyo, Roche, Takeda, Sanofi-Aventis, and Eli Lilly.

It’s an impressive list of Glaxo’s competitors, including Takeda, the maker of Avandia’s most direct competitor, Actose. Well, how about that!

Via Kevin M.D.

Acute decompensated heart failure: management in 2007

A review article in the March 13 2007 issue of CMAJ covers the initial evaluation and management and cites the supporting literature. A few points of interest follow.

Loop diuretics: Mainstay of initial therapy; should be combined with other modalities.

Peripheral venous ultrafiltration: Promising, with role in the general care of acute heart failure to be determined.

Nitroglycerine intravenously: Beneficial for patients with adequate blood pressure, underutilized.

Nesiritide: Controversial. Large mortality and cost effectiveness trial about to begin.

CPAP, BiPAP: Now considered first line as initial short term therapy in acute cardiogenic pulmonary edema. (Invasive mechanical ventilation may be more appropriate in some patients presenting with acute myocardial infarction).

Inotropes, PDE inhibitors: Generally avoided and limited to short term palliative use. May increase mortality.

“What to do with long-term ß-blocker therapy in the setting of acute decompensated heart failure remains a clinical conundrum. Our practice is to reduce the dose proportionate to the degree of hemodynamic compromise; the ß-blocker dose may be decreased by about half in patients with evidence of hypoperfusion, and stopped in patients with frank cardiogenic shock, although there is little evidence to support this approach. Following an episode of acute decompensated heart failure, ß-blocker therapy should be titrated upward slowly.”