Month: May 2013

Are you interested in making your AMI diagnostic evaluation even less specific?  Good!  Because Brahms Thermo Fisher et al want to sell you a rapid copeptin assay to help with that.

Copeptin is a stable, terminal portion of the arginine vasopressin peptide.  This peptide is released from the pituitary in response to cardiovascular hemodynamic stress and has a theoretical role in the diagnosis of acute myocardial infarction.  The advantage copeptin may have over conventional troponin assays is detectable release in circulation preceding troponin.

In 1971 patients collected through their multi-center trial, 156 were diagnosed with AMI (7.9%).  Upon presentation to the Emergency Department, 40 were STEMI.  281 patients had cTnI greater than 40ng/L, 97 of whom were subsequently diagnosed with nSTEMI.  1646 had cTnI less than 40ng/L, 19 of whom eventually were diagnosed with nSTEMI – a miss rate of 1.1%.  Pretty good – but, obviously, we practice in a zero-miss world.  Adding copeptin to this troponin-negative population with a cut-off of 14pmol/L decreased the miss rate to 0.5%.  The specificity, of course, was useless – only 10 of 493 patients with positive initial copeptin and negative inital troponin went on to receive a diagnosis of nSTEMI.

So, the question is – would a negative copeptin change your practice?  Is there a clinically important difference between a 1 in 100 miss rate vs. a 1 in 200 miss rate?  These authors think adding copeptin to troponin will allow you to discharge a patient after the inital biomarker result – but I think this minimal incremental improvement in diagnostic performance doesn’t change whatever pathway the patient was already on, nor add much to a discussion of shared decision-making with the patient.  They also don’t address a performance advantage compared to high-sensitivity troponin assays (which have, of course, their own issues).

These authors are pretty high on copeptin – but, then again, many of them are employed by or sponsored by the manufacturers of the copeptin assay.

“Copeptin Helps in the Early Detection Of Patients with Acute Myocardial Infarction: the primary results of the CHOPIN Trial”
http://www.ncbi.nlm.nih.gov/pubmed/23643595

The prevailing notion has been that women present with symptoms of angina that are “atypical” from men – headaches, jaw pain, generalized malaise – rather than definitive anginal-type chest pain or pressure.  These authors would like to suggest this global characterization is incorrect.

These authors enrolled a sample of 128 men and 109 women who underwent coronary angiogram following an abnormal stress test.  Patients with obstructive coronary artery disease on their angiogram were surveyed regarding the symptoms that prompted them to seek care.  Of this cohort, 89 men had obstructive disease compared with 50 women.

Overall, there was no significant statistical difference in the rate of most descriptors used by men or women.  Surprisingly, women were statistically more likely to use “typical” terms such as “discomfort”, “crushing”, “pressing” and “aching” to describe their chest pain.  Therefore, these authors conclude the clinical construct of “atypical angina” in women is incorrect.

I would tend to agree – excepting their study suffers from selection bias.  If patients are only referred for testing due to suspected coronary artery disease, then the population with “atypical” symptoms might not be fully captured.  That being said, it does look as though the female population in their study encompassed a number of patients who potentially were referred for atypical symptoms, considering the yield of their coronary angiography was much lower in women.  It would have been interesting to compare the referral symptoms to the subset with demonstrated obstructive CAD.

“Reconstructing Angina: Cardiac Symptoms Are the Same in Women and Men”
www.ncbi.nlm.nih.gov/pubmed/23567974‎