In One-Hour: A Diagnosis of Heart Attack made possible by one Blood Test
Reporter: Larry H Bernstein, MD, FCAP
Voice of Dr. Larry:
This presents a dilemma for medicine with the pressure to discharge patients, and to save money for the system. The practice of decision-making is still quite elemental.
TRAPID-AMI is a prospective observational study supported by Roche and investigated more than 1,200 patients with acute chest pain during 2011-2014. The study was conducted in twelve institutions from nine countries and three continents, led by Professors Christian Mueller, University of Basel (Switzerland), and Bertil Lindahl, University of Uppsala (Sweden).
I have great respect for Mueller and Lindahl. This is a prospective observational study and does not carry the same weight as a randomized study. Moreover, there is nothing new in this, as you must know.
I think that the Roche hsTNT is the best method out there, but the study will not spur laboratories to switch from hsTnI. The only condition for such a decision would be performing the test in the ED, which might be the case here. POCT is not without problems.
Only in the last 5 years we have seen much confusion about interpreting the hsTnT and hsTnI. There is a sensitivity not achieved in earlier methods of the same proteins. However, there was a tradeoff in specificity and accuracy of diagnosis. It was great for cardiologists, and the measurement of a second assay in 3 hours was warranted. However, it was certainly reasonable to carry out the one hour study because patients arrive at the ED perhaps 6 hrs after onset. There was a time that while the CK-MB was increased and the second assay was in decline, The LD1 assay was needed for a late arrival because of placement on the curve. LD1 is no longer done, and patient awareness is much better than 15-20 years ago. I had a patent on an LD1 assay that could be done on a centrifugal fast analyzer using the forward reaction PYR–LAC, with NADH oxdation rather than LAC–PYR.
This study indicates that a validation of the suspect diagnosis can be done in 1 hour based on the increase in a shorter time span. It resolves some of the problem of hsTn’s. I’m not at all convinced that it is sufficient. I would have to see something more definitive.
There is consensus on the reclassification of Acute Coronary Syndrome into plaque rupture and not plaque rupture.
This creates a problem for relying on a so called “magic bullet” approach. It would certainly indicate that in order to classify correctly there has to be a minimum of two tests. All patients with CKD would fall into the not plaque rupture category. There are other patients who might have 50-60% narrowing and experience precordial symptoms, pressure, but without elevation. Are they very early AMI presentation, as my grandfather some 48 years ago?
SOURCE
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Every facility was doing a second assay at 3 hrs. You could argue that they had a second variable by taking the optimum change at 3 hours. I published on the slope of the CKMB rise in 1983, and then I later published with Jack Good a computer calculated probability based on two values taken at 6 and 18 hours (it could have been cut to 12 hours) in 1986. They finished the algorithm while I was in the hospital with a tibial fracture and we published in Clinical Chemistry.
I would be more comfortable if they did #1 at presentation, #2 at 1 hour later, and #3 at 3 hours after presenting. It being an observational study, the physician would benefit from having the 3 hour result. Action might be taken after the second assay, but the observational study would be consistent with the standard of practice going into the study. The expected benefit would be in having a three point linear curve to better determine the optimum increase in 1 hour after presentation. This could result in a more accurate evaluation of the data.
It would remain that patients with CKD would have minor elevations that don’t change. Patients with ACS would have a rapid increase. Then there would be patients with 65% decrease in lumen diameter who have CKD, and perhaps decreased cardiac output from CHF or who have AFib that would account for acute ischemia. The rise in hsTnT would be less than for plaque rupture. Of course, this is a hypothetical.