Guest post: Reviewing the Fourth Universal Definition of MI
By Howard Rodenberg, MD, MPH, CCDS
You’ve certainly heard the phrase, “timing is everything.” Turns out that like most age-old aphorisms, this one’s mostly true, whether you’re talking about relationships or hand grenades.
This adage applies to the ACDIS Blog as well. Loyal readers (both of them) may recall a post a few weeks ago about Takotsubo cardiomyopathy. The article was originally drafted in late June and submitted in early July. It then went through an editorial process to take out all the offensive material (a.k.a., “the stuff I really like”) until it reached you, Gentle Reader, in a format of which both my high school English teacher Nora Lampkin and Miss Manners would approve.
(Shameless Plug Department: The unaltered versions are posted on my own blog site, WritingwithScissors.blogspot.com. Subscribe and be a follower, not a leader.)
About a week before that piece was posted in the early fall, I became aware that it was already going to be an anachronism. The Third Universal Definition of Myocardial Infarction (MI) was being superseded that very day by the surprisingly-named Fourth Universal Definition of MI. I felt personally dissed. Imagine, all those cardiologists getting together to wed themselves to some new terminology and I never even got so much as an invitation to the reception. Elitist snobs.
(Admittedly, my irritation may have been keto rage, fueled by the fact that I’ve recently started the diet of the same name as a Symbol of Relationship Commitment to my significant other, the Dental Empress. This unabashed anger prompted my erstwhile colleague Dr. Douglas Campbell to tape a sign on the door to my office claiming I had “Acute Psychosis due to Carbohydrate Deficiency, ICD-10-CM R134.65.”)
So, with great haste, I got myself a copy of the Fourth Universal Definition. The biggest change in for us in the CDI world involves a new overarching concept of myocardial injury. The baseline characteristic of myocardial injury is an elevated troponin. Myocardial injury can be acute or chronic. Acute myocardial injury, suggested by a “rise and fall” of troponin values, can be seen in both MI (types 1-5) and non-ischemic causes of elevated troponins (acute congestive heart failure [CHF], myocarditis, Takotsubo cardiomyopathy). Common origins of chronic myocardial injury (troponins elevated but flat) include chronic CHF and chronic kidney disease (CKD).
To be fair, myocardial injury was not ignored within the Third Universal Definition. However, it seems to be described simply as the origin of elevated cardiac biomarkers, rather than the over-arching conceptual framework as within the newer document.
There’s also some clarification of what exactly constitutes a Type 2 MI. Given our use of the term “demand ischemia” in times past, there’s an impression remaining (one that I regrettably shared) that the Type 2 MI is a supply-demand mismatch in the absence of coronary disease. The Fourth Definition makes it clear that the difference between a Type 1 and a Type 2 MI is the presence of an acute coronary thrombosis in a Type 1 event; you can have significant coronary disease as part of the reason for the supply demand mismatch in a Type 2 scenario without the acute interruption of blood flow that accompanies an acute coronary thrombosis. This distinction, now made clear in the newer document, may help retire the term “demand ischemia” under the banner of acute coronary syndrome and/or Type 2 MI. It’s also noted that there is a rare subset of patients with MI in the absence of any coronary disease. These patients are considered as having MI with non-occlusive coronary arteries, or MINOCA. (Nope, no code for that, don’t even try.)
While we’re talking about demand ischemia, is there any time the term is still of value? I’m starting to think the answer is no. If we recognize that coronary disease does not preclude a Type 2 MI, then demand ischemia would only apply if you knew the patient’s ischemic symptoms occurred due to excess myocardial oxygen demand in the presence of pristine coronary anatomy. Otherwise, the ischemic event (in the absence of elevated troponin or other evidence of infarction) would seem to be an example of acute coronary syndrome (ACS).
CDI finally gets thrown a bone towards the back of the document. (Maybe I did get an invite to the party after all!). Under the alluring title of “Individual and Public Implications of the Myocardial Infarction Definition,” it’s noted that “the diagnosis is also associated with societal implications with regards to diagnosis-related coding, hospital reimbursement, public health statistics, sick leave, and disability actions.” There is a call for educational materials, and even a small recognition of what we might term clinical validation in a call for a computable phenotype of MI, which sounds like a good grad student project if anyone has a kid who needs one.
As we know, Coding World and CDI World lag behind Clinical World, and terms such as acute and chronic myocardial injury don’t exist within the current lexicon. The only kind of heart injury I can currently find in ICD-10-CM clearly deals with trauma. I’m hopeful the terminology will catch up ASAP, and that that both acute and chronic myocardial injury will be recognized as a comorbid/complicating conditions Has a patient with an elevated troponin for any reason not been subject to additional assessment and monitoring? Probably only if they’re holding a hand grenade.
Editor’s note: Rodenberg is the adult physician advisor for CDI at Baptist Health in Jacksonville, Florida. Contact him at howard.rodenberg@bmcjax.com or follow his personal blog at writingwithscissors.blogspot.com. Advice given is general. Readers should consult professional counsel for specific legal, ethical, clinical, or coding questions. Opinions expressed are that of the author and do not represent HCPro or ACDIS.