Beyond the Dichotomy: A Call to Cardiologists to Rethink AMI and Takotsubo

  

For decades, cardiology has drawn a firm line between two conditions: acute myocardial infarction (AMI), caused by coronary blockage, and Takotsubo syndrome (TTS), caused by a catecholamine surge. These have been treated as mutually exclusive diagnoses—two separate diseases with separate mechanisms, separate protocols, separate mental models at the bedside.

We believe this line is drawn in the wrong place, and we invite the cardiology community to examine why.

Our framework, STAMI (Superimposed Takotsubo and Acute Myocardial Infarction), rests on a physiological fact no one disputes: every heart attack triggers a massive catecholamine surge. That surge doesn't stop at the infarct border. It acts on myocardium throughout the heart, including tissue far from the blocked artery. This means a Takotsubo-like process is, to some degree, present in every AMI patient. The real clinical question isn't "infarction or Takotsubo?"—it's "how much of each, and in which patient?"

Viewed this way, pure AMI and pure TTS aren't separate diseases. They're opposite poles of a single spectrum. Between them lies a broad, clinically important middle ground that our current binary classification simply doesn't capture—and that has real consequences for diagnosis and treatment.

Why This Matters at the Bedside

The spectrum model explains clinical puzzles that standard frameworks struggle to account for:

• Wall motion abnormalities beyond the culprit artery's territory, often dismissed as "remote stunning," may reflect catecholamine-mediated injury operating independently.

• Hemodynamic instability disproportionate to infarct size may signal an invisible catecholaminergic injury burden that angiography cannot detect.

• Marked QT prolongation atypical for focal infarction may be a direct signature of superimposed Takotsubo physiology.

We've also outlined four clinical phenotypes—ranging from large infarcts with minimal Takotsubo overlay to small infarcts masked by dominant apical ballooning—each representing a different balance point on this spectrum, each with distinct risk profiles and prognostic implications.

An Invitation, Not a Final Word

This is not a hypothesis awaiting its first evidence. It's a theory built from decades of case reports, catecholamine cardiotoxicity research, inflammatory repair biology, and our own prior clinical and experimental work. But it needs what only the broader cardiology community can provide: prospective cohort studies, systematic cardiac MRI of remote myocardium in AMI patients, and biomarker research capable of separating catecholaminergic injury from ischemic injury.

We're not asking clinicians to discard the ischemic paradigm. We're asking them to look for what may be hiding alongside it—and to consider how recognizing this dual injury pattern might change risk stratification, treatment timing, or monitoring for patients whose presentations don't quite fit the textbook.

The full theoretical framework, spectrum model, phenotype descriptions, and complete evidence base are available in our paper, Beyond the AMI–Takotsubo Dichotomy: A Spectrum Model of Catecholamine-Mediated and Ischemic Myocardial Injury. We invite specialists to read it critically, test it against their own case series, and help determine whether this reframing changes how patients are managed at the bedside.

This spectrum model also connects to a broader argument developed in The Science of Healing: Optimality and New Understanding of Myocardial Infarction by Mykola Iabluchanskyi—the idea that myocardial infarction itself is not simply necrosis from blocked blood flow, but a unique form of acute aseptic inflammation with its own healing logic. Together, these frameworks suggest that recognizing the true, dual-injury nature of myocardial damage—and the natural trajectory of its healing—may open new pathways for treatment that work with the heart's biology rather than against it.

Mykola Iabluchanskyi together with Vladimir Evgeny Shlyakhover