Spontaneous Coronary Artery Dissection: Anatomy, Physiology, and Restraint

A young female patient, without relevant previous medical history, presented with chest pain. The troponin showed a clear dynamic rise, fulfilling rule-in criteria for myocardial infarction. The ECG was not normal, showing anterior repolarization changes, most pronounced in the precordial leads. Echocardiography demonstrated a mild apical hypokinesia.

At first glance, this is a familiar pathway: chest pain, dynamic troponin, ECG changes, regional wall motion abnormality.

So she was treated initially as an acute coronary syndrome with aspirin and heparin. After that, she became symptom-free. Nevertheless, because of the biomarker dynamics, ECG changes, and echo finding, coronary angiography was indicated.

The cath lab then changed the discussion.

The angiographic appearance was highly suspicious for spontaneous coronary artery dissection — SCAD, most likely involving the LAD territory. Rather than a typical focal atherosclerotic plaque rupture, the image suggested a long, smooth, diffuse narrowing pattern, compatible with the classic angiographic appearance of SCAD, especially type 2.

This distinction matters.

SCAD is not simply “ACS in a young patient.” It is a different mechanism of myocardial infarction.

In SCAD, the problem is usually not plaque rupture with thrombotic occlusion, but a spontaneous tear or bleeding within the arterial wall, creating an intramural hematoma and compressing the true lumen. The patient may present exactly like an ACS patient: chest pain, troponin rise, ECG changes, wall motion abnormalities. But the interventional strategy is very different.

The important teaching point is restraint.

In atherosclerotic ACS, we are trained to look for the culprit lesion and fix it. In SCAD, fixing the lesion mechanically can make things worse.

PCI in SCAD can be technically difficult and carries a relevant risk of extending the dissection, losing side branches, propagating the intramural hematoma, or even causing left main involvement. Intracoronary imaging may help in uncertain cases, but it is not harmless either and should be used selectively, with minimal manipulation.

Conservative management is preferred whenever possible, especially when the patient is clinically stable, symptoms have resolved, flow is preserved, and there is no ongoing ischemia. Many SCAD lesions heal spontaneously on follow-up angiography.

PCI should be reserved for specific high-risk situations:

ongoing ST elevation or profound ST depression, total occlusion with TIMI 0–1 flow, cardiogenic shock, or clear ongoing ischemia despite medical stabilization.

In this case, the patient was symptom-free after initial treatment, without hemodynamic instability, and the angiographic situation did not suggest a scenario where aggressive intervention would clearly improve the outcome. The key was recognizing the pattern and not treating it like ordinary plaque rupture.

For me, this case has one central message:

In SCAD, the diagnosis is not only about seeing the lesion. It is about understanding when not to intervene.

This is one of the situations where good interventional cardiology means careful angiography, gentle catheter handling, minimal unnecessary injections, and respect for the biology of the vessel wall.

Not every ACS needs a stent. Not every impressive angiographic finding should be “fixed.” Sometimes the best treatment decision is the one that avoids converting a stable SCAD into an unstable complication.

Question for colleagues: When you suspect SCAD in the cath lab, what is your threshold for intracoronary imaging or PCI?

Educational case discussion only. Patient details are anonymized and simplified for teaching purposes.

#Cardiology #SCAD #InterventionalCardiology #AcuteCoronarySyndrome #ClinicalReasoning