Chronic Coronary Artery Dissection: Persistent LAD Dissection After Unrecognized SCAD

A 44-year-old woman with no cardiovascular risk factors and no prior medical history presented with recurrent oppressive chest pain radiating to the left shoulder, lasting several minutes and subsiding spontaneously. The pain occurred unpredictably — both at rest and with minimal exertion — and had worsened over the preceding week. She reported a similar but more severe and prolonged episode two years earlier, diagnosed at that time as an anterior STEMI, which had never been formally worked up or followed up. She had received no cardiovascular care in the intervening period.

On examination, blood pressure was 130/70 mmHg bilaterally and heart rate was 62 bpm. The cardiovascular exam was unremarkable. Troponin levels were within the normal range on presentation.

Figure 1

EKG — Prior Anterior Infarction Pattern

Sinus rhythm at 62 bpm with poor R-wave progression in the anteroseptal and apical leads (black stars) and low voltage in the apico-lateral leads with biphasic T waves (arrows) — findings consistent with prior anterior wall infarction. The absence of acute ST changes and a normal troponin shifted the presentation toward a chronic or subacute process rather than an active STEMI equivalent.

Transthoracic echocardiography demonstrated akinesia of the apex and adjacent segments with a preserved LVEF of 53% — a scar pattern consistent with prior anterior infarction involving the LAD territory. Coronary angiography was performed given the clinical history of prior STEMI plus recurrent chest pain.

Figure 2

Coronary Angiography — Multiple Parallel Channels in LAD

Angiography revealing multiple parallel contrast-filled channels in the mid-LAD coronary artery (arrows), consistent with a Type 1 dissection pattern — the angiographic hallmark of SCAD, in which the intimal tear allows contrast to fill both the true and false lumen. No significant atherosclerotic disease was identified, fitting the clinical profile of SCAD in a young woman without risk factors.

Angiography revealed a long segment of the mid-LAD artery with multiple contrast-filled linear channels — a Type 1 dissection pattern. No significant atherosclerotic disease was identified. IVUS and OCT were not available at the center, limiting diagnostic certainty; alternative diagnoses (recanalized thrombus, woven coronary artery) could not be definitively excluded. Given preserved TIMI 3 flow, the absence of active ischemia, and the known risks of PCI in SCAD (including dissection propagation and iatrogenic injury), a conservative approach was adopted: aspirin 75 mg daily, bisoprolol 2.5 mg, and ramipril 5 mg. The patient was discharged with planned six-month follow-up angiography.

Three months later she returned with symptom recurrence not fully controlled on medical therapy. An earlier-than-planned repeat coronary angiogram was performed and showed unchanged morphology — persistent dissection without new stenosis or ischemic features.

Figure 3

Follow-Up Angiography — Persistent Dissection at 3 Months

Repeat coronary angiography demonstrating persistent radiolucency in the distal LAD (arrows) at the three-month follow-up — angiographic stability over time supporting the diagnosis of chronic coronary artery dissection (CCAD). The lack of new stenosis, absence of active hematoma, and preserved TIMI 3 flow validated continuation of conservative management.

Conservative management was continued. At 12-month follow-up the patient remained free of major cardiac events. The diagnosis of chronic coronary artery dissection was supported by the angiographic stability over time, the retrospective assessment of the initial STEMI as an unrecognized SCAD, the patient's demographic profile (young woman, no risk factors, LAD involvement), and the absence of atherosclerotic disease.

Discussion

Spontaneous coronary artery dissection accounts for 25–35% of myocardial infarctions in women under 50, making it the most common cause of MI in young women — yet it remains systematically underdiagnosed because most clinicians approach chest pain presentations with an atherosclerotic framework. The LAD is the most frequently affected vessel (32–46% of SCAD cases), and the typical patient is a young or middle-aged woman without traditional cardiovascular risk factors. SCAD may present as STEMI, NSTEMI, or stable angina depending on the degree of luminal compromise; when the initial event is unrecognized or inadequately worked up, the dissection flap or intramural hematoma may persist without healing, evolving into what is termed chronic coronary artery dissection (CCAD). This entity is poorly defined in the literature — no consensus time-based definition exists — but is suggested by persistent angiographic double-lumen or linear filling defects in the absence of active ischemia or expanding hematoma.

Management of CCAD remains empirical. Conservative therapy — beta-blockers to reduce coronary shear stress, low-dose aspirin, ACE inhibitors, and avoidance of triggers including extreme physical or emotional stress and hormonal fluctuations — is the preferred approach in patients with TIMI 3 flow and no ongoing ischemia. PCI in SCAD carries unique risks: stents in fragile, non-atherosclerotic arterial walls may propagate the dissection or create edge hematomas, and wiring the false lumen can precipitate acute closure. CABG is reserved for refractory high-risk anatomy but carries the risk of competitive native flow causing graft failure. The role of dual antiplatelet therapy is controversial — DAPT may increase intramural hemorrhage risk, and most SCAD experts favor single antiplatelet therapy. The 10–30% SCAD recurrence rate over 10 years underscores the need for long-term surveillance, patient education on symptom recognition, and careful counseling around precipitating factors.