Chronic Spontaneous Coronary Artery Dissection in a Young Woman Managed With Coronary Artery Bypass Grafting: A Case Report With Literature Review

ABSTRACT

Spontaneous coronary artery dissection (SCAD) is an uncommon, non‐atherosclerotic cause of acute coronary syndrome, typically occurring in young to middle‐aged women. Although most cases resolve spontaneously with conservative therapy, a small proportion develop chronic dissections that require revascularization. We report the case of a 39‐year‐old Ethiopian woman with a 7‐year history of coronary artery disease who had been managed medically but presented with worsening exertional chest pain. Invasive coronary angiography during the current presentation demonstrated a long‐segment dissection of the left anterior descending (LAD) artery along with a 60% mid‐right coronary artery (RCA) stenosis of uncertain etiology. Coronary angiography performed 1 year and 5 months earlier had shown a proximal LAD dissection and a 50% mid‐RCA stenosis. Despite prolonged medical therapy, her symptoms persisted. She subsequently underwent successful coronary artery bypass grafting (CABG), with an uneventful perioperative course. This case highlights the rare occurrence of chronic SCAD with persistent ischemia despite conservative therapy. It underscores the potential role of follow‐up coronary angiography in selected symptomatic patients to guide individualized management. CABG may be considered in refractory cases when medical therapy fails and PCI is not feasible or unlikely to achieve durable revascularization.

Key Clinical Message

Chronic SCAD may rarely present with persistent ischemia despite optimal conservative therapy. Management should be individualized, and CABG should be considered when symptoms or ischemia persist and PCI is not a viable option.

1. Background

Spontaneous coronary artery dissection (SCAD) is an uncommon, nonatherosclerotic, nontraumatic intimal tear of the coronary artery and an underrecognized cause of acute coronary syndrome (ACS). Estimating its true incidence remains challenging due to underdiagnosis, limited awareness, and variable diagnostic resources, especially in low‐ and middle‐income settings. Available data suggest SCAD accounts for 1%–4% of all ACS cases and up to 25% in women under 50 years [1, 2, 3, 4].

In SCAD, myocardial injury primarily results from coronary artery obstruction caused by the formation of an intramural hematoma or intimal disruption rather than plaque rupture or thrombus. Presenting symptoms are consistent with atherosclerotic ACS, with chest pain being the most prevalent [5]. SCAD most characteristically affects young and middle‐aged individuals with a strong female predominance (80%–90%) [3, 5, 6].

Accurate diagnosis of SCAD is essential, as its management differs from atherosclerotic disease. Coronary angiography remains instrumental in the diagnosis of SCAD, with optical coherence tomography or intravascular ultrasound aiding in nondiagnostic cases [3, 7].

SCAD frequently demonstrates spontaneous angiographic healing; therefore, conservative management is preferred in hemodynamically stable patients. However, a small subset of cases shows no angiographic improvement on follow‐up despite optimal medical therapy, representing chronic SCAD, which for the purpose of this report is defined as persistent angiographic SCAD without evidence of healing on serial imaging. Such cases require individualized management and close surveillance. Revascularization is indicated in patients with ongoing ischemia, hemodynamic instability, or high‐risk anatomy. When intervention is required, percutaneous coronary intervention (PCI) is generally preferred, while coronary artery bypass grafting (CABG) is reserved for failed PCI, technical infeasibility, or large myocardial territory at risk [7, 8, 9, 10, 11, 12].

We report a rare case of chronic SCAD in a young Ethiopian woman managed with CABG.

2. Case History and Examination

We report the case of a 39‐year‐old Ethiopian woman with a 7‐year history of coronary artery disease, first diagnosed in the immediate postpartum period, who currently presented with a 2‐month history of progressively worsening exertional chest pain. The pain was described as squeezing in nature, radiating to the neck, left shoulder, and arm, and associated with shortness of breath. Her medications included aspirin 81 mg once daily, atorvastatin 80 mg once daily, bisoprolol 10 mg once daily, enalapril 5 mg twice daily, and spironolactone 25 mg once daily. She had experienced a similar worsening of symptoms 1 year and 5 months earlier when coronary angiography had revealed a proximal left anterior descending artery (LAD) dissection and a 50% mid‐right coronary artery (RCA) stenosis of uncertain etiology. She was managed conservatively at that time; however, her symptoms persisted, prompting a repeat angiographic evaluation at the current presentation.

Upon further inquiry, the patient reported two full‐term pregnancies and one first‐trimester medical abortion. Her past medical history was notable for dyslipidemia, pregnancy‐induced hypertension, combined oral contraceptive use, and a recent diagnosis of diabetes mellitus. Socially, she reported occasional shisha smoking, exposure to secondhand cigarette smoke, and khat chewing. She had previously received empirical treatment for pulmonary tuberculosis. She denied a history of chronic hypertension, alcohol use, headaches, sleep disturbances, psychiatric illness, recent intense emotional or physical stressors, or financial hardship.

Upon physical examination, her blood pressure was 120/75 mmHg, heart rate was 68 beats per minute, respiratory rate was 18 breaths per minute, and oxygen saturation was 96% on room air. Her weight was 96 kg, height 163 cm, and body mass index (BMI) 36 kg/m². Physical examination of the cardiovascular and other systems revealed no abnormal findings.

3. Differential Diagnosis, Investigations, and Treatment

In this patient, chronic SCAD is a leading differential. Her proximal LAD dissection represents a classic SCAD phenotype, and cohort studies and scientific statements show that recurrent or de novo SCAD, extension of prior dissection, or incomplete arterial healing can present months to years later with progressive exertional angina rather than ACS, even after conservative management [1, 3, 7, 9]. Progressive atherosclerotic chronic coronary syndrome is plausible given her cardiometabolic risk factors including diabetes, dyslipidemia, obesity, pregnancy‐induced hypertension, and tobacco exposure. Moderate lesions can progress to flow‐limiting stenosis over time, and worsening of her previously documented moderate RCA lesion could explain her typical progressively worsening exertional angina [13, 14]. Coronary microvascular dysfunction should also be considered, as it is common in symptomatic women and can cause ischemia through impaired coronary flow reserve and endothelial dysfunction despite nonobstructive epicardial disease [15].

Laboratory investigations revealed borderline hs‐troponin level, abnormal lipid profiles, and elevated glycated hemoglobin level. Other results, including complete blood count, renal function tests, and viral markers, were within normal limits and are summarized in Table 1.

TABLE 1.

Laboratory results.

Laboratory tests	Results	Reference ranges (unit)
White blood cell count	5.05	3.98–10.04 (×103/μL)
Hemoglobin	14.9	11.2–15.7 (g/dL)
Platelet	211	182–369 (×103/μL)
hs‐Troponin	0.05	< 0.05 ng/mL
Glycated hemoglobin	7	< 5.7%
LDL	142	< 100 mg/dL
HDL	39	> 40 mg/dL
Total cholesterol	259	< 200 mg/dL
Triglycerides	393	< 150 mg/dL
HBsAg	Negative	—
HCAb	Negative	—
HIV serology	Negative	—
Creatinine	0.7	0.51–0.95 mg/dL
Sodium	133.5	136–145 mmol/L
Potassium	4.4	3.5–5.1 mmol/L
INR	0.73	0.6–1.3 mmol/L

Abbreviations: HBsAg, hepatitis B surface antigen; HCAb, hepatitis C antibody; HDL, high‐density lipoprotein cholesterol; HIV, human immunodeficiency virus; hs‐troponin, high‐sensitivity cardiac troponin; INR, international normalized ratio; LDL, low‐density lipoprotein cholesterol.

Her electrocardiogram (ECG) showed sinus rhythm at a rate of 75 beats per minute, with deep Q waves, T‐wave inversions, and poor R‐wave progression in leads V1–V3, findings suggestive of prior anterior wall myocardial infarction. Echocardiography revealed hypokinesis of the anterior and anteroseptal left ventricular wall segments, with a moderately reduced left ventricular ejection fraction of 35%–40%. The chest X‐ray was largely unremarkable, except for fibrotic changes in the right upper lobe. A repeat invasive coronary angiography performed at the current presentation demonstrated a long‐segment type 1 spontaneous coronary artery dissection extending from the proximal to distal left anterior descending artery (LAD) (Figure 1) and a 60% mid‐RCA stenosis of uncertain etiology (Figure 2), consistent with persistent angiographic SCAD on follow‐up imaging.

FIGURE 1.

Right anterior oblique cranial view of the left coronary artery demonstrating a long‐segment type 1 spontaneous dissection of the left anterior descending artery extending from the proximal to distal segments (white arrows).

FIGURE 2.

Left anterior oblique view of the coronary angiogram showing a 60% stenosis of the mid‐right coronary artery (black arrow).

Intracoronary imaging with optical coherence tomography (OCT) and intravascular ultrasound (IVUS) was not available at the treating institution, and referral to a higher‐level center was not feasible due to worsening clinical condition requiring definitive management. Coronary computed tomography angiography, a non‐invasive modality for SCAD follow‐up, as well as systematic screening for extracoronary arteriopathies, particularly fibromuscular dysplasia, was not performed due to resource limitations.

After establishing a diagnosis of chronic SCAD, the patient underwent CABG using great saphenous vein grafts harvested from the left lower limb and anastomosed to the left anterior descending (LAD) and right coronary artery (RCA), with an uneventful perioperative course. Although the left internal mammary artery (LIMA) is the preferred conduit, it was of small caliber (< 1 mm) with poor flow and therefore deemed unsuitable for grafting. A combination of papaverine and lidocaine was administered both topically and intraluminally; however, no appreciable improvement in vessel caliber or flow was observed.

4. Outcome and Follow‐Up

She remained in the intensive care unit for 3 days before being transferred to the general ward in stable condition and was discharged after a total hospital stay of 9 days on dual antiplatelet therapy (aspirin 81 mg daily, clopidogrel 75 mg daily), atorvastatin 40 mg daily, and metoprolol 12.5 mg twice daily.

Two weeks post‐CABG, the patient developed post‐pericardiotomy pericarditis, manifested by left anterior pleuritic chest pain exacerbated by inspiration and a mild pericardial effusion on echocardiography. She was initiated on high‐dose aspirin (650 mg orally three times daily, getting tapered over 4 weeks) and colchicine 0.5 mg twice daily to be taken for a total of 3 months. At follow‐up after 3 months, no notable symptoms were reported.

The patient's full clinical course, encompassing the initial diagnosis, previous treatments, surgical intervention, postoperative complications, and follow‐up outcomes, is summarized in Table 2.

TABLE 2.

Timeline of the patient's clinical course.

Time point	Event/clinical course	Investigations/interventions	Outcome/remarks
Immediate postpartum (7 years prior)	Diagnosed with coronary artery disease and dyslipidemia	Clinical evaluation, ECG, and echocardiography	Initiated on medical therapy
1 year and 5 months prior to the current presentation	Worsening exertional chest pain	Coronary angiography: Proximal LAD dissection and 50% mid‐RCA stenosis	Managed conservatively; persistent symptoms
Current presentation	Progressive exertional chest pain for 2 months	ECG: deep Q waves, T‐wave inversion in V1–V3; Echocardiography: anterior wall hypokinesis, LVEF 35%–40%	Referred for repeat coronary angiography
Current angiography		Long‐segment Type 1 LAD dissection (proximal–distal) and 60% mid‐RCA stenosis	Persistent angiographic features suggestive of SCAD
Post‐diagnosis	Underwent surgical revascularization	CABG with great saphenous vein grafts to LAD and RCA	Uncomplicated intra‐ and postoperative course; discharged on dual antiplatelets, statin, and beta‐blocker
2 weeks post‐CABG	Left anterior chest pain exacerbated by inspiration	Echocardiography: mild pericardial effusion	Diagnosed post‐pericardiotomy pericarditis; treated with aspirin 650 mg TID (tapered over 4 weeks) and colchicine 0.5 mg BID
3 months post‐CABG	Follow‐up evaluation	Clinical assessment and echocardiography	Asymptomatic; no recurrent pericardial effusion

Abbreviations: BID, twice daily; CABG, coronary artery bypass grafting; ECG, electrocardiography; LAD, left anterior descending artery; LVEF, left ventricular ejection fraction; RCA, right coronary artery; SCAD, spontaneous coronary artery dissection; TID, three times daily.

5. Discussion

SCAD, characterized by an epicardial coronary artery tear that occurs independently of atherosclerosis, trauma, or iatrogenic injury, commonly presents as ACS [3, 10]. Most patients present with chest pain, elevated cardiac biomarkers, and ECG findings indicative of myocardial infarction [16, 17]. However, SCAD can occasionally present without evidence of myocardial infarction, as described in rare case reports [18, 19]. Our case illustrates a rare chronic presentation of SCAD characterized by persistent ischemic symptoms without ACS features at the time of re‐evaluation.

Although SCAD is classically described in patients without conventional atherosclerotic risk factors [17], conditions such as hypertension, dyslipidaemia, smoking, and obesity may still be present [20]. Female‐specific factors, including pregnancy, migraine, and psychosocial stressors such as depression or low socioeconomic status, have also been implicated [21]. Estrogen‐only oral contraceptives have been reported as associated exposures, whereas the role of combined oral hormone therapy, which our patient used, remains uncertain [1, 21]. Precipitating stressors, seen in about two‐thirds of cases, often involve intense emotional or physical exertion [4]. In our patient, dyslipidemia, obesity, diabetes mellitus, and prior history of combined oral contraceptive use were present, with no emotional or physical triggers elicited on history, highlighting the variable clinical profile of SCAD.

Coronary angiography classifies SCAD into three types. Type 1 (29.1%) is characterized by an intimal tear, contrast staining, a false lumen, and delayed contrast clearance. Type 2, the most common (67%), appears as a long, smooth narrowing from intramural hematoma without a visible tear. Type 3 (3.9%) also involves intramural hematoma but resembles atherosclerotic stenosis, making diagnosis difficult without intracoronary imaging [1]. SCAD usually affects a single vessel, most often the LAD [22]. In our patient, angiography demonstrated type 1 SCAD involving the LAD. A concurrent lesion in the mid‐RCA was angiographically indeterminate, with differential considerations including focal atherosclerotic stenosis versus type 3 SCAD; however, definitive classification was not possible in the absence of intracoronary imaging.

Most SCAD lesions heal spontaneously, but a small proportion persist, with unclear mechanisms and the potential for delayed healing [3, 6, 23]. In a prospective observational study of conservatively treated patients, repeat angiography ≥ 26 days later demonstrated complete healing in all 79 patients, whereas only 3 of 73 patients in a long‐term Swiss cohort had persistent dissection at 6 months [1, 24]. Healing is often detectable within days and frequently observed by 1 month [1, 6, 23]. Persistent or chronic SCAD should be distinguished from recurrent SCAD, which occurs at a different location and is associated with ACS symptoms and biomarker elevation [25]. In our patient, ongoing symptoms and angiographic findings represent a rare instance of chronic SCAD, underscoring the importance of follow‐up angiography to guide timely intervention.

Conservative management is recommended in stable SCAD, while revascularization is reserved for high‐risk anatomy or clinical instability, with PCI generally first‐line and CABG used when PCI is not feasible [23, 24, 26]. Cohort studies and registry data show that PCI in extensive SCAD has variable success and significant technical limitations, whereas CABG is rarely performed (< 1%–5%) and mainly reserved for left main, multivessel, or anatomically unsuitable disease [1, 6, 27]. Guideline statements and expert reviews support CABG as a bailout or anatomy‐driven strategy in such cases [3, 7, 9, 28, 29].

In this patient, coronary angiography demonstrated a long‐segment LAD dissection from proximal to distal vessel without a distal landing zone, consistent with diffuse involvement and large myocardial territory at risk. This made PCI unfavorable due to the need for long‐segment stenting, risk of intramural hematoma propagation, and incomplete lesion sealing. CABG was therefore selected after Heart Team discussion, acknowledging its limitations including competitive flow–related graft failure [11].

This case has several limitations. First, the absence of intracoronary imaging (OCT or IVUS) precluded definitive tissue‐level characterization of the mid‐RCA lesion, limiting differentiation between atherosclerotic disease and type 3 SCAD. Second, the lack of long‐term angiographic and clinical follow‐up after surgical revascularization limits assessment of graft patency and the potential for late recurrent or de novo SCAD in untreated coronary segments. Finally, systematic screening for extracoronary arteriopathies, particularly fibromuscular dysplasia, was not performed due to resource constraints.

6. Conclusions

This case highlights the rare occurrence of chronic SCAD with persistent ischemia despite conservative therapy. It underscores the potential role of follow‐up coronary angiography in selected symptomatic patients to guide individualized management. CABG may be considered in refractory cases when medical therapy fails and PCI is not feasible or unlikely to achieve durable revascularization.

Author Contributions

Gashaw Solela: conceptualization, data curation, investigation, writing – original draft, writing – review and editing. Desalew Mekonnen: conceptualization, data curation, writing – review and editing. Nish Patel: investigation, validation, visualization. Jim Kauten: data curation, validation, writing – review and editing. Chala Fekadu Oljira: data curation, investigation, validation. Adane Petros: conceptualization, investigation, supervision. Siraj Kemal Mussa: investigation, writing – original draft. Gashayeneh Genetu Tiruneh: investigation, writing – original draft. Getu Kusa Wakoya: data curation, investigation, writing – review and editing. Tesfamariam Aklilu Betemariam: data curation, investigation, writing – review and editing. Dagmawit Mesfin Tasew: investigation, validation. Clifford J. Kavinsky: data curation, validation. Tesfaye Telila: conceptualization, resources, supervision, validation. Obsinet Merid: conceptualization, resources, supervision, validation.

Funding

The authors have nothing to report.

Ethics Statement

The authors have nothing to report.

Consent

Written informed consent was obtained from the patient for the publication of this case report.

Conflicts of Interest

The authors declare no conflicts of interest.

Data Availability Statement

Data supporting this case report are available from the corresponding author upon reasonable request.