Idiopathic Spontaneous Coronary Artery Dissection (SCAD): Disease Characteristics Research Report

Executive summary

Idiopathic spontaneous coronary artery dissection (SCAD) is a non-atherosclerotic cause of acute coronary syndrome (ACS) caused by separation within the coronary arterial wall that produces an intramural hematoma and/or intimal tear, compressing the true lumen and causing myocardial ischemia/infarction. Contemporary evidence supports conservative-first management for clinically stable patients due to high spontaneous healing rates, with selective revascularization for high-risk anatomy or ongoing ischemia; systematic screening for extracoronary arteriopathies—especially fibromuscular dysplasia (FMD)—is commonly recommended. Despite rapidly growing registry-based knowledge, randomized controlled trial (RCT) evidence remains limited, and many recommendations are based on expert consensus and observational studies. (morena2024advancesinthe pages 1-2, dang2024spontaneouscoronaryartery pages 6-6, smirnova2023spontaneouscoronaryartery pages 1-2, petrovic2024managementandoutcomes pages 1-2)

1. Disease information

1.1 Definition and overview

SCAD is described as a non-atherosclerotic, non-traumatic, non-iatrogenic separation of the coronary arterial wall resulting in a false lumen and/or intramural hematoma that compresses the true lumen and presents as ACS. (morena2024advancesinthe pages 1-2, smirnova2023spontaneouscoronaryartery pages 1-2, pender2025spontaneouscoronaryartery pages 1-2)

Abstract-supported quotes - “SCAD is caused by separation occurring within or between any of the three tunics of the coronary artery wall. This leads to intramural hematoma and/or formation of false lumen in the artery, which leads to ischemic changes or infarction of the myocardium.” (Frontiers review abstract) (dang2024spontaneouscoronaryartery pages 6-7) - “Spontaneous coronary artery dissection (SCAD) is a non-traumatic and non-iatrogenic separation of the coronary arterial wall.” (systematic review/meta-analysis abstract) (apostolovic2024spontaneouscoronaryartery pages 1-2)

1.2 Key identifiers (from retrieved evidence)

• ICD-10-CM: I25.42 used to identify SCAD in U.S. administrative datasets. (mughal2022contemporarytrendsin pages 1-3, krittanawong2020recurrentspontaneouscoronary pages 1-2)
• ICD-9-CM: 414.12 used to identify SCAD before the ICD-10 transition. (mughal2022contemporarytrendsin pages 1-3, krittanawong2020recurrentspontaneouscoronary pages 1-2)

Not confirmed in retrieved full texts: MeSH term(s), MONDO ID, Orphanet ID, OMIM entry specifically for “idiopathic SCAD” (these identifiers exist in external ontologies but are not present in the retrieved documents and are not inferred here). (mughal2022contemporarytrendsin pages 1-3, krittanawong2020recurrentspontaneouscoronary pages 1-2)

1.3 Synonyms / alternative names

• Spontaneous coronary artery dissection (SCAD) (morena2024advancesinthe pages 1-2)
• Non-atherosclerotic coronary artery dissection / non-iatrogenic coronary artery dissection (descriptive usage across reviews) (smirnova2023spontaneouscoronaryartery pages 1-2, pender2025spontaneouscoronaryartery pages 1-2)

1.4 Evidence provenance

The current understanding summarized here is derived largely from aggregated disease-level evidence: systematic reviews/meta-analyses, narrative reviews, and registry/administrative cohort analyses, with some mechanistic inference from intracoronary imaging and pathology discussions. (dang2024spontaneouscoronaryartery pages 6-6, petrovic2024managementandoutcomes pages 1-2)

2. Etiology

2.1 Disease causal factors (current mechanistic framing)

SCAD is thought to arise via two nonexclusive mechanisms: 1) “Inside–out”: an intimal tear allows blood to enter the arterial wall, forming a false lumen. 2) “Outside–in”: spontaneous hemorrhage (e.g., from vasa vasorum) causes intramural hematoma within the media, compressing the lumen. (rusali2025spontaneouscoronaryartery pages 3-5, pender2025spontaneouscoronaryartery pages 1-2)

2.2 Risk factors

Predisposing conditions (non-exhaustive)

• Fibromuscular dysplasia (FMD): the most consistently associated extracoronary arteriopathy; prevalence among SCAD patients varies widely (in part due to screening modality/intensity). (dang2024spontaneouscoronaryartery pages 6-6, gori2023contemporaryreviewon pages 3-4)
• Pregnancy/peripartum state (pregnancy-associated SCAD often more severe). (smirnova2023spontaneouscoronaryartery pages 1-2, gori2023contemporaryreviewon pages 3-4, apostolovic2024spontaneouscoronaryartery pages 1-2)
• Inherited connective tissue disorders (rare; often in syndromic/non-syndromic connective tissue disease contexts). (smirnova2023spontaneouscoronaryartery pages 1-2, gori2023contemporaryreviewon pages 3-4)
• Hypertension (frequent “traditional” risk factor reported in multiple reviews). (gori2023contemporaryreviewon pages 3-4)
• Migraine and other neuropsychiatric conditions are reported in SCAD cohorts and may associate with recurrence risk. (dang2024spontaneouscoronaryartery pages 6-6, krittanawong2020recurrentspontaneouscoronary pages 1-2)

Precipitating triggers

Reviews report that emotional stress (more often in women) and physical stress/exertion (more often in men) commonly precede symptoms; stimulant exposure (e.g., cocaine/amphetamines) is also discussed as a precipitating factor in risk-factor reviews. (gori2023contemporaryreviewon pages 3-4)

2.3 Protective factors

No specific protective genetic variants or protective exposures were identified in the retrieved evidence set.

2.4 Gene–environment interactions

The retrieved evidence supports a conceptual model of arterial vulnerability (predisposition) + trigger (stress/hemodynamic/hormonal changes) but does not provide quantified gene–environment interaction estimates. (rusali2025spontaneouscoronaryartery pages 3-5, gori2023contemporaryreviewon pages 3-4)

3. Phenotypes

3.1 Clinical presentation

SCAD most commonly presents as ACS with chest pain and biomarker/ECG changes consistent with MI.

Abstract-supported quote - “Spontaneous coronary artery dissection (SCAD) represents a quite rare event but with potentially serious prognostic implications. Meanwhile, SCAD typically presents as an acute coronary syndrome (ACS).” (review abstract) (morena2024advancesinthe pages 1-2)

Frequencies / ranges reported in recent syntheses

• Systematic review (n=1,801): NSTEMI ~48.5%, STEMI ~36.8%, unstable angina ~3.4%, stable angina ~0.56%. (petrovic2024managementandoutcomes pages 1-2)
• In women of reproductive age meta-analysis (n=2,145): STEMI ~47.4% (pooled). (apostolovic2024spontaneouscoronaryartery pages 1-2)

Complications/severe presentations (examples)

A 2023 review reports cardiogenic shock (~2%), sudden cardiac death (~0.8% in autopsy series), and ventricular arrhythmias (~5%) among reported presentations/complications, and notes Takotsubo syndrome overlap. (smirnova2023spontaneouscoronaryartery pages 1-2)

3.2 Quality-of-life impacts

Post-event psychological morbidity is common; a 2024 narrative review highlights depression/anxiety/PTSD and recommends mental-health screening and peer support as part of follow-up care. (dang2024spontaneouscoronaryartery pages 6-6)

3.3 Suggested HPO terms (for knowledge base entry; not exhaustive)

• Chest pain HP:0100749
• Acute myocardial infarction HP:0001658
• ST elevation HP:0031557 / Abnormal ST segment HP:0031425
• Elevated cardiac troponin HP:0031195
• Ventricular arrhythmia HP:0001663
• Cardiogenic shock HP:0030144
• Dyspnea HP:0002094
• Nausea HP:0002018

(These HPO codes are provided as ontology suggestions; they were not explicitly enumerated in the retrieved articles.)

4. Genetic / molecular information

4.1 Current understanding

SCAD is generally not strongly inherited; familial cases are uncommon in the reviewed literature, and monogenic causes are considered rare and more often linked to connective tissue disorders. (gori2023contemporaryreviewon pages 3-4, smirnova2023spontaneouscoronaryartery pages 1-2)

A 2024 narrative review discusses reported genetic associations/case reports including PHACTR1/EDN1 locus, SMAD3 mutation cases, and variants in fibrillar collagens; however, the excerpted evidence does not provide a comprehensive gene list or variant-level frequencies. (dang2024spontaneouscoronaryartery pages 6-7)

4.2 When to consider genetic testing (practice-oriented guidance)

Genetic testing is described as low-yield and not routine, but may be considered in SCAD patients with recurrent SCAD, multivessel disease, extracoronary vascular abnormalities, or a family history/features suggestive of a heritable connective tissue disorder, with appropriate counselling and possible aortopathy/connective tissue gene panels. (dang2024spontaneouscoronaryartery pages 6-6)

4.3 Variants/modifier genes/epigenetics/chromosomal abnormalities

The retrieved evidence does not provide curated variant-level data (e.g., ACMG classifications, allele frequencies) or epigenetic/chromosomal abnormality findings specific to idiopathic SCAD.

5. Environmental information

5.1 Environmental/lifestyle factors

The evidence set primarily emphasizes stress-related triggers (emotional/physical) rather than classic lifestyle risk factors; traditional atherosclerotic risk factors are often less prevalent, though hypertension is frequently reported. (gori2023contemporaryreviewon pages 3-4)

5.2 Infectious agents

No specific infectious agent etiology was identified in the retrieved evidence.

6. Mechanism / pathophysiology

6.1 Causal chain (high-level)

Predisposing arteriopathy/hormonal milieu/stress exposure → arterial wall vulnerability → intramural bleeding and/or intimal disruption → intramural hematoma/false lumen → true-lumen compression → myocardial ischemia/infarction → ACS presentation and complications. (rusali2025spontaneouscoronaryartery pages 3-5, pender2025spontaneouscoronaryartery pages 1-2, smirnova2023spontaneouscoronaryartery pages 1-2)

6.2 Cellular processes and tissue injury (conceptual mapping)

• Vessel wall injury leading to intramural hematoma with downstream ischemia is central to SCAD pathophysiology. (rusali2025spontaneouscoronaryartery pages 3-5, pender2025spontaneouscoronaryartery pages 1-2)

6.3 Suggested GO (biological process) and CL (cell type) terms (ontology suggestions)

• GO:0001525 angiogenesis (vasa vasorum biology; conceptual)
• GO:0007596 blood coagulation (intramural hemorrhage context; conceptual)
• GO:0006954 inflammatory response (discussed as unclear/variable in reviews; conceptual) (rusali2025spontaneouscoronaryartery pages 3-5)
• CL:0002131 vascular smooth muscle cell
• CL:0002543 endothelial cell

(These are ontology suggestions; the retrieved evidence does not provide explicit GO/CL annotations.)

7. Anatomical structures affected

7.1 Primary structures

• Coronary arteries (often LAD as culprit). (petrovic2024managementandoutcomes pages 1-2, apostolovic2024spontaneouscoronaryartery pages 1-2)

7.2 Secondary involvement/complications

• Myocardium (ischemia/infarction); potential for heart failure, arrhythmias, cardiogenic shock. (smirnova2023spontaneouscoronaryartery pages 1-2, petrovic2024managementandoutcomes pages 1-2)

7.3 Suggested UBERON terms (ontology suggestions)

• Coronary artery UBERON:0001621
• Left anterior descending coronary artery (LAD) (UBERON term varies by subset; provide as “LAD coronary artery” mapping in your implementation)
• Myocardium UBERON:0002349

8. Diagnostics

8.1 Imaging and diagnostic approach

• Invasive coronary angiography (ICA) is emphasized as the diagnostic gold standard, with adjunctive intracoronary imaging (IVUS/OCT) improving diagnostic performance and clarifying mechanism. (morena2024advancesinthe pages 1-2, bollati2024spontaneouscoronarydissection pages 4-7)
• Extracoronary vascular imaging: head-to-pelvis CT angiography is described as a method for FMD screening; MRA is an alternative but may have lower spatial resolution. (dang2024spontaneouscoronaryartery pages 6-6)

8.2 Angiographic classification (Saw types)

Recent reviews describe an ICA-based SCAD classification (Types 1–4) used in practice; Table/Figure evidence is available from a 2024 review, including examples of Types 1, 2A, 3, and 4 and management flow-chart context. (bollati2024spontaneouscoronarydissection pages 4-7, bollati2024spontaneouscoronarydissection media ffbb95a5, bollati2024spontaneouscoronarydissection media 8d0f25c2, bollati2024spontaneouscoronarydissection media 8c541a8a, bollati2024spontaneouscoronarydissection media 353fb04a, bollati2024spontaneouscoronarydissection media 94fd0b42, bollati2024spontaneouscoronarydissection media df824cb3)

8.3 Differential diagnosis

SCAD can mimic atherosclerotic ACS and requires careful angiographic interpretation; intracoronary imaging can help in ambiguous cases. (gori2023contemporaryreviewon pages 3-4)

9. Treatment

9.1 Acute management strategy (current practice pattern)

• Conservative management is preferred in clinically stable SCAD because spontaneous healing is common, while PCI success is limited by technical challenges and risks of propagation/iatrogenic dissection. (bollati2024spontaneouscoronarydissection pages 4-7, petrovic2024managementandoutcomes pages 1-2)
• Revascularization (PCI; CABG rarely) is reserved for high-risk presentations (e.g., left main/proximal multivessel, TIMI 0/1 flow, hemodynamic/electrical instability, ongoing ischemia). (bollati2024spontaneouscoronarydissection pages 4-7, bollati2024spontaneouscoronarydissection pages 7-8)

9.2 Medical therapy themes

• Beta-blockers are commonly used; observational evidence associates beta-blockers with lower recurrence. (dang2024spontaneouscoronaryartery pages 6-6)
• ACE inhibitor/ARB is recommended when LVEF is reduced after SCAD-related ACS. (dang2024spontaneouscoronaryartery pages 6-6)
• Antiplatelet strategy in conservatively managed SCAD remains debated in reviews due to concern about intramural hematoma expansion; practice varies and RCT data are limited. (morena2024advancesinthe pages 1-2, bollati2024spontaneouscoronarydissection pages 4-7)
• Statins are generally not routine unless indicated for dyslipidemia/atherosclerotic disease. (smirnova2023spontaneouscoronaryartery pages 1-2)

9.3 Cardiac rehabilitation and psychosocial care

Cardiac rehabilitation is described as safe and recommended for SCAD patients; low/moderate-intensity aerobic and low-resistance programs are favored, along with avoidance of high-intensity abrupt-movement activities, and psychological screening/support is emphasized. (dang2024spontaneouscoronaryartery pages 6-6)

9.4 Current clinical trials (real-world implementations of evidence generation)

• NCT04850417: “Randomized Study of Beta-Blockers and Antiplatelets in Patients With Spontaneous Coronary Artery Dissection” (Phase 4; planned enrollment 600; Spanish Society of Cardiology). (clinical trial record) (dang2024spontaneouscoronaryartery pages 6-6)
• NCT06955663: Exercise support/rehabilitation after SCAD (planned enrollment 120). (dang2024spontaneouscoronaryartery pages 6-6)
• NCT04251039: RESPONSE observational study in SCAD patients undergoing complex PCI. (dang2024spontaneouscoronaryartery pages 6-6)

9.5 Suggested MAXO terms (ontology suggestions)

• Conservative management / medical management (MAXO “medical therapy” class; implement with local MAXO mapping)
• Percutaneous coronary intervention PCI
• Coronary artery bypass grafting CABG
• Cardiac rehabilitation
• CT angiography screening for extracoronary arteriopathy

10. Prevention

10.1 Primary prevention

No established primary prevention is supported by RCT evidence in the retrieved set; prevention is largely framed as managing predispositions (e.g., blood pressure), avoiding extreme triggers, and individualized counselling. (dang2024spontaneouscoronaryartery pages 6-6, gori2023contemporaryreviewon pages 3-4)

10.2 Secondary/tertiary prevention

• Recurrence risk mitigation: beta-blockers are associated with lower recurrence in observational data and are commonly used; follow-up and monitoring are emphasized. (dang2024spontaneouscoronaryartery pages 6-6)
• Screening for FMD and other extracoronary vascular abnormalities is commonly recommended; FMD is associated with higher recurrence risk in review-level evidence. (dang2024spontaneouscoronaryartery pages 6-6)

11. Outcomes / prognosis

11.1 Mortality and major adverse cardiovascular events

A 2024 systematic review (13 observational studies, n=1,801) reported in-hospital mortality ~1.2% and follow-up mortality ~1.3%, with MACE including recurrent SCAD up to 31% across studies and other events (ACS, target vessel revascularization, HF, stroke) reported variably. (petrovic2024managementandoutcomes pages 1-2)

A 2024 meta-analysis in reproductive-age women reported pooled recurrent SCAD ~15.2% (95% CI 9.1–21.3). (apostolovic2024spontaneouscoronaryartery pages 1-2)

11.2 Recurrence and prognostic factors

• Reviews report recurrence risk persists for years and may vary widely depending on definitions and cohorts; recurrence has been reported up to ~30% historically, with more recent prospective series reporting lower values in certain follow-up windows. (smirnova2023spontaneouscoronaryartery pages 1-2)
• FMD is linked to higher recurrence risk (RR 2.02 in review summary). (dang2024spontaneouscoronaryartery pages 6-6)

12. Temporal development

12.1 Onset

SCAD often occurs in younger to middle-aged adults, with strong female predominance and particular relevance in peripartum settings. (smirnova2023spontaneouscoronaryartery pages 1-2, apostolovic2024spontaneouscoronaryartery pages 1-2)

12.2 Course

• Early in-hospital period: risk of early extension/worsening in the first days is noted in reviews (reported ~5–10% in one review summary). (bollati2024spontaneouscoronarydissection pages 4-7)
• Longer term: recurrence risk and chronic symptoms (e.g., persistent chest pain syndromes discussed in later reviews) can require ongoing follow-up care. (rusali2025spontaneouscoronaryartery pages 14-16)

13. Inheritance and population

13.1 Epidemiology

• SCAD is commonly cited as accounting for ~1–4% of ACS. (gori2023contemporaryreviewon pages 3-4)
• Administrative incidence trend analysis (U.S. National Inpatient Sample) reported rising crude incidence per 1,000,000 discharges from ~4.95 (2010) to ~14.81 (2017), identified using ICD-9/10 SCAD codes. (mughal2022contemporarytrendsin pages 1-3)

13.2 Demographics

• Female predominance is consistently reported; many reviews cite ~80–90% of cases in women. (gori2023contemporaryreviewon pages 3-4, petrovic2024managementandoutcomes pages 1-2)

13.3 Inheritance pattern

The evidence supports mostly complex/polygenic susceptibility with rare monogenic syndromic cases, rather than a single Mendelian inheritance pattern for idiopathic SCAD. (smirnova2023spontaneouscoronaryartery pages 1-2, gori2023contemporaryreviewon pages 3-4)

14. Other species / natural disease

No evidence for naturally occurring SCAD as a defined veterinary disease entity was identified in the retrieved materials.

15. Model organisms

No SCAD-specific validated animal model descriptions were found in the retrieved evidence excerpts; current literature in this evidence set emphasizes human imaging/registry studies and connective-tissue disease genetics rather than experimental organism models. (dang2024spontaneouscoronaryartery pages 6-6, petrovic2024managementandoutcomes pages 1-2)

Visual evidence (angiographic types and management algorithm)

The following extracted visuals provide practical depictions of SCAD angiographic types and a management flow chart from a 2024 review; they can be used to support knowledge base UI elements and clinician-facing summaries. (bollati2024spontaneouscoronarydissection media ffbb95a5, bollati2024spontaneouscoronarydissection media 8d0f25c2, bollati2024spontaneouscoronarydissection media df824cb3)

Structured evidence table

Table: This table condenses high-yield evidence on spontaneous coronary artery dissection, including definition, epidemiology, risk factors, diagnostics, management, outcomes, coding, and current trial identifiers. It is useful as a compact reference for building a structured disease knowledge base entry.

Recent developments and expert analysis (2023–2024 emphasis)

• Registry-driven science has accelerated SCAD understanding, but reviews emphasize that RCT evidence is still scarce, prompting active trials such as BA-SCAD. (dang2024spontaneouscoronaryartery pages 6-6)
• Reviews highlight system-level care gaps and practice variation, including incomplete FMD screening and variable rehabilitation referral; meta-analytic estimates suggest substantial heterogeneity across regions and eras. (petrovic2024managementandoutcomes pages 1-2)

URLs and publication dates (from retrieved sources)

• Dang Q. et al. npj Cardiovascular Health (May 2024). https://doi.org/10.1038/s44325-024-00004-y (dang2024spontaneouscoronaryartery pages 6-6)
• Petrović M. et al. Frontiers in Cardiovascular Medicine (Jan 2024). https://doi.org/10.3389/fcvm.2024.1276521 (petrovic2024managementandoutcomes pages 1-2)
• Apostolović S. et al. Frontiers in Cardiovascular Medicine (Feb 2024). https://doi.org/10.3389/fcvm.2024.1277604 (apostolovic2024spontaneouscoronaryartery pages 1-2)
• Smirnova A. et al. European Heart Journal Supplements (Apr 2023). https://doi.org/10.1093/eurheartjsupp/suad059 (smirnova2023spontaneouscoronaryartery pages 1-2)
• Mughal M.S. et al. Expert Review of Cardiovascular Therapy (May 2022). https://doi.org/10.1080/14779072.2022.2080055 (mughal2022contemporarytrendsin pages 1-3)

Evidence gaps (important for knowledge base provenance)

• MONDO/MeSH/Orphanet/OMIM identifiers were not extractable from the retrieved full texts; adding them will require direct ontology lookups outside this evidence set.
• Variant-level genetics (ClinVar-style curation), epigenetic signatures, and experimental model organism evidence are not provided in the retrieved excerpts and remain incomplete here.

References

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2. (dang2024spontaneouscoronaryartery pages 6-6): Quan Dang, Sonya Burgess, Peter J. Psaltis, Sarah Fairley, Jacqueline Saw, and Sarah Zaman. Spontaneous coronary artery dissection: a clinically oriented narrative review. npj Cardiovascular Health, May 2024. URL: https://doi.org/10.1038/s44325-024-00004-y, doi:10.1038/s44325-024-00004-y. This article has 14 citations.

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13. (bollati2024spontaneouscoronarydissection media ffbb95a5): Mario Bollati, Vincenzo Ercolano, and Pietro Mazzarotto. Spontaneous coronary dissection review: a complex picture. Reviews in Cardiovascular Medicine, Dec 2024. URL: https://doi.org/10.31083/j.rcm2512448, doi:10.31083/j.rcm2512448. This article has 6 citations and is from a peer-reviewed journal.

14. (bollati2024spontaneouscoronarydissection media 8d0f25c2): Mario Bollati, Vincenzo Ercolano, and Pietro Mazzarotto. Spontaneous coronary dissection review: a complex picture. Reviews in Cardiovascular Medicine, Dec 2024. URL: https://doi.org/10.31083/j.rcm2512448, doi:10.31083/j.rcm2512448. This article has 6 citations and is from a peer-reviewed journal.

15. (bollati2024spontaneouscoronarydissection media 8c541a8a): Mario Bollati, Vincenzo Ercolano, and Pietro Mazzarotto. Spontaneous coronary dissection review: a complex picture. Reviews in Cardiovascular Medicine, Dec 2024. URL: https://doi.org/10.31083/j.rcm2512448, doi:10.31083/j.rcm2512448. This article has 6 citations and is from a peer-reviewed journal.

16. (bollati2024spontaneouscoronarydissection media 353fb04a): Mario Bollati, Vincenzo Ercolano, and Pietro Mazzarotto. Spontaneous coronary dissection review: a complex picture. Reviews in Cardiovascular Medicine, Dec 2024. URL: https://doi.org/10.31083/j.rcm2512448, doi:10.31083/j.rcm2512448. This article has 6 citations and is from a peer-reviewed journal.

17. (bollati2024spontaneouscoronarydissection media 94fd0b42): Mario Bollati, Vincenzo Ercolano, and Pietro Mazzarotto. Spontaneous coronary dissection review: a complex picture. Reviews in Cardiovascular Medicine, Dec 2024. URL: https://doi.org/10.31083/j.rcm2512448, doi:10.31083/j.rcm2512448. This article has 6 citations and is from a peer-reviewed journal.

18. (bollati2024spontaneouscoronarydissection media df824cb3): Mario Bollati, Vincenzo Ercolano, and Pietro Mazzarotto. Spontaneous coronary dissection review: a complex picture. Reviews in Cardiovascular Medicine, Dec 2024. URL: https://doi.org/10.31083/j.rcm2512448, doi:10.31083/j.rcm2512448. This article has 6 citations and is from a peer-reviewed journal.

19. (bollati2024spontaneouscoronarydissection pages 7-8): Mario Bollati, Vincenzo Ercolano, and Pietro Mazzarotto. Spontaneous coronary dissection review: a complex picture. Reviews in Cardiovascular Medicine, Dec 2024. URL: https://doi.org/10.31083/j.rcm2512448, doi:10.31083/j.rcm2512448. This article has 6 citations and is from a peer-reviewed journal.

20. (rusali2025spontaneouscoronaryartery pages 14-16): Andrei Constantin Rusali, Ioana Caterina Lupu, Lavinia Maria Rusali, and Lucia Cojocaru. Spontaneous coronary artery dissection unveiled: pathophysiology, imaging, and evolving management strategies. Jun 2025. URL: https://doi.org/10.20944/preprints202506.0355.v1, doi:10.20944/preprints202506.0355.v1.

21. (singulane2025spontaneouscoronaryartery pages 1-2): Cristiane C. Singulane, Shuo Wang, Kelsey Watts, Macy E. Stahl, LeAnn Denlinger, Rachel Lloyd, Pranavi Pallinti, Lauren Preston, Mohamed Morsy, Odayme Quesada, Angela Taylor, Randy K. Ramcharitar, Mete Civelek, and Patricia F. Rodriguez-Lozano. Spontaneous coronary artery dissection (scad): unveiling the enigma of the unexpected coronary event. Current Atherosclerosis Reports, Aug 2025. URL: https://doi.org/10.1007/s11883-025-01328-5, doi:10.1007/s11883-025-01328-5. This article has 8 citations and is from a peer-reviewed journal.