Pathophysiology of spontaneous coronary artery dissection: hematoma, not thrombus

Djokovic, Aleksandra; Krljanac, Gordana; Matic, Predrag; Zivic, Rastko; Djulejic, Vuk; Marjanovic Haljilji, Marija; Popovic, Dusan; Filipovic, Branka; Apostolovic, Svetlana

doi:10.3389/fcvm.2023.1260478

Cited by 3 publications

(1 citation statement)

References 84 publications

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“…The pathophysiology of SCAD and its management is different to type 1 AMI. The latter is based on the well-known atherosclerotic plaque disruption complicated by coronary atherothrombosis [2,22]. Regarding SCAD, instead, two main pathogenetic mechanisms have been described: (i) a mechanism concerning the more external arterial wall layers characterized by a possible vasa vasorum rupture with consequent arterial wall bleeding; (ii) a mechanism starting from the inner wall layers characterized by intima tearing and consequent false lumen formation with media hemorrhage and true lumen compression.…”

Section: Pathophysiology Of Spontaneous Coronary Artery Dissectionmentioning

confidence: 99%

Spontaneous Coronary Artery Dissection in Clinical Practice: Pathophysiology and Therapeutic Approaches

D’Amato,

Mariani,

Prosperi

et al. 2024

Medicina

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Spontaneous coronary artery dissection (SCAD) is a cause of myocardial infarction without obstructive coronary artery disease (MINOCA). It is determined by a coronary artery wall layers separation, which occurs regardless of traumatic or iatrogenic injuries. Even if it is often a missed diagnosis, its incidence is growing along with the improvement of intracoronary imaging techniques that allow for better detection. The main angiographical classification distinguishes three different forms, with slightly different prognoses at long-term follow up. SCAD is a recurrent condition, severely hampering the life quality of affected patients. The predominantly young age of patients with SCAD and the high prevalence of females among them have made the topic increasingly important, especially regarding therapeutic strategies. According to the data, the most recommended treatment is conservative, based on the use of antiplatelet agents and supportive anti-ischemic therapy. However, there are conflicting opinions concerning the need for dual antiplatelet therapy and its duration. In the case of invasive treatment, the choice between percutaneous coronary intervention and coronary artery bypass graft depends on the patient’s clinical stability and the interested vessel. The purpose of the current review is to revise the pathophysiological mechanisms underlying SCAD and the current knowledge of its treatment.

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Section: Pathophysiology Of Spontaneous Coronary Artery Dissectionmentioning

confidence: 99%

Spontaneous Coronary Artery Dissection in Clinical Practice: Pathophysiology and Therapeutic Approaches

D’Amato,

Mariani,

Prosperi

et al. 2024

Medicina

View full text Add to dashboard Cite

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Surgical stress as a potential trigger for spontaneous coronary artery dissection: A case report

Rivera,

Plumber,

Louis

et al. 2025

International Journal of Surgery Case Reports

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Spontaneous coronary artery dissection and fibromuscular dysplasia: insights into recent developments

Eltabbakh,

Khudair,

Khudair

et al. 2024

Front. Cardiovasc. Med.

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Spontaneous coronary artery dissection (SCAD), an uncommon cause of acute coronary syndrome, continues to be a poorly understood disease predominantly affecting females. It is characterized by an abrupt separation in the coronary arterial wall due to intramural bleeding. Fibromuscular dysplasia (FMD) is a non-atherosclerotic arteriopathy manifesting in medium and small-sized arteries. It is a concomitant disease found among SCAD patients. In some studies, FMD prevalence in SCAD patients ranges between 25%–86%, which can be explained through varying screening techniques or modalities. The potential association has been elucidated in some studies; notably, not only has a genetic link been recently delineated between SCAD and FMD, but there is data to suggest that FMD not only can predispose to SCAD but can also be a potential predictor of its recurrence. However, a clear-cut correlation between the two has still not been established due to conflicting reports in the literature. To further dive into its pathology, it is crucial to highlight the importance of systematic screening in SCAD in order to identify associated risk factors and to be used as a method of FMD detection in such patients. Together, the two pathologies pose unique challenges in understanding its pathophysiology, diagnosis and management, as there is no clear evidence of a definitive treatment plan for patients with SCAD and FMD. A potentially beneficial modality of management is physical exercise, which is currently understudied in the long-term approach to treatment for patients with concomitant SCAD and FMD. Limited research in this field brings disadvantages to the understanding of the association between these two diseases, in order to give rise to better management recommendations. This mini-review aims to highlight the recent developments in the association between SCAD and FMD, its potential genetic association and some insights in screening, diagnosis, and management.

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Pathophysiology of spontaneous coronary artery dissection: hematoma, not thrombus

Cited by 3 publications

References 84 publications

Spontaneous Coronary Artery Dissection in Clinical Practice: Pathophysiology and Therapeutic Approaches

Spontaneous Coronary Artery Dissection in Clinical Practice: Pathophysiology and Therapeutic Approaches

Surgical stress as a potential trigger for spontaneous coronary artery dissection: A case report

Spontaneous coronary artery dissection and fibromuscular dysplasia: insights into recent developments

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