Pathophysiology of Spontaneous Coronary Artery Dissection Determines Anticoagulation Strategy.

Philip Houck

doi:10.7759/cureus.17437

Abstract

Spontaneous coronary dissection is an uncommon disorder, lacking convincing pathophysiologic evidence. Scientific statements and state-of-the-art articles suggest intramural hematoma from bleeding vasa vasorum is the cause. Evidence is based on limited invasive evaluation with optical coherence tomography. This assumption, therefore, suggests anti-coagulation be discontinued. Mechanical shear forces, intraluminal pressures do not support bleeding vasa vasorum closing a higher luminal pressure vessel.The endothelium’s role in inflammation, thrombosis, and repair suggests the pathophysiology is failure to repair endothelium with the lack of repair as the nidus of disruption. A tear ensues and can spontaneously reseal. The lack of inflammatory cells in pathological specimens and association with another poorly understood disease fibromuscular dysplasia supports the etiology of both entities as failure to replace endothelium. The endothelium is the fulcrum of both inflammation and thrombosis. The ability to heal the rift supports conservative therapy.Anticoagulants and antiplatelet reduce thrombosis and inflammation which will ensue when the endothelium is disrupted. These agents will substitute for the failed endothelium allowing thrombosis to be kept in check, reduce inflammation, and promote healing. This thesis and the state-of-the-art articles do not present clinical outcome data. Both support conservative interventions. Anticoagulation recommendations are however in opposite realms. Failure to repair endothelium suggest additional therapies of statins, exercise, smoking cessation will increase circulating stem cells may reduce future events and slow the progression of fibromuscular dysplasia. Future directions in understanding this disease and new therapies requires measurement of repair mechanisms such as the quantity of circulating endothelial progenitor cells.

Highlights

BackgroundSpontaneous coronary artery dissection is an unusual cause of myocardial infarction occurring in young women, frequently peripartum, and is associated with another unusual condition of fibromuscular dysplasia
The pathophysiology of this condition supported by this article is intramural hematoma from bleeding vasa vasorum, the “outside-in” hypothesis, and anticoagulation is to be avoided
Forgotten endothelium exists in lymphatic vessels one of the major components of the immune system and runs with the vasa vasorum

Summary

Introduction

Spontaneous coronary artery dissection is an unusual cause of myocardial infarction occurring in young women, frequently peripartum, and is associated with another unusual condition of fibromuscular dysplasia. Hemorrhage is unlikely to compress the artery This same pressure is likely to tamponade bleeding from an inflammatory disruption of the vasa vasorum. Forgotten endothelium exists in lymphatic vessels one of the major components of the immune system and runs with the vasa vasorum This system participates and is affected by both inflammation and thrombosis. The blood vessel inflammatory, thrombosis, and repair introduction is necessary to propose a mechanism for coronary artery dissection. Heparin anticoagulants and antiplatelet medication decrease the inflammatory response caused by dissection and promotes healing of the disrupted endothelium. Yes denudation of endothelium Yes incomplete healing after denudation with fibrosis Yes reduced circulating stem cells estrogen associated [26] Yes Yes. Bleeding into the vasa vasorum is unlikely to close the vessel. Plasmapheresis, intravenous immune globulin, and steroids were necessary to reverse the fetal antigen-mediated multivessel immune-mediated coronary syndrome

Conclusions

Findings

Disclosures