Spontaneous coronary artery dissection pathophysiology
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Spontaneous Coronary Artery Dissection Microchapters |
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Differentiating Spontaneous coronary artery dissection from other Diseases |
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Diagnosis |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Nate Michalak, B.A., Arzu Kalayci, M.D. [2]
Synonyms and keywords: SCAD
Overview
Pathophysiology
At present the pathophysiology of SCAD continues to be poorly understood due to the rarity of this condition and its heterogeneous pathology. In SCAD the affected coronary artery develops a tear, causing blood to flow between the coronary arterial layers eventually forcing them apart. The pattern of dissection in SCAD is different from the pattern observed in patients with pre-existing atherosclerosis. In SCAD the plane of dissection lies within the outer third of the tunica media or between the media and adventitia. Dissections can be present in either one artery or several arteries concomitantly.[1] The dissecting plane between intima and media creates a false lumen and the resulting hematoma compresses the vessel lumen causing myocardial ischemia or myocardial infarction (MI).
Spontaneous arterial dissection can develop in any layer (intima , media, or adventitia) of the coronary artery wall. Two possible mechanisms may be responsible for the arterial wall separation.[2] The first one is, the intimal tear hypothesis, in which intramural blood accumulation may develop through a primary entry tear which occurs due to the damaged intimal surface and causes separation of the arterial wall. The second one is, medial hemorrhage hypothesis, in which spontaneous rupture of newly formed vasa vasorum in response to injury can cause a haemorrhage in between the arterial wall layers. High pressure of the haematoma within the aortic wall may rupture through the intima and create a “reverse” intimal rupture. Both result in creation of a false lumen filled with intramural hematoma. [3] False lumen dilatation due to the increasing pressure of enlarging hematoma may lead to luminal compression and precipitate myocardial ischemia and infarction. Atherosclerotic variant of SCAD has basically different characteristic which only includes medial atrophy and scarring. [4] However, NA-SCAD can have an expanded dissection, particularly in the presence of an underlying arteriopathy which makes the arterial wall more fragile. It has been clearly demonstrated by intracoronary imaging studies that these cases have a normal intimal structure. [5] [6] Some negative effects of hormones and elevated hemodynamic stress make the coronary arterial wall weaker (more fragile) during pregnancy.[7] Multiparty causes a longer exposure to pregnancy-associated changes which result in an increased risk of SCAD.[8] Histological analyses revealed a periarteritis including eosinophilic infiltrates in the tunica adventitia that may lead to a disintegration of the medial and adventitial layers resulting in dissection. On the other hand this inflammatory state could be a response to the dissection instead of being an underlying mechanism. </ref> [6]
Although intimal tear or bleeding of vasa vasorum with intramedial hemorrhage seems to be most probable reason, the exact underlying mechanism of non-atherosclerotic spontaneous coronary artery dissection (NA-SCAD) is still unknown [1]. Consequently intramural hematoma creates a false lumen [2]. Progressive expansion of the false lumen may cause subsequent myocardial ischemia and infarction.
References
- ↑ Choi JW, Davidson CJ (2002). "Spontaneous multivessel coronary artery dissection in a long-distance runner successfully treated with oral antiplatelet therapy". The Journal of Invasive Cardiology. 14 (11): 675–8. PMID 12403896.
- ↑ Saw J, Mancini GBJ, Humphries KH (2016). "Contemporary Review on Spontaneous Coronary Artery Dissection". J Am Coll Cardiol. 68 (3): 297–312. doi:10.1016/j.jacc.2016.05.034. PMID 27417009.
- ↑ Alfonso F, Bastante T (2014). "Spontaneous coronary artery dissection: novel diagnostic insights from large series of patients". Circ Cardiovasc Interv. 7 (5): 638–41. doi:10.1161/CIRCINTERVENTIONS.114.001984. PMID 25336602.
- ↑ Isner JM, Donaldson RF, Fortin AH, Tischler A, Clarke RH (1986). "Attenuation of the media of coronary arteries in advanced atherosclerosis". Am J Cardiol. 58 (10): 937–9. PMID 3776849.
- ↑ Saw J, Mancini GB, Humphries K, Fung A, Boone R, Starovoytov A; et al. (2016). "Angiographic appearance of spontaneous coronary artery dissection with intramural hematoma proven on intracoronary imaging". Catheter Cardiovasc Interv. 87 (2): E54–61. doi:10.1002/ccd.26022. PMID 26198289.
- ↑ 6.0 6.1 Alfonso F, Paulo M, Gonzalo N, Dutary J, Jimenez-Quevedo P, Lennie V; et al. (2012). "Diagnosis of spontaneous coronary artery dissection by optical coherence tomography". J Am Coll Cardiol. 59 (12): 1073–9. doi:10.1016/j.jacc.2011.08.082. PMID 22421300.
- ↑ Basso C, Morgagni GL, Thiene G (1996). "Spontaneous coronary artery dissection: a neglected cause of acute myocardial ischaemia and sudden death". Heart. 75 (5): 451–4. PMC 484340. PMID 8665336.
- ↑ Vijayaraghavan R, Verma S, Gupta N, Saw J (2014). "Pregnancy-related spontaneous coronary artery dissection". Circulation. 130 (21): 1915–20. doi:10.1161/CIRCULATIONAHA.114.011422. PMID 25403597.