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: Arzu Kalayci, M.D. [2], Nate Michalak, B.A.
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).
At present the pathophysiology of spontaneous coronary artery dissection (SCAD) continues to be poorly understood due to the rarity of this condition and its heterogeneous pathology. Although intimal tear or bleeding of vasa vasorum with intramedial hemorrhage seems to be most probable reasons, the exact underlying mechanism is still unknown.[2] SCAD can develop in any layer (intima , media, or adventitia) of the coronary artery wall. However, the initiation and the pattern of dissection in SCAD is different from the pattern observed in patients with pre-existing atherosclerosis. In SCAD the plane of dissection mostly occurs within the outer third of the tunica media or between the media and adventitia. In addition dissections can be present within either one artery or several arteries concomitantly.[1]
Two possible mechanisms have been described for the arterial wall separation.[3] The first one is, 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 within between the arterial wall layers. Both result in creation of a false lumen filled with intramural hematoma. [4]High pressure of the haematoma within the arterial wall may lead to a rupture through the intima and create a “reverse” intimal rupture. False lumen dilatation due to the increasing pressure of enlarging hematoma may lead to luminal compression and precipitate myocardial ischemia and infarction. Thrombus can occur in both true and false lumen. It mostly originates from intimal rupture sites in the true lumen. The current literature remains controversial regarding whether there is a thrombus in the true lumen in patients with SCAD. Two angiographic and one optical coherence tomography (OCT) studies have proposed that there was no thrombus in the arterial true lumen. [5] [6] [7] However, another OCT study has detected some insignificant thrombosis in the false and true lumen.[8]
Atherosclerotic variant of SCAD has basically different characteristic which only includes medial atrophy and scarring. [9] 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. [7] [8]
Some negative effects of hormones and elevated hemodynamic stress make the coronary arterial wall weaker (more fragile) during pregnancy.[10] Multiparty causes a longer exposure to pregnancy-associated changes which result in an increased risk of SCAD.[11] Histological analyses revealed a periarteritis including eosinophilic infiltrates in the tunica adventitia that may lead to a separation of the arterial wall layers resulting in dissection. On the other hand this inflammatory state could be a response to the dissection instead of being an underlying mechanism. [8] A retrospective study has shown the relationship between coronary artery tortuosity and SCAD. [12]. An association has also been described between coronary tortuosity and fibromuscular dysplasia. Most likely, tortuosity is also a consequence of an underlying vasculopathy likewise dissection. [13] [3]
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. 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).
References
- ↑ 1.0 1.1 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.
- ↑ Alfonso F (2012). "Spontaneous coronary artery dissection: new insights from the tip of the iceberg?". Circulation. 126 (6): 667–70. doi:10.1161/CIRCULATIONAHA.112.122093. PMID 22800852.
- ↑ 3.0 3.1 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.
- ↑ Saw J, Aymong E, Sedlak T, Buller CE, Starovoytov A, Ricci D; et al. (2014). "Spontaneous coronary artery dissection: association with predisposing arteriopathies and precipitating stressors and cardiovascular outcomes". Circ Cardiovasc Interv. 7 (5): 645–55. doi:10.1161/CIRCINTERVENTIONS.114.001760. PMID 25294399.
- ↑ Tweet MS, Eleid MF, Best PJ, Lennon RJ, Lerman A, Rihal CS; et al. (2014). "Spontaneous coronary artery dissection: revascularization versus conservative therapy". Circ Cardiovasc Interv. 7 (6): 777–86. doi:10.1161/CIRCINTERVENTIONS.114.001659. PMID 25406203.
- ↑ 7.0 7.1 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.
- ↑ 8.0 8.1 8.2 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.
- ↑ 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.
- ↑ 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.
- ↑ Eleid MF, Guddeti RR, Tweet MS, Lerman A, Singh M, Best PJ; et al. (2014). "Coronary artery tortuosity in spontaneous coronary artery dissection: angiographic characteristics and clinical implications". Circ Cardiovasc Interv. 7 (5): 656–62. doi:10.1161/CIRCINTERVENTIONS.114.001676. PMID 25138034.
- ↑ Saw J, Bezerra H, Gornik HL, Machan L, Mancini GB (2016). "Angiographic and Intracoronary Manifestations of Coronary Fibromuscular Dysplasia". Circulation. 133 (16): 1548–59. doi:10.1161/CIRCULATIONAHA.115.020282. PMID 26957531.