Spontaneous coronary artery dissection pathophysiology: Difference between revisions
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==Genetics== | |||
[Disease name] is transmitted in [mode of genetic transmission] pattern. | |||
OR | |||
Genes involved in the pathogenesis of [disease name] include: | |||
*[Gene1] | |||
*[Gene2] | |||
*[Gene3] | |||
OR | |||
The development of [disease name] is the result of multiple genetic mutations such as: | |||
*[Mutation 1] | |||
*[Mutation 2] | |||
*[Mutation 3] | |||
==Associated Conditions== | |||
Conditions associated with [disease name] include: | |||
*[Condition 1] | |||
*[Condition 2] | |||
*[Condition 3] | |||
==Gross Pathology== | |||
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name]. | |||
==Microscopic Pathology== | |||
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name]. | |||
==References== | ==References== | ||
Revision as of 20:56, 8 April 2020
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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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Treatment |
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Case Studies |
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Type 1 Type 2A Type 2B Type 3 |
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
At present the pathophysiology of non-atherosclerotic spontaneous coronary artery dissection (NA-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.
Pathophysiology
NA-SCAD can develop in any layer (intima , media, or adventitia) of the coronary artery wall. However, the initiation and the pattern of dissection in NA-SCAD is different from the pattern observed in patients with pre-existing atherosclerosis. The plane of dissection mostly occurs within the outer third of the tunica media or between the media and adventitia in NA-SCAD. In addition dissections can be present within either one artery or several arteries concomitantly in this state.[1][2]
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 haemorrhage 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 of them result in a creation of false lumen filled with intramural haematoma. [4]High pressure of the haematoma within the arterial wall may lead to a rupture through the intima and create a “reverse” intimal rupture.
Furthermore, increasing pressure of enlarging haematoma in the false lumen may also lead to luminal compression and precipitate myocardial ischemia and infarction. Thrombus can occur in both true and false lumen. Thrombosis of the true lumen mostly originates from intimal rupture sites. The current literature remains controversial regarding whether there is a thrombus in the true lumen in patients with NA-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 also true lumen.[8]
Atherosclerotic variant of SCAD has basically different characteristic which only includes medial atrophy and scarring. [9] Unlike the atherosclerotic pattern, 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 NA-SCAD cases have a normal intimal structure. [7] [8]
It is clearly known that pregnancy is a significant risk factor for NA-SCAD. Some negative effects of hormones and elevated hemodynamic stress make the coronary arterial wall weak 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]
 (Adapted from Br J Sports Med. 2012; 46(Suppl_1): i15–i21. under CC BY-NC license) [14] |
Genetics
[Disease name] is transmitted in [mode of genetic transmission] pattern.
OR
Genes involved in the pathogenesis of [disease name] include:
- [Gene1]
- [Gene2]
- [Gene3]
OR
The development of [disease name] is the result of multiple genetic mutations such as:
- [Mutation 1]
- [Mutation 2]
- [Mutation 3]
Associated Conditions
Conditions associated with [disease name] include:
- [Condition 1]
- [Condition 2]
- [Condition 3]
Gross Pathology
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
References
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Sheppard MN (2012). "Aetiology of sudden cardiac death in sport: a histopathologist's perspective". Br J Sports Med. 46 Suppl 1: i15–21. doi:10.1136/bjsports-2012-091415. PMC 3603681. PMID 23097474.
