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Spontaneous Coronary Artery Dissection: Pathophysiological Insights From Optical Coherence Tomography

R. Jackson, A. Al-Hussaini, S. Joseph, G. van Soest, A. Wood, F. Macaya, N. Gonzalo, J. Cade, A. Caixeta, O. Hlinomaz, P. Leinveber, P. O'Kane, M. García-Guimaraes, B. Cortese, NJ. Samani, J. Escaned, F. Alfonso, T. Johnson, D. Adlam,

. 2019 ; 12 (12) : 2475-2488. [pub] 20190313

Language English Country United States

Document type Journal Article, Multicenter Study, Observational Study, Research Support, Non-U.S. Gov't

Persistent link   https://www.medvik.cz/link/bmc20025444

Grant support
PG/13/96/30608 British Heart Foundation - United Kingdom
Department of Health - United Kingdom

OBJECTIVES: This study used optical coherence tomography to investigate the mechanism of false lumen (FL) formation in spontaneous coronary artery dissection (SCAD) by studying: 1) differences between fenestrated and nonfenestrated SCAD; 2) vasa vasorum density; and 3) light attenuation characteristics of the FL. BACKGROUND: SCAD is an increasingly recognized cause of acute coronary syndromes, characterized by FL formation and compression of the true lumen (TL). The mechanisms underlying FL formation remain poorly understood. METHODS: A total of 65 SCAD patients (68 vessels) who underwent acute OCT imaging as part of routine clinical care were included. Images were classified by the absence or presence of a connection (fenestration) between the TL and FL. Indexed measurements of TL stenosis, external elastic lamina (EEL) area, FL area, and light attenuation of the FL were assessed. Vasa vasorum densities of SCAD cases were compared with those in control non-SCAD myocardial infarction cases. RESULTS: In nonfenestrated cases, there was significantly larger expansion of the EEL area (9.1% vs. -1.9%; p <0.05) and a larger FL area (73.6% vs. 53.2%, respectively; p <0.05) in dissected segments. No significant differences were found between vasa vasorum density in SCAD and those in control subjects. The FL contents were heterogeneous but attenuated less light than whole blood or thrombus (4.28 ± 0.55 mm-1 vs. 5.08 ± 0.56 mm-1; p < 0.05; vs. 4.96 ± 0.56 mm-1; p < 0.05). CONCLUSIONS: These observational data suggest that the absence of a fenestration leads to increased FL pressure and compression of the TL. Although vasa vasorum may still be implicated in pathogenesis, increased vasa vasorum density could be an epiphenomenon of vascular healing.

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$a OBJECTIVES: This study used optical coherence tomography to investigate the mechanism of false lumen (FL) formation in spontaneous coronary artery dissection (SCAD) by studying: 1) differences between fenestrated and nonfenestrated SCAD; 2) vasa vasorum density; and 3) light attenuation characteristics of the FL. BACKGROUND: SCAD is an increasingly recognized cause of acute coronary syndromes, characterized by FL formation and compression of the true lumen (TL). The mechanisms underlying FL formation remain poorly understood. METHODS: A total of 65 SCAD patients (68 vessels) who underwent acute OCT imaging as part of routine clinical care were included. Images were classified by the absence or presence of a connection (fenestration) between the TL and FL. Indexed measurements of TL stenosis, external elastic lamina (EEL) area, FL area, and light attenuation of the FL were assessed. Vasa vasorum densities of SCAD cases were compared with those in control non-SCAD myocardial infarction cases. RESULTS: In nonfenestrated cases, there was significantly larger expansion of the EEL area (9.1% vs. -1.9%; p <0.05) and a larger FL area (73.6% vs. 53.2%, respectively; p <0.05) in dissected segments. No significant differences were found between vasa vasorum density in SCAD and those in control subjects. The FL contents were heterogeneous but attenuated less light than whole blood or thrombus (4.28 ± 0.55 mm-1 vs. 5.08 ± 0.56 mm-1; p < 0.05; vs. 4.96 ± 0.56 mm-1; p < 0.05). CONCLUSIONS: These observational data suggest that the absence of a fenestration leads to increased FL pressure and compression of the TL. Although vasa vasorum may still be implicated in pathogenesis, increased vasa vasorum density could be an epiphenomenon of vascular healing.
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$a Al-Hussaini, Abtehale $u Department of Cardiovascular Sciences, Glenfield Hospital, Leicester, United Kingdom, and National Institute for Health Research Leicester Biomedical Research Centre, Glenfield Hospital, Leicester, United Kingdom; Department of Cardiology, Royal Brompton Hospital, London, United Kingdom.
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$a Joseph, Shiju $u Department of Cardiovascular Sciences, Glenfield Hospital, Leicester, United Kingdom, and National Institute for Health Research Leicester Biomedical Research Centre, Glenfield Hospital, Leicester, United Kingdom.
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$a van Soest, Gijs $u Erasmus MC, University Medical Centre Rotterdam, Rotterdam, the Netherlands.
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$a Wood, Alice $u Department of Cardiovascular Sciences, Glenfield Hospital, Leicester, United Kingdom, and National Institute for Health Research Leicester Biomedical Research Centre, Glenfield Hospital, Leicester, United Kingdom.
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$a Macaya, Fernando $u Hospital Clínico San Carlos and Universidad Complutense, Madrid, Spain; Department of Cardiology, King's College Hospital, London, United Kingdom.
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$a Cade, Jamil $u Department of Cardiology, Hospital Israelita Albert Einstein, São Paulo, São Paulo, Brazil.
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$a Caixeta, Adriano $u Department of Cardiology, Hospital Israelita Albert Einstein, São Paulo, São Paulo, Brazil.
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$a O'Kane, Peter $u Department of Cardiology, Bournemouth Hospital, Bournemouth, United Kingdom.
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$a García-Guimaraes, Marcos $u Department of Cardiology, Hospital Universitario de La Princesa, Madrid, Spain.
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$a Cortese, Bernardo $u San Carlo Clinic, Milano, Italy.
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$a Samani, Nilesh J $u Department of Cardiovascular Sciences, Glenfield Hospital, Leicester, United Kingdom, and National Institute for Health Research Leicester Biomedical Research Centre, Glenfield Hospital, Leicester, United Kingdom.
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$a Johnson, Thomas $u Department of Cardiology, Bristol Heart Institute, Bristol Royal Infirmary, Bristol, United Kingdom.
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