Repeated epicardial coronary artery endothelial injuries lead to a global spontaneous coronary artery spasm

Saitoh, Shu‐ichi; Muto, Misturu; Osugi, Taku; Aikawa, Kazuhiko; Matsumoto, Ken; Onogi, Futoshi; Maehara, Kazuhira; Ishibashi, Toshiyuki; Maruyama, Yukio

doi:10.1097/00019501-200405000-00002

Cited by 12 publications

(21 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…36) They also showed that the levels of 5-HT1B receptor mRNA of coronary arteries are increased compared with those of brain arteries in WHHL rabbits, indicating a difference in receptor number among different vascular beds. Together with their observation, we can speculate Finally, it would be expected from the results of both the present and previous studies that the coronary artery is highly susceptible to mechanical stress, 37) as well as to various noxious stimuli such as hyperlipidemia and hypertension. Moreover, atherosclerotic progression, vascular remodeling, and regulation of vascular tone by various vasoactive substances following repeatedly induced intimal injury might be altered in a vessel-specific manner, although the direct clinical application of the present results must be considered carefully because of the species differences.…”

Section: Alterations Of Responses To Various Vasoactive Agentssupporting

confidence: 81%

Specificity of Vascular Reactivity and Remodeling After Repeated Endothelial Injury in a Swine Model

et al. 2006

Self Cite

View full text Add to dashboard Cite

SUMMARYWe investigated the difference in vascular responses and remodeling between coronary and iliac arteries after repeated endothelial denudation. Endothelial denudation of the left anterior descending coronary artery (LAD) and the right common iliac artery (RIA) was repeated 4 times twice a month using a Fogarty catheter in 21 pigs. Vascular responses to vasoactive drugs were evaluated as % luminal diameter changes on contrast angiography 2 weeks after the last denudation. Corresponding nondenuded sites, ie, the left circumflex coronary artery (LCX) and the left common iliac artery (LIA), were used as references. Acetylcholine (1 µg/kg) did not constrict the LCX (0 ± 1%) and the LAD (1 ± 1%, P < 0.05), whereas it constricted the RIA (20 ± 6%) but not the LIA (−3 ± 3%, P < 0.01). Alternatively, serotonin (10 µg/kg) constricted the LAD strikingly (88 ± 5%, P < 0.01 versus LCX and RIA), as well as the RIA (35 ± 10%, P < 0.05 versus LIA). Vasodilator responses to substance P and isosorbide dinitrate were not different after injury in both arteries. The intima-to-media ratio and adventitia-to-media ratio of the relevant site in cross section of tissue sample from LAD were greater than those from LCX, and were more prominent than those from RIA. The results show that vascular tone regulation after the endothelial injury and vascular remodeling might be altered in a vesselspecific manner. (Int Heart J 2006; 47: 297-310)

show abstract

Section: Alterations Of Responses To Various Vasoactive Agentssupporting

confidence: 81%

Specificity of Vascular Reactivity and Remodeling After Repeated Endothelial Injury in a Swine Model

et al. 2006

Self Cite

View full text Add to dashboard Cite

show abstract

“…From our previous report 32) , it is likely that microvessels may more easily acquire heightened sensitivity to various pathological stimuli than the large coronary artery and that global spontaneous coronary spasm, including downstream microvessels, might finally occur in this model. As the downstream coronary microvessel is never directly damaged during our experimental procedure, abnormal stimuli produced in the epicardial coronary artery may induce microvascular spasm.…”

Section: Study Limitationsmentioning

confidence: 77%

Preventive Effect of Chronic Endothelin Type A Receptor Antagonist on Coronary Microvascular Spasm Induced by Repeated Epicardial Coronary Artery Endothelial Denudation in Pigs

Osugi

Saitoh

Matumoto

et al. 2010

JAT

Self Cite

View full text Add to dashboard Cite

“…1). 23) Through this examination, we found that this model is suitable as a global spontaneous coronary artery spasm model. This model in- Fig.…”

Section: Development Of a Pig Coronary Artery Spasm Modelmentioning

confidence: 89%

“…We have developed such a model in the conscious and unrestrained state using repeated coronary artery endothelial injury, 23,24) which may be linked to vascular smooth muscle hypercontraction ; this type of injury is likely to occur repeatedly over the course of a lifetime as a result of local shear forces and various risk factors (such as hypercholesterolemia, diabetes mellitus, and hypertension). 9) Using this original spasm model, we investigated the mechanism of coronary vasospasm in which impaired endothelial functioning leads to heightened vascular smooth muscle reactivity and provokes intense conduit coronary artery constriction; we also examined the possibility of therapeutic agents such as antioxidants, β1 -blockers, and endothelin type -A antagonist 25 -28) as therapeutic approaches.…”

mentioning

confidence: 99%

“…We hypothesized that microvascular spasm is caused by a diffuse increase in arteriolar sensitivity to vasoconstrictor stimuli because of upstream epicardial coronary artery endothelial dysfunction, and we confirmed that the repeated endothelial injuries of the epicardial coronary artery induced not only spontaneous conduit coronary artery spasm but also downstream microvascular spontaneous spasm. 23) …”

mentioning

confidence: 99%

See 1 more Smart Citation

Mechanistic Insights of Coronary Vasospasm and New Therapeutic Approaches

Saitoh

Takeishi

Maruyama

2015

FJMS

Self Cite

View full text Add to dashboard Cite

PREFACECoronary vasospasm is a major health problem in Japan because of its high incidence and severity. Great advances have been made in clinical research and therapy focusing on coronary vasospastic angina. In particular, the Ca antagonist has contributed to improvements in the quality of life of patients with coronary vasospastic angina. Moreover, several animal models of coronary vasospasm have provided insight into the pathophysiology of this disease. However, the mechanisms of coronary vasospasm and microvascular spasm remain elusive. We have studied the mechanisms of coronary vasospasm, including microvascular spasm, in an animal model. The present study was designed to develop an animal model of coronary vasospasm and to elucidate the mechanisms and pathophysiology of coronary vasospasm and new therapeutic approaches. The topics discussed in this article include : (1) the role of endothelial and smooth muscle function on the genesis of coronary vasospasm, (2) the participation of reactive oxygen species in coronary vasospasm, and (3) aging and spasm. We hope that the contents of this volume will be useful to "students of coronary vasospasm" at many levels, including the clinician involved in cardiovascular studies and scientists in various disciplines who are interested in a comprehensive, in -depth review of coronary vasospasm.Coronary vasospasm can be defined as a reversible, focal, and intense coronary vasoconstriction that typically occurs in an epicardial conduit artery segment. The definitive diagnosis of a coronary artery spasm is determined by the direct visualization of such a reversible focal subtotal coronary occlusion at a site distal to the catheter tip. This is generally associated with regional ST segment elevation and angina. The first description of coronary artery spasm was likely made by Heberden in 1802 when he described angina as spasmodic, occurring at rest and related to emotional factors. 1) For over 100 years, this presumed vasoconstrictor phenomenon was implicated in myocardial infarction and angina pectoris. It was not until the mid -twentieth century that the correlation between atherosclerotic plaques and angina pectoris was realized. 2) This observation lessened the interest in vasospasms as an etiology of angina, particularly because later investigations failed to observe spasms very often in patients with angina pectoris. 3) In the latter third of the twentieth century, the demonstration of coronary vasospasm during angina (Prinzmetal's angina) and as a precursor to myocardial infarction 4) resurrected interest in the vasomotor etiology of angina pectoris. 5) In recent years, our understanding of the endothelial modulation of coronary tone has evolved, and substantial insight has been provided from a number of studies over the past three decades. However, the mechanism of coronary vasospasm remains elusive.Some investigations have reported that endothelial dysfunction is present at the site of a coronary vasospasm. 6,7) However, several lines of evidence indicate that coro...

show abstract

Repeated epicardial coronary artery endothelial injuries lead to a global spontaneous coronary artery spasm

Abstract: Epicardial coronary artery endothelial injury may induce spontaneous vasospasticity in the downstream coronary microvessels as well as in the denuded portion, suggesting functional abnormality through the entire coronary arterial tree.

Cited by 12 publications

References 18 publications

Specificity of Vascular Reactivity and Remodeling After Repeated Endothelial Injury in a Swine Model

Specificity of Vascular Reactivity and Remodeling After Repeated Endothelial Injury in a Swine Model

Preventive Effect of Chronic Endothelin Type A Receptor Antagonist on Coronary Microvascular Spasm Induced by Repeated Epicardial Coronary Artery Endothelial Denudation in Pigs

Mechanistic Insights of Coronary Vasospasm and New Therapeutic Approaches

Contact Info

Product

Resources

About