2011
DOI: 10.1161/circulationaha.111.037283
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Mechanisms of Coronary Artery Spasm

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Cited by 333 publications
(297 citation statements)
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References 119 publications
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“…[1,3] Vasospasm is predominantly caused by hyper-reactive vascular smooth muscle cells and probably endothelial dysfunction. [4] It is also reported that prolonged VSA may cause acute myocardial infarction. [2] The prevalence of VSA is known to be as low as 1% to 1.5% of angina admissions.…”
Section: Introductionmentioning
confidence: 98%
“…[1,3] Vasospasm is predominantly caused by hyper-reactive vascular smooth muscle cells and probably endothelial dysfunction. [4] It is also reported that prolonged VSA may cause acute myocardial infarction. [2] The prevalence of VSA is known to be as low as 1% to 1.5% of angina admissions.…”
Section: Introductionmentioning
confidence: 98%
“…U podłoża dolegliwości dławicowych, oprócz najczęściej stwierdzanego tła miażdżycowego, mogą leżeć inne mechanizmy, które istotnie ograniczają przepływ krwi w naczyniach wieńcowych. Są to między innymi dysfunkcja mikrokrążenia, ogniskowy lub uogólniony skurcz tętnicy, stan zapalny czy mechanizm restenozy [1,2]. Pozamiażdżycowe czynniki wpływające na ograniczenie przepływu w naczyniach wieńcowych należy rozważać szczególnie u chorych z objawami, u których wyniki badań dodatkowych nie potwierdzają istotności zwężenia naczyń wieńcowych.…”
Section: Dyskusjaunclassified
“…1 In our article, we questioned that endothelial dysfunction (ED) can by itself be the main pathophysiological substrate for CAS in the clinical setting for 2 main reasons: (1) the discrepancy between the high prevalence of ED and the low prevalence of vasospastic angina; (2) the lack of any significant relation between most cardiovascular risk factors (CVRFs) known to cause ED and CAS.…”
mentioning
confidence: 98%
“…1 In our article, we questioned that endothelial dysfunction (ED) can by itself be the main pathophysiological substrate for CAS in the clinical setting for 2 main reasons: (1) the discrepancy between the high prevalence of ED and the low prevalence of vasospastic angina; (2) the lack of any significant relation between most cardiovascular risk factors (CVRFs) known to cause ED and CAS.In their letter, instead, Yasue et al propose that ED is the central abnormality in the mechanisms of CAS; specifically, they propose that smooth muscle cell (SMC) hyperreactivity, ultimately responsible for CAS, is caused by chronic ED.Yasue et al speculate that the reason why chronic ED does not frequently cause CAS in Western countries, despite its large diffusion, depends on the fact that the high prevalence of dyslipidemia in these populations also results in the frequent development of atherosclerotic coronary plaques, which would constitute an inadequate milieu for the development of SMC hyperreactivity. In contrast, in Japanese people, the low prevalence of dyslipidemia would result in a low prevalence of coronary plaques, whereas the high prevalence of smoking would induce a chronic ED that, in the absence of dyslipidemia-related coronary plaques, would result in SMC hyperreactivity and CAS.…”
mentioning
confidence: 99%