Coronary artery spasm: Current knowledge and residual uncertainties☆

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Abstract

Myocardial ischaemia results from a direct mismatch between oxygen supply and demand, commonly arising as a result of coronary atherosclerosis, microvascular dysfunction or acute thrombosis and luminal obstruction. However, transient ischaemia may also occur due to coronary spasm leading to acute and unexpected myocardial ischaemia without obvious visible coronary pathology. Aside from symptoms of chest pain, coronary spasm can cause infarction, LV impairment, promote life threatening arrhythmias and ultimately sudden cardiac death. While therapeutic options are available, controversies exist around diagnosis, pathology, management and prognosis. This review summarises some of the common questions in this area. In particular we explore and discuss the available evidence for the pharmacological treatment of coronary spasm, and strategies for identification and management of very high risk patients to try and reduce the incidence of sudden premature death.

Highlights

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Myocardial ischaemia results from a mismatch between oxygen supply and demand.
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Spasm might lead to myocardial ischaemia without visible coronary pathology.
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Coronary spasm can cause infarction, LV impairment and sudden cardiac death.

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Most cited references 94

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Increase in circulating products of lipid peroxidation (F2-isoprostanes) in smokers. Smoking as a cause of oxidative damage.

J Morrow, B Frei, A Longmire … (1995)

It has been hypothesized that the pathogenesis of diseases induced by cigarette smoking involves oxidative damage by free radicals. However, definitive evidence that smoking causes the oxidative modification of target molecules in vivo is lacking. We conducted a study to determine whether the production of F2-isoprostanes, which are novel products of lipid peroxidation, is enhanced in persons who smoke. We measured the levels of free F2-isoprostanes in plasma, the levels of F2-isoprostanes esterified to plasma lipids, and the urinary excretion of metabolites of F2-isoprostanes in 10 smokers and 10 nonsmokers matched for age and sex. The short-term effects of smoking (three cigarettes smoked over 30 minutes) and the effects of two weeks of abstinence from smoking on levels of F2-isoprostanes in the circulation were also determined in the smokers. Plasma levels of free and esterified F2-isoprostanes were significantly higher in the smokers (242 +/- 147 and 574 +/- 217 pmol per liter, respectively) than in the nonsmokers (103 +/- 19 and 345 +/- 65 pmol per liter; P = 0.02 for free F2-isoprostanes and P = 0.03 for esterified F2-isoprostanes). Smoking had no short-term effects on the circulating levels of F2-isoprostanes. However, the levels of free and esterified F2-isoprostanes fell significantly after two weeks of abstinence from smoking (250 +/- 156 and 624 +/- 214 pmol per liter, respectively, before the cessation of smoking, as compared with 156 +/- 67 and 469 +/- 108 pmol per liter after two weeks' cessation; P = 0.03 for free F2-isoprostanes and P = 0.02 for esterified F2-isoprostanes). The increased levels of F2-isoprostanes in the circulation of persons who smoke support the hypothesis that smoking can cause the oxidative modification of important biologic molecules in vivo.

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Coronary artery spasm--clinical features, diagnosis, pathogenesis, and treatment.

Hirofumi Yasue, Hitoshi Nakagawa, Teruhiko Itoh … (2008)

Coronary (artery) spasm plays an important role in the pathogenesis of ischemic heart disease, including stable angina, unstable angina, myocardial infarction, and sudden death. The prevalence of coronary spasm differs among populations, is higher in Japan and Korea than in the Western countries probably due to genetic as well as environmental factors. Coronary spasm occurs most often from midnight to early morning and is usually not induced by exercise in the daytime. The attacks of coronary spasm are associated with either ST segment elevation or depression, or negative U wave on ECG. Patients with multi-vessel coronary spasm may suffer from lethal arrhythmia, including advanced AV block, ventricular tachycardia or fibrillation, or even sudden death, and they are often resistant to conventional medical therapy including Ca-channel blockers (CCBs). Endothelial nitric oxide (NO) activity is reduced and markers of oxidative stress are elevated in patients with coronary spasm. Thrombogenesis is enhanced and plasma levels of hsCRP and P-selection are elevated in patients with coronary spasm. Thus, patients with coronary spasm have endothelial dysfunction and are suffering from a low-grade chronic inflammation. Polymorphisms of endothelial NO synthase, smoking, and low-grade inflammation are the most important risk factors for coronary spasm. Coronary spasm is a hyper-contraction of coronary smooth muscle triggered by an increase of intracellular Ca2+ in the presence of an increased Ca2+ sensitivity. It has been shown that RhoA/ROCK pathway is involved in Ca2+ sensitivity and that the reduced endothelial NO activity results in increased Ca2+ sensitivity through enhanced RhoA/ROCK pathway. Accordingly, it is possible that in addition to CCBs, RhoA/ROCK pathway blockers may prove to be useful for the treatment of coronary spasm.

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Mechanisms of coronary artery spasm.

Filippo Crea, G Careri, Gaetano Lanza (2011)

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Author and article information

Contributors

Massimo Slavich

Journal

Journal ID (nlm-ta): Int J Cardiol Heart Vasc

Journal ID (iso-abbrev): Int J Cardiol Heart Vasc

Title: International Journal of Cardiology. Heart & Vasculature

Publisher: Elsevier

ISSN (Electronic): 2352-9067

Publication date PMC-release: 23 January 2016

Publication date Collection: March 2016

Publication date (Electronic): 23 January 2016

Volume: 10

Pages: 47-53

Affiliations

[a ]Dept. of Cardiology, The Heart Hospital, University College London NHS Trust, London, UK

[b ]Unità Terapia Intensiva Coronarica, IRCCS Ospedale San Raffale, Via Olgettina 58, Milan, Italy

[c ]Institute of Cardiovascular Sciences, University College London, London, UK

Author notes

[* ]Corresponding author at: Unità Terapia Intensiva Coronarica, IRCCS Ospedale San Raffale, Via Olgettina 58, Milan, Italy.Unità Terapia Intensiva CoronaricaIRCCS Ospedale San RaffaleVia Olgettina 58MilanItaly slavich.massimo@ 123456hsr.it

Article

Publisher ID: S2352-9067(16)30003-3

DOI: 10.1016/j.ijcha.2016.01.003

PMC ID: 5462634

PubMed ID: 28616515

SO-VID: 7df5bf20-928f-4ee6-810a-8905ae25c572

License:

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

History

Date received : 9 November 2015

Date accepted : 10 January 2016

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