The Mystery of Coronary Artery Spasm

Ajani, A.; Yan, Bryan P.

doi:10.1016/j.hlc.2006.11.003

Cited by 28 publications

(30 citation statements)

References 77 publications

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“…However, they are major sites where vasospasm occurs resulting in symptoms of myocardial ischemia (1). A previous in vivo study (25) demonstrated that, after ischemia-reperfusion injury, hypoxemia causes constrictions of epicardial arteries that can be prevented by an inhibitor of NO synthase, which is line with the present assumption that cIMP synthesized by NO-activated sGC mediates hypoxic vasoconstriction.…”

Section: Discussionsupporting

confidence: 79%

cIMP synthesized by sGC as a mediator of hypoxic contraction of coronary arteries

Chen

Zhang

Lei

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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. cIMP synthesized by sGC as a mediator of hypoxic contraction of coronary arteries. Am J Physiol Heart Circ Physiol 307: H328 -H336, 2014. First published June 6, 2014; doi:10.1152/ajpheart.00132.2014cGMP is considered the only mediator synthesized by soluble guanylyl cyclase (sGC) in response to nitric oxide (NO). However, purified sGC can synthesize several other cyclic nucleotides, including inosine 3=,5=-cyclic monophosphate (cIMP). The present study was designed to determine the role of cIMP in hypoxic contractions of isolated porcine coronary arteries. Vascular responses were examined by measuring isometric tension. Cyclic nucleotides were assayed by HPLC tandem mass spectroscopy. Rho kinase (ROCK) activity was determined by measuring the phosphorylation of myosin phosphatase target subunit 1 using Western blot analysis and an ELISA kit. The level of cIMP, but not that of cGMP, was elevated by hypoxia in arteries with, but not in those without, endothelium [except if treated with diethylenetriamine (DETA) NONOate]; the increases in cIMP were inhibited by the sGC inhibitor 1H-[1,2,4]oxadiazolo[4,3,-a]quinoxalin-1-one (ODQ). Hypoxia (PO2: 25-30 mmHg) augmented contractions of arteries with and without endothelium if treated with DETA NONOate; these hypoxic contractions were blocked by ODQ. In arteries without endothelium, hypoxic augmentation of contraction was also obtained with exogenous cIMP. In arteries with endothelium, hypoxic augmentation of contraction was further enhanced by inosine 5=-triphosphate, the precursor for cIMP. The augmentation of contraction caused by hypoxia or cIMP was accompanied by increased phosphorylation of myosin phosphatase target subunit 1 at Thr 853 , which was prevented by the ROCK inhibitor Y-27632. ROCK activity in the supernatant of isolated arteries was stimulated by cIMP in a concentration-dependent fashion. These results demonstrate that cIMP synthesized by sGC is the likely mediator of hypoxic augmentation of coronary vasoconstriction, in part by activating ROCK. soluble guanylyl cyclase; inosine 3=,5=-cyclic monophosphate; hypoxic vasoconstriction; endothelium A PREVIOUS STUDY reported that acute hypoxia caused a rapid further increase in tension of contracted canine saphenous veins (31). Subsequent findings demonstrated that such a phenomenon, termed hypoxic augmentation of vasoconstriction (5, 15), occurs in a number of blood vessel types (5,7,8,15,21,23,25,26) contracted with norepinephrine (7, 8), phenylephrine (23), PGF 2␣ (15,25), and the TP receptor agonist U-46619 (21), indicating that it is not unique for a specific vasoconstrictor. It occurs in isolated coronary arteries with but not without endothelium (5,15,25,26). The phenomenon is not affected by bosentan, a blocker of endothelin receptors (5), but is prevented by inhibitors of nitric oxide (NO) synthase (5,15,25). Hypoxic augmentation also occurs in arteries without endothelium treated with an exogenous NO donor (5) However, hypoxic augmentation is not accompanied by changes in the intracellular leve...

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Section: Discussionsupporting

confidence: 79%

cIMP synthesized by sGC as a mediator of hypoxic contraction of coronary arteries

Chen

Zhang

Lei

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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“…Ich wystąpienie nie ma związku z zaawansowaniem współistniejącej miażdżycy tętnic wień -cowych, a zależy głównie od tego, która tętnica objęta jest skurczem. Gdy uniesienie dominuje w odprowadzeniach znad ściany dolnej, zwykle towarzyszą mu bradyarytmie, a gdy dotyczy ściany przedniej -obserwujemy arytmie komorowe [25].…”

Section: Dyskusjaunclassified

Myocardial infarction with transient ST-segment elevation as a clinical manifestation of a Prinzmetal’s angina in patients with primary non-significant coronary artery stenosis. s

Noll¹,

Suchcicki²,

Karwowski³

et al. 2010

pwki

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“…Vagal withdrawal is usually the mechanism leading to spontaneous spasm, although sympathetic activity alteration may also be responsible [1]. Coronary spasm may not be limited to normal coronary arteries, and up to 60% of cases occur superimposed on fixed coronary lesions [2]. Coronary spasm is generally manifested by ST-segment elevation on the electrocardiogram.…”

mentioning

confidence: 99%

“…Rarely myocardial infarction, cardiac arrest, and sudden death can occur with variant angina without obstructive coronary stenosis. Prinzmetal angina is an uncommon etiology for myocardial infarction (MI) unless coronary obstruction is severe and prolonged [2]. Coronary spasm is suggested by reversible hypercontractility of coronary arteries.…”

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confidence: 99%

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Coronary spasm provocation with cold pressor test

Ghaffari

Pourafkari

2010

Intern Emerg Med

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A 66-year-old man was admitted to our emergency department (ED) with acute retrosternal chest pain for a duration of 30 min. This was his first episode of chest pain, and the past medical history was unremarkable. He did not have a history of smoking, drinking alcohol or using illicit drugs, and had not been under any medication. Electrocardiogram (ECG) on admission showed 3-4 mm of ST-segment elevation in leads V1 to V5. He was prescribed aspirin, nitroglycerin and morphine. Just a few minutes after admission he developed ventricular fibrillation that was successfully terminated by DC shock. Twenty minutes later and concomitant with his pain subsiding, a repeat ECG showed resolution of ST-segment elevation. He was admitted to the cardiac care unit. No change was observed in serial ECGs, and chest pain did not recur. He had an elevated cardiac troponin I (cTnI) of 2.5 ng/ml (normal = 0.1-1 ng/ml). Coronary angiography showed normal coronary arteries except for mild irregularity at the proximal left anterior descending artery (LAD) (Fig. 1). Upon suspicion of coronary spasm, a cold pressor test was performed that provoked 99% vasoconstriction in the proximal LAD (Fig. 2) accompanied by chest pain and ST-segment elevation. The spasm rapidly resolved with the administration of intracoronary nitrates. Based on these findings a diagnosis of Prinzmetal (variant) angina was made, and the patient was discharged on clopidogrel, diltiazem, isosorbide dinitrate and atorvastatin. At 1 year follow up the patient remains well and symptom free.Prinzmetal et al. introduced the first description of chest pain resulting from coronary artery spasm as episodes of ''temporary increased tonus '' in 1959 [1]. Coronary spasm is described as an exaggerated contractile reaction of coronary artery smooth muscle to different stimuli. Vagal withdrawal is usually the mechanism leading to spontaneous spasm, although sympathetic activity alteration may also be responsible [1]. Coronary spasm may not be limited to normal coronary arteries, and up to 60% of cases occur superimposed on fixed coronary lesions [2]. Coronary spasm is generally manifested by ST-segment elevation on the electrocardiogram. Rarely myocardial infarction, cardiac arrest, and sudden death can occur with variant angina without obstructive coronary stenosis. Prinzmetal angina is an uncommon etiology for myocardial infarction (MI) unless coronary obstruction is severe and prolonged [2]. Coronary spasm is suggested by reversible hypercontractility of coronary arteries. Severe chest pain, commonly without physical exertion and with a simultaneous transient ST-segment elevation in the ECG, is the key for the diagnosis. In the ED, especially during the initial care, it may be difficult to differentiate episodes of Prinzmetal angina from an acute MI, and this may lead to inappropriate thrombolytic injection. Resting pain especially during early morning (midnight to 8 am), together with a rapid resolution of the pain and ST elevation with sublingual nitroglycerine along with a lack ...

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The Mystery of Coronary Artery Spasm

Cited by 28 publications

References 77 publications

cIMP synthesized by sGC as a mediator of hypoxic contraction of coronary arteries

cIMP synthesized by sGC as a mediator of hypoxic contraction of coronary arteries

Myocardial infarction with transient ST-segment elevation as a clinical manifestation of a Prinzmetal’s angina in patients with primary non-significant coronary artery stenosis. s

Coronary spasm provocation with cold pressor test

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