A 62-year-old lady was admitted with clinical and electrocardiograph features of acute myocardial infarction. Urgent coronary arteriography was performed, demonstrating a single discrete stenosis of one coronary artery. Following intracoronary injection of GTN, this stenosis completely resolved, as the symptoms did. The causes of acute myocardial infarction with normal coronary arteries are reviewed

Gosai, J.

Grech, E.D.

Malkin, C.J.

PubMed

J. Gosai

C. J. Malkin

E. D. Grech

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The Vanishing Stenosis: ST Elevation Myocardial Infarction and Rhythm Disturbance due to Coronary Artery Spasm—Case Report and Review of the Literature

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Hindawi Publishing CorporationCase Reports in MedicineVolume 2010, Article ID 132902, 4 pagesdoi:10.1155/2010/132902Case ReportThe Vanishing Stenosis: ST Elevation MyocardialInfarction and Rhythm Disturbance due to Coronary ArterySpasm—Case Report and Review of the LiteratureJ. Gosai, C. J. Malkin, and E. D. GrechDepartment of Cardiology, Sheffield Teaching Hospitals NHS Foundation Trust, Northern General Hospital, Sheffield S5 7AU, UKCorrespondence should be addressed to J. Gosai, jiv@doctors.org.ukReceived 4 October 2009; Accepted 8 February 2010Academic Editor: Robert SouferCopyright © 2010 J. Gosai et al. This is an open access article distributed under the Creative Commons Attribution License, whichpermits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.A 62-year-old lady was admitted with clinical and electrocardiograph features of acute myocardial infarction. Urgent coronaryarteriography was performed, demonstrating a single discrete stenosis of one coronary artery. Following intracoronary injectionof GTN, this stenosis completely resolved, as the symptoms did. The causes of acute myocardial infarction with normal coronaryarteries are reviewed.1. Case PresentationA 62-year-old lady with a history of treated hypothyroidismand obesity presented with a 12 hour history of severe centralchest pain radiating to her left arm and not respondingto sublingual nitrates. On arrival, she appeared in severepain, and electrocardiogram (ECG) showed intermittentheart block and ST elevation in leads II, III and aVF withST depression and deep T wave inversions in leads V2—V5 (Figure 1). A diagnosis of infero-posterior ST elevationmyocardial infarction was made and she was transferred tothe cardiac catheterisation suite for primary angioplasty.The patient had no known risk factors for coronaryartery disease except for obesity (BMI 44). She had previouslyhad a diagnosis of ischaemic heart disease and anginaand previous ECGs had shown T wave inversion in theinferolateral leads. There had been extensive correspondenceabout her problematic exertional chest pain and non-compliance with therapy.Coronary angiography showed an 80% discrete stenosisof the proximal circumflex artery (Figure 2).Initially the circumflex lesion was crossed with a hydro-philic floppy guide wire, and 200 micrograms intracoronaryglyceryl trinitrate (GTN) was administered. Following this,there was an immediate and complete resolution of the appa-rent luminal stenosis, with marked increase in the calibre ofthe coronary artery throughout. The ECG and symptomsimmediately improved (Figures 3 and 4).The patient was treated overnight with intravenousGTN infusion and converted to a long acting oral nitratepreparation. She had no further symptoms and troponin Iwas measured at 0.07 ng/mL at 12 hours post pain (normalrange <0.05). The patient was discharged. At 6 months shewas reported to have few ongoing symptoms and improvedexercise tolerance.2. DiscussionCoronary spasm as a mimic of acute coronary syndromeincluding acute myocardial infarction (AMI) is a well doc-umented phenomenon, associated with chest pain, hospitaladmissions and treatment as for atherosclerotic heart diseaseincluding angiography. It can also cause life threateningarrhythmia and other complications related to ischaemicmyocardium.Coronary spasm may occur in normal coronary arter-ies, but is more common in vessels with non-obstructiveatheroma which do not cause significant flow limitation atangiography but reduce the reserve capacity for flow throughthe vessel. The prevalence is higher in Japanese and Koreanpopulations than in the Western population, probably dueto a combination of genetic and environmental factors.2 Case Reports in MedicineIIIIIIIIaVRaVLaVFV1V2V3V4V5V6Figure 1: ECG demonstrating Inferior ST elevation, T waveinversions.LAO cranial. Figure 2Polymorphisms of the endothelial nitric oxide synthase andangiotensin II type 1 receptor have been put forward as pro-vasospastic with reduced endothelial nitric oxide activity andincreased inflammatory markers. Several authors have alsosuggested that smoking is a strong independent risk factorfor coronary artery spasm. This spasm may be dynamic,and can involve both large and small coronary arteries,sometimes multiple. This may explain acute myocardialinfarction without a definite 100% stenosis seen.The recently reported CASPAR study by Ong et al. took alarge series of patients presenting with chest pain progressingto coronary angiography. 28% (138 of 488) had no demon-strable culprit lesion, and of these 86% underwent acetyl-choline provocation testing. 49% (n= 42) demonstratedevidence of significant coronary spasm defined as a reductionin vessel calibre of at least 75% [1].Animal models have demonstrated upregulation ofcoronary artery Rho-Kinase (ROCK) activity, resultingin increased myosin light chain phosphorylation (viamyosin light chain phosphatase inhibition). An abnormalvasoconstrictor response to acetylcholine is seen. This formsthe basis of the ergonovine provocation test used to assesspropensity to vasospasm in those with chest pain and nonflow limiting disease at angiography.Table 1: Associations of coronary artery vasospasm.SmokingThyroid dysfunctionRaynaud’s phenomenonSclerodermaCold exposureMigraine (conflicting evidence)Drugs CocaineEthanolAmphetaminesCalcium channel blockers(withdrawal)CapecitabineMartı́nez-Sellés et al. demonstrated ergonovine inducedspasm in 20% of 346 patients who had presented withchest pain and normal coronary arteries, and that induciblevasospasm was a positive predictor for future presentationwith vasospasm. However the same authors also foundthat the baseline ECG and any ECG changes seen did notcorrelate with the presence of vasospasm. Hattori et al. alsodescribe cases of an ergonovine provocation test producingvasospasm, and subsequent delivery of GTN failing to reverseor possibly even exacerbating this [2–6].Intense vasospasm is seen in AMI following cocaineuse (and certain amphetamine like compounds such asCatha edulis—khat), capecitabine administration, ethanolintoxication and following abrupt withdrawal of calciumchannel blocking drugs. The alpha-adrenoceptor agonisteffects of cocaine were thought to be the primary mechanismfor cocaine induced coronary spasm, although it seemslikely that this occurs in individuals predisposed to coronaryspasm. There are case reports of pseudoephedrine inducedacute myocardial infarction with normal coronary arteriesin those using the drug for viral upper respiratory tractinfections [5, 7–9] (see Table 1).The anti-migraine triptan drugs are contra-indicated inthose with known atherosclerotic coronary artery disease,and are though to induce vasoconstriction. However a recentstudy to quantify this showed only a modest vasoconstrictiveeffect of up to 6.8% of coronary artery diameter with twodifferent triptan drugs in those with stable angina [10].Unsurprisingly, associations have been made betweenRaynaud’s disease, or limited systemic sclerosis (sclero-derma) and coronary artery spasm, as well as one studyfinding an increased prevalence of migraine in those withcoronary vasospasm (but not an increased prevalence ofRaynaud’s). As such, in one case report, iloprost was usedas therapy and appeared to reverse the coronary spasm. Inanother, an emotional upset was thought to have triggeredthe event in a patient with CREST and acquired protein Sdeficiency. One small study of patients with documentedcoronary artery spasm demonstrated reproducible myocar-dial perfusion defects when the patients were exposed tothe cold. Control subjects with atherosclerosis did not. Thedefects were reversed on rewarming [11–13].Case Reports in Medicine 3IIIIIIIIaVRaVLaVFV1V2V3V4V5V6Measurement results:QRS: 86 msQT/QTcB: 394/451 msPR: 180 msP: 120 msPR/PP: 784/755 msP/QRS/T: 58/33/57 degreesInterpretation:Unconfirmed report.−90aVR aVL0 IIIIII+90aVF< P< T< QRSFigure 3: ECG immediately post angiography and IC GTN.Post GTN-LAO caudal Figure 4Other associations with coronary artery spasm are hyper-thyroidism (classically described in young Asian women andresolving on establishing euthyroidism). There are also a twocase reports of hypothyroidism associated with Raynaud’sphenomenon and coronary artery spasm [14–18].In the acute setting, nitrates are the preferred treatmentfor coronary spasm, although efficacy is variable. Rarelyother interventions are required in the context of spasmcausing myocardial infarction.Maintenance therapy is based on nitrates and calciumchannel blockers. Ninomiya et al. demonstrated in a smallstudy of patients on either long term long acting nitrates orcalcium channel blocker with anginal symptoms and normalor near normal coronary arteries and segments displayinga vasoconstrictive response to acetylcholine that the degreeof flow restriction when challenged with acetylcholine wasgreater in the nitrate group than the calcium channel blockergroup. The conclusions were that treatment with calciumchannel blockers may be more effective than nitrates in thelong term. Beta blockers should be avoided, as there is a riskof precipitating spasm with these [19].Learning Points. (i) Coronary artery spasm well is a docu-mented cause of chest pain and presentation as acute coro-nary syndrome. (ii) Coronary arteriography may demon-strate normal arteries or disease at a level inconsistentwith symptoms. The stenosis may be dynamic, involvinglarge or small and often multiple coronary arteries. (iii)It can cause acute myocardial infarction, including suddendeath. (iv) Treatment acutely is with nitrate. (v) Treatmentacutely is with nitrate. (vi) It is most commonly seenin Asian populations, young women and smokers. (vii)Other associations include drugs, thyroid dysfunction, andscleroderma. The underlying pathophysiology is unclear butthought to be EDRF related. (ix) Maintenance treatmentis with calcium channelblocking drugs or nitrates. Betablockers are best avoided.References[1] P. Ong, A. Athanasiadis, S. Hill, H. Vogelsberg, M. Voehringer,and U. Sechtem, “Coronary artery pasm as a frequent causeof acute coronary syndrome: the CASPAR (Coronary ArterySpasm in Patients with Acute Coronary Syndrome) Study,”Journal of the American College of Cardiology, vol. 52, no. 7,pp. 528–530, 2008.4 Case Reports in Medicine[2] J. Sztajzel, F. Mach, and A. Righetti, “Role of the vascularendothelium in patients with angina pectoris or acute myocar-dial infarction with normal coronary arteries,” PostgraduateMedical Journal, vol. 76, no. 891, pp. 16–21, 2000.[3] M. Martı́nez-Sellés, T. Datino, A. M. Pello, and F. F. Avilés,“Predictors of coronary spasm in patientswith chest painand no significant coronary stenosis,” International Journal ofCardiology. In press.[4] R. Hattori, Y. Takatsu, Y. Yui, H. Nonogi, and C. Kawai,“Unusual vasomotor coronary arterial responses after reversalof ergonovine induced spasm with glyceryl trinitrate,” BritishHeart Journal, vol. 51, no. 3, pp. 312–315, 1984.[5] H. Yasue, H. Nakagawa, T. Itoh, E. Harada, and Y. Mizuno,“Coronary artery spasm—clinical features, diagnosis, patho-genesis, and treatment,” Journal of Cardiology, vol. 51, no. 1,pp. 2–17, 2008.[6] K. Miwa, M. Fujita, and S. Sasayama, “Recent insights intothe mechanisms, predisposing factors, and racial differencesof coronary vasospasm,” Heart and Vessels, vol. 20, no. 1, pp.1–7, 2005.[7] P. A. Scott, L. Ferchow, A. Hobson, and N. P. Curzen, “Coro-nary spasm induced by capecitabine mimicks ST elevationmyocardial infarction,” Emergency Medicine Journal, vol. 25,no. 10, pp. 699–700, 2008.[8] M. Al-Habori, “The potential adverse effects of habitual use ofCatha edulis (khat),” Expert Opinion on Drug Safety, vol. 4, no.6, pp. 1145–1154, 2005.[9] S. Akay and M. Ozdemir, “Acute coronary syndrome pre-senting after pseudoephedrine use and regression with beta-blocker therapy,” Canadian Journal of Cardiology, vol. 24, no.11, pp. e86–e88, 2008.[10] C. M. H. Newman, I. Starkey, N. Buller, et al., “Effects ofsumatriptan and eletriptan on diseased epicardial coronaryarteries,” European Journal of Clinical Pharmacology, vol. 61,no. 10, pp. 733–742, 2005.[11] K. A. Kovacs, G. W. Burggraf, and C. L. Dewar, “Reversiblecardiogenic shock in an angry woman—case report andreview of the literature,” Canadian Journal of Cardiology, vol.12, no. 7, pp. 689–693, 1996.[12] Y. Nakamura, N. Shinozaki, M. Hirasawa, et al., “Prevalenceof migraine and Raynaud’s phenomenon in Japanese patientswith vasospastic angina,” Japanese Circulation Journal, vol. 64,no. 4, pp. 239–242, 2000.[13] T. Stefenelli, H. Sochor, B. Slama, J. Czernin, O. Pachinger,and P. Probst, “Transient myocardial perfusion abnormalitiesduring cold provocation test in patients with arterial hyper-reactivity,” Zeitschrift für Kardiologie, vol. 80, no. 10, pp. 622–626, 1991.[14] R. Patel, G. Peterson, A. Rohatgi, et al., “Hyperthyroidism-associated coronary vasospasm with myocardial infarctionand subsequent euthyroid angina,” Thyroid, vol. 18, no. 2, pp.273–276, 2008.[15] S. M. Lee, T. S. Jung, J. R. Hahm, et al., “Thyrotoxicosis withcoronary spasm that required coronary artery bypass surgery,”Internal Medicine, vol. 46, no. 23, pp. 1915–1918, 2007.[16] Y. H. Choi, J. H. Chung, S. W. Bae, et al., “Severe coronaryartery spasm can be associated with hyperthyroidism,” Coro-nary Artery Disease, vol. 16, no. 3, pp. 135–139, 2005.[17] R. Sipilä, K. Viitasalo, and J. Heikkilä, “Hypothyroidism,Raynaud’s phenomenon, and acute myocardial infarction in ayoung woman,” Clinical Cardiology, vol. 6, no. 6, pp. 304–306,1983.[18] C. Tschöpe, D. Westermann, P. Steendijk, et al., “Coronaryvasospasm-induced acute diastolic dysfunction in a patientwith Raynaud’s phenomenon,” Clinical Research in Cardiology,vol. 95, no. 6, pp. 344–348, 2006.[19] Y. Ninomiya, S. Hamasaki, K. Saihara, et al., “Comparisonof effect between nitrates and calcium channel antagonist onvascular function in patients with normal or mildly diseasedcoronary arteries,” Heart and Vessels, vol. 23, no. 2, pp. 83–90,2008.

The Vanishing Stenosis: ST Elevation Myocardial Infarction and Rhythm Disturbance due to Coronary Artery Spasm-Case Report and Review of the Literature

Directory of Open Access Journals

Case Reports in Medicine

Acute coronary syndrome presenting after pseudoephedrine use and regression with betablocker therapy,”

C h o i ,J .H .C h u n g ,S .W .B a e ,e ta l . ,“ S e v e r ec o r o n a r y artery spasm can be associated with hyperthyroidism,”

Comparison of eﬀect between nitrates and calcium channel antagonist on vascular function in patients with normal or mildly diseased coronary arteries,” Heart and Vessels,

Coronary artery pasm as a frequent cause of acute coronary syndrome: the CASPAR (Coronary Artery Spasm in Patients with

Coronary artery spasm—clinical features, diagnosis, pathogenesis, and treatment,”

Coronary vasospasm-induced acute diastolic dysfunction in a patient withRaynaud’sphenomenon,”ClinicalResearchinCardiology,

Eﬀects of sumatriptan and eletriptan on diseased epicardial coronary arteries,”

Hyperthyroidismassociated coronary vasospasm with myocardial infarction and subsequent euthyroid angina,”

ınez-Sell´ e s ,T .D a t i n o ,A .M .P e l l o ,a n dF .F .A v i l ´ es, “Predictors of coronary spasm in patientswith chest pain and no signiﬁcant coronary stenosis,” International Journal of Cardiology.

l - H a b o ri ,“T h ep o t e n t i a la d v e r s ee ﬀects of habitual use of Catha edulis (khat),”

Prevalence of migraine and Raynaud’s phenomenon in Japanese patients with vasospastic angina,”

Raynaud’s phenomenon, and acute myocardial infarction in a young woman,”

Recent insights into the mechanisms, predisposing factors, and racial diﬀerences of coronary vasospasm,”

Reversible cardiogenic shock in an angry woman—case report and review of the literature,”

Role of the vascular endotheliuminpatientswithanginapectorisoracutemyocardial infarction with normal coronary arteries,”

S c o t t ,L .F e r c h o w ,A .H o b s o n ,a n dN .P .C u r z e n ,“ C o r o -nary spasm induced by capecitabine mimicks ST elevation myocardial infarction,”

Thyrotoxicosis with coronary spasm that required coronary artery bypass surgery,”

Transient myocardial perfusion abnormalities during cold provocation test in patients with arterial hyperreactivity,”

Unusual vasomotor coronary arterial responses after reversal of ergonovine induced spasm with glyceryl trinitrate,”

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The Vanishing Stenosis: ST Elevation Myocardial Infarction and Rhythm Disturbance due to Coronary Artery Spasm-Case Report and Review of the Literature

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