Exercise-Induced Spastic Coronary Artery Occlusion at the Site of a Moderate Stenosis
2010; Lippincott Williams & Wilkins; Volume: 122; Issue: 23 Linguagem: Inglês
10.1161/circulationaha.110.984823
ISSN1524-4539
AutoresAli Yılmaz, Stephan Hill, Tim Schäufele, Matthias Vöhringer, Angela Geissler, Udo Sechtem,
Tópico(s)Coronary Artery Anomalies
ResumoHomeCirculationVol. 122, No. 23Exercise-Induced Spastic Coronary Artery Occlusion at the Site of a Moderate Stenosis Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialFree AccessResearch ArticlePDF/EPUBExercise-Induced Spastic Coronary Artery Occlusion at the Site of a Moderate StenosisNeither Prinzmetal's Angina nor Cardiac Syndrome X but "Prinzmetal X" Ali Yilmaz, MD, Stephan Hill, MD, Tim Schäufele, MD, Matthias Vöhringer, MD, Angela Geissler, MD and Udo Sechtem, MD Ali YilmazAli Yilmaz From the Division of Cardiology (A.Y., S.H., T.S., M.V., U.S.) and Division of Radiology (A.G.), Robert Bosch Krankenhaus, Stuttgart, Germany. , Stephan HillStephan Hill From the Division of Cardiology (A.Y., S.H., T.S., M.V., U.S.) and Division of Radiology (A.G.), Robert Bosch Krankenhaus, Stuttgart, Germany. , Tim SchäufeleTim Schäufele From the Division of Cardiology (A.Y., S.H., T.S., M.V., U.S.) and Division of Radiology (A.G.), Robert Bosch Krankenhaus, Stuttgart, Germany. , Matthias VöhringerMatthias Vöhringer From the Division of Cardiology (A.Y., S.H., T.S., M.V., U.S.) and Division of Radiology (A.G.), Robert Bosch Krankenhaus, Stuttgart, Germany. , Angela GeisslerAngela Geissler From the Division of Cardiology (A.Y., S.H., T.S., M.V., U.S.) and Division of Radiology (A.G.), Robert Bosch Krankenhaus, Stuttgart, Germany. and Udo SechtemUdo Sechtem From the Division of Cardiology (A.Y., S.H., T.S., M.V., U.S.) and Division of Radiology (A.G.), Robert Bosch Krankenhaus, Stuttgart, Germany. Originally published7 Dec 2010https://doi.org/10.1161/CIRCULATIONAHA.110.984823Circulation. 2010;122:e570–e574A 44-year-old man was referred to our hospital to undergo coronary angiography because of suspected coronary artery disease. For approximately 2 weeks, the patient had been experiencing typical symptoms of angina pectoris that occurred exclusively during physical exercise and predominantly in the morning hours when he bicycled to work. His general practitioner had performed a bicycle exercise test. In his written report, the practitioner noted that he suspected hemodynamically significant coronary artery disease because of reproduction of typical angina pectoris in addition to ischemic ECG changes.On admission, the patient was in good general condition with no symptoms at rest. Coronary angiography revealed an ≈80% stenosis in the small right coronary artery and an ≈50% stenosis in the proximal segment of the left anterior descending artery (LAD), although systolic left ventricular function was normal (Figure 1). Fractional flow measurements (fractional flow reserve) were performed in the right coronary artery and the LAD and revealed a significantly impaired fractional flow reserve only in the right coronary artery (fractional flow reserve 70%) and not in the LAD (fractional flow reserve 85%). Thus, the right coronary artery stenosis was treated with a drug-eluting stent (Figure 1), and the patient was discharged on medical therapy.Download figureDownload PowerPointFigure 1. Coronary angiograms of the left coronary artery (LCA) and right coronary artery (RCA) at first presentation. A stenosis of ≈50% was observed in the proximal segment of the LAD (left; black arrow), and an ≈80% stenosis was observed in the RCA (middle; black arrow). The stenosis of the RCA was stented successfully with a drug-eluting stent (right; black arrow). PCI indicates percutaneous coronary intervention.Six weeks later, the patient was referred again to our department because of unchanged symptoms of exercise-induced typical angina pectoris. Again, his general practitioner had performed a bicycle exercise test and observed ischemic ECG changes accompanied by typical angina pectoris. Coronary angiography was repeated and revealed only minor lumen irregularities in the right coronary artery and an unchanged ≈50% stenosis in the proximal LAD (Figure 2). Because only stress echocardiography has a satisfactory diagnostic specificity for the detection of significant epicardial coronary artery disease in patients with potential microvascular disease,1 we decided to perform stress echocardiography the next day.Download figureDownload PowerPointFigure 2. Coronary angiograms of the left coronary artery (LCA) and right coronary artery (RCA) at second presentation. An unchanged ≈50% stenosis was observed in the proximal LAD (left; black arrow), and only minor lumen irregularities were observed in the RCA (right; black arrow).At the beginning of stress echocardiography (with bicycle exercise), the patient was free of any symptoms, and echocardiography demonstrated normal wall motion. At 50-W stress exposure, he began feeling some angina. Concurrently, his ECG demonstrated subtle ST-segment changes, whereas echocardiography revealed hypokinesis in the anteroseptal wall. At 75-W stress exposure, his symptoms and ECG changes increased rapidly and severely, and echocardiography demonstrated akinesis of the anteroseptal wall. Further aggravation of angina and ECG changes at 100 W of stress exposure forced us to stop the test. After stopping exercise, the patient recovered spontaneously and quickly, his ECG changes disappeared, and wall motion in the anteroseptal segments normalized (Figures 3A through 3D; full-motion Movies 1A through 1D in the online-only Data Supplement). Taken together, these findings were suggestive of exercise-induced transmural ischemia in the anteroseptal wall with reciprocal ST-segment depressions in the inferolateral leads. To identify the cause of this unusual presentation, it was decided to take the patient once more to the catheterization laboratory and perform a coronary vasomotion test with intracoronary acetylcholine provocation.Download figureDownload PowerPointFigure 3. First stress echocardiography (bicycle exercise) with respective ECG recordings. At rest, the ECG was normal, and echocardiography demonstrated normal wall motion (A). At 50 W of stress exposure, minor ECG changes were observed (subtle ST-segment elevation in leads V1 through V2 and ST-segment depression in leads II, III, and aVF), whereas echocardiography revealed hypokinesis in the anteroseptal wall (B, gray arrow). At 100 W of stress exposure, ECG changes increased, and echocardiography demonstrated akinesis of the anteroseptal wall (C, gray arrow). After exercise was stopped, the ECG changes disappeared, and wall motion in the anteroseptal segments normalized (D).In the first angiogram of the left coronary artery, the proximal LAD stenosis appeared more narrowed (≈75%;Figure 4A) than in the prior angiograms. Even at the smallest dose of 2 μg of acetylcholine infused into the left coronary artery, severe vasoconstriction occurred at the site of the LAD stenosis, with impaired coronary blood flow distal to this stenosis (Figure 4B). Minor ECG changes were observed; however, the patient was still asymptomatic. At the next dose of 20 μg of acetylcholine, the LAD occluded completely at the site of the former stenosis (Figure 4C). At this time, severe ECG changes occurred, and the patient began to experience his usual angina pain. Therefore, 0.4 mg of nitroglycerin was injected into the left coronary artery, and after 2 minutes, the LAD occlusion disappeared, and the LAD stenosis was unmasked with only ≈50% remaining luminal occlusion (Figure 4D).Download figureDownload PowerPointFigure 4. Angiograms and respective ECG recordings during coronary vasomotion testing with intracoronary acetylcholine (ACH) provocation. At baseline, the proximal LAD stenosis appeared more narrowed (≈75%, white arrow; A). After infusion of 2 μg of acetylcholine, severe vasoconstriction occurred at the site of the LAD stenosis (B, white arrow), although only minor ECG changes were observed. After infusion of 20 μg of acetylcholine, the LAD occluded completely at the site of the former stenosis (C, white arrow), whereas severe ECG changes (ST-segment elevation in leads V1 through V4 and ST-segment depression in leads II, III, and aVF) occurred. After infusion of 0.4 mg of nitroglycerin, the LAD occlusion disappeared, and the LAD stenosis was unmasked with only ≈50% luminal occlusion (D, white arrow).A coronary computed tomography study revealed a focal atheromatous plaque at the site of the LAD stenosis (Figure 5). Consequently, a diagnosis of exercise-induced spastic LAD occlusion at the site of an atheromatous plaque was made. The implantation of another stent at the site of this moderate LAD stenosis was weighed against an antispastic medical treatment with a calcium antagonist. It was decided to start an antispastic treatment with diltiazem 120 mg twice daily and to continue monitoring the patient as an inpatient.Download figureDownload PowerPointFigure 5. Coronary computed tomography angiography was performed with a dual-source computed tomography system (Definition Flash, Siemens Healthcare, 2×128 slices, spiral acquisition, effective dose ≤1 mSv). Curved multiplanar reconstruction of the LAD demonstrated a focal atheromatous plaque at the site of the LAD stenosis (left; white arrow), whereas curved multiplanar reconstruction of the right coronary artery (RCA) demonstrated the RCA stent.Two days after medical treatment with diltiazem was started, stress echocardiography was repeated. At this time, workload could be increased stepwise up to 175 W, and the bicycle test only had to be terminated because lower-extremity muscle exhaustion occurred. The patient did not feel any chest discomfort throughout the test, and echocardiography demonstrated normal wall-motion behavior during all levels of stress exposure (Figures 6A through 6D; full-motion Movies 2A through 2D in the online-only Data Supplement). Thus, successful treatment of the exercise-induced spastic LAD occlusion was achieved with medical therapy.Download figureDownload PowerPointFigure 6. Second stress echocardiography (bicycle exercise) with respective ECG recordings after the patient began treatment with diltiazem. Echocardiography demonstrated normal wall-motion behavior during all levels of stress exposure (A–D). The ECG was normal until 100 W of stress exposure, and minor asymptomatic ST-segment depressions were observed in leads II, III, aVF, and V3 through V5 after 125 W (C) that disappeared after exercise was stopped.Our results suggest that (1) the coronary wall at the site of an atheromatous plaque is not simply fixed and immobile but may even be hyperdynamic and cause spastic coronary occlusion in response to exercise; (2) assessment of luminal diameters only or performance of fractional flow reserve measurements (without physical exercise) does not allow the detection of dynamic exercise-induced coronary obstructions; and (3) dramatically improved stress test results may be obtained in such patients within a few days as a result of successful medical therapy. Currently used denotations such as Prinzmetal's angina2 or cardiac syndrome X3 do not really cover our observation of a strictly exercise-induced spastic occlusion of the LAD at the site of a moderate stenosis. Because this case resembles some aspects of Prinzmetal's angina and other aspects of cardiac syndrome X, we suggest calling such a pathophysiology "Prinzmetal X."DisclosuresNone.FootnotesThe online-only Data Supplement is available with this article at http://circ.ahajournals.org/cgi/content/full/122/23/e570/DC1.Correspondence to Ali Yilmaz, MD, Robert Bosch Krankenhaus, Division of Cardiology, Auerbachstrasse 110, 70376 Stuttgart, Germany. E-mail ali.[email protected]deReferences1. Fragasso G, Lu C, Dabrowski P, Pagnotta P, Sheiban I, Chierchia SL. Comparison of stress/rest myocardial perfusion tomography, dipyridamole and dobutamine stress echocardiography for the detection of coronary disease in hypertensive patients with chest pain and positive exercise test. J Am Coll Cardiol. 1999; 34:441–447.CrossrefMedlineGoogle Scholar2. Prinzmetal M, Kennamer R, Merliss R, Wada T, Bor N. Angina pectoris, I: a variant form of angina pectoris: preliminary report. Am J Med. 1959; 27:375–388.CrossrefMedlineGoogle Scholar3. Cannon RO. Microvascular angina and the continuing dilemma of chest pain with normal coronary angiograms. J Am Coll Cardiol. 2009; 54:877–885.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Sechtem U, Seitz A, Ong P and Bekeredjian R (2022) Management des chronischen KoronarsyndromsManagement of chronic coronary syndrome, Herz, 10.1007/s00059-022-05137-3, 47:5, (472-482), Online publication date: 1-Oct-2022. Seitz A, Martínez Pereyra V, Sechtem U and Ong P (2022) Update on coronary artery spasm 2022 – A narrative review, International Journal of Cardiology, 10.1016/j.ijcard.2022.04.011, 359, (1-6), Online publication date: 1-Jul-2022. 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December 7, 2010Vol 122, Issue 23 Advertisement Article InformationMetrics © 2010 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.110.984823PMID: 21135367 Originally publishedDecember 7, 2010 PDF download Advertisement SubjectsContractile FunctionEchocardiographyEndothelium/Vascular Type/Nitric OxideImagingPathophysiologyRehabilitation
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