International Journal of Cardiology 102 (2005) 371 – 373 www.elsevier.com/locate/ijcard
Letter to the Editor
Microvascular angina due to microvascular coronary vasospasm Fernando Sarnago Cebada*, Fernardo Sarnago Bullo´n, Pablo Avanzas, Manuel Abeytua, Miriam Juarez, Toma´s Datino, Jesu´s Almendral Cardiology Department, Gregorio Maran˜o´n Hospital, Madrid, Spain Received 25 May 2004; accepted 7 June 2005 Available online 17 May 2005
Keywords: Angina; Spasm
We read with interest an article from the journal by Masumoto et al. [1] reporting three-year follow-up data of Japanese patients with microvascular angina attributable to coronary microvascular spasm. This time in a Caucasian patient, we report an unusual case of angina pectoris with angiographically normal coronary arteries and positive results (chest pain and typical ST-segment shifts) of provocative tests of coronary spasm, in the absence of epicardial coronary vasoconstriction. A 53-year-old white man with a history of asthma and systemic hypertension was admitted to our institution for the assessment of chest pain at rest. He had a longstanding history of chest pain both at rest and on exertion for which he underwent coronary arteriography on two previous occasions (1982 and 1999). On both occasions, his coronary arteriograms were completely normal. His exertional chest pain was typically brought on by moderate or severe effort and relieved by rest, sublingual nitrates or both. His exercise ECG test was positive with chest pain and N1 mm horizontal ST-segment depression. This man’s angina threshold was dramatically impaired 15 days prior to the hospital admission and he had suffered repeated episodes of angina at rest, relieved by sublingual nitrates. Physical examination, a chest X-ray and a transthoracic echocardiogram were all normal. The baseline ECG recorded whilst the patient was asymptomatic showed sinus rhythm and negative T waves in leads III and aVF. During hospital admission, he had several episodes of angina with ST-segment depression in leads V4, V5 and V6. Myocardial perfusion scintigraphy (Fig. 1) showed transient perfusion defects in the lateral and * Corresponding author. Tel.: +34 915868286; fax: +34 915868276. E-mail address:
[email protected] (F. Sarnago Cebada). 0167-5273/$ - see front matter D 2004 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2004.06.003
inferior walls, which were associated with chest pain and transient ST-segment depression. Coronary angiography was repeated, which showed normal arteries. An ergonovine test carried out during cardiac catheterisation was positive, with typical chest pain and ST-segment depression in leads V4, V5 and V6, but no coronary spasm or severe epicardial vasoconstriction was observed (Fig. 2). The patient received treatment with oral nitrates and diltiazem. Theophylline was prescribed together with bronchodilator sprays for management of his bronchial asthma. Symptoms and ECG changes were abolished by the medication and the patient was discharged form hospital on the above mentioned tablets. A repeat dipyridamole myocardial perfusion scintigraphy was carried out 1 week after hospital discharge and showed a mild fixed perfusion defect in the lateral and inferior walls. Patients with angina who have normal coronary angiograms without epicardic coronary vasospasm account for 20–30% of all patients who undergo coronary angiography [2] . Cardiac syndrome X is commonly diagnosed in patients with typical chest pain in the presence of ischaemic ECG changes on exercise stress testing and normal coronary arteriograms. The syndrome is heterogeneous and there is no consensus in the pathogenesis of this cardiovascular disorder. A common and single underlying pathophysiological mechanism has not yet been identified. Mohri et al. [3] suggested microvascular spasm as the cause of angina in this group of patients. Our findings agree with this notion and suggest coronary microvascular spasm as the underlying mechanism responsible for our patient’s symptoms and electrocardiographic changes. Microvascular spasm has been previously reported in oriental population [1,4], but has not been described so far in Caucasians. Presentation of these patients is usually compatible with unstable angina.
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Fig. 1. Pharmacologic myocardial perfusion imaging test showing the existence of a perfusion defect in lateral and inferior walls. The patient had chest pain and the test was electrically positive with ST segment depression in V3, V4, V5 and V6 leads. Left, basal ECG; Middle, ECG while patient suffers chest pain; Right, myocardial perfusion imaging test. STR, stress; RST, rest; ANT, anterior wall; INF, inferior wall; LAT, lateral wall; SEPT: septum.
Patients with chest pain and normal coronary angiograms have a favourable long-term prognosis [5], with an incidence of myocardial infarction and cardiovascular death similar to
the general population [6], although some cases progress to dilated cardiomyopathies, particularly if left bundle branch blocked [7] or raised endothelin-1 levels [8] are present. This
Fig. 2. Intracoronary ergonovine vasospasm test. The test was angiographically negative (middle up) and clinically and electrically positive (middle down left: Basal ECG; middle down right: ECG performed while patient suffers chest pain). Transthoracic echocardiogram performed during the test did not reveal any anomalies in cardiac contractility.
F. Sarnago Cebada et al. / International Journal of Cardiology 102 (2005) 371–373
case has potential clinical implications. Prognosis of patients with epicardic coronary spasm is different compared to patients with microvascular spasm. Both spasm aetiologies have to be considered in the diagnosis of patients with angina and normal coronary angiograms. Ergonovine test conducted with angiography was crucial in the differential diagnosis of this patient’s spasm, a technique not usually performed in patients with angina, but particularly suited to exclude the presence of epicardial spasm.
References [1] Masumoto A, Mohri M, Takeshita A. Three-year follow-up of the Japanese patients with microvascular angina attributable to coronary microvascular spasm. Int J Cardiol 2001;81:151 – 6. [2] Kemp Jr HG. Left ventricular function in patients with the anginal syndrome and normal coronary arteriograms. Am J Cardiol 1973;32: 375 – 376.
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[3] Mohri M, Koyanagi M, Egashira K, et al. Angina pectoris caused by coronary microvascular spasm. Lancet 1998;351:1165 – 9. [4] Sun H, Mohri M, Shimokawa H, Usui M, Urakami L, Takeshita A. Coronary microvascular spasm causes myocardial ischemia in patients with vasospastic angina. J Am Coll Cardiol 2002;39:847 – 51. [5] Bemiller CR, Pepine CJ, Rogers AK. Long-term observations in patients with angina and normal coronary arteriograms. Circulation 1973;47:36 – 43. [6] Kaski JC, Rosano GM, Collins P, Nihoyannopoulos P, Maseri A, PooleWilson PA. Cardiac syndrome X: clinical characteristics and left ventricular function. Long-term follow-up study. J Am Coll Cardiol 1995;25:807 – 14. [7] Opherk D, Schuler G, Wetterauer K, Manthey J, Schwarz F, Kubler W. Four-year follow-up study in patients with angina pectoris and normal coronary arteriograms (bsyndrome XQ). Circulation 1989;80:1610 – 6. [8] Kaski JC, Cox ID, Crook JR, et al. Differential plasma endothelin levels in subgroups of patients with angina and angiographically normal coronary arteries. Coronary Artery Disease Research Group. Am Heart J 1998;136:412 – 7.
