All Title Author
Keywords Abstract

Publish in OALib Journal
ISSN: 2333-9721
APC: Only $99


Relative Articles


Nitroglycerine Induced Acute Myocardial Infarction in a Patient with Myocardial Bridging

DOI: 10.1155/2014/289879

Full-Text   Cite this paper   Add to My Lib


Muscle overlying an intramyocardial segment of a coronary artery is termed a myocardial bridge. The intramyocardial segment, the tunneled artery, is compressed during systole. The condition is generally benign but may occasionally cause myocardial ischemia, infarction, arrhythmia, or sudden cardiac death. We present a case regarding a 52-year-old man with exercise-induced angina who was diagnosed with a myocardial bridge overlying the left anterior descending artery. He was initially treated with beta-blockers and later received coronary bypass graft surgery. 1. Introduction The major coronary arteries are normally distributed epicardially, that is, on the surface of the myocardium. Occasionally, these vessels have a segmental intramyocardial course. During systole, this segment is compressed either partially or completely. Muscle overlying the intramyocardial segment is called a myocardial bridge, and the artery coursing within the myocardium is termed a tunneled artery [1–3]. 2. Case Presentation A 52-year-old man with a long-standing history of smoking and a positive family history of coronary artery disease (CAD) had undergone multiple admissions and investigations in several different hospitals during the last 13 years due to exercise-induced chest pain, shortness of breath, and palpitations. The electrocardiogram (ECG) showed sinus rhythm with complete right bundle branch block. The concentration of the myocardial tissue-specific biomarker, troponin T, was within the reference range during each hospitalization. A 7-day Holter-monitor recording and an exercise stress test also showed normal results. A transthoracic echocardiogram showed a slightly increased tricuspid regurgitation jet peak gradient (38?mmHg), and a subsequent computed tomography (CT) of the heart revealed dilatation of the right-sided chambers with a sinus venosus-type atrial septal defect (ASD) with partial anomalous pulmonary venous return (abnormal return of the right upper pulmonary vein into sinus venosus) and poor contrast enhancement of the left anterior descending artery (LAD), but no coronary artery calcification. The anomalous anatomical findings were confirmed by transesophageal echocardiography. To further examine the coronary anatomy, the patient underwent invasive coronary angiography, revealing a myocardial bridge confined to the LAD with mild systolic compression (Figure 1), which worsened during intravenous administration of nitroglycerin (Figure 2). During the angiography, he developed mild chest pain, which continued thereafter in the ward. Despite the


[1]  S. M?hlenkamp, W. Hort, J. Ge, and R. Erbel, “Update on myocardial bridging,” Circulation, vol. 106, no. 20, pp. 2616–2622, 2002.
[2]  J. R. Alegria, J. Herrmann, D. R. Holmes Jr., A. Lerman, and C. S. Rihal, “Myocardial bridging,” European Heart Journal, vol. 26, no. 12, pp. 1159–1168, 2005.
[3]  R. Nakanishi, R. Rajani, Y. Ishikawa, T. Ishii, and D. S. Berman, “Myocardial bridging on coronary cta: an innocent bystander or a culprit in myocardial infarction?” Journal of Cardiovascular Computed Tomography, vol. 6, no. 1, pp. 3–13, 2012.
[4]  T. Ishii, N. Asuwa, S. Masuda, and Y. Ishikawa, “The effects of a myocardial bridge on coronary atherosclerosis and ischaemia,” Journal of Pathology, vol. 185, no. 1, pp. 4–9, 1998.
[5]  T. Masuda, Y. Ishikawa, Y. Akasaka, K. Itoh, H. Kiguchi, and T. Ishii, “The effect of myocardial bridging of the coronary artery on vasoactive agents and atherosclerosis localization,” Journal of Pathology, vol. 193, no. 3, pp. 408–414, 2001.
[6]  J. Ge, A. Jeremias, A. Rupp et al., “New signs characteristic of myocardial bridging demonstrated by intracoronary ultrasound and Doppler,” European Heart Journal, vol. 20, no. 23, pp. 1707–1716, 1999.
[7]  J. Ge, R. Erbel, H. Rupprecht et al., “Comparison of intravascular ultrasound and angiography in the assessment of myocardial bridging,” Circulation, vol. 89, no. 4, pp. 1725–1732, 1994.
[8]  J. Noble, M. G. Bourassa, R. Petitclerc, and I. Dyrda, “Myocardial bridging and milking effect of the left anterior descending coronary artery. Normal variant or obstruction?” American Journal of Cardiology, vol. 37, no. 7, pp. 993–999, 1976.
[9]  T. Ishimori, A. E. Raizner, and R. A. Chahine, “Myocardial bridges in man: clinical correlations and angiographic accentuation with nitroglycerin,” Catheterization and Cardiovascular Diagnosis, vol. 3, no. 1, pp. 59–65, 1977.
[10]  Y. Hongo, H. Tada, K. Ito, Y. Yasumura, K. Miyatake, and M. Yamagishi, “Augmentation of vessel squeezing at coronary-myocardial bridge by nitroglycerin: study by quantitative coronary angiography and intravascular ultrasound,” American Heart Journal, vol. 138, no. 2 I, pp. 345–350, 1999.
[11]  E. R. Schwarz, H. G. Klues, J. Vom Dahl, I. Klein, W. Krebs, and P. Hanrath, “Functional, angiographic and intracoronary Doppler flow characteristics in symptomatic patients with myocardial bridging: effect of short-term intravenous beta-blocker medication,” Journal of the American College of Cardiology, vol. 27, no. 7, pp. 1637–1645, 1996.
[12]  P. K. Haager, E. R. Schwarz, J. Vom Dahl, H. G. Klues, T. Reffelmann, and P. Hanrath, “Long term angiographic and clinical follow up in patients with stent implantation for symptomatic myocardial bridging,” Heart, vol. 84, no. 4, pp. 403–408, 2000.
[13]  K. Tsujita, A. Maehara, G. S. Mintz et al., “Impact of myocardial bridge on clinical outcome after coronary stent placement,” American Journal of Cardiology, vol. 103, no. 10, pp. 1344–1348, 2009.


comments powered by Disqus

Contact Us


WhatsApp +8615387084133

WeChat 1538708413