Printer Friendly

Bridge over troubled coronary artery/ muscular bridge causing non-ST-segment elevation myocardial infarction/Tehlikedeki koroner arterin koprusu/ST-elevasyonsuz miyokard infarktusune neden olan miyokardiyal kopruleme.

Dear Editor,

Myocardial bridging is a congenital condition, defined as the intramyocardial course of a portion of the coronary artery. It was first described by Reyman in 1737 (1) and the artery coursing within the myocardium is called the "tunneled artery" (2). The left anterior descending is the most common artery affected. The coronary arteries are not necessarily epicardial in all the mammals. For example the rodents do have intramyocardial vessels and the chimpanzees have intramural coronary arteries (2).

The significance of the presence of the bridging is also controversial. There is a significant discrepancy between the autopsy series and angiographic series in terms of the incidence of myocardial bridging. Some autopsy series have reported the incidence to be as high as 85%, whereas the angiographic incidence remains only in the 1.5% to 16% range (3, 4). Some have advocated that, by careful review of the coronary angiograms, for the specific purpose of identifying the muscle bridge, there would be a higher incidence of myocardial bridging (5). Nevertheless, the true significance of the myocardial bridging is debatable since only 15% of the coronary blood flow occurs during systole. There are numerous reports of patients with myocardial bridges with unstable angina (6), myocardial infarction (7-9), dysrhythmias (10, 11) and sudden death (12, 13) but in general this abnormality is considered to be clinically harmless.

Intravascular ultrasound (IVUS) and Doppler evaluation of the myocardial bridges have provided valuable insight to the problem. Ge et al. described the highly specific echolucent half moon phenomenon over the bridge segment that existed throughout the cardiac cycle (3). Ge et al. also showed a high incidence of atherosclerotic plaque proximal to the area of the muscle bridge (3). Thus, the hemodynamic impairment of the coronary blood flow by the bridging can be accentuated by the formation of atherosclerosis at the proximal segment of the artery and may explain some of the presentations of angina, dysrhythmias and myocardial infarction. When intracoronary Doppler was used, the characteristic early diastolic fingertip phenomenon was observed (3). This fingertip phenomenon represents a sudden increase in the blood flow velocity due to an increase in the blood flow with early diastole due to the relaxation of myocardial tension and microcirculation but persistent decrease in the vessel diameter. Both the Doppler findings and the systolic compression of the coronary artery can be accentuated by the use of nitroglycerine (14) and rapid pacing (15). This has important implications for the treatment of myocardial bridging. Beta-blockers are the mainstay of treatment and avoidance of nitrates might be necessary.

In the December issue of your Journal Aytan et al. (16) describe a patient with a myocardial bridging of the left anterior descending artery presenting with a non ST segment elevation myocardial infarction. Since this patient had already had a coronary angiogram 4 years before the presentation and no report of a bridge was given, one possibility is that the use of antianginal agents presumably including nitroglycerine might have contributed to the augmentation of the angiographic appearance of the bridging. The other mechanism would be the formation of thrombus proximal to the area of bridging. Whatever the mechanism was in this patient it would have been interesting to have a follow-up SPECT imaging to see if the anterior ischemia reported in the previous study had resolved.

Myocardial bridging of the coronary arteries, although mostly asymptomatic, might not be so innocent after all. Coronary angiograms should be carefully scrutinized to identify this abnormality.

Ali E. Denktas

University of Texas at Houston

MSB 1.246, 6431 Fannin

Houston, TX 77030, USA

References

(1.) Reyman H. Dissertatis de vasis cordis propriis. Bibl Anat 1737; 2: 359-79.

(2.) Mohlenkamp S, Hort W, Ge J, Erbel R. Update on myocardial bridging. Circulation 2002; 106: 2616-22.

(3.) Ge J, Jeremias A, Rupp A, Abels M, Baumgart D, Liu F, et al. New signs characteristic of myocardial bridging demonstrated by intracoronary ultrasound and Doppler. Eur Heart J 1999; 20: 1707-16.

(4.) Alegria JR, Herrmann J, Holmes DR, Jr, Lerman A, Rihal CS. Myocardial bridging. Eur Heart J 2005; 26: 1159-68.

(5.) Irvin RG. The angiographic prevalence of myocardial bridging in man. Chest 1982; 81: 198-202.

(6.) Bestetti RB, Finzi LA, Amaral FT, Secches AL, Oliveira JS. Myocardial bridging of coronary arteries associated with an impending acute myocardial infarction. Clin Cardiol 1987; 10: 129-31.

(7.) Vasan RS, Bahl VK, Rajani M. Myocardial infarction associated with a myocardial bridge. Int J Cardiol 1989; 25: 240-1.

(8.) Tauth J, Sullebarger T. Myocardial infarction associated with myocardial bridging: case history and review of the literature. Cathet Cardiovasc Diagn 1997; 40: 364-7.

(9.) Smith SC, Taber MT, Robiolio PA, Lasala JM. Acute myocardial infarction caused by a myocardial bridge treated with intracoronary stenting. Cathet Cardiovasc Diagn 1997; 42: 209-12.

(10). den Dulk K, Brugada P, Braat S, Heddle B, Wellens HJ. Myocardial bridging as a cause of paroxysmal atrioventricular block. J Am Coll Cardiol 1983; 1: 965-9.

(11.) Kracoff OH, Ovsyshcher I, Gueron M. Malignant course of a benign anomaly: myocardial bridging. Chest 1987; 92: 1113-5.

(12.) Morales AR, Romanelli R, Boucek RJ. The mural left anterior descending coronary artery, strenuous exercise and sudden death. Circulation 1980; 62: 230-7.

(13.) Desseigne P, Tabib A, Loire R. [Myocardial bridging on the left anterior descending coronary artery and sudden death. Apropos of 19 cases with autopsy]. Arch Mal Coeur Vaiss 1991; 84: 511-6.

(14.) Ishimori T, Raizner AE, Chahine RA, Awdeh M, Luchi RJ. Myocardial bridges in man: clinical correlations and angiographic accentuation with nitroglycerin. Cathet Cardiovasc Diagn 1977; 3: 59-65.

(15.) Schwarz ER, Klues HG, vom Dahl J, Klein I, Krebs W, Hanrath P. Functional characteristics of myocardial bridging. A combined angiographic and intracoronary Doppler flow study. Eur Heart J 1997; 18: 434-42.

(16.) Aytan P, Ulusal G, Yenigun EC, Yildirim O, Pirpir A, Yildirim S. Muscular bridge causing non-ST-segment elevation myocardial infarction. Anadolu Kardiyol Derg 2006; 6: 374-5.

Author's reply

Dear Editor,

We appreciate the comments of our colleague regarding our report, as well as the additional data that had been provided. The possible mechanisms for the detection failure of the myocardial bridging by angiography that had been done 4 years ago were very well outlined in the letter; use of antianginal agents presumably including nitroglycerine might contribute in augmenting the angiographic appearance of the bridging and secondly the formation of thrombus may be proximal to the area of bridging. The first angiography was done in another center and the patient had not been followed up. As a result we could not have any idea of why in the first angiography no report of a bridge was given. With his admission to the emergency department of our center antianginal therapy was started. At the 3rd day of the onset of angina cardiac catheterization was performed. Coronary angiography revealed suspicion of thrombosis and 95% luminal narrowing by systolic compression in the mid segment of the left anterior descending coronary artery at left anterior oblique cranial position. The gold standard diagnostic tool for diagnosing myocardial bridge is selective coronary artery angiography. But the new imaging techniques like intravascular ultrasound, intracoronary Doppler ultrasound, and intracoronary pressure devices as invasive techniques (1, 2) and electron beam tomography, multislice computed tomography, magnetic resonance tomography, or transthoracic Doppler echocardiography as noninvasive imaging techniques (3) can be used for diagnosis of functional and morphological status of bridges.

Single photon emission computed tomography (SPECT) has been proposed for further investigation in such cases (4) and at the 7th day of the onset of symptoms a SPECT was performed. Moderately extended, mildly severe (+1) reversible ischemic defect was reported.

It is prudent to follow these patients with a SPECT imaging as it has been suggested by our colleague. It was planned to follow-up the patient with another SPECT imaging during his follow-ups to see if the anterior ischemia had resolved; however, the patient did not come to his follow-up examination.

Pelin Aytan, * Ozgur Yildirim, I. Safa Yildirim The 3rd Internal Medicine Clinic Ministry of Social Insurance Yildirim Beyazit Educational and Research Hospital, Ankara, Turkey * Clinic of Cardiovascular Surgery, Kosuyolu Heart Education and Research Hospital, Istanbul, Turkey

References

(1.) Ge J, Jeremias A, Rupp A, Abels M, Baumgart D, Liu F, et al. New signs characteristic of myocardial bridging demonstrated by intracoronary ultrasound and Doppler. Eur Heart J 1999; 20: 1707-16.

(2.) Bourassa MG, Butnaru A, Lesperance J, Tardif JC. Symptomatic myocardial bridges: overview of ischemic mechanisms and current diagnostic and treatment strategies. J Am Coll Cardiol 2003; 41: 351-9.

(3.) Mohlenkamp S, Hort W, Ge J, Erbel R. Update on myocardial bridging. Circulation 2002;106: 2616-22.

(4.) Huang WS, Chang HD, Yang SP, Tsao TP, Cheng CY, Cherng SC. Abnormal 201 TI myocardial single photon emission computed tomography in energetic male patients with myocardial bridge. Nucl Med Commun 2002; 23:1123-8.

Address for Correspondence: Ali E. Denktas, FACC, FSCAI, Assistant Professor of Medicine University of Texas at Houston SB 1.246, 6431 Fannin, Houston, TX 77030 Telephone: +1 (713) 500-6590, Fax: +1 (713) 500-6556 E-mail: Ali.E.Denktas@uth.tmc.edu
COPYRIGHT 2007 Galenos Yayincilik
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2007 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Author:Denktas, Ali E.; Aytan, Pelin
Publication:The Anatolian Journal of Cardiology (Anadolu Kardiyoloji Dergisi)
Article Type:Letter to the editor
Date:Mar 1, 2007
Words:1504
Previous Article:Coronary rupture to the right ventricle during PTCA for myocardial bridge/"Miyokardiyal Bridge" tedavisinde uygulanan PTKA sirasinda koroner arterin...
Next Article:Today and tomorrow of the Anadolu Kardiyoloji Dergisi/Anadolu Kardiyoloji Dergisi'nin bugunu ve yarini.


Related Articles
Koroner arter cerrahisinde insulin ve koroner sinus laktat seviyeleri/Coronary sinus lactate levels and insulin in coronary artery bypass surgery.
No-reflow'a guncel yaklasim/Current management of no-reflow.
Muscular bridge causing non- ST-segment elevation myocardial infarction/ST-elevasyonsuz miyokard infarktusune neden olan miyokardiyal kopruleme.
Myocardial bridge: a bridge to atherosclerosis/Miyokardiyal kopruleme: Ateroskleroza kopru.
Pre-hospital thrombolytic therapy/Hastane oncesi trombolitik tedavi.
Spontaneous coronary artery dissection / Spontan koroner arter disseksiyonu.
Role of leucocytes in microvascular malperfusion in reperfused acute myocardial infarction/Reperfuze akut miyokard infarktusunde mikrovaskuler...

Terms of use | Privacy policy | Copyright © 2019 Farlex, Inc. | Feedback | For webmasters