International Journal of Cardiology 115 (2007) e49 – e51 www.elsevier.com/locate/ijcard
Letter to the Editor
Myocardial bridging causing transmural ischemia Successful coronary artery bypass surgery Caio B. Vianna ⁎, Maria M. Gonzalez, Fabio B. Jatene, Marcus N. Gama, Sergio Timerman, Luiz A. Cesar Heart Institute (InCor), University of São Paulo Medical School, Brazil Received 4 April 2006; received in revised form 28 July 2006; accepted 29 July 2006 Available online 23 October 2006
Abstract Myocardial bridging is a common and usually benign inborn coronary anomaly. We report on a 51-year-old man who presented with recent angina on minimum physical effort. Cineangiography showed myocardial bridging of the mid-left anterior descending artery (LAD), and intracoronary ultrasonography excluded atherosclerotic disease. Gated single-photon emission computed tomography (SPECT), with exercise stress, showed an extensive anterior perfusion defect, and remarkable ST-segment elevation (up to 10 mm) in recovery. Vasospasm of the LAD was the main hypothesis. Additional oral drugs did not bring about improvement, as indicated on a new SPECT; disabling angina persisted. Surgical revascularization of the LAD by left internal mammary artery graft was performed. Two years later, SPECT and exercise tests returned to normal. The patient remains asymptomatic. © 2006 Elsevier Ireland Ltd. All rights reserved. Keywords: Myocardial bridging; Ischemia; Coronary vasospasm; Coronary artery bypass; Intravascular ultrasound
1. Case report We report the case of a 43-year-old man who presented with angina on effort (class-II, Cardiovascular Canadian Society). A cineangiography showed myocardial bridging in the midsegment of the left anterior descending artery (LAD). The patient was medicated with atenolol and simvastatin, and the angina was alleviated considerably. Eight years later, at age 51, the angina suddenly worsened, to class-III, and the patient was transferred to this University Hospital. The patient never smoked and had no family history of heart disease. He did have hypertension and hypercholesterolemia. The physical examination was unremarkable. An electrocardiogram recorded sinus bradycardia, slow progression of the R-wave from V1 to V3, and a flat inverted T-wave in I, aVL, V5, and V6 leads. Transthoracic echocardiogram was normal. ⁎ Corresponding author. Av. Doutor Enéas Carvalho Aguiar 44, 05403.900, São Paulo, Brazil. Tel.: +55 1130695387; fax: +55 1130695348. E-mail address:
[email protected] (C.B. Vianna). 0167-5273/$ - see front matter © 2006 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2006.07.159
Gated single-photon emission computed-tomography (SPECT) imaging of myocardial perfusion (Tc-99 m sestamibi tracer) with an exercise stress test was performed. All medication was withdrawn 7 days before testing. Treadmill testing (Bruce-protocol) had a maximal duration of 8:50 min (Fig. 1). At peak exercise, ST-segment elevation was recorded in V1, V2, and V3 leads, maximum of 3 mm in V3. A few seconds into the recovery phase, a remarkable ST-segment elevation was observed in all precordial leads, maximum of 10 mm in V3. These ischemic changes persisted for at least 10 min during recovery (Fig. 1). The patient experienced discrete chest pain. SPECT imaging showed reversible anterior, septal, and apical perfusion defects. At rest, only a small area of perfusion abnormality was noted in the apex. A new cineangiography confirmed myocardial bridging in the mid-LAD (Fig. 2). The bridge caused strong systolic compression (“milking effect”) (Fig. 2B). Left ventriculography showed discrete apical hypokinesia. Simultaneous intravascular ultrasonography showed the “half moon” sign surrounding the tunneled segment, during all cardiac cycle, and mild thickening of the intima was seen in all segments of the LAD (Fig. 3).
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Fig. 1. Initial treadmill exercise test, performed 7 days after all drugs had been withdrawn. At peak exercise, ST-segment elevation was recorded in V1, V2, and V3 leads, maximum of 3 mm in V3. After only 15 s in recovery phase, remarkable ST-segment elevation occurred in all precordial leads. At 1:50 min in recovery, STsegment elevation achieved 10 mm in V3 lead. Ischemic changes persisted for at least 10 min. See also simultaneous gated single-photon emission computed tomography in the text.
However, no atherosclerotic plaques were observed, including in the segment proximal to the bridge. LAD vasospasm was the main clinical hypothesis. Oral medication was increased (atenolol, simvastatin, amlodipine, and nitrate). Two weeks later, SPECT was repeated with this oral therapy, and very similar results were observed, without any improvement. Oral nitrate was withdrawn. During 2 weeks under clinical observation, the disabling angina persisted, in spite of oral medication. The patient was then operated on. Surgery was performed by median sternotomy, cardiopulmonary bypass, and cardioplegia. Myotomy was not performed because the bridge was very extensive and deep. LAD revascularization by a left internal mammary artery graft was preferred.
Fig. 2. Left coronary angiogram, from cranial right anterior oblique projection, in diastole (A) and systole (B). Arrowhead indicates strong systolic compression (“milking effect”) on the left anterior descending artery (LAD) during systole.
The patient was discharged using atenolol, amlodipine, simvastatin, and acetylsalicylic acid. He became asymptomatic. After discharge, 2 SPECT with near-maximum exercise stress testing were performed, with transitory oral drugs withdrawn, and neither showed ischemic defects. Two years later, the patient remains with no symptoms and has a satisfactory quality of life. 2. Discussion In theory, myocardial bridging cannot cause myocardial ischemia, because only 15–20% of the coronary flow occurs during systole. However, complications have been reported,
Fig. 3. Intravascular ultrasound in the tunneled segment of the left anterior descending artery (LAD) at end-diastole (A) and end-systole (B). Strong compression of the lumen is observed during systole. A “half-moon-like” area surround the tunneled segment (arrows) was seen during all cardiac cycle. In the intima, only mild thickening was observed in all segments of the LAD (arrowheads).
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such as chronic or unstable angina, myocardial infarction, coronary spasm, arrhythmias, and sudden death [1,2]. Recently, it has been demonstrated that mechanical compression of the LAD in systole persists throughout a large portion of diastole [1,2]. In normal conditions, the maximum vessel area is achieved at end systole and early diastole. On the contrary, in the tunneled segment, the minimum vessel area occurs at end-systole leading to a delay in relaxation in early diastole. Over time, systolic mechanical compression and modified coronary flow pattern during all cardiac cycle can cause structural and functional damage to the endothelium. Bioavailability of vasoactive substances, such as nitric oxide and endothelin-1, can progressively (or even suddenly) change. In addition, adhesion and aggregation of platelets can be facilitated. Therefore, the initially benign systolic compression can cause endothelial dysfunction and then promotes inadequate coronary dilation during diastole [1–3]. In periods of high heart rate (when systolic/diastolic ratio increases), especially during physical effort or other conditions of sympathetic activation, diastolic flow can be extensively impaired due to vasoconstriction. In addition, even vigorous vasospasm can occur in some cases [4–6]. In the present case transmural myocardial ischemia was revealed by accentuated ST-segment elevation and extensive perfusion defect in the anterior wall of the left ventricle at the SPECT. Spasm of the LAD was a probable alternative since it has been described in some reports [4–6]. There are other reasons suggesting vasospasm. In both treadmill tests before the surgery, ST-segment elevation started suddenly, persisted during a long period in the recovery phase, and increased while heart rate slowed down. Two aspects are specially relevant for this discussion. One refers to alternative diagnostic modalities recently described. Currently, coronary angiography by magnetic resonance, electron-beam tomography and multidetector computed tomography are newer non-invasive techniques which provide excellent visualization of myocardial bridges. Intracoronary Doppler and ultrasound had provided interesting physiopathology data. Intracoronary Doppler shows a characteristic flow pattern in the bridge segment: a steep rise in the flow velocity at early diastole followed by a sharp deceleration and subsequent plateau (the “fingertip” or “spike-and-dome” pattern). Retrograde flow can occur during systole in the segment of the LAD proximal to the bridge. Another method is the intravascular ultrasound. It shows squeezing of the coronary artery during systole and the half-moon-like echolucent area (Fig. 3). This morphological sign is incompletely understood. It appears to be a specific sign since it is only found surrounding the tunneled segment during all cardiac cycle. Mild thickening of the intima can be seen in all segments of the LAD, including the tunneled one (Fig. 3) [1,2]. However, it is well known that the intima beneath the bridge segment is protected from atherosclerosis. Otherwise, atherosclerotic plaques are very frequently founded in the LAD proximal to the bridge [1,2].This proximal segment can be apparently normal at coronary angiography, but intravas-
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cular ultrasound frequently demonstrates atherosclerotic plaques. In the present case, we performed intravascular ultrasound to rule out incipient plaques that could facilitate coronary spasms. The second aspect refers to currently available therapeutic options. Mainly, three strategies are usually available: pharmacological therapy; stenting of the tunneled segment; and surgical treatment by myotomy or coronary artery bypass graft. Initially, we tried and exhausted drug regimens with high doses of beta-blocker, amlodipine, nitrate, and statin, but a new SPECT showed no improvement of the ischemia. Nitrates were maintained initially due to the clear evidence of coronary spasms. However, as nitrates can worsen systolic compression in the tunneled segment of the bridges, they were withdrawn. As all strategies with drugs were ineffective, and the angina persisted unaltered and disabling, revascularization became imperative. Stenting of the tunneled segment was not attempted because the results are still unclear and, at 7 weeks, high incidence of in-stent restenosis has been described [1,7]. Surgical treatment was then performed. Myotomy was initially planned, but during the surgery the bridge was considered extensive and deep. There was considerable risk of complications such as perforation of the right ventricle or injury to the LAD. Coronary artery bypass grafting of LAD was an effective treatment in this patient. Surgical myocardial revascularization is a very uncommon procedure for treating myocardial bridges, but it has been successfully reported, including minimally invasive technique of coronary artery bypass grafting [1,8]. However, long-term results are still unknown. References [1] Alegria JR, Herrmann J, Holmes Jr DR, Lerman A, Rihal CS. Myocardial bridging. Eur Heart J 2005;26:1159–68. [2] Ge J, Jeremias A, Rupp A, et al. New signs characteristic of myocardial bridging demonstrated by intracoronary ultrasound and Doppler. Eur Heart J 1999;20:1707–16. [3] Teragawa H, Fukuda Y, Matsuda K, et al. Myocardial bridging increases the risk of coronary spasm. Clin Cardiol 2003;26:377–83. [4] Ciampricotti R, el Gamal M. Vasospastic coronary occlusion associated with a myocardial bridge. Cathet Cardiovasc Diagn 1988;14:118–20. [5] Kodama K, Morioka N, Hara Y, et al. Coronary vasospasm at the site of myocardial bridge. Report of two cases. Angiology 1998;49:659–63. [6] Low AF, Chia BL, Ng WL, Lim YT. Bridge over troubling spasm: is the association of myocardial bridging and coronary artery spasm a distinct entity? Three case reports. Angiology 2004;55:217–20. [7] Haager PK, Schwartz ER, vom Dahl J, Klues HG, Reffelmann T, Hanrath P. Long-term angiographic and clinical follow up in patients with stent implantation for symptomatic myocardial bridging. Heart 2000;84:403–8. [8] Pratt JW, Michler RE, Pala J, Brown DA. Minimally invasive coronary artery bypass grafting for myocardial muscle bridging. Heart Surg Forum 1999;2:250–3.
