|Year : 2022 | Volume
| Issue : 2 | Page : 87-91
Adenosine-Induced Myocardial Ischemia in a Patient with Myocardial Bridge: A Case Report
Bingqing Bai1, Huan Ma1, Lan Guo1, Xueju Yu2, Haochen Wang3, Yuting Liu3, Ha Yin2, Fengyao Liu3, Qingshan Geng1
1 Department of Cardiology, Guangdong Provincial Cardiovascular Institute; Department of Cardiology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China
2 Department of Cardiology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China
3 Department of Cardiology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences; Department of Cardiology, School of Medicine, South China University of Technology, Guangzhou, China
|Date of Submission||24-May-2021|
|Date of Acceptance||10-Aug-2021|
|Date of Web Publication||16-May-2022|
Dr. Qingshan Geng
Guangdong Provincial Cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences,106, 2nd Zhongshan Road, Yuexiu District, Guangzhou 510080
Source of Support: None, Conflict of Interest: None
The adenosine stress test and exercise stress test have been widely used in the diagnosis of coronary heart disease, which has high sensitivity and specificity for diagnosis of coronary heart disease. The myocardial bridge is a congenital dysplasia of the coronary artery which may cause severe myocardial ischemia, acute myocardial infarction, arrhythmia, and sudden death. Although drug therapy for this disease is clear and widely used, indication for open-chest surgery is still vague. This case shows a patient with long-term chest pain undergoing the coronary computed tomographic angiography in our hospital 1 month ago, which showed the mild myocardial bridge in the left anterior descending (LAD) branch. Then, she did the mental stress-induced myocardial ischemia and cardiopulmonary exercise test which the results were negative. After the informed consent, the patient took the adenosine stress test and severe angina occurred during the test. Later, coronary angiography showed that the myocardial bridge caused 70% contraction of the middle segment of the LAD branch. In the case of long-term ineffective drug treatment, the patient underwent a open-chest surgery called coronary artery myotomy and her chest discomfort eventually recovered. To a degree, adenosine stress test may be more sensitive than exercise stress test in predicting the severity of coronary artery stenosis. Moreover, we may provide a unique direction of indication for surgeons to operate open-chest surgery on the myocardial bridge.
Keywords: Adenosine stress test, exercise stress test, myocardial bridge, myocardial ischemia, open-chest surgery
|How to cite this article:|
Bai B, Ma H, Guo L, Yu X, Wang H, Liu Y, Yin H, Liu F, Geng Q. Adenosine-Induced Myocardial Ischemia in a Patient with Myocardial Bridge: A Case Report. Heart Mind 2022;6:87-91
|How to cite this URL:|
Bai B, Ma H, Guo L, Yu X, Wang H, Liu Y, Yin H, Liu F, Geng Q. Adenosine-Induced Myocardial Ischemia in a Patient with Myocardial Bridge: A Case Report. Heart Mind [serial online] 2022 [cited 2022 Jul 1];6:87-91. Available from: http://www.heartmindjournal.org/text.asp?2022/6/2/87/345282
| Introduction|| |
Pharmacologic stress tests and exercise stress tests are widely used for noninvasive diagnosis of coronary heart disease. With a prominent role in the cardiovascular system, it has been extensively studied for both its therapeutic and diagnostic effects. Because of a rapid onset of action, short duration, low cost, and no significant side effects, adenosine has become the most conventional method of pharmacologically induced vasodilation.
The myocardial bridge is a congenital coronary artery malformation; in other words, a segment of the coronary artery or its branches runs through the myocardial fibers. According to the literature, the prevalence rate of the myocardial bridge varies from 5% to 86% by necropsy, meanwhile, from 0.5% to 12% in resting conditions and to 40% during provocative tests by coronary angiography (CAG). Moreover, it has been proven that it is related to myocardial ischemia, acute myocardial infarction, arrhythmia, and sudden death.
It is rarely reported that patients with myocardial bridges occurred chest pain during adenosine stress test, but it happened in our case.
| Patient Information|| |
Here is a 58-year-old postmenopausal woman, who has suffered from chest pain and tightness for more than 30 years and has obviously aggravated for the past 6 months. The symptoms of this patient mainly included limited and fixed pain in the precordial area but no shoulder radiation pain, belch, and acid reflux. Moreover, after taking a 10-min rest, the above symptoms had a remission. Furthermore, she once underwent coronary computed tomographic angiography (CTA) in Guangdong Provincial People's Hospital 1 month ago, which showed a mild myocardial bridge in the left anterior descending (LAD) branch. Besides, she has had high blood pressure for more than 8 years and irregularly took bisoprolol and losartan. The report indicated that this woman patient has been suffering from depression, loss of energy, and interest for a long time.
[TAG:2]Clinical Findings [/TAG:2]
| Physical examination and auxiliary examination|| |
Her blood pressure was 153 mmHg systolic and 86 mmHg diastolic, and her body temperature, pulse, heart rate, and breathing were normal. Other physical examinations showed no apparent abnormalities. Her blood tests, ranging from complete blood count, cardiac enzymes, coagulation index to D-dimer and inflammatory indicators, were all within a normal range. Electrocardiogram (ECG) demonstrated sinus rhythm and ST-T changes. Holter electrocardiogram showed occasional atrial premature beats and premature ventricular contraction. Furthermore, echocardiography displayed a reduction of left ventricular function and mild aortic valve regurgitation. Equally unpromising, the chest radiography indicated aortosclerosis.[Table 1]
| Mental Stress-Induced Myocardial Ischemia|| |
Three mental stress tests were used to assess whether this woman patient suffered from mental stress-induced myocardial ischemia or not. The entire duration of the mental stress test is 12 min and each one lasts for 4 min. (We have thoroughly elaborated the mental stress procedure in a protocol.) Apart from that, 13NH3 should be injected for positron emission tomography (PET) scanning when comes 7 min into the test. Finally, after three mental stress tests and through PET-computed tomography scanning, we found that she did not present an evident myocardial ischemia.
| Cardiopulmonary Exercise Test|| |
This woman patient performed the cardiopulmonary exercise test (CPET). Before the first test, she took β-blockers orally 10 mg/day. Although her maximum heart rate increases to 171 beats/min, the ST-T segment changed slightly and could not meet the positive diagnostic criteria [Figure 1]b. Furthermore, her rest ECG before CPET and recovery ECG after CPET were both in normal ranges [Figure 1]a.
|Figure 1: ECG changes during the diagnosis and treatment. (a) Rest and recovery ECG; (b) Maximum exercise load ECG during cardiopulmonary exercise test with β-blockers orally 10 mg/day; (c) Maximum exercise load ECG during cardiopulmonary exercise test without taking β-blockers at least 48 h; (d) Normal ECG after the myotomy surgery. ECG = Electrocardiogram|
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| Adenosine-Induced Myocardial Ischemia|| |
Because coronary CTA does not include obstructive coronary arteries and we dare not make sure if the patient suffers from a microvascular disorder, we performed adenosine myocardial perfusion imaging. Two intravenous lines were used to inject the radiopharmaceutical, without interrupting the adenosine infusion. Adenosine was infused with a syringe pump at a constant rate of 140 μg/kg/min for 6 min.
In the beginning, the resting electrocardiogram showed ST-segment depression in leads V3–V6 <0.05 mv and slightly T-wave inversions [Figure 2]a. Within 1 min 20 s of commencing the adenosine infusion, the patient occurred a fixed chest pain. Her heart rate increased, ECG showed settling of ST segment in leads V3–V6, and T-wave inversions became deeper [Figure 2]b. In the 2nd min, the patient still had chest discomfort and cold sweat. Her heart rate kept rising up, ST-segment depression in leads V3–V6 has become 0.1–0.3 mV and T-wave developed coronary T-wave inversions [Figure 2]c. In the 3rd min of infusion, ECG changes were similar to the former. After 3-min 40-s intravenous administration of adenosine, at this point, her clinical symptoms did not improve better. ECG started to reveal premature ventricular contraction [Figure 2]d.
|Figure 2: Dynamic electrocardiogram changes during intravenous administration of adenosine. (a) Resting electrocardiogram: ST-segment depression in leads V3–V6 <0.05 mV and slightly T-wave inversions; (b) ECG showed settling of ST segment in leads V3–V6 and T-wave inversions became deeper; (c) ST-segment depression in leads V3–V6 has become 0.1–0.3 mV and T-wave developed coronary T-wave inversions; (d) ECG started to reveal premature ventricular contraction; (e) Heart rate and ECG ST-segment depression gradually recovered to the baseline. ECG = Electrocardiogram|
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When we stopped the intravenous administration of adenosine at the 4th min, her heart rate and ECG ST-segment depression gradually recovered to the baseline in the next 20 s. Subsequently, the patient's chest discomfort disappeared [Figure 2]e.
Because of the patient's severe clinical symptoms, we did not get the result of myocardial perfusion imaging.
Given that intravenous administration of adenosine developed myocardial ischemia changes in V3–V6 leads, the anterior descending branch that governs V3–V6 leads had more than 50% stenosis, which was inconsistent with the results of coronary CTA.
We compared results between CPET and adenosine stress test. Then, we considered whether the patient had a false negative in CPET or not. There might be a possible reason: the patient still took β-blockers orally. Since the half-life of bisoprolol is generally 10–12 h, the patient was told to stop the β-blocker for more than 48 h to eliminate the drug effects and took the second CPET. However, the result was still negative [Figure 1]c.
After 2 days of the adenosine stress test, the patient underwent clinically indicated CAG. It presented that the patient had a myocardial bridge over the LAD branch, which caused 70% constriction of the middle segment of the coronary artery in the systole while no constriction in the diastole [Figure 3]a. Furthermore, there were no obstructive lesions in the right coronary artery [Figure 3]b.
|Figure 3: Coronary angiography results. (a) 70% constriction of the middle segment of coronary artery in the systole (left anterior descending artery); (b) Right coronary artery (with no obstructive lesions)|
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| Treatment and Outcomes|| |
After the above examinations, the patient was asked to take the highest doses of β-blockers and calcium channel blockers orally for about 1 month. Nevertheless, she still suffered from chest pain and tightness. Furthermore, she underwent coronary artery myotomy and cardiotomy in cardiac surgery. During the surgery, she presented slight heart enlargement. The myocardial bridge was visible in the mid-anterior descending branch for 1 cm which constricted 80% of LAD in the systole. Subsequently, the patient recovered gradually, the symptoms of chest discomfort disappeared, and the ECG also returned to normal [Figure 1]d. Then, she followed the doctor's advice to take isosorbide mononitrate, furosemide, and antisterone for 1 month to stabilize postoperative condition. After 2 months of cardiac surgery, this patient has suffered from community infectious pneumonia. She has recovered from it after 1-week effective anti-infection treatment. Furthermore, we have followed up this patient for 1.5 years, while she did not show obvious chest discomfort and continually took bisoprolol and losartan to control the blood pressure well.
| Discussion|| |
Adenosine is a coronary vasodilator that is widely used as a pharmacologic stress agent during myocardial perfusion studies. It acts on four subtypes of adenosine receptors (A1, A2a, A2b, and A3). The A1 and A2 receptors are responsible for the alteration of the cardiovascular system. By binding to the A2 receptor, vasodilatation is induced, which can result in a 4- to 5-fold increase in coronary blood flow in healthy individuals. Adenosine can rapidly dilate normal coronary arteries or limit dilating obstructive coronary arteries. As a result, the blood flow in the obstructive coronary supply area is relatively reduced; at the same time, the potential myocardial ischemia appears, helping us to figure out the location, range, and extent of myocardial ischemia and find criminal blood vessel. Due to the 80% constriction of LAD in the systole phase in this woman patient, the above mechanism may play an important role in clinical manifestations. In addition, adenosine can also evaluate the coronary microvascular disorder, which may cause angina in patients with nonobstructive coronary artery. However, in this case, the patient suffered from unendurable clinical symptoms during the adenosine stress test, so we did not finish the assessment of microvascular function.
The exercise stress test is a method that may induce myocardial ischemia and electrocardiogram ischemic changes by increasing cardiac workload through exercise. It is convenient to operate and is completely noninvasive. It has 67% sensitivity and 80% specificity in diagnosing coronary heart disease. However, our patient did not present clinical symptoms and the exercise ECG either did not reach the positive diagnostic criteria. This might indicate that, to some extent, the adenosine stress test is more sensitive than the traditional exercise stress test in the diagnosis. We might not exclude the effects of β-blockers. In a previous study, the lower incidence of anginal complaints during exercise may indicate a protective effect of β-blocker treatment.
As for the myocardial bridge, the detection rate of it by CAG is about 0.5%–12%. Furthermore, it is mostly found in the LAD artery (70%–98%). Drug therapy, such as β-blockers and calcium channel blockers, is popular for patients with long-term symptoms. Surgical treatment can be used for patients with difficult to control by medicines or with severe myocardial ischemia and myocardial infarction. According to a previous study, myotomy can be the priority surgical option for a simple myocardial bridge, which appears to be more effective in controlling symptoms than stenting. However, there is no official indication to operate open-chest surgery on a patient with a myocardial bridge. Our patient suffered from long-term chest discomfort while long-term drug therapy could not improve her condition. According to the myocardial ischemia under the adenosine stress test and CAG results, myotomy is a more appropriate treatment for our patients. Furthermore, the surgical treatment was indeed obviously effective for our patient.
However, in this case, we cannot exclude an unusual complication of intravenous administration of adenosine, coronary artery spasm, especially when our patient has a myocardial bridge. Coronary spasm is thought to be indirectly a result of the abrupt withdrawal of the short-acting vasodilator effect of adenosine. Nevertheless, it is not well clear how exactly adenosine causes coronary spasm yet. In view of the patient's physical state and personal interest, we did not further conduct provocating tests such as ergoxin or acetylcholine to exclude coronary spasm.
| Conclusion|| |
We presented a rare case of a myocardial bridge with long-term chest discomfort. After adhesive and exercise stress tests, we finally diagnosed precisely by CAG. Based on all the test results and ineffective drug therapy, we proposed myotomy as a better treatment. This case demonstrates that the adenosine stress test may be more sensitive than the exercise stress tests in predicting the degree of coronary artery stenosis, especially when patients take β-blockers. In addition, this case may break new ground for myocardial bridge's indication of open-chest surgery.
The patient declared that she did not suffer from chest discomforts since myotomy and she thanked all the doctors who once helped her.
Financial support and sponsorship
This work was supported by the grants of the Natural Science Foundation of Guangdong Province(2019A1515011224) and Guangdong Medical Science and Technology Research Fund (2019118152336191) and Guangdong Provincial Bureau of Traditional Chinese Medicine (20201008) and the High-level Hospital Construction Project of Guangdong Provincial People's Hospital (DFJH201811, DFJH201922, and DFJH2020003).
Prof. Qingshan Geng is the Executive Editor-in-Chief of the Heart and Mind journal. The article was subject to the journal's standard procedures, with peer review handled independently of Prof. Qingshan Geng and their research groups. There are no conflicts of interest.
The authors would like to thank the patient for agreeing and providing her clinical results.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
| References|| |
Juilliére Y, Berder V, Suty-Selton C, Buffet P, Danchin N, Cherrier F. Isolated myocardial bridges with angiographic milking of the left anterior descending coronary artery: A long-term follow-up study. Am Heart J 1995;129:663-5.
Layland J, Carrick D, Lee M, Oldroyd K, Berry C. Adenosine: Physiology, pharmacology, and clinical applications. JACC Cardiovasc Interv 2014;7:581-91.
Liao S, Li X, Zhang X. One-stage minimally surgical treatment for myocardial bridge with other cardiac malformations. Gen Thorac Cardiovasc Surg 2020;68:1495-8.
Cerrato E, Barbero U, D'Ascenzo F, Taha S, Biondi-Zoccai G, Omedè P, et al.
What is the optimal treatment for symptomatic patients with isolated coronary myocardial bridge? A systematic review and pooled analysis. J Cardiovasc Med (Hagerstown) 2017;18:758-70.
Ma H, Guo L, Fei H, Yin H, Wang H, Bai B, et al.
Assessing mental stress on myocardial perfusion and myocardial blood flow in women without obstructive coronary disease: Protocol for a mechanistic clinical trial. BMJ Open 2020;10:e038362.
Anagnostopoulos C, Harbinson M, Kelion A, Kundley K, Loong CY, Notghi A, et al.
Procedure guidelines for radionuclide myocardial perfusion imaging. Heart 2004;90 Suppl 1:i1-10.
van der Hiel B, Scholte AJ, Stokkel MP. Intermittent ST-segment depressions during adenosine stress test. Clin Nucl Med 2007;32:927-9.
Spoladore R, Garroni D, Fragasso G, Palloshi A, Amadio S, Montano C, et al.
Post cardiac surgery diaphragmatic spasm successfully treated with gabapentin. Int J Cardiol 2006;109:282-3.
Kansal S, Roitman D, Sheffield LT. Stress testing with ST-segment depression at rest. An angiographic correlation. Circulation 1976;54:636-9.
Müller-Suur R, Eriksson SV, Strandberg LE, Mesko L. Comparison of adenosine and exercise stress test for quantitative perfusion imaging in patients on beta-blocker therapy. Cardiology 2001;95:112-8.
Tarantini G, Migliore F, Cademartiri F, Fraccaro C, Iliceto S. Left Anterior descending artery myocardial bridging: A clinical approach. J Am Coll Cardiol 2016;68:2887-99.
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