Left anterior descending artery myocardial bridge manifesting as episodic, symptomatic exertional non-sustained ventricular tachycardia

Abstract

A 48-year-old man presented to the emergency department (ED) with exertional chest pressure associated with palpitations and lightheadedness. He was found to have non-sustained ventricular tachycardia (NSVT) in the ED, which resolved spontaneously. Given his history of hyperlipidaemia, unknown family history due to being adopted and episode of NSVT in the ED, he underwent cardiac catheterisation, which showed non-obstructive coronary artery disease and distal left anterior descending artery myocardial bridge (MB). The patient subsequently underwent ECG treadmill stress test with reproduction of chest pressure and NSVT. The patient was referred to cardiac surgery for definitive management of symptomatic MB and underwent resection of MB.

Background

Myocardial bridge (MB) refers to portion of the myocardium overlying an intracardiac segment of coronary artery, usually the left anterior descending (LAD) artery. It can range in presentation from being asymptomatic to causing acute coronary syndrome, ventricular tachycardia and sudden death. It is important to identify patients with an MB who require more urgent and invasive intervention due to risk factors for malignant arrhythmias and sudden cardiac death.

Case presentation

A 48-year-old man with medical history of hyperlipidaemia presented to the emergency department (ED) with exertional chest pressure associated with palpitations and lightheadedness. Chest pressure was left-sided, non-radiating, exacerbated by exercise and lifting heavy weights and relieved with rest. This was associated with palpitations and presyncope. The patient described similar episodes precipitated by exertion for many months but acutely worsening over the last 2 weeks. He previously had ECG and Holter monitor testing, which did not reveal any arrhythmia. This time in the ED, the patient had an episode of non-sustained ventricular tachycardia (NSVT), which resolved spontaneously while using the restroom as shown in figure 1.

Figure 1.

Initial ECG from the emergency department showing non-sustained ventricular tachycardia.

The patient has a history of hyperlipidaemia with last low-density lipoprotein (LDL) level being 137 mg/dL in 2016. He was not on a statin. He chewed tobacco for the last 20 years. He did not smoke cigarettes currently but reported smoking cigarettes in his teenage years. He did not know his family history as he was adopted. His average weekly alcohol intake was 5.2 standard US drinks.

Investigations

Serial ECG and troponin levels were normal. The patient had an episode of NSVT in the ED while going to the bathroom as shown in figure 1.

Lipid panel showed elevated LDL at 159 mg/dL and total cholesterol elevated at 249 mg/dL with a high-density lipoprotein level of 51 mg/dL.

Echocardiogram was obtained to evaluate for any wall motion abnormalities, and it showed mild global hypokinesis of left ventricle, moderate bi-atrial enlargement and ejection fraction of 45%–50%.

Given the patient’s chest pressure, NSVT on ECG and echocardiogram findings, decision was made to proceed with left heart catheterisation (LHC) to ascertain whether the NSVT was a manifestation of ischaemia. LHC showed non-obstructive coronary arteries and a mid LAD MB as shown in figure 2 and video 1.

Figure 2.

Left coronary angiogram is shown in systole (left frame) and diastole (right frame). There is marked systolic narrowing of the left anterior descending artery consistent with myocardial bridging.

Video 1.

bcr-2021-244810supp002.mp4 ^{(668.9KB, mp4)}

DOI: 10.1136/bcr-2021-244810.video01

An exercise ECG stress test was done to see if the patient’s symptoms were reproducible. Five minutes into the exercise stress test, the patient announced that he was feeling similar symptoms to presentation. Ventricular tachycardia beats were noticed in leads II, III, V1, V2, V3, V4, V5 and V6. The stress test was stopped at this point. He had multiple beats of NSVT during the recovery phase as shown in figures 3 and 4, but eventually, his symptoms resolved after resting for a while.

Figure 3.

Preoperative ECG recording during stress test recovery time 0.48 s showing non-sustained ventricular tachycardia. HR, heart rate; PVC, premature ventricular complex; CPLT, Ventricular couplet (2 PVCs); aVR, augmented vector right; aVL, augmented vector left; aVF, augmented vector foot; GE, general electronics; FRF, finite impulse response residual filtering algorithm; MD, doctor of medicine.

Figure 4.

Preoperative ECG recording during stress test recovery time 1.48 s showing non-sustained ventricular tachycardia. HR, heart rate; PVC, premature ventricular complex; aVR, augmented vector right; aVL, augmented vector left; aVF, augmented vector foot; GE, general electronics; FRF, finite impulse response residual filtering algorithm; MD, doctor of medicine.

At this point, the patient’s symptoms were attributed to MB causing reversible myocardial ischaemia and ventricular tachycardia.

Treatment

The patient was initially started on a beta-blocker but was unable to tolerate it due to bradycardia and hypotension. For the same reason, a calcium channel blocker was not used.

In light of the patient’s reproducible ventricular tachycardia and risk of sudden cardiac death, decision was made to consult cardiothoracic surgery for possible resection (deroofing) of MB as a definitive treatment.

The patient was deemed a candidate for sternotomy, and resection of MB was done. Intraoperatively, a 2 cm proximal to mid-LAD MB was observed as shown in figure 5. After excision of MB, the diameter of LAD increased from 1 mm prior to excision to 3–4 mm post excision.

Figure 5.

Intraoperative image showing left anterior descending artery after excision of myocardial bridge.

Postoperative course was remarkable for frequent premature ventricular complexes for which amiodarone was started. He was started on dual platelet therapy with aspirin and clopidogrel for 6 months. Patient was discharged to outpatient care.

Outcome and follow-up

The patient followed up in clinic with cardiothoracic surgery at 2 weeks and did not have any episodes of chest pressure or lightheadedness. He had an exercise treadmill stress test 1 month after MB excision, the ECG tracing did not show any ventricular tachycardia and he achieved target heart rate, as shown in figure 6. He had a final follow-up with cardiovascular surgery at 6 weeks where he had returned to work and denied further symptoms of chest pressure.

Figure 6.

Postoperative ECG recording during stress test did not show any non-sustained ventricular tachycardia. aVR; augmented vector right; aVL, augmented vector left; aVF, augmented vector foot.

Discussion

Lee and Chen note that Reyaman first described the phenomenon of MB during an autopsy as myocardial muscle overlying the epicardial coronary artery, called a tunnelled artery, in 1737.¹ In 1951, Geiringer et al published a detailed analysis of autopsy samples describing the same phenomenon.² However, myocardial bridging was not considered clinically significant until the first angiographic description of the bridge was done in vivo by Porstmann in 1960, as noted by Loukas et al.³

MB is usually asymptomatic and benign, but it can lead to ischaemia, angina, acute coronary syndromes, arrhythmia, and even sudden cardiac death.^{4 5} The prevalence of myocardial bridging depends on the mode of evaluation. It is reported more commonly in autopsy series than via angiogram. Alegria et al report that the largest autopsy study reported a rate of 26% in 1056 patients.⁶ Angiography typically reports systolic compression of bridging, which can be a reason for lower reported rates of 0.5%–12%. In patients with normal coronaries on angiogram, use of provocation testing with intracoronary nitroglycerin enhances systolic compression and reveals bridges more often.⁷ MB can be present in any epicardial artery, but majority occur in the LAD artery and lesser extent in the circumflex, diagonal. It has been observed that patients with hypertrophic cardiomyopathy and heart transplant have significantly higher rates of bridging.⁸ The thickness, length of the bridge, orientation of overlying myocardial fibres, presence of loose connective tissue or adipose tissue all determine the physiological effect of the bridge.⁹

The myocardium is perfused predominantly during the diastole because systolic contraction transiently reduces intracoronary blood flow. Tachycardia during activities with high sympathetic drive such as exercise or emotional distress further impedes blood flow and myocardial perfusion by decreasing diastolic time. Increased sympathetic drive also causes epicardial coronary vasoconstriction, and contraction of MB further reduces coronary blood flow.^{10 11} Our patient presented with exertional chest pressure, palpitations and near syncope. He was seen by primary care and ED physicians previously and discharged home as he did not have any ECG changes at rest and on Holter monitor. This time, he developed dizziness in the ED while using the restroom, and ECG done at the same time showed NSVT, which prompted an angiogram showing LAD bridging. To find out if the bridging is causing his symptoms, a treadmill stress test was done, which reproduced both his symptoms and ECG findings. Question arises why this patient was asymptomatic all his life. As patients age, certain changes in them like left ventricular hypertrophy, increased diastolic dysfunction and atherosclerosis worsen supply–demand mismatch imposed by the presence of bridging.¹² Intravascular ultrasound (IVUS) and autopsy studies have shown that bridged portion and distal segments of the vessels are free from atherosclerosis, but proximal segment is more prone to atherosclerosis, as seen in our patient proximal, and mid-LAD have 20% stenosis. This can be explained by low shear stress, haemodynamic forces, increased local wall tension and stretch. Low shear stress is known to potentiate atherosclerotic plaque formation, and high shear stress in the tunnelled arteries is protective.^{13 14}

Diagnosis of bridging not only includes identifying the anomaly but also demonstrating the haemodynamic significance of myocardial bridging. Various diagnostic modalities such as IVUS, coronary computed tomographic angiography (CCTA), intracoronary Doppler and fractional flow reserve (FFR) have enabled better understanding of the physiological and anatomical changes of systolic compression in MBs. Resting ECGs are usually normal, but stress testing can reproduce symptoms and induce ischaemia, arrhythmias or new conduction abnormalities like in our patient.¹⁵ CCTA can provide anatomical information, but coronary angiography is considered gold standard; it is used to determine the haemodynamic significance of tunnelled arteries.¹⁶ Classic findings are the ‘milking effect’ and ‘step down-step up’ phenomenon during systole. Sometimes when angiographic diagnosis is not clear, provocation with dobutamine and diastolic FFR measurement or intracoronary nitroglycerin are used to assess the physiological impact of the compression. Newer diagnostic modalities like IVUS and intracoronary ultrasound (ICD) can be used to both visualise and measure MB quantitatively if angiography is not conclusive.^{17 18} The half-moon phenomenon on IVUS is characteristic of MB, as much it is only present in the tunnelled segment but not proximal or distal to it. The presence of ‘fingertip phenomenon’ or ‘spike-and-dome pattern’ on pullback of the Doppler flow wire during ICD study is also characteristic of MBs.^{19 20}

Treatment is generally reserved to symptomatic patients to improve quality of life once symptoms are proven to be attributable to the bridge. Three treatment strategies are generally used: negative inotropic/chronotropic agents like β-blockers and calcium channel blockers, surgical myotomy with or without coronary artery bypass grafting (CABG) and rarely stenting of the tunnelled segment. Evidence behind medical therapy is not extensive. β-Blockers decrease heart rate, increase diastolic filling time and decrease contractility and compression of the artery.^{21 22} Similarly, calcium channel blockers prevent compression of the artery. Nitrates are thought to worsen compression and ischaemia by vasodilating the adjacent coronary segments and increase the systolic compression of bridged segments.²³ Coronary artery stenting has been associated with high rates of restenosis, stent fracture, target lesion revascularisation and reported cases of perforation of the artery so not the preferred therapy.^{24 25} Surgical approaches are CABG and surgical myotomy. In long (>25 mm) and deep (>5 mm) MBs because of concern of entering the right ventricle, aneurysm formation or bleeding CABG is preferred over surgical myotomy.^{26 27} Surgical myotomy is the choice of treatment for short and relatively superficial bridges.

In 2009, Schwarz et al proposed a new classification used to guide therapy in the absence of significant coronary artery disease. This is particularly important as it is linked to clinical outcomes. According to Schwarz classification, MB can be divided into three types: (1) type A—MB is incidentally found on angiography but no concern for ischaemia related to MB, (2) type B—presence of symptoms concerning for ischaemia on non-invasive stress test and (3) type C—presence of ischaemic symptoms along with measured altered intracoronary haemodynamic changes. On 5-year follow-up, patients with type A did well with no treatment, but type B and C had symptomatic improvement with β-blockers and calcium channel blockers. Patients with type C who were refractory to medical therapy were considered for intervention.²⁸ Our patient can be considered type B as symptoms were reproduced on stress testing but did not tolerate negative ionotropic agents, so he was a candidate for invasive treatment.

In the subject’s refractory to medications, Binet et al first time reported surgical myotomy in 1975, which showed improvement in clinical symptoms, reversal of local ischaemia and increase in coronary blood flow. It involves resecting the overlying muscle fibres, and over the years, minimally invasive surgical myotomy is also being performed.²⁹ Our patient could not tolerate negative inotropic agents because of hypotension/bradycardia; his bridge was short and relatively superficial, so he underwent surgical myomectomy.

Patient’s perspective.

Below is a recap of the issues I have had regarding my heart.

I started experiencing symptoms of what felt like heart palpitations. I was coaching fall baseball, and that’s when I experienced it the most. As I was trying to warm up my baseball team hitting them baseballs back-and-forth, I got to the point to where I felt like I was going to faint or pass out, so I had to stop hitting baseballs. My heart felt like it was racing and hard to catch my breath. I experienced it a couple weeks later while throwing BP to my players while they were hitting for warm-ups; I once again had to stop throwing. After this, I became worrisome, so I set up an appointment with my primary physician. He then did an ECG on me at that time, found nothing wrong and gave me some breathing exercises to do.

I still continued to have them on and off throughout the fall; however, none of them were to the extreme of what it was back in the fall. I would be working at my baseball facility and find that I would feel it a couple times, and then, it would go away and then 20 min later a couple more times and then go away. Feeling of my heart skipping beats. I never realised that the more active I was, the more often it happened.

I was helping assist a crew due to all the pipe freezers we had. I was moving around some small equipment and started to feel the same palpitations, dizziness and feeling of fainting. I stopped what I was doing try to catch my breath; I did that for about 5 min and then went back as soon as I started to exert myself again; the same feelings came, I went out to the front of the building and my boss and another employee came out saw me and rushed me to the emergency room. At that time, they did the same thing; they did an ECG and Holter monitored, they did an X-ray, they did bloodwork and they found that my potassium levels were low. They sent me home and told me to take more potassium and all would be well.

I spent most of the day just doing things around the house, organising doing spring cleaning. I felt several heart palpitations throughout the day; none of them were severe enough, but they were multiple ones throughout the day. Then on Sunday, I spent the morning cleaning up, felt a few but nothing serious. I was getting ready to go see a friend and have been going up and down the stairs. I suddenly felt my heart racing, dizziness and feeling of fainting. I contacted my friend who is also a PA at an emergency room; he came over saw how I was doing; he checked my pulse. When he checked my pulse, he stated when I was feeling the heart palpitations I would have no pulse for 3–5 s at a time. He contacted 911; I went to the ER. I was told I experienced V-tach’s then had them again at the ER. I experienced similar symptoms while on the treadmill, which have disappeared completely post surgery. It has been 2 months now, and I feel like I can exert myself without feeling palpitations.

Learning points.

• Myocardial bridge (MB) can range in presentation from being asymptomatic to causing significant cardiac ischaemia leading to acute coronary syndrome and sudden cardiac death.

• Diagnosis is usually on cardiac angiography showing collapsed segment of coronary artery during systole.

• Schwarz classification can be used to guide therapy in symptomatic patients due to MB without significant coronary artery disease.

• Treatment for symptomatic MB involves beta-blockers or calcium channel blockers. Nitrates are contraindicated.

• For patients not tolerating pharmacological methods or patients showing imminent signs of cardiac ischaemia and/or malignant arrhythmias like ventricular tachycardia, surgical excision of MB may be required.

Ethics statements

Patient consent for publication

Obtained.