Management of Coronary Bridge Lesions and Kinks
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Anum Ijaz M.B.B.S., M.D.[2]
Overview
A myocardial bridge is a congenital coronary artery anomaly in which a segment of an epicardial coronary artery runs within the myocardium rather than over it. The overlying muscle is the bridge and the intramyocardial segment is the tunneled artery. Most bridges involve the mid or distal left anterior descending artery and most are incidental. A minority produce angina, ischaemia, arrhythmia or an acute coronary syndrome, and these are the patients in whom treatment is considered.
The bridge is a dynamic rather than a fixed lesion, so the usual angiographic and physiological tools mislead. Angiography shows systolic compression, the so-called milking effect, but underestimates how many bridges are present. Fractional flow reserve obtained after adenosine underestimates the bridge, and inotropic challenge with dobutamine is required to unmask it. Diastolic fractional flow reserve is the reference index but is not commercially available at the point of care, so a non-hyperaemic pressure ratio measured during dobutamine stress is used in its place. Because endothelial dysfunction, epicardial spasm and microvascular dysfunction frequently coexist with a bridge and are not corrected by treating it, vasomotor and microvascular testing belong in the same study.
Beta-blockers and non-dihydropyridine calcium channel blockers are first-line treatment. Nitrates worsen systolic compression and should be avoided. Revascularization is reserved for symptoms that persist on maximally tolerated medical therapy. Percutaneous coronary intervention of a bridged segment carries a higher risk of in-stent restenosis, stent fracture and perforation than percutaneous coronary intervention elsewhere, and expert recommendations conflict over whether a bridged segment should be stented at all. Where a proximal atherosclerotic lesion is treated, the stent should be landed short of the tunneled artery. Surgical unroofing is the alternative where the bridge is deep or long, and competitive flow through the native vessel limits the durability of arterial grafts if coronary artery bypass grafting is chosen instead.
Coronary kinks arise two ways and are managed differently. A stiff guidewire in a tortuous vessel straightens and shortens the artery and generates transient eccentric pseudolesions, which resolve on withdrawing the wire and must not be stented. A native angulation that flexes through the cardiac cycle, termed hinge motion, is a durable mechanical problem that predicts stent fracture and subsequent in-stent restenosis once a stent is placed across it.
The Bridge Lesion
Lesion Assessment
- A myocardial bridge should be suspected where angiography shows systolic compression of an epicardial segment with delayed relaxation extending into early diastole.[1]
- The great majority of bridges lie in the left anterior descending artery, and the reported frequency depends almost entirely on the modality used: roughly 42% at autopsy, 22% on CT and 6% on coronary angiography.[2]
- A bridge missed on angiography is not excluded; the mean bridge is approximately 19 mm long and 2.5 mm thick, and many tunneled segments produce no angiographic compression at all.[2]
- Depth and length should be recorded because they determine which treatment is feasible. A superficial bridge has 1 to 2 mm of overlying myocardium, a deep bridge 2 mm or more, a very deep bridge 5 mm or more, and a long bridge measures 25 mm or more.[3]
- Intravascular ultrasound should be used to confirm the bridge and to measure it, and demonstrates a characteristic echolucent half-moon band overlying the tunneled segment.[3]
- Fractional flow reserve measured after adenosine underestimates the significance of a bridge and should not be used alone to decide treatment.[4][5]
- Systolic pressure overshoot across the bridge raises the mean-pressure index and is the reason conventional fractional flow reserve misleads; diastolic fractional flow reserve is the index of choice.[5]
- Physiological assessment should be performed during dobutamine challenge rather than at rest or after adenosine, since inotropic stimulation is what reproduces the compression.[5][4]
- A diastolic fractional flow reserve of 0.76 or less during dobutamine stress defines a haemodynamically significant bridge.[5][6]
- Diastolic fractional flow reserve is not commercially available at the point of care. A non-hyperaemic pressure ratio, either instantaneous wave-free ratio or resting full-cycle ratio, should be recorded during dobutamine stress in its place.[7]
- The provocation protocol should be specified rather than left to operator discretion. Intravenous dobutamine is titrated in increments to 50 µg/kg/min, atropine is added as required to reach 85% of the maximum predicted heart rate, and the diastolic index is then recorded.[7]
- Instantaneous wave-free ratio and resting full-cycle ratio measured during dobutamine stress correlate closely with dobutamine diastolic fractional flow reserve.[8]
- Acetylcholine provocation testing and microvascular assessment by coronary flow reserve and index of microcirculatory resistance should be performed during the same study, before any decision on bridge-directed revascularization.[3][9]
- Coexisting endothelial dysfunction should be expected and sought, since it is present in the large majority of patients with angina, non-obstructive coronary artery disease and a bridge, and will not be corrected by treating the bridge alone.[6]
- Atherosclerosis develops preferentially in the segment immediately proximal to the bridge, while the tunneled segment itself is typically spared, so a proximal plaque and a bridge frequently coexist and each requires separate assessment.[1][3]
Medical Therapy
- Beta-blockers should be used first line in the symptomatic patient, since reducing contractility lessens systolic compression and slowing the heart rate lengthens diastolic filling.[3][1]
- Non-dihydropyridine calcium channel blockers should be used where beta-blockers are not tolerated, and are preferred where vasospasm is also suspected.[3]
- Nitrates should be avoided. They intensify systolic compression of the tunneled artery, dilate the segments adjacent to the bridge, exacerbate retrograde flow and worsen symptoms, and they may precipitate reflex tachycardia.[3]
- Nitrates retain a role only where coronary vasospasm coexists and is the dominant mechanism.[3]
- Ivabradine may be considered where beta-blockers and calcium channel blockers are not tolerated or fail to control the heart rate, but its use in this setting is off-label.[3]
- Availability should be checked before prescribing. The brand-name ivabradine preparation was discontinued in the United States with effect from 1 January 2026.[10]
- Revascularization should not be offered until symptoms have persisted on maximally tolerated medical therapy.[3]
- Where atherosclerosis has been demonstrated, risk factor modification and antiplatelet therapy should be instituted irrespective of how the bridge itself is managed.[3]
Percutaneous Coronary Intervention
- There are no randomised data comparing percutaneous coronary intervention with medical therapy in symptomatic myocardial bridging, and the decision rests on anatomy, local expertise and patient preference.[3]
- Recommendations conflict on whether a bridged segment should be stented at all. A state-of-the-art review of angina with non-obstructive coronary arteries advises against stenting a bridge, citing reported stent fracture, restenosis and rupture, and favours surgical unroofing for refractory symptoms.[9]
- Where a proximal atherosclerotic lesion is being treated, the stent should be landed short of the tunneled segment. Extending stent coverage into the bridge carries a substantially higher rate of target vessel revascularization than ending the stent proximal to it, and this should govern the landing zone.[11]
- A shorter bridge and a superficial tunneled segment of less than 2 mm depth favour percutaneous coronary intervention where it is undertaken.[3]
- A deep or long bridge, particularly one that cannot be covered by a single stent, should prompt assessment for surgical revascularization rather than stenting.[3]
- A second-generation drug-eluting stent with high radial strength should be selected, to resist cyclical systolic compression.[3]
- Dobutamine challenge should be used to size stent length before implantation, because incomplete coverage of the bridge is hazardous.[3]
- Intravascular ultrasound should be used to size the stent and to define the extent of the tunneled segment.[3]
- Perforation at the time of stent deployment in a bridged segment has been reported in up to 6% of cases, and stent fracture and stent thrombosis have both been described.[3]
- In-stent restenosis is more frequent after stenting a bridged segment than after percutaneous coronary intervention elsewhere.[3]
- Most reported complications arose with bare metal stents or first-generation drug-eluting platforms, which limits how far they should be applied to contemporary practice.[3]
Surgical Unroofing and Bypass
- Supra-arterial myotomy, in which the myocardial fibres overlying the tunneled artery are divided, is the operation performed for symptoms refractory to maximally tolerated medical therapy.[12][3]
- Unroofing for isolated left anterior descending artery bridging can be performed without cardiac-related death, and most patients are free of chest pain afterwards.[12]
- Recurrent non-ischaemic chest pain should be anticipated and discussed before operation. Around a third of patients remain symptomatic despite relief of coronary compression, and medical therapy is often continued.[12]
- Right ventricular perforation is the characteristic operative hazard, and is a consequence of a deep endomyocardial course of the tunneled artery. Coronary perforation, incomplete unroofing, ventricular aneurysm and postoperative bleeding are also recognised.[12]
- Coronary artery bypass grafting is the alternative where anatomy is unfavourable for unroofing, and the choice between the two rests on bridge depth and length, operator experience and patient preference rather than on randomised evidence.[3]
- Conduit selection should account for competitive flow through the native vessel, which is intermittent rather than continuous in a bridge. Only around 10% of left internal mammary artery grafts to the left anterior descending artery remain patent at 18 months, whereas saphenous vein graft patency is approximately 80%.[3]
- Competitive flow also argues against coronary artery bypass grafting altogether where the bridge produces only intermittent ischaemia.[3]
Coronary Kinks
Guidewire-Induced Pseudolesions
- A stiff guidewire advanced through a tortuous coronary artery straightens and shortens the vessel and produces multiple transient eccentric narrowings, known as the accordion or concertina phenomenon.[13]
- A pseudolesion should be suspected when several new narrowings appear along a tortuous segment immediately after wiring, rather than at the site being treated.[13]
- Pseudolesions do not respond to intracoronary nitroglycerin. Failure to respond to a vasodilator is the finding that separates them from spasm.[13]
- Dissection, thrombus and spasm are the differential diagnoses and should be excluded before any further device is deployed.[13]
- Ischaemia, electrocardiographic change and haemodynamic compromise can occur if a pseudolesion is not recognised promptly.[13]
- The guidewire should be withdrawn or repositioned so that its floppy segment lies across the tortuous portion and native curvature is restored; the narrowings then resolve.[13]
- A pseudolesion should never be stented. Treating a reversible finding converts it into a permanent iatrogenic one.[13]
Hinge Motion and Stent Kinking
- Hinge motion is the change in coronary angulation between diastole and systole at a given point, and a change of 16° or more has been used to define it.[14]
- A stent placed across a hinge point should be expected to fracture there. The fracture site corresponds closely to the point of maximal angulation change.[14]
- Hinge motion, right coronary artery location, a stainless steel platform, stent length greater than 25 mm, stent overlap, a stent-to-vessel ratio below 0.8 and the use of multiple stents are independent predictors of stent fracture.[15]
- Hinge motion remains a predictor of fracture with contemporary thin-strut platinum-chromium platforms, so newer stent generations do not remove the need to plan around it.[16]
- Pre-existing in-stent restenosis at the treated site is itself a strong predictor of subsequent fracture, and a repeat stent layer across a hinge point compounds the risk.[16]
- Stent fracture occurs in approximately 5% of patients after drug-eluting stent implantation, and reported incidence has risen over the past two decades as complex lesions have been treated and surveillance imaging has increased.[17]
- Stent fracture carries a higher rate of in-stent restenosis, target lesion revascularization and definite stent thrombosis, so it is a clinical event rather than an imaging curiosity.[15]
- The shortest stent that covers the lesion should be chosen, overlap across an angulated segment avoided, and aggressive high-pressure post-dilatation with an oversized balloon avoided, since each of these is an independent predictor of fracture.[15]
- Where hinge motion is severe and persistent, a shorter stent, a drug-coated balloon or coronary artery bypass grafting may be considered in preference to stenting across the hinge point, but this is supported only by case-level observation and should not be regarded as established.[18]
- Angiography alone under-detects stent fracture; cine fluoroscopy, intravascular ultrasound, optical coherence tomography and CT all improve detection and should be used when restenosis recurs at an angulated site.[17]
Summary of management for coronary bridge lesion and kinks
Step 1: Establish which entity is present
- Systolic compression of an epicardial segment with delayed early-diastolic relaxation → bridge lesion, go to Step 2
- New multiple narrowings appearing along a tortuous segment after wiring → guidewire-induced pseudolesion, go to Step 6
- Fixed angulation that flexes through the cardiac cycle at the intended landing zone → hinge motion, go to Step 7
Step 2: Characterise the bridge
- Intravascular ultrasound to confirm the tunneled segment and measure depth and length
- Depth 1 to 2 mm → superficial; 2 mm or more → deep; 5 mm or more → very deep; length 25 mm or more → long
Step 3: Establish haemodynamic significance and test for coexisting mechanisms
- Do not rely on adenosine fractional flow reserve
- Intravenous dobutamine titrated to 50 µg/kg/min, with atropine as required to reach 85% of maximum predicted heart rate
- Diastolic fractional flow reserve 0.76 or less → significant; where diastolic fractional flow reserve is unavailable, record instantaneous wave-free ratio or resting full-cycle ratio during the same challenge
- Add acetylcholine provocation and coronary flow reserve with index of microcirculatory resistance in the same study
Step 4: Medical therapy first
- Beta-blocker first line; non-dihydropyridine calcium channel blocker if not tolerated or if vasospasm coexists
- Stop nitrates unless coronary vasospasm is the dominant mechanism
- Ivabradine if rate control remains inadequate, off-label and subject to availability
- Treat any spasm or microvascular dysfunction identified at Step 3 on its own terms
- Symptoms controlled → continue medical therapy
Step 5: Select the revascularization modality for refractory symptoms
- Proximal atherosclerotic lesion requiring treatment → land the stent short of the tunneled segment; do not extend coverage into the bridge
- Bridge itself symptomatic despite maximal therapy → recognise that recommendations conflict, and weigh stenting against unroofing explicitly with the patient
- Short and superficial bridge, coverable by a single stent, where stenting is chosen → high-radial-strength second-generation drug-eluting stent, sized under dobutamine challenge
- Deep or long bridge, or not coverable by a single stent → surgical unroofing
- Anatomy unfavourable for unroofing → coronary artery bypass grafting with a saphenous vein graft rather than an arterial conduit; avoid grafting where ischaemia is only intermittent
Step 6: Manage a guidewire-induced pseudolesion
- Give intracoronary nitroglycerin; resolution → spasm, not a pseudolesion
- No response → withdraw or reposition the guidewire so the floppy segment lies across the tortuosity
- Narrowings resolve → do not stent
- Narrowings persist after wire removal → exclude dissection and thrombus with intravascular ultrasound
Step 7: Plan around hinge motion
- Angulation change of 16° or more at the landing zone → hinge point
- Shortest stent that covers the lesion; avoid overlap across the hinge; avoid oversized high-pressure post-dilatation
- Severe and persistent hinge motion → consider a drug-coated balloon or coronary artery bypass grafting instead of stenting across the hinge
- Recurrent restenosis at an angulated site → image for stent fracture rather than treating angiographically
Complications
The bridged segment and the hinge point are both sites at which a stent is subjected to repeated mechanical loading, and the complications of treating them follow from that. Guidewire-induced pseudolesions are reversible, and their principal hazard is that they are mistaken for a real lesion.
- Perforation during stent deployment in a bridged segment has been reported in up to 6% of cases.[3]
- In-stent restenosis, stent fracture and stent thrombosis are all more frequent after stenting a bridged segment.[3]
- Stent fracture at a hinge point carries increased in-stent restenosis, target lesion revascularization and definite stent thrombosis.[15]
- Right ventricular perforation, coronary perforation, incomplete unroofing, ventricular aneurysm and postoperative bleeding are the recognised hazards of surgical unroofing.[12]
- Around a third of patients have recurrent chest pain after unroofing despite relief of coronary compression.[12]
- An unrecognised guidewire-induced pseudolesion can cause ischaemia, electrocardiographic change and haemodynamic compromise, and can lead to stenting of a reversible finding.[13]
- Left internal mammary artery grafts placed for myocardial bridging fail from competitive flow, with only around 10% patent at 18 months.[3]
- Extending a stent into the bridged segment when treating a proximal lesion carries a substantially higher rate of target vessel revascularization than landing it proximal to the bridge.[11]
References
- ↑ 1.0 1.1 1.2 Tarantini G, Migliore F, Cademartiri F, Fraccaro C, Iliceto S (2016). "Left Anterior Descending Artery Myocardial Bridging: A Clinical Approach". Journal of the American College of Cardiology. 68 (25): 2887–2899. doi:10.1016/j.jacc.2016.09.973. PMID 28007148. Unknown parameter
|month=ignored (help);|access-date=requires|url=(help) - ↑ 2.0 2.1 Hostiuc S, Negoi I, Rusu MC, Hostiuc M (2018). "Myocardial Bridging: A Meta-Analysis of Prevalence". Journal of Forensic Sciences. 63: 1176–1185. PMID 29044562.
|access-date=requires|url=(help) - ↑ 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 3.13 3.14 3.15 3.16 3.17 3.18 3.19 3.20 3.21 3.22 3.23 3.24 3.25 3.26 Sternheim D, Power DA, Samtani R, Kini A, Fuster V, Sharma S (2021). "Myocardial Bridging: Diagnosis, Functional Assessment, and Management: JACC State-of-the-Art Review". Journal of the American College of Cardiology. 78 (22): 2196–2212. doi:10.1016/j.jacc.2021.09.859. PMID 34823663 Check
|pmid=value (help). Unknown parameter|month=ignored (help);|access-date=requires|url=(help) - ↑ 4.0 4.1 Hakeem A, Cilingiroglu M, Leesar MA (2010). "Hemodynamic and intravascular ultrasound assessment of myocardial bridging: fractional flow reserve paradox with dobutamine versus adenosine". Catheterization and Cardiovascular Interventions. 75 (2): 229–36. doi:10.1002/ccd.22237. PMID 19753633. Unknown parameter
|month=ignored (help);|access-date=requires|url=(help) - ↑ 5.0 5.1 5.2 5.3 Escaned J, Cortés J, Flores A, Goicolea J, Alfonso F, Hernández R, Fernández-Ortiz A, Sabaté M, Bañuelos C, Macaya C (2003). "Importance of diastolic fractional flow reserve and dobutamine challenge in physiologic assessment of myocardial bridging". Journal of the American College of Cardiology. 42 (2): 226–33. doi:10.1016/S0735-1097(03)00588-6. PMID 12875756. Unknown parameter
|month=ignored (help);|access-date=requires|url=(help) - ↑ 6.0 6.1 Pargaonkar VS, Kimura T, Kameda R, Tanaka S, Yamada R, Schwartz JG, Tremmel JA, Schnittger I (2021). "Invasive assessment of myocardial bridging in patients with angina and no obstructive coronary artery disease". EuroIntervention. 16: 1070–8. doi:10.4244/EIJ-D-20-00779.
|access-date=requires|url=(help) - ↑ 7.0 7.1 Bangalore S, Fearon WF, Fugar S, Dangas GD, Iqbal S, Johnson NP, Power D, Tamis-Holland J, Kern MJ (2025). "Evidence-Based Practices in the Cardiac Catheterization Laboratory: Invasive Epicardial Coronary Physiologic Assessment: A Scientific Statement From the American Heart Association". Circulation. 153: e25–e41. doi:10.1161/CIR.0000000000001389.
|access-date=requires|url=(help) - ↑ Otsuki H, Yoshida A, Pargaonkar VS, Takahashi K, Honda Y, Fitzgerald PJ, Schnittger I, Tremmel JA (2025). "Comparison of Coronary Physiological Indices in Identifying Functionally Significant Myocardial Bridges in ANOCA". Circulation: Cardiovascular Interventions. 18 (6): e014824. doi:10.1161/CIRCINTERVENTIONS.124.014824. PMID 40365677 Check
|pmid=value (help). Unknown parameter|month=ignored (help);|access-date=requires|url=(help) - ↑ 9.0 9.1 Smilowitz NR, Prasad M, Widmer RJ, Toleva O, Quesada O, Sutton NR, Lerman A, Reynolds HR, Tremmel JA (2023). "Comprehensive Management of ANOCA, Part 2—Program Development, Treatment, and Research Initiatives: JACC State-of-the-Art Review". Journal of the American College of Cardiology. 82 (12): 1264–1279. doi:10.1016/j.jacc.2023.06.044. PMID 37704316 Check
|pmid=value (help). Unknown parameter|month=ignored (help);|access-date=requires|url=(help) - ↑ "Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book)". U.S. Food and Drug Administration. Retrieved 2026-09-15.
- ↑ 11.0 11.1 Corban MT, Hung OY, Eshtehardi P, Rasoul-Arzrumly E, McDaniel M, Mekonnen G, Timmins LH, Lutz J, Guyton RA, Samady H (2014). "Myocardial bridging: contemporary understanding of pathophysiology with implications for diagnostic and therapeutic strategies". Journal of the American College of Cardiology. 63 (22): 2346–2355. doi:10.1016/j.jacc.2014.01.049. PMID 24583304. Unknown parameter
|month=ignored (help);|access-date=requires|url=(help) - ↑ 12.0 12.1 12.2 12.3 12.4 12.5 Hemmati P, Schaff HV, Dearani JA, Daly RC, Lahr BD, Lerman A (2020). "Clinical Outcomes of Surgical Unroofing of Myocardial Bridging in Symptomatic Patients". The Annals of Thoracic Surgery. 109 (2): 452–457. doi:10.1016/j.athoracsur.2019.07.005. PMID 31376377. Unknown parameter
|month=ignored (help);|access-date=requires|url=(help) - ↑ 13.0 13.1 13.2 13.3 13.4 13.5 13.6 13.7 Abool Maaly CA, Rafie I, Alkindi F (2017). "Pseudo-lesions of a Tortuous Right Coronary Artery During Percutaneous Coronary Intervention: Accordion Phenomena". Heart Views. 18 (2): 47–49. doi:10.4103/HEARTVIEWS.HEARTVIEWS_44_17. PMID 28706595.
|access-date=requires|url=(help) - ↑ 14.0 14.1 Kuramitsu S, Iwabuchi M, Haraguchi T, Domei T, Nagae A, Hyodo M, Yamaji K, Soga Y, Arita T, Shirai S, Kondo K, Ando K, Sakai K, Goya M, Takabatake Y, Sonoda S, Yokoi H, Toyota F, Nosaka H, Nobuyoshi M (2012). "Incidence and clinical impact of stent fracture after everolimus-eluting stent implantation". Circulation: Cardiovascular Interventions. 5 (5): 663–71. doi:10.1161/CIRCINTERVENTIONS.112.969238. PMID 23011266. Unknown parameter
|month=ignored (help);|access-date=requires|url=(help) - ↑ 15.0 15.1 15.2 15.3 Kan J, Ge Z, Zhang JJ, Liu ZZ, Tian NL, Ye F, Li SJ, Qian XS, Yang S, Chen MX, Rab T, Chen SL (2016). "Incidence and Clinical Outcomes of Stent Fractures on the Basis of 6,555 Patients and 16,482 Drug-Eluting Stents From 4 Centers". JACC: Cardiovascular Interventions. 9 (11): 1115–23. doi:10.1016/j.jcin.2016.02.025. PMID 27009464. Unknown parameter
|month=ignored (help);|access-date=requires|url=(help) - ↑ 16.0 16.1 Kuramitsu S, Hiromasa T, Enomoto S, Shinozaki T, Iwabuchi M, Mazaki T, Domei T, Yamaji K, Soga Y, Hyodo M, Shirai S, Ando K (2015). "Incidence and Clinical Impact of Stent Fracture After PROMUS Element Platinum Chromium Everolimus-Eluting Stent Implantation". JACC: Cardiovascular Interventions. 8 (9): 1180–1188. doi:10.1016/j.jcin.2015.02.029. PMID 26210803. Unknown parameter
|month=ignored (help);|access-date=requires|url=(help) - ↑ 17.0 17.1 Chen Y, Li D, Liao Y, Yao X, Ruan Y, Zou K, Liao H, Ding J, Qin H, Yu Z, Zhao Y, Hu L, Yang R (2022). "Incidence of coronary drug-eluting stent fracture: A systematic review and meta-analysis". Frontiers in Cardiovascular Medicine. 9: 925912. doi:10.3389/fcvm.2022.925912. PMID 36082117 Check
|pmid=value (help). Unknown parameter|month=ignored (help);|access-date=requires|url=(help) - ↑ Liu J, Hau WK, Li Y, Wang L, Dong F, Chen Y, Huang X (2026). "Multiple PCI Failures Due to Excessive Coronary Hinge Motion". JACC: Case Reports. 31 (15): 107380. doi:10.1016/j.jaccas.2026.107380. PMID 41837928 Check
|pmid=value (help). Unknown parameter|month=ignored (help);|access-date=requires|url=(help)