Arteriopathy of the Internal Mammary Artery

Abstract

Background

Spontaneous coronary artery dissection (SCAD) is frequently associated with systemic arteriopathies, particularly fibromuscular dysplasia. Although extracoronary arterial screening is recommended, abnormalities of the internal mammary artery (IMA), the usual preferred conduit for coronary artery bypass grafting, is rarely described.

Case Summary

We report 2 women with systemic arteriopathy and recurrent SCAD who had structural abnormalities of the IMA. The first had Loeys-Dietz syndrome and prior cervical artery dissections, presented with neck pain, and was found to have vertebral artery dissection and focal aneurysmal dilation and suspected dissection of the left IMA. The second had multifocal fibromuscular dysplasia involving renal, cervicocephalic, and thoracic arteries, and presented with recurrent SCAD myocardial infarction. Beaded irregularity of the left IMA was noted. Both patients were managed conservatively.

Discussion

These cases highlight under-recognized IMA involvement in patients with SCAD and systemic arteriopathy, raising considerations regarding conduit assessment when surgical revascularization is contemplated.

Visual Summary

Visual Summary.

Internal Mammary Artery Abnormalities in Patients With Spontaneous Coronary Artery Dissection–Associated Arteriopathy

CABG = coronary artery bypass grafting; FMD = fibromuscular dysplasia; IMA = internal mammary artery; SCAD = spontaneous coronary artery dissection.

Spontaneous coronary artery dissection (SCAD) is an important cause of acute coronary syndrome in women without traditional atherosclerotic risk factors and is frequently associated with systemic arteriopathies, most often fibromuscular dysplasia (FMD).¹ Inherited connective tissue disorders are also present in a small subset of patients with SCAD.¹ Current practice favors conservative management for most SCAD presentations; however, coronary artery bypass grafting (CABG) may be required in selected patients with ongoing ischemia, left main involvement, or hemodynamic instability.² In general, the internal mammary artery (IMA) is the preferred conduit for CABG because of superior long-term patency.³ However, this may not be true for patients with SCAD. Importantly, follow-up imaging in SCAD patients has shown atretic left internal mammary artery (LIMA) grafts likely given healing of the native vessel and competitive flow.⁴

Take-Home Messages

• •IMA abnormalities may be present in patients with SCAD and systemic arteriopathy, including fibromuscular dysplasia and connective tissue disorders.
• •Although the IMA is usually the preferred conduit for coronary artery bypass grafting, IMA arteriopathy may have implications for surgical planning.
• •Individualized assessment may be reasonable in SCAD patients with diffuse arteriopathy when revascularization is contemplated.

FMD is a nonatherosclerotic, noninflammatory arteriopathy that commonly involves renal, carotid, and vertebral arteries but may affect virtually any medium-sized artery.⁵ Although extracoronary arterial screening is recommended in SCAD,^2,6 the IMA is not routinely assessed. The presence of IMA abnormalities in patients with SCAD and systemic arteriopathy raises important considerations regarding conduit selection should surgical revascularization become necessary.

We present 2 patients with SCAD and diffuse arteriopathy in whom imaging demonstrated structural abnormalities of the LIMA, highlighting a potential knowledge gap in preoperative vascular assessment.

Patient 1

Presentation

A 55-year-old woman with Loeys-Dietz syndrome type 3 with a SMAD3 pathogenic variant presented to the emergency department after an episode of nocturnal chest pain that resolved with sublingual nitroglycerin, followed by persistent posterior neck pain over the subsequent 2 days. Her neck pain resembled symptoms she had experienced during prior cervical artery dissections, raising concern for recurrent arterial dissection.

On presentation, she was hemodynamically stable and free of chest pain or dyspnea. Vital signs included blood pressure 142/92 mm Hg and heart rate 95 beats/min. Physical examination revealed no focal neurologic deficits, and cardiopulmonary examination was unremarkable.

Her medical history included 3 separate SCAD myocardial infarctions (MIs), prior bilateral carotid artery dissections and vertebral artery dissection (VAD) (Figure 1), coronary vasospasm with microvascular dysfunction, dilated aortic root under surveillance, unprovoked pulmonary embolism on chronic apixaban therapy, hypertension, and hyperlipidemia. Family history was noncontributory.

Figure 1.

Computed Tomography Angiography of the Neck

(A) Axial image demonstrating right vertebral artery dissection (arrow). (B) Three-dimensional volume-rendered CTA showing bilateral internal carotid artery fibromuscular dysplasia with arterial irregularity (arrow). CTA = computed tomography angiography.

Initial diagnostic work-up

Electrocardiogram (ECG) demonstrated sinus rhythm with premature ventricular complexes and findings suggesting a prior inferior infarction unchanged compared to her prior ECG. High-sensitivity troponin I was mildly elevated with a downtrending pattern (124→120→101 ng/L). Complete blood count and renal function were normal.

Magnetic resonance angiography of the neck demonstrated a new dissection involving the distal V2 segment of the right vertebral artery. Brain magnetic resonance imaging showed no evidence of acute stroke.

ECG-gated cardiac computed tomography angiography (CTA) demonstrated focal aneurysmal dilation of the proximal LIMA measuring up to 9 mm with suspected focal dissection. The vessel also showed luminal irregularity suggestive of FMD (Figure 2A, Video 1). In addition, the study showed interval enlargement of the aortic root, with the sinuses of Valsalva measuring up to 43 mm. No aortic dissection, intramural hematoma, or penetrating atherosclerotic ulcer was identified. There was no obstructive coronary disease. Focal wall thinning and subendocardial hypoattenuation of the mid inferolateral left ventricular wall were consistent with her known past MIs. Transthoracic echocardiography demonstrated preserved left ventricular systolic function with a chronic mild inferior wall motion abnormality.

Figure 2.

Internal Mammary Artery Abnormalities in Patients with SCAD and Systemic Arteriopathy

(A) ECG-gated cardiac CTA in patient 1 demonstrating focal aneurysmal dilation of the proximal LIMA with suspected focal dissection (orange arrow) and luminal irregularity suggestive of FMD (yellow arrows). (B) ECG-gated CTA in patient 2 demonstrating multifocal beaded irregularity of the LIMA consistent with FMD (arrows). ECG = electrocardiogram; CTA = computed tomography angiography; FMD = fibromuscular dysplasia; LIMA = left internal mammary artery; SCAD = spontaneous coronary artery dissection.

Taken together, these findings suggested ongoing multifocal arteriopathy with new VAD, progressive aortic root dilation, and suspected LIMA dissection.

Management

A conservative management strategy was pursued because the patient remained hemodynamically stable, neurologically intact, and free of ongoing chest pain. Heparin was discontinued after completion of diagnostic evaluation, and long-term antithrombotic therapy was resumed with reduced-dose apixaban in combination with aspirin. for history of unprovoked pulmonary embolism Blood pressure control was intensified with a target of <120/80 mm Hg, supported by home monitoring and adjustment of antihypertensive therapy. The patient was advised to avoid heavy lifting and significant physical or emotional stress.

Because there was no evidence of rupture, organ malperfusion, refractory ischemia, or neurologic deterioration, both the VAD and the LIMA aneurysmal/dissection abnormality were managed conservatively with close surveillance. Care was coordinated through the cardiology and vascular medicine teams, with continued monitoring of the aortic root.

Outcome and follow-up

The patient remained clinically stable during hospitalization without neurologic deficits, recurrent chest pain, or hemodynamic deterioration. She was discharged with outpatient follow-up appointments including vascular imaging of the head, neck, and thorax to monitor healing of the VAD, the LIMA abnormality, and the dilated aortic root.

Patient 2

Presentation

A 46-year-old woman with a history of MI due to SCAD presented to the emergency department with chest pain. Several days before presentation, she developed substernal chest pain radiating to the right arm and scapula that resolved after approximately 15 minutes. She subsequently experienced recurrent chest pain that awakened her from sleep and was associated with exertional dyspnea. Because the symptoms resembled those of her past MI, she sought emergency evaluation.

On presentation, her blood pressure was 137/94 mm Hg and heart rate was 74 beats/min. Physical examination revealed a soft systolic ejection murmur without signs of heart failure; lung and neurologic examinations were normal.

Her medical history included renal artery FMD, hypertension, migraine headaches, and impaired fasting glucose. She denied tobacco or illicit drug use. Family history was notable for significant vascular disease in her mother, including splenic artery rupture and celiac artery aneurysm.

Initial diagnostic work-up

ECG demonstrated sinus rhythm with premature ventricular complexes without significant ST-segment changes. High-sensitivity troponin T was elevated with an uptrending pattern (87→147→ 210 ng/L), consistent with non–ST-segment elevation myocardial infarction. Complete blood count and renal function were normal.

Coronary angiography demonstrated dissection of the first septal perforator artery with severe luminal narrowing but preserved distal flow (TIMI flow grade 3). The remaining epicardial coronary arteries were angiographically normal. Additional findings included mild myocardial bridging of the mid left anterior descending artery (LAD) and evidence of healed SCAD in the distal obtuse marginal branch.

Transthoracic echocardiography showed normal left ventricular size with preserved systolic function (ejection fraction: 61%) and regional wall motion abnormalities unchanged from prior imaging.

Because the patient remained hemodynamically stable with preserved distal coronary flow, a conservative management strategy was pursued. Diltiazem was discontinued and replaced with beta-blocker therapy (metoprolol), while low-dose aspirin was continued. Her symptoms improved, and she was discharged with outpatient follow-up.

Early re-presentation and repeat evaluation

Two days after discharge, the patient returned with recurrent severe chest pain radiating to the back and both arms. Sublingual nitroglycerin did not provide relief, and she experienced syncope after repeated dosing. On arrival, she appeared pale and unwell but remained hemodynamically stable.

ECG demonstrated transient mild ST-segment elevation in the high lateral leads with reciprocal inferior changes. Troponin remained elevated but was lower than the previous peak value. Because of recurrent chest pain radiating to the back, ECG-gated CTA using a triple-rule-out computed tomography protocol was performed to exclude pulmonary embolism and acute aortic pathology. The study demonstrated mild luminal narrowing of the mid LAD and resting subendocardial perfusion abnormalities without new major coronary obstruction.

Cardiac magnetic resonance imaging demonstrated a new anterior and anteroseptal MI compared with prior studies, while the chronic inferolateral and apical infarction remained unchanged. Biventricular chamber size and systolic function were preserved.

Repeat coronary angiography demonstrated dissection of the mid LAD with extension toward the septal and diagonal branches, with preserved TIMI flow grade 3. The first septal branch remained narrowed without clear angiographic progression. Because distal coronary flow remained preserved and there was no clear progression, conservative management was continued.

The patient's symptoms improved, electrocardiographic changes resolved, and she was discharged with close follow-up in the specialized SCAD clinic.

Advanced imaging and diagnostic clarification

Given the history of recurrent SCAD and renovascular FMD, comprehensive arterial imaging was performed to evaluate systemic arteriopathy.

CTA of the head and neck demonstrated fusiform narrowing of the basilar artery and progressive tortuosity with mild luminal irregularity of the vertebral and distal internal carotid arteries, suggestive of FMD. Beaded irregularity of the LIMA and the right costocervical trunk was also identified, suggestive of FMD (Figure 2B).

CTA of the abdomen and pelvis demonstrated multifocal beading of the right renal artery and distal left renal artery, confirming renovascular FMD, with subtle irregularity of the external iliac arteries suggesting additional arterial involvement. Given the family history of arterial rupture and aneurysm, the patient was referred for genetic evaluation, which did not identify any pathogenic variants.

Management and outcome

The patient was managed conservatively with antiplatelet therapy, beta-blockade, and careful blood pressure control. Sublingual nitroglycerin was used for recurrent chest pain.

She was referred to cardiac rehabilitation and counseled regarding SCAD recurrence risk and avoidance of heavy isometric exertion, Valsalva maneuvers, and activities involving extreme head or neck positioning.

At follow-up, she remained clinically stable without further major ischemic events. Left ventricular systolic function remained preserved, although regional wall motion abnormalities and a small apical aneurysm persisted as sequelae of prior infarction. Serial vascular imaging showed stable multivessel FMD involving renal, cervicocephalic, and thoracic arterial beds, including the IMA, consistent with systemic arteriopathy.

Discussion

This case series illustrates arteriopathic involvement of the IMA in patients with SCAD and systemic arteriopathy, including imaging findings consistent with dissection, aneurysmal change, or multifocal beading suggestive of FMD. Although FMD and connective tissue disorders are recognized causes of systemic arteriopathy affecting medium-sized vessels,⁷ characterization of IMA abnormalities in the setting of SCAD, and their implications for conduit selection, has been less well emphasized.

These observations have important clinical implications. Conservative management remains the cornerstone of therapy for the vast majority of patients with SCAD, with spontaneous healing observed in most patients. Revascularization is reserved for a minority of high-risk patients, such as those with ongoing ischemia, left main or proximal coronary involvement, or hemodynamic instability.² Observational data suggest that emergency CABG is required in approximately 2.2% to 7.4% of patients, whereas an initial CABG strategy is used in 0.6% to 3.7%.² In atherosclerotic coronary disease, the IMA is the preferred conduit for CABG because of its superior long-term durability. Accordingly, the clinical relevance of conduit selection is limited to this relatively small subgroup of patients.³

However, long-term durability of the IMA grafts has not been shown among SCAD patients; rather, atretic LIMA grafts have been noted on follow-up images.⁴ Additionally, there have been reports of LIMA dissection in patients with FMD, which may compromise myocardial perfusion.⁸ The presence of focal aneurysm, dissection, or multifocal beading in the IMA could compromise graft durability, increase technical complexity, or predispose to future graft failure. These observations raise considerations regarding conduit integrity and potential long-term outcomes in patients with diffuse vascular disease.

Contemporary recommendations support comprehensive arterial imaging from brain to pelvis in patients with SCAD.^2,9 However, the IMA is not routinely emphasized in screening protocols, as it is not typically considered an at-risk vascular territory.^7,10 Our cases demonstrate that clinically silent IMA abnormalities may be detectable on cross-sectional imaging performed for other indications. Although the findings of the 2 patient cases presented do not support routine imaging to assess the IMA, they demonstrate the value of careful review of prior imaging and consideration of targeted preoperative assessment of potential conduit vessels in patients with SCAD, FMD, heritable connective tissue disorders, or recurrent arterial dissections.

Ultimately, larger studies are needed to determine the prevalence and clinical significance of IMA involvement in SCAD-associated arteriopathy and whether selective evaluation of the IMA should be considered when CABG is contemplated.

Conclusions

IMA abnormalities may be present in patients with SCAD and systemic arteriopathy. Although the IMA remains the preferred surgical conduit in general practice, underlying arterial abnormalities of the IMA may have implications for operative planning. Further study is needed to clarify the prevalence and clinical impact of IMA arteriopathy in this population.

Funding Support and Author Disclosures

Dr Tweet is supported by the National Heart, Lung, and Blood Institute, National Institutes of Health (K23HL155506), Bethesda, Maryland, USA. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Appendix

Video 1

Axial ECG-Gated Cardiac Computed Tomography Images of Patient 1 Scrolling Through the Proximal Left Internal Mammary Artery

Arrow highlights focal aneurysmal dilation with suspected dissection.