Obstructive CAD Masquerading as Chronic Neck and Shoulder Pain

A 56-year-old Caucasian man with a history of premature atherosclerotic CAD — previously stented in the LAD 14 years earlier — was transferred to hospital after three witnessed syncopal episodes within an hour. He had experienced three presyncopal episodes in the preceding six months. None of these episodes were preceded by postural change, chest pain, palpitations, or exertion.

Critically, he also described a full year of persistent, non-exertional left-sided neck and shoulder dull ache and tightness — rated 3–4/10 on good days, 10/10 on bad days, sometimes disrupting sleep. The pain had begun shortly after a road traffic collision and had been attributed by his primary care to musculoskeletal injury. A normal cervical radiograph and failed response to codeine-paracetamol and physiotherapy had not prompted cardiac reassessment. He was physically active, mountain biking 50 miles twice weekly, without any exacerbation of the neck/shoulder pain during exercise — an atypical feature for obstructive CAD but one explained by the RCA distribution of his ischaemia.

On admission: BP 150/105 mmHg, HR 52 bpm (bradycardia). ECG at admission showed sinus bradycardia at 50 bpm with a borderline first-degree AV block — initial troponin was normal.

Figure 1

ECG at Admission — Sinus Bradycardia with Borderline 1° AV Block

Sinus bradycardia at 50 bpm with a borderline first-degree AV block. In retrospect, this combination in a patient with neck and shoulder pain should raise suspicion for RCA-territory ischaemia affecting the sinoatrial and atrioventricular nodes. The initial troponin was normal, which is characteristic of chronic stable ischaemia rather than acute infarction.

After four days on a cardiac monitoring unit, the patient experienced a five-minute episode of retrosternal chest discomfort while shaving, accompanied by waxing of his left-sided neck and shoulder pain. Initial post-event ECG showed ST-segment elevation in inferior leads II, III, and aVF with reciprocal ST depression in lateral leads I and aVL — triggering a STEMI pathway activation.

Figure 2

ECG After Chest Discomfort — Inferior ST-Segment Elevation

ST-segment elevation in leads II, III, and aVF (inferior leads) with reciprocal depression in I and aVL, consistent with RCA-territory ischaemia. The co-occurrence of neck and shoulder waxing at the same moment as chest discomfort retrospectively confirmed both symptoms were manifestations of the same ischaemic event. The high-sensitivity troponin T subsequently rose to 30 ng/L (reference <14 ng/L).

Figure 3

Repeat ECG — Resolution of Inferior ST Elevation

Complete resolution of inferior ST-segment elevation and lateral reciprocal changes within minutes, consistent with transient ischaemia rather than completed infarction. Transient ST elevation with non-persistent ECG changes and a modest troponin rise identifies a high-risk NSTEMI subset warranting early invasive coronary angiography within 24 hours per ESC guidelines.

Coronary angiography at the PCI centre revealed two-vessel obstructive disease: severe proximal RCA stenosis and moderate-to-severe mid-LAD stenosis (the previously stented segment had new disease). The patient underwent PCI with drug-eluting stent implantation in the RCA, followed three days later by staged IVUS-guided PCI in the LAD. Echocardiogram was normal. He was discharged without complications.

Figure 4

Coronary Angiograms — Pre-PCI (Two-Vessel Disease)

A) LAO projection of the RCA: blue arrows indicate severe proximal RCA stenosis; red arrow marks the posterior descending artery branch (right-dominant circulation). B) RAO caudal view of the left coronary artery: blue arrows show moderate-to-severe mid-LAD stenosis. The severe proximal RCA stenosis explains the sinus and AV node dysfunction — the RCA supplies the sinoatrial node in ~67% of individuals and the AV node in ~80% of right-dominant systems.

Figure 5

Coronary Angiograms — Post-PCI (Drug-Eluting Stents in RCA and LAD)

A) LAO cranial view post-RCA PCI: blue arrows mark the DES implantation site in the proximal RCA with excellent angiographic result; red arrow marks the posterior descending artery. B) RAO cranial view post-LAD PCI: blue arrow indicates the DES site in the mid-LAD. Complete revascularisation of both culprit lesions resulted in immediate and permanent resolution of the patient's year-long neck and shoulder pain.

Figure 6

ESC Risk Factor-Weighted Clinical Likelihood (RF-CL) Model for Obstructive CAD

The RF-CL model estimates the pre-test clinical likelihood of obstructive atherosclerotic CAD based on age, sex, symptom character, and risk factors. Retrospective application to this patient (age 56, male, symptom score 1, three risk factors) yields a 7% clinical likelihood — in the "low" range, which would ordinarily prompt coronary CTA rather than invasive angiography. This highlights how persistent, non-exertional pain patterns cause underestimation of CAD probability using standard tools. Image reproduced under fair use for educational purposes from Vrints et al., ESC 2024 guidelines. CAD = coronary artery disease; RF-CL = risk factor-weighted clinical likelihood.

At six-month follow-up by telephone, the patient reported complete and immediate resolution of his left-sided neck and shoulder pain after the first PCI session — with no recurrence. He had no further presyncopal or syncopal episodes after discharge. He independently noted that the neck and shoulder pain had felt different from his previous musculoskeletal experiences, raising his own doubts about the initial diagnosis.

Discussion

The complete and immediate resolution of chronic neck and shoulder pain following RCA PCI is the definitional proof that these symptoms were an anginal equivalent — cardiac referred pain mediated by the convergence of afferent signals from the heart and the ipsilateral shoulder/neck dermatomes onto shared spinal cord neurons. The RCA's supply to the SA and AV nodes explains the patient's bradycardia and syncopal episodes, while inferior wall ischaemia from the dominant RCA accounts for the transient ST changes. What makes this case instructive is the interaction between the trauma history and the symptom chronicity: the road traffic collision provided a plausible musculoskeletal explanation that deferred cardiac assessment for a full year. When symptoms attributable to a benign cause fail to respond to appropriate treatment, the index of suspicion for an organic diagnosis — including CAD — should rise with each failed intervention.

Retrospective application of the ESC Risk Factor-Weighted Clinical Likelihood model placed this patient at only 7% pre-test probability for obstructive CAD based on his symptom character — low enough that current guidelines would direct him toward coronary CTA rather than invasive angiography. This underlines a systematic limitation: clinical likelihood models score symptom location, onset, exertion-relationship, and relief by rest or nitrates, but the unremitting character of his pain scored against a cardiac diagnosis. Future guideline iterations may need to accommodate persistent, non-exertional anginal equivalents as a recognised presentation of obstructive CAD, distinct from both typical CCS and classic unstable angina, particularly when alternative treatments have been exhausted.