A Case of Severe Aortic Stenosis Mimicking Acute Coronary Syndrome: Diagnostic Challenges and Surgical Management

A 52-year-old man with well-controlled essential hypertension presented to the emergency department with a three-day history of recurrent, pressure-like, non-radiating chest tightness rated 6/10 in intensity and exertional in character, accompanied by progressive dyspnea over the preceding week. He had completed a course of oral antibiotics for a urinary tract infection one week before admission. On examination he was febrile at 37.8°C, hypertensive (BP 140/95 mmHg), and tachycardic (HR 105 bpm). Bilateral basal crackles were present, and a prominent ejection systolic murmur was audible at the right second intercostal space.

Initial ECG showed lateral ST-segment depression. Given exertional chest pain, troponin elevation, and dynamic ECG changes, an acute coronary syndrome (ACS) diagnosis was initially assumed. Coronary angiography was performed — and revealed entirely normal coronary arteries. This finding redirected the diagnostic workup toward structural pathology. A transesophageal echocardiogram (TEE) was then performed, which confirmed a bicuspid aortic valve (BAV) with severe aortic stenosis (maximum velocity 5.0 m/s), moderate aortic regurgitation, impaired LV systolic function, and a markedly dilated ascending aorta with measurements of 4.1 cm at the Valsalva sinuses, 4.6 cm at the sinotubular junction, and 4.9 cm in the proximal ascending aorta. Blood cultures were negative.

Figure 1

Transesophageal Echocardiogram — Bicuspid Aortic Valve

TEE images in the aortic valve short-axis view (left) and long-axis view (right) confirming a bicuspid aortic valve morphology. The short-axis view demonstrates the characteristic "fish-mouth" opening pattern with fusion of the right and left coronary cusps. The long-axis view shows restricted cusp excursion consistent with severe stenosis. The combination of BAV, severe AS, and aortic root dilation in a 52-year-old signals complex underlying pathology beyond simple calcific degeneration.

The differential had evolved dramatically. ACS was definitively excluded by normal coronary anatomy. Severe symptomatic AS due to BAV emerged as the primary diagnosis. Acute aortic syndrome was considered due to chest pain and aortic dilation but excluded by imaging. Infective endocarditis was not suspected pre-operatively because blood cultures were negative and TEE showed no vegetations — yet the possibility was noted given the recent UTI, fever, and markedly elevated troponin disproportionate to isolated AS alone (typical AS-related troponin elevation is generally below 500 ng/L; this patient's 1,938 ng/L suggested an additional insult).

A multidisciplinary team reviewed the combined findings — severe symptomatic AS, moderate AR, BAV, impaired LV function, and ascending aortic aneurysm — and recommended urgent surgical intervention. The patient underwent a Bentall procedure: composite graft replacement of the aortic valve, aortic root, and ascending aorta with bilateral coronary ostial reimplantation. Intraoperatively, two unexpected findings emerged: a small intimal tear in the ascending aorta, and — most significantly — an abscess cavity beneath the annulus of the right coronary cusp with partial tissue destruction, findings consistent with previously unrecognized culture-negative infective endocarditis (IE). The negative blood cultures and absence of pre-operative vegetations on TEE made this a "silent" IE, revealed only on direct surgical inspection.

Postoperative management included six weeks of IV flucloxacillin for the culture-negative IE, lifelong warfarin with a target INR of 2.5 (range 2.0–3.0) for the mechanical valve, and a PET scan to assess for deep-seated infection. Recovery was uneventful: the patient was extubated successfully, transferred from the ICU to cardiology, completed the antibiotic course, and was discharged in stable condition.

Discussion

This case exemplifies what has been termed the "AS-ACS paradox" — the well-documented but diagnostically challenging phenomenon where severe aortic stenosis produces a clinical picture indistinguishable from acute myocardial ischemia. Up to 70% of patients with severe AS report anginal chest pain, and 20–30% present with ACS-like features despite normal coronary arteries. The mechanism involves subendocardial ischemia driven by pressure overload-induced LV hypertrophy with reduced capillary density, impaired coronary flow reserve (often reduced to 1.5–2.0 versus a normal 3.5–5.0), and supply-demand mismatch during exertion or tachycardia. Moderate troponin elevation is expected in this setting, but levels above 500 ng/L — as in this patient at 1,938 ng/L — should trigger consideration of a complicating etiology such as annular abscess, embolic phenomena, or direct cytokine-mediated myocardial damage from concurrent endocarditis.

The intraoperative discovery of a peri-annular abscess in the absence of pre-operative blood culture positivity or echocardiographic vegetations highlights the limits of non-invasive diagnosis in culture-negative endocarditis. TEE has excellent sensitivity for detecting vegetations but can miss deep annular abscesses, particularly when the valve is heavily calcified and echogenic. The presence of triple pathology — severe AS with BAV, aortic root dilation, and annular abscess — made the Bentall procedure the only appropriate operative strategy. This case reinforces that when troponin elevation is disproportionate to the expected degree from AS alone, clinicians should maintain a high index of suspicion for concurrent structural complications and not be reassured by negative blood cultures or the absence of classic endocarditis stigmata on pre-operative imaging.