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Introduction

Takayasu arteritis (TA) is a granulomatous large-vessel vasculitis that primarily involves the aorta, its major branches and, in some cases, the pulmonary arteries (1-5). It is a chronic inflammatory disease of unknown etiology that predominantly affects young women and is most frequent in Asian populations (1-5).

TA is divided into two phases: an initial systemic inflammatory phase characterized by nonspecific symptoms, and a chronic vascular phase dominated by structural complications of the large vessels (1). Consequently, depending on the stage of disease progression, patients with TA may present with clinical manifestations such as carotidynia, absent pulses, blood pressure discrepancies between limbs, claudication, cerebral hypoperfusion symptoms (transient visual disturbances, transient ischemic attacks, stroke), and arterial hypertension with its associated complications (1,3,4). In the early stages, it typically manifests with general, nonspecific symptoms such as headache, fever, fatigue, and weight loss, which often delays timely diagnosis (1). As the disease progresses, vascular wall thickening occurs, leading to stenosis, thrombosis, occlusions, dilatations, or aneurysm formation (2,3,5). Although uncommon, cardiac dysfunction may be one of the initial manifestations. Similarly, there are reports of dilated cardiomyopathy, valvular regurgitation, secondary hypertension, and coronary involvement resulting from the inflammatory process in patients with TA (2).

Given the diverse clinical spectrum of TA, a comprehensive and targeted diagnostic approach is essential to prevent delays in identification that could compromise patient outcomes.

Case presentation

An 18-year-old female from Guamo, Tolima (Colombia), with no relevant medical or family history of cardiovascular or autoimmune diseases, presented to the emergency department of a secondary care center due to a two-week history of progressive dyspnea—initially on moderate exertion and eventually at rest—lower limb edema, non-productive cough, palpitations, and a decline in functional capacity. This decline was suspected considering the limitations she experienced for performing activities of daily living and was confirmed by reviewing her medical history.

Due to the progression of symptoms, she was referred on July 11, 2025, to a tertiary care hospital in Ibagué (Tolima). Upon admission, the physical examination revealed that the patient was conscious, oriented, and hemodynamically stable, with elevated blood pressure (155/105 mmHg), tachycardia (127 bpm), a normal respiratory rate (20 rpm), and a temperature of 37°C. Oxygen saturation was 98% on room air, and her body mass index was 26.78 kg/m2. The abdomen was soft, non-tender, and non-distended, with no palpable masses or organomegaly. The limbs were eutrophic, without edema, and distal pulses were palpable and symmetric.

Cardiac auscultation revealed rhythmic heart sounds without murmurs or gallops; however, physical examination of the neck identified bilateral carotid bruits. Lung auscultation showed normal vesicular breath sounds, with no rales or signs of respiratory distress. The initial neurological exam showed no alterations in consciousness or motor or sensory deficits.

Admission laboratory tests (Table 1 and Table 2) revealed preserved renal function, mild anemia (11.90 g/dL), marked thrombocytosis (639x103/µL), and normal electrolyte and troponin levels. C-reactive protein (CRP) levels were elevated (5.85 mg/L), while serum procalcitonin was normal (0.020 ng/mL) —findings consistent with an active inflammatory process of likely non-infectious origin—. Infectious and autoimmune etiologies were ruled out, as serology for Chagas disease and HIV was negative, while the autoimmune profile (antinuclear antibodies, anti-DNA antibodies, and complement levels) was within normal limits. Ferritin levels were normal, and vitamin B12 was at the lower limit of normal (Table 2).

Table 1. Basic admission laboratory tests.

Test	Results	Reference values
Thyroid-stimulating hormone	3.764µUI/mL	0.34-4.82µUI/mL
Serum creatinine	0.82mg/dL	0.7-1.3mg/dL
Potassium	4.54mEQ/L	3.5-5.5mEQ/L
Sodium	132.54mEQ/L	135-145mEQ/L
Glucose	87.5mg/dL	70-100mg/dL
Blood urea nitrogen	11.9mg/dL	7-23mg/dL
Cardiac troponin I (quantitative)	14.6ng/L	0-47ng/L
Free thyroxine	1.21ng/dL	0.89–1.76ng/dL
N-terminal pro-b-type natriuretic peptide	1014pg/mL	125 pg/mL in people <75 years of age
Hemoglobin	11.90g/dL	14-16g/dL
Hematocrit	35.70%	38-48%
Red blood cell count	5.03x106/µL	4.2-5.4x106/µL
Mean corpuscular volume	71fL	80-99fL
Mean corpuscular hemoglobin	19.6pg	27-31pg
Mean corpuscular hemoglobin concentration	27.6g/dL	33-37g/dL
Red cell distribution width	15%	11.5-14.5%
White blood cell count	10.45x103/µL	4.5-10.6x103/µL
Neutrophil percentage	61.10%	40-74%
Absolute neutrophil count	6.39x103/µL	1.9-8x103/µL
Lymphocyte percentage	27.50%	19-48%
Absolute lymphocyte count	2.88x103/µL	0.9-5.2x103/µL
Eosinophil percentage	2.70%	0-7%
Absolute eosinophil count	0.28x103/µL	0-0.8x103/µL
Monocyte percentage	6.50%	3.4-9%
Absolute monocyte count	0.68x103/µL	0.1-1x103/µL
Basophil percentage	0.40%	0-1.5%
Absolute basophil count	0.04x103/µL	0-0.2x103/µL
Platelet count	639x103/µL	130-400x103/µL
Mean platelet volume	6.80fL	7.2-11.1fL
Large unstained cells (LUC) percentage	1.90%	0-4%

Source: Own elaboration.

Table 2. Complementary admission laboratory tests.

Test	Results	Reference values
Serum procalcitonin	0.020ng/mL	0-0.1ng/mL
High-sensitivity C-reactive protein	5.85mg/L	< mg/L: low risk 1–3 mg/L: moderate risk ≥ 3 mg/L: high risk
Aspartate aminotransferase	19.31U/L	10-35U/L
Alanine aminotransferase	39.75U/L	30-65U/L
Direct bilirubin	0.07mg/dL	0-0.3mg/dL
Indirect bilirubin	0.19mg/dL	0-0.7mg/dL
Total bilirubin	0.26mg/dL	0-1mg/dL
Alkaline phosphatase	70.2U/L	50-260U/L
Total serum protein	6.50g/dL	6-8.3g/dL
Transferrin saturation index	7.51%	20-50%
Serum transferrin	226.8mg/dL	200-400mg/dL
Serum ferritin	116.8ng/mL	15-150ng/mL
Total iron	28.36ug/dL	65-175ug/dL
Folic acid	7.76ng/mL	2.7-17ng/mL
Vitamin B12 (cyanocobalamin)	102pg/mL	180.0-914.0pg/mL
Glycated hemoglobin	5.7%	Non-diabetics: 3-5.6% Prediabetes: 5.7-6.4%
HDL cholesterol	37mg/dL	High risk: <40mg/dL Low risk: ≥60 mg/dL
LDL cholesterol	60mg/dL	Low risk: <130mg/dL
Total cholesterol	111mg/dL	100-200mg/dL
Triglycerides	71mg/dL	40-150mg/dL
Activated partial thromboplastin time	30.1 seconds	25-35 seconds
Antinuclear antibodies	Negative	Negative: ≤1.0U Weak positive: 1.1-2.9U. Positive: ≥3.0U
Anti-double-stranded DNA	Negative	Negative: <10UI/mL. Indeterminate: 10-15UI/mL Positive: >15-25UI/mL
Serology for Trypanosoma cruzi	Negative	Negative: <1:32 or absence of antibodies. Indeterminate: borderline titers that require repeat testing. 1:16 or values close to the kit’s cutoff point. Positive: ≥1:32
Treponemal test for syphilis	Non-reactive	Reactive Non-reactive
Serum complement C3	128mg/dL	80-180mg/dL
Serum complement C4	20.2mg/dL	10 and 40mg/dL

Source: Own elaboration.

On the day of admission, an electrocardiogram revealed sinus tachycardia and T-wave inversions in the precordial leads (Figure 1). A transthoracic echocardiogram (Figure 2) confirmed dilated cardiomyopathy with eccentric left ventricular hypertrophy, a left ventricular ejection fraction (LVEF) of 27%, severe global hypokinesis, severe diastolic dysfunction with increased filling pressures, and severe left atrial dilatation, without significant valvular disease or relevant signs of pulmonary hypertension. Based on these findings, myocarditis was suspected. Consequently, standard supportive management for heart failure with reduced ejection fraction—the therapeutic mainstay for myocarditis—was initiated while the underlying etiology was determined.

Figure 1. Admission electrocardiogram.

Source: Image obtained while conducting the study.

Figure 2. Admission transthoracic echocardiogram.

Source: Image obtained while conducting the study.

To determine the etiology of the ventricular dysfunction, a cardiac MRI was performed on July 12. It showed a mildly dilated left ventricle with eccentric hypertrophy, moderate global hypokinesis, and an LVEF of 31%. There was no evidence of myocardial edema or late gadolinium enhancement. These findings suggested a low probability of active myocarditis, though it could not be entirely ruled out.

On July 14, the patient experienced an episode of syncope with transient loss of consciousness (without loss of sphincter control) associated with hypertension, prompting a neurology consultation. That same day, a carotid Doppler ultrasound was performed, revealing diffuse bilateral wall thickening of the carotid arteries. It showed significant bilateral stenosis (approximately 70%) and complete thrombosis of the distal segment of the right common carotid artery, extending into its internal and external branches. These findings, suggestive of large-vessel vasculitis, shifted the clinical suspicion toward TA.

On July 15, a cerebral angiography (Figure 3) was performed, revealing stenosis of the right subclavian artery and the ostium of the right vertebral artery. Additionally, it showed complete thrombosis of the right common carotid artery from its origin, as well as string sign in the left common carotid artery with multisegmental stenosis. Intracranial collateral circulation dependent on the vertebrobasilar system was also observed; all these findings were consistent with the occlusive-stenotic phase of TA. That same day, an abdominal aortogram (Figure 4) revealed an active 21x32x21 mm pseudoaneurysm in the right inguinal region arising from the right common femoral artery.

Figure 3. Cerebral angiography. Complete thrombosis of the distal right common carotid artery and string sign on the left side are observed.

Source: Images obtained while conducting the study.

Figure 4. Abdominal aortogram and lower limb study. An active 21x32x21 mm pseudoaneurysm is observed in the right inguinal region.

Source: Images obtained while conducting the study.

On July 16, to establish the extent of large-vessel involvement, a CT angiography with 3D reconstruction of the thoracic and abdominal aorta was requested (Figure 5). While a “beaded” pattern was not observed, the study revealed diffuse involvement of the aortic axis, characterized by luminal diameter irregularities and structural alterations of the thoracoabdominal aorta and its bifurcation into the iliac arteries—findings consistent with Takayasu arteritis

Figure 5. CT angiography with 3D reconstruction of the thoracic and abdominal aorta. A) Left anterolateral oblique view of the aortic axis; B) Anterior view of the heart and aorta; C) Lower thoracoabdominal segment.

Source: Images obtained while conducting the study.

On July 16, following the confirmation of the TA diagnosis, immunosuppressive treatment was initiated with intravenous methylprednisolone pulses (1 g every 24 hours) for 3 days, followed by oral prednisone (50 mg daily). Steroid-sparing therapy was also started with methotrexate (5 mg orally every 12 hours, using a weekly split dose to reach a total of 20 mg) and folic acid (1 mg orally every 24 hours) from Wednesday to Sunday. Additionally, as antiparasitic prophylaxis, albendazole (400 mg orally every 24 hours) was prescribed for 3 days, according to the institutional protocol.

On the same day, management for heart failure was optimized with sacubitril/valsartan (50 mg every 12 hours), metoprolol (50 mg every 12 hours), ivabradine (7.5 mg every 12 hours), spironolactone (12.5 mg daily), empagliflozin (10 mg daily), furosemide (20 mg orally every 24 hours), acetylsalicylic acid
(100 mg daily), and atorvastatin (80 mg daily). Dosages were established based on the patient’s hemodynamic tolerance.

Given the carotid artery involvement, anticoagulation with therapeutic doses of low-molecular-weight heparin (60 mg subcutaneously every 12 hours) was also started on July 16, along with adjuvant care including omeprazole (20 mg daily), sucralfate (1 g orally every 8 hours), and acetaminophen (1 g every 8 hours for pain). This medication regimen was instituted without a predefined duration, to be adjusted based on clinical progress and subsequent findings.

During the first few days of her hospital stay, the patient remained hemodynamically and clinically stable, showing no adverse effects from the immunosuppressive therapy. On July 21, 2025, due to the TA diagnosis, severe thrombotic phenomena, and multisystem involvement, the rheumatology service recommended transfer to a quaternary care center for advanced studies and specialized multidisciplinary management; the referral process was then initiated.

On July 29, the patient reported pain in the right inguinal region. Physical examination revealed local swelling, suggesting a vascular complication. An inguinal ultrasound performed the next day confirmed an active 21×32×21 mm pseudoaneurysm originating from the right common femoral artery, with no evidence of inflammatory collections or associated lymphadenopathy. Consequently, endovascular management was performed on July 31 via the placement of a 10×57 mm covered stent.

On August 3, while awaiting transfer, she presented with episodes of hypertension refractory to fluid resuscitation associated with progressive hemodynamic compromise. She was admitted to the intensive care unit (ICU) with a diagnosis of undifferentiated shock, with a suspected cardiogenic component given her severe ventricular dysfunction and polypharmacy.

During the ICU stay, due to her immunosuppressed state, the patient required vasopressor support with norepinephrine (0.1 mcg/kg/min), continuous non-invasive monitoring, and broad-spectrum antibiotics (intravenous [IV] meropenem 2 g every 8 hours and IV linezolid 600 mg every 12 hours). This antibiotic regimen was maintained for 5 days.

On August 4, samples were taken for microbiological studies. Multiple cultures (including blood cultures and other sites according to protocol) were negative, ruling out an infectious source or sepsis. By August 6, blood pressure normalized, allowing for the gradual tapering of vasopressor support. During her ICU stay, the patient did not require mechanical ventilation and experienced no further neurological, thromboembolic, or infectious complications.

Considering the complexity of the clinical case—characterized by TA with severe multisegmental vascular involvement, persistent heart failure with reduced ejection fraction, and the presence of thrombi—as well as the need for advanced studies to establish large-vessel involvement and adjust immunosuppressive and cardiovascular therapy, the decision was made to transfer the patient to a quaternary care institution. Recommendations included follow-up by rheumatology, cardiology, and vascular surgery, as well as serial echocardiographic follow-up and vascular studies every 3–6 months to evaluate the progression of ventricular function and arterial disease activity. However, the patient was lost to follow-up after the referral.

Discussion

Upon admission, despite having no prior cardiovascular history, the patient exhibited clear manifestations of heart failure, such as progressive dyspnea, edema, and palpitations, which represented an atypical finding for her age. Similarly, the echocardiogram showed severe systolic dysfunction (LVEF of 27%), a rare finding in young patients without a relevant medical history (2). Initially, myocarditis was suspected; however, cardiac magnetic resonance imaging showed no late gadolinium enhancement or signs of active inflammation. However, while this indicates a low probability of said condition, it does not entirely rule it out

The subsequent appearance of transient neurological symptoms (presyncope, paresthesia, and paraparesis), combined with the detection of bilateral carotid bruits on physical examination, shifted the diagnostic suspicion toward vascular involvement beyond the heart. Consequently, a carotid Doppler ultrasound was performed, revealing arterial wall thickening and critical bilateral stenosis of the carotid arteries, with complete thrombosis of the distal segment of the right carotid artery—findings characteristic of the stenotic-occlusive phase of TA (3).

Ventricular dysfunction in cases of large-vessel vasculitis such as TA may be due to multiple factors, including arterial hypertension caused by aortic or renal artery stenosis, direct myocardial inflammation, coronary ostial involvement, and hemodynamic overload from aortic regurgitation (6). In the present case, the coexistence of recently diagnosed arterial hypertension, eccentric left ventricular hypertrophy, and severe systolic dysfunction—in the absence of documented coronary artery disease or significant structural valvular disease—suggests that the ventricular dysfunction was caused by multiple factors, such as the persistent systemic inflammation inherent to TA, hemodynamic overload associated with arterial hypertension, and large-vessel involvement, which could have favored the development of adverse left ventricular remodeling.

In the present case, the American College of Rheumatology (ACR)
criteria (4) were used to establish the diagnosis: the patient was under 60 years of age, presented arterial bruits (bilateral carotid bruits), and imaging tests evidenced vascular stenosis. Furthermore, despite the absence of specific serum biomarkers for TA and the low specificity of acute phase reactants (elevated CRP and normal procalcitonin), the clinical and imaging correlation allowed for the establishment of the TA diagnosis (1). It should be noted that timely clinical suspicion led to the performance of vascular imaging studies (Doppler ultrasound and angiography) that enabled an adequate diagnosis (4); however, the definitive diagnosis was delayed due to the non-specificity of the symptoms, reflecting a common problem in this type of vasculitis (1,3). The diagnosis was established based on clinical and imaging findings compatible with large-vessel vasculitis, fulfilling ACR criteria and supported by CT angiography, which evidenced multisegmental involvement of the aortic axis.

In our patient, the early initiation of immunosuppressive treatment with pulse methylprednisolone followed by high-dose prednisone and methotrexate as a steroid-sparing therapy (the therapeutic standard in active phases of the disease) (3) was fundamental in halting the progression of the inflammatory process. However, chronic vascular progression had already caused structural complications, such as a femoral pseudoaneurysm that required endovascular intervention with the placement of a covered stent, albeit with partial persistence of the lesion.

The present case is of relevance to the literature because it exemplifies an atypical presentation of TA, in which heart failure constitutes the initial manifestation of the disease (2). Furthermore, it emphasizes the necessity of considering systemic vasculitis in young patients with heart failure of no apparent etiology, highlighting how the combination of systemic symptoms, transient neurologic symptoms, and vascular findings on imaging can be pivotal in guiding the diagnosis. This case also underscores the value of a comprehensive and multidisciplinary approach, in which clinical suspicion and the judicious use of diagnostic tools can prevent significant delays in identifying complex conditions such as TA.

Similarly, our case highlights that the shock episode during hospitalization was the major adverse event experienced by the patient. From a pathophysiological standpoint, this was initially classified as undifferentiated shock; although a state of hypoperfusion was documented, the absence of an evident infectious focus and the coexistence of multiple predisposing factors precluded the immediate identification of a specific etiology, which is consistent with the definition of this type of shock described in the literature (7). However, a predominantly cardiogenic origin was proposed due to persistent severe systolic dysfunction, adverse left ventricular remodeling, and inflammatory involvement of large vessels, factors that increase afterload and diminish contractile reserve.

Nevertheless, a distributive or subclinical septic component cannot be entirely ruled out, particularly in the context of recent immunosuppression with pulse glucocorticoids and methotrexate. These agents can attenuate systemic inflammatory response and mask the clinical and paraclinical manifestations of infection (8), which justified the initiation of empirical broad-spectrum antibiotic therapy in our patient. However, the absence of microbiological isolates, the lack of clinical or paraclinical evidence of sepsis, and the favorable response to vasopressor support without the need for mechanical ventilation suggest that the infectious component, had it existed, was not predominant (9).

The present case report has limitations that should be considered. First, the nonspecific nature of the initial symptoms delayed the definitive diagnosis; this is consistent with the literature, which reports that the diagnosis may be late since the initial systemic phase of TA is characterized by nonspecific systemic symptoms (1). Second, the lack of mid- and long-term clinical and imaging follow-up hinders a more precise assessment of the sustained response to immunosuppressive therapy, the potential reversibility of ventricular remodeling, and the evolution of multisegmental vascular involvement. Third, as this is an individual case report, it is not possible to establish definitive causal inferences or generalize the findings.

Despite the aforementioned limitations, this case report makes a significant contribution to the medical literature because it illustrates an atypical presentation of TA and underscores the need to maintain a high index of diagnostic suspicion for this condition in young patients with heart failure of unknown etiology.

Conclusions

Even though TA is a rare disease, it has a profound impact on those affected. The onset of severe ventricular dysfunction in young patients with no cardiovascular history should raise alarm regarding inflammatory or vascular etiologies, particularly when heart failure is the initial manifestation. Early identification of TA allows for the timely initiation of appropriate immunosuppressive therapy, which is vital for controlling the disease and preventing serious long-term complications.

Ethical considerations

For the preparation of this case report, informed consent was obtained from the patient for the publication of her clinical data.

Conflicts of interest

None stated by the authors.

Funding

None stated by the authors.

Acknowledgments

To the Clínica Avidanti in Ibagué for facilitating the development of this case report, which provides valuable insights into the clinical management of Takayasu Arteritis.

References

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