International Journal of Research in Medical Sciences
Sharma PK et al. Int J Res Med Sci. 2024 Aug;12(8):3033-3035
[Link] pISSN 2320-6071 | eISSN 2320-6012
DOI: [Link]
Case Report
Beyond the pulse: unusual presentations of Takayasu’s arteritis
Pallav K. Sharma*, Chandan Kumar, Suraj Kumar
Department of Medicine, Patna Medical College and Hospital, Patna, Bihar, India
Received: 24 May 2024
Revised: 17 June 2024
Accepted: 29 June 2024
*Correspondence:
Dr. Pallav K. Sharma,
E-mail: pallavkumarsharma@[Link]
Copyright: © the author(s), publisher and licensee Medip Academy. This is an open-access article distributed under
the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial
use, distribution, and reproduction in any medium, provided the original work is properly cited.
ABSTRACT
Takayasu’s arteritis (TA) a.k.a pulseless disease is a chronic inflammatory occlusive thrombo-aortopathy. It is a rare
inflammatory disease affecting large arteries, often leading to significant diagnostic challenges, especially when
presenting with atypical symptoms. This case report explores a patient, whose primary complaints were chest pain
and no neurological or constitutional symptoms, diverging from the common presentations of diminished pulses or
limb claudication. Advanced imaging, including CT Aortogram and interventions like cardiac angiography, played a
crucial role in detecting vascular inflammation and stenosis, facilitating accurate diagnosis and management. The case
underscores the importance of considering Takayasu arteritis in differential diagnoses, even with non-classical
presentations. This present case demonstrates rare and unique presentation of TA where patient presents with
myocardial infarction and cardiogenic shock and also explains the diagnostic dilemma of TA with such unusual
presentation.
Keywords: CT Aortogram, Myocardial infarction, Takayasu’s arteritis
INTRODUCTION and stroke.4 Myocardial infarction at presentation is rare.5
This case involves a patient presenting with NSTEMI and
Takayasu’s arteritis (TA) predominantly affects cardiogenic shock, without prior history or other
individuals in Asian countries, with approximately 25% symptoms of TA.
of cases beginning before age 20.1 It involves chronic
inflammation of the vessel wall, leading to stenosis, CASE REPORT
thrombosis, or aneurysm formation. The late phase of TA
features intimal proliferation with atherosclerosis, medial A 22-year-old married housewife developed mild
necrosis with scarring, and adventitial fibrosis.2 Many dyspnoea on exertion on March 7, 2024. This persisted
patients with TA have anti-endothelial cell antibodies that for 10 days with little discomfort and was left untreated.
damage vessels by inducing endothelial inflammatory Few days after, she experienced acute chest pain and
cytokine production, adhesion, and apoptosis.3 It mainly dizziness, leading to her admission to a private hospital in
affects aorta and its branches such as subclavian artery, Madhubani, Bihar (On March 17, 2024). Her attendants
common carotid artery, renal artery, vertebral artery etc. reported no prior similar illnesses. Initial examination
TA’s manifestations are diverse, ranging from revealed non-palpable peripheral pulses and unrecordable
constitutional symptoms like fever, malaise, light- blood pressure. She was dyspneic at presentation. ECG
headedness, and musculoskeletal pain to upper limb indicated NSTEMI with ST-T changes in leads V1-V6,
claudication, secondary hypertension, aortic III, and aVF, and elevated cardiac enzymes (positive
regurgitation, congestive heart failure, retinal ischemia, Troponin T). She was treated with inotropes, nitrates,
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Sharma PK et al. Int J Res Med Sci. 2024 Aug;12(8):3033-3035
aspirin, clopidogrel, atorvastatin and enoxaparin. Her AR causes left ventricular (LV) remodelling, resulting in
general condition improved, and chest pain subsided, but LV dilatation and increased LV mass (hypertrophy).6
peripheral pulses remained non-palpable, and BP was
unrecordable. She was referred to Patna Medical College
and Hospital, diagnosed with NSTEMI and cardiogenic
shock. On March 18, 2024, at PMCH, she was enquired
thoroughly and reported no prior illnesses. There was not
any history of prior such illness since childhood. Her
birth was uneventful. There weren’t any chronic
symptoms except for dyspnoea for last 10 days.
Examination revealed non-palpable peripheral pulses and
non-recordable BP in all limbs, mild pallor, without
icterus, cyanosis, clubbing or lymphadenopathy. Chest A B
examination revealed bilateral basal fine crepitations, and
a low-intensity, soft diastolic murmur in the aortic area.
She had decreased urine output. Blood tests showed Figure 1 (A and B): CT aortogram findings.
moderate anaemia (9 g/dl), raised ESR (106 mm/hr), and
raised CRP with normal liver and kidney function, lipid
Table 1: Examination findings.
profile, thyroid profile, serum homocysteine level, ANA,
ANCA, and APLA. ECG still showed ST-T changes, and
Findings Observations
chest radiography revealed cardiomegaly.
General Examination
Echocardiography indicated global hypokinesia of the left
ventricle, left ventricular hypertrophy (18 mm), mild MR, Pulse Non recordable
moderate AR, and a reduced ejection fraction (37%). Blood pressure Non recordable
Abdominal ultrasonography and renal vessel Doppler Temperature 99oF
were unremarkable. Next day, on March 19, 2024, her Pallor Present
lower limb pulses became palpable, however the upper Icterus, Cyanosis, Clubbing,
Absent
limb (radial, brachial) pulses were absent, and BP in Lymphadenopathy, Edema
lower limb was 100/70 mm Hg. Inotropes were tapered Biochemical Investigation
and discontinued as her condition improved. On further CBC 10300 Cells/dl
examining the patient a pronounced carotid bruit, more Hb 9g/dl
on the left than the right, was noted. A CT aortogram was Bilirubin-1.2mg/dl
performed and showed wall thickening of the thoracic LFT and KFT SGPT/SGOT-40/44
and abdominal aorta with stenosis in the left CCA and Creatinine-1.3mg/dl
left subclavian artery (figure 1) with aortic root dilatation ESR 109 mm/hour
(figure 2). Coronary angiography revealed no
Suggestive of
abnormalities. She was started on prednisolone
Iron profile anaemia of chronic
1mg/kg/day. Diuretics, Beta blockers and ARNI were
disease
started for heart failure and LVH after which she was
discharged. Reticulocyte count 0.6%
Normal, no any
PBS
Follow Up immature cell present
HIV/HBsAg/HCV Non-reactive
On one moth follow up, there was no relapse of Other Investigations
symptoms and initial remission was achieved. Patient ANA by IFA Non-reactive
showed marked improvement in symptoms (dyspnoea on c-ANCA and p-ANCA Non-reactive
exertion and chest pain). Biochemical investigations were APLA profile Negative
normal and 2D ECHO revealed no deterioration in USG whole abdomen and
cardiac function. Prednisolone and other medications Unremarkable
Renal artery Doppler study
were continued till the next follow up. Could not be
Arterial biopsy
performed
DISCUSSION
Prolonged LV hypertrophy and dilatation, combined with
A spectrum of disorders can cause myocardial infarction ongoing inflammation, can precipitate myocardial
(MI) in young individuals, including antiphospholipid ischemia due to an oxygen supply-demand mismatch,
antibody syndrome (APLA), familial dyslipidaemia, potentially leading to MI. It may also result in LV
hypercoagulable states, and Kawasaki disease. Takayasu aneurysm or septal/free wall rupture. In this patient,
arteritis is a rare cause. Chronic inflammation of the prolonged LV hypertrophy likely caused the MI. Lesion
aorta, especially the aortic arch, leads to aortic root in Coronary artery causing stenosis or aneurysm due to
dilatation and aortic regurgitation (AR). Long-standing inflammation can also lead to acute MI but on coronary
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Sharma PK et al. Int J Res Med Sci. 2024 Aug;12(8):3033-3035
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Funding: No funding sources Cite this article as: Sharma PK, Kumar C, Kumar S.
Conflict of interest: None declared Beyond the pulse: unusual presentations of
Ethical approval: Not required Takayasu’s arteritis. Int J Res Med Sci
2024;12:3033-5.
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