A case of Takayasu arteritis misdiagnosed as dilated cardiomyopathy: a case report

A 34-year-old female patient was admitted to our hospital with a 6-year history of recurrent chest tightness, which had significantly worsened over the past three days. The clinical presentation was notable for accompanying refractory hypertension. Interestingly, the clinical presentations were inconsistent with typical heart failure (HF), creating a diagnostic challenge that obscured the underlying aetiology.

We reported a case of a patient who presented with dilated cardiomyopathy (DCM), because of the significant symptoms of HF. However, the concurrent presence of refractory hypertension introduced diagnostic complexity, potentially confounding the final diagnosis. After comprehensive diagnostic evaluation including echocardiography, ancillary laboratory tests, and computed tomographic angiography (CTA) were finished, the underlying aetiology of this complex case ultimately revealed.

Takayasu arteritis (TA) is a rare, chronic, idiopathic granulomatous vasculitis affecting the entire aorta and its primary branches. TA demonstrates heterogeneous clinical manifestations that vary according to lesion location, frequently resulting in diagnostic delays. We report a case of a young female presenting with an atypical manifestation of TA, who presentation manifesting as HF and refractory hypertension. Previous misdiagnoses at referring institutions included DCM, with subsequent management involving antihypertensive therapy and symptomatic blood transfusions. Comprehensive examinations confirmed a diagnosis of TA, featuring severe renal artery stenosis that induced secondary hypertension. Uncontrolled or active TA can exacerbate valvular regurgitation, potentially precipitating severe HF, eventually resulting in global cardiac enlargement, resembling DCM. This case illustrates a diagnostically challenging presentation of TA, where HF with reduced ejection fraction (HFrEF) emerged as the initial clinical manifestation amidst multiple confounding factors. Notably, TA may manifest with a DCM phenotype. The development of HFrEF in these patients is primarily driven by two TA-related mechanisms: (i) secondary hypertension from renal artery stenosis, and (ii) volume overload due to aortic regurgitation during active disease phases.