Key result
Long-term telmisartan linked to severe anemia, resolving after drug discontinuation.
Why the study?
Angiotensin receptor blockers may suppress erythropoietin production and worsen anemia, potentially contributing to heart failure decompensation.
Case Report (n=1)
No
Long-term ARB therapy may exacerbate iron deficiency anemia and precipitate high-output heart failure, highlighting the need to monitor hemoglobin in susceptible patients.
Single case links long-term telmisartan to anemia and high-output HF; leaves open whether ARBs require hemoglobin monitoring in susceptible patients.
Anemia is a common comorbidity in patients with cardiovascular disease and may contribute to heart failure. Angiotensin receptor blockers (ARBs), through inhibition of the renin-angiotensin–aldosterone system (RAAS), may suppress erythropoietin production and erythropoiesis. We report the case of a 67-year-old female with ischemic heart disease and hypertension on long-term telmisartan therapy who presented with breathlessness and bilateral pedal edema. Investigations revealed severe microcytic anemia (hemoglobin: 6.1 g/dL) with iron deficiency. Imaging showed cardiomegaly with bilateral pleural effusion, and the patient developed high-output heart failure with type II respiratory failure. ARB therapy was discontinued, and the patient was managed with blood transfusion and diuretics, resulting in clinical improvement and hemoglobin increase to 10.6 g/dL. This case highlights the potential contribution of RAAS blockade to worsening anemia and subsequent cardiac decompensation.
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Khambhaliawala et al. (2026) conducted a case report in High output heart failure and iron deficiency anemia (n=1). Telmisartan was evaluated on Hemoglobin level.
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