Hypertension is a common comorbidity in patients with heart failure and most drugs that have demonstrated to improve prognosis in this population have the potential to reduce blood pressure. Nonetheless, the relationship between blood pressure and clinical outcomes and the relevance of blood pressure reduction in heart failure remains unclear. This narrative review summarises the evidence currently available to guide blood pressure treatment in this patient group and highlights key questions for further research. In patients with heart failure with reduced ejection fraction, guidelines consensually recommend treating hypertension with drugs that have compelling indications in heart failure, with a target blood pressure of 130/80 mmHg. In patients with heart failure with preserved ejection fraction, guidelines acknowledge that the optimal treatment strategy remains unclear and thus recommend adopting a similar treatment strategy to patients with reduced ejection fraction. In any case, low blood pressure should not deter uptitration of drugs otherwise indicated to improve prognosis in heart failure, provided that patients tolerate drugs without adverse events. In the absence of evidence for modification of treatment efficacy and safety by baseline blood pressure, it is likely that treatment may actually lead to higher absolute risk reduction in patients with the lowest blood pressure. Special considerations and treatment adjustments are needed in the elderly as well as in patients with diabetes, chronic kidney disease and atrial fibrillation. More evidence is needed on blood pressure management in patients with heart failure in general, in whom the increasing burden of multimorbidity adds further complexity to treatment.
- heart failure with preserved ejection fraction
- heart failure with reduced ejection fraction
- heart failure
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Patient consent for publication Not required.
Contributors ACP-G contributed to planning and writing this review article. KR supervised ACP-G and reviewed the manuscript. ACP-G is responsible for the overall content of this review.
Funding This project was supported by the Oxford Martin School grant for the Deep Medicine programme, the National Institute of Health Research (NIHR), Oxford Biomedical Research Centre and the British Heart Foundation.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
Data sharing statement There is no additional data.
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