Monitoring drug therapy for HFrEF

The response to therapy and the need for additional or adjusted therapy for HFrEF is primarily guided by ongoing assessment of the patient’s symptoms, functional status and left ventricular ejection fraction.

While plasma b-type natriuretic polypeptide (BNP) or N-terminal proBNP (NT-proBNP) concentrations can be used to monitor the response to therapy, the clinical and cost effectiveness of this approach remain uncertain. Reserve BNP and NT-proBNP monitoring for patients with HFrEF who have not responded to conventional managementMcLellan, 2016.

Common issues encountered in the management of heart failure are an asymptomatic fall in blood pressure or a rise in serum creatinine (up to 30%) or serum potassium (within the normal range) when drug therapy is started, or doses are increased. This may be transient and should not necessarily prompt dose reduction or cessation of treatment; consider the clinical context of these changes—for example, whether they have occurred in isolation, or if other signs or symptoms are present.

If a patient taking combination therapy has symptomatic hypotension, consider changing the timing of doses (eg split into morning and night) and review the patient’s volume status and other medical therapy. Consider stopping treatments that reduce blood pressure but have not been shown to improve outcomes in HFrEF (eg treatments for prostate enlargement, calcium channel blockers). If the patient remains symptomatic, especially in the absence of congestion, reduce the dose of the renin-angiotensin system inhibitor (or other vasodilators) and loop diuretic in preference to reducing the beta blocker dose (unless the heart rate is less than 50 beats/minute).

If kidney function continues to deteriorate, review the patient’s volume status and medical therapy. If there are no clinical symptoms or signs of congestion, initially reduce or withhold the loop diuretic. If the patient is taking a nonsteroidal anti-inflammatory drug, this should be stopped. Consider decreasing the dose of the renin-angiotensin system inhibitor or mineralocorticoid receptor antagonist.

If the patient has hyperkalaemia, ensure they are not taking a potassium supplement and review their diet. Consider decreasing the dose of the renin-angiotensin system inhibitor or mineralocorticoid receptor antagonist. If the serum potassium is greater than 5 mmol/L, withhold the mineralocorticoid receptor antagonist.

Patients with heart failure are at increased risk of developing iron deficiency. In patients with heart failure, iron deficiency (with or without anaemia) is strongly associated with increased mortalityJankowska, 2014. Intravenous iron therapy in patients with HFrEF and iron deficiency (with or without anaemia) improves symptoms, exercise tolerance and quality of life, and may reduce hospitalisationAnker, 2009Ponikowski, 2015. Consider investigations to identify the cause of iron deficiency if appropriate.