Wait, what happened to diastolic heart failure?
This is now called heart failure with preserved ejection fraction .The preferred terms are now:
- heart failure with preserved ejection fraction (HFpEF) – 50% or more
- heart failure with mildly reduced ejection fraction (HFmrEF) – 40% to 49%
- heart failure with reduced ejection fraction (HFrEF) – 40% or less
Traditionally, support of HFpEF was mostly supportive, but there is now a role of SGLT-2 and MLA for improving the prognosis for HFpEF.
Why all the excitement about SGLT-2s and cardio-renal protection?
SGLT-2s block glucose reabsorption in the renal proximal tubule. However, the studies show no glucose dependency for cardiorenal protection, suggesting the protection happens through a non-glucose mechanism. On the CKD side, they may improve tubule-glomerular feedback and reduce the filtration pressures. On the CHF side, they affect the sodium-hypgoren exchanges, and may reduce oxidative stress/inflammation.
So we should have everyone with DM on SGLT-2?
I’m starting to think of metformin, SGLT-2 and GLP-1 agonists as my ‘A-team’. They all promote weight loss to some degree and have some sort of cardio-renal benefit.
The others antidiabetic meds have a role for lowering glucose, but don’t have the weight loss/cardio-renal protective effects.
The NICE guidelines promote two of the three ‘A-team’ early on (metformin and SGLT-2), especially if cardio-renal risk.
When exactly is ACE used in CKD?
I used to think this was pretty much default for most people with CKD. On closer reading of the guidelines, you can think of it as a sliding scale against ACR:
3 + -> Only if diabetes 30 + -> Only if hypertension 70 + -> everyone (and refer to nephrology unless known attributed to diabetic nephropathy, and drop clinic BP target to 130/80 mmHg)
When do you use an SGLT-2 in CKD, and which one?
Dapagliflozin and empagliflozin have subtly different indications for eGFR range, and it’s easiest to use empagliflozin as it has a wider range and more permissive indications. Assuming the person is already on the max-tolerated dose of ACE-i/ARB:
- 20 mL/min/1.73 m2 to less than 45 mL/min/1.73 m2, or
- 45 mL/min/1.73 m2 to 90 mL/min/1.73 m2 and either an ACR of 22.6 mg/mmol or more, or type 2 diabetes
So did you start empagliflozin in this case?
Yes. We discussed rechecking BP once it was started, warning signs of DKA, pausing on sick days, UTIs, balanitis and the rare risk fo Fournier’s gangrene.
What did you learn about clinical inertia during this?
I realised that quite often I/we don't think to escalate treatments for LTCs unless reviewing that specific LTC. I thought of all the times we see someone with CKD or CHF, and how rarely we optimise medications unless they've had a trigger event e.g. a flare, brought up a specific symptom or there's a test result relating to the condition to review. According to this article on Clinical Inertia, this may be because we overestimate the care already given, or find soft reasons not to escalate care at this time, or because of a lack of training/confidence. I realise I therefore don't need to just learn about SGLT-2 for CKD/CHF, but to know about them with confidence and believe in their importance to improve patient outcomes. This will encourage me to consider these optimisations even outside of those trigger events.
What have you learnt going forwards?
I should be more confident initiating SGLT-2s in people with CHF and CKD who meet the criteria, even without diabetes. I need to also believe in the value of using them to make me more likely consider these changes even when there is no trigger event.