This MedCase explores the diagnosis and management of heart failure with reduced ejection fraction (HFrEF) alongside type 2 diabetes (T2D) – two conditions that frequently coexist and profoundly amplify one another, leading to significant morbidity and premature mortality.
The case provides an opportunity to address multiple clinical challenges simultaneously while keeping equity and whānau at the centre of care.
Hemi is a 56-year-old Māori man presenting for a routine diabetes review and ongoing management of chronic back pain.
Six months ago, he injured his back at work while lifting heavy stock during a night shift. Because his sick leave is limited and he cannot afford to lose income, he has continued working and self-managed the pain with over-the-counter NSAIDs for the past two months. He says he "didn't want to make a fuss" or burden the practice.
He is a former smoker with a 20-pack-year history and switched to vaping 18 months ago.
His wife accompanies him and mentions that he has been "a bit puffed" lately, especially when walking to the letterbox. Hemi initially attributes this to poor sleep from back pain, but on further questioning, he admits to increasing dyspnoea on exertion and needing an extra pillow to sleep comfortably (orthopnoea).
Past medical history
- T2D | Hypertension | Dyslipidaemia
Medications
- Metformin 1 g twice daily (total 2 g/day)
- Candesartan 8 mg daily
- Atorvastatin 20 mg daily.
Social history
- Lives with his wife and mokopuna. Works as a machine operator in a food processing plant.
- Night shifts, limited flexibility, and financial pressure make it difficult to attend appointments or take time off.
- Former smoker, currently vaping.
Physical examination
- BP: 155/95 mmHg | Weight: 82 kg | BMI: 28 kg/m²
- Raised JVP | Mild bilateral ankle oedema | Reduced air entry and fine crackles at both lung bases.
Clinical impression
Hemi has symptoms and signs consistent with heart failure and fluid overload:
- exertional dyspnoea
- orthopnoea (extra pillow)
- raised JVP
- peripheral oedema
- basal crackles.
Epidemiology and health equity
Heart failure is the inability of the heart to pump blood sufficiently to meet the body's metabolic demands. In Aotearoa New Zealand, Māori and Pacific peoples experience a disproportionately higher burden of heart failure with HFrEF and T2D1.
- The mortality rate for Māori with heart failure is significantly higher than for non-Māori (relative risk 2.80 for males, 1.70 for females).
- Māori men are 4 times more likely, and Māori women 4.5 times more likely, to be hospitalised with heart failure than non-Māori.
- Heart failure occurs 10–15 years earlier in Māori compared with non-Māori.
- Māori and Pacific people under 50 are six times more likely to be hospitalised with heart failure than non-Māori, non-Pacific people.
These disparities reflect the cumulative effects of systemic inequity, socioeconomic hardship, limited access to preventive care, and the compounding burden of diabetes, hypertension, and obesity – conditions that are themselves more prevalent and less well-managed in Māori and Pacific communities.
Initial management of Hemi's HFrEF with T2D
Stop NSAIDs immediately: NSAIDs cause sodium and water retention, reduce renal perfusion, increase blood pressure, and can acutely decompensate heart failure, particularly in people with diabetes and hypertension.
Start oral furosemide 40 mg once daily for symptomatic fluid overload (can increase to 40 mg twice daily if response is inadequate).
Investigations
- Blood tests: FBC, U&Es, creatinine/eGFR, LFTs, BNP or NT-proBNP, HbA1c, lipids
- Urine ACR
- ECG
- Urgent echocardiography.
For Hemi's back pain
- Advise paracetamol (up to 1 g four times daily).
- Refer for physiotherapy.
- Discuss workplace modification and manual-handling support.
Initiating treatment while awaiting echocardiogram
The echocardiogram remains the gold standard for distinguishing HFrEF (LVEF ≤40%) from HFpEF (LVEF ≥50%), as ejection fraction is the critical determinant of which medications are life-prolonging2,3. However, given the current public system wait times, treatment need not be delayed.
Several clinical features help differentiate HFrEF from HFpEF when imaging is delayed, but are non-specific:
| Feature | HFrEF | HFpEF |
|---|---|---|
| Typical age | Younger (50–65) | Older (>70) |
| Sex | Male predominance (60–70%) | Female predominance |
| BMI | Lower | Higher (obesity common) |
| BNP/NT-proBNP | Markedly elevated (>1000–2000 pg/mL) | Moderately elevated (300–1000 pg/mL) |
| Common aetiology | Ischaemic, prior MI, dilated cardiomyopathy | Hypertension, atrial fibrillation, obesity |
Two days later, you review Hemi. He reports feeling less breathless, and you visibly notice has improved:
- Dyspnoea has eased
- Weight down from 82 kg to 80 kg
- Ankle oedema resolved
- Lung fields clearer.
Results from presentation day
- HbA1c: 65 mmol/mol
- LDL-C: 2.5 mmol/L, total cholesterol: 5.8 mmol/L
- Urine ACR: >100 mg/mmol (significant albuminuria)
- eGFR: 60 mL/min/1.73 m², K+ 4.0 mmol/L
- ECG: sinus rhythm
- BNP: 1400 pg/mL (markedly elevated).
The markedly elevated BNP supports heart failure in this clinical context. Given his symptoms, elevated BNP, and likely delays to echocardiography, it is reasonable to proceed with treatment on the assumption of HFrEF while awaiting imaging.
The four pillars of HFrEF therapy
International guidelines, including the 2024 ACC Expert Consensus Decision Pathway, 2022 ACC/AHA/HFSA guidelines, and the 2023 ESC focused update, consistently recommend quadruple therapy as the foundation of HFrEF management. When all four pillars are used, the aggregate treatment effect reduces the hazard of cardiovascular death or hospitalisation for heart failure significantly (HR 0.38; 95% CI 0.30–0.47) compared with an ACE inhibitor/ARB plus beta-blocker alone2.
All four agents should be initiated and uptitrated to maximally tolerated doses2,3.
| Pillar | Agent Class | Examples | Key Considerations |
|---|---|---|---|
| 1 | ACE inhibitor / ARB / ARNI |
ARB: candesartan; ARNI: sacubitril/valsartan |
ARNI preferred if tolerated – discuss with cardiology. Avoid ACEi: higher cough risk in Māori and Pacific peoples. |
| 2 | Cardioselective beta-blocker | Bisoprolol, carvedilol, metoprolol succinate | Initiate only when euvolaemic; check HR and BP at each uptitration. |
| 3 | Mineralocorticoid receptor antagonist (MRA) | Spironolactone 25 mg | Monitor potassium (risk of hyperkalaemia) and eGFR closely – especially with macroalbuminuria. |
| 4 | SGLT2 inhibitor | Empagliflozin 10 mg, Dapagliflozin 10 mg | Dual benefit: HFrEF mortality reduction AND diabetes management. |
Rapid uptitration of all four pillars after hospitalisation significantly reduced 180-day readmission risk and improved quality of life9. In primary care, aim for early initiation and stepwise uptitration at each review visit, checking BP, HR, renal function, and electrolytes.
Guideline-directed treatment for Hemi
International guidelines emphasise early introduction of all four pillars of guideline-directed medical therapy (GDMT) rather than slow stepwise escalation.
The following changes and introductions of medication are made with Hemi. He is concerned about the number of medications; with reassurance and the shared goal of returning to work, he agrees to the plan.
Regular follow-up is arranged to monitor fluid status, blood pressure, creatinine/eGFR, and electrolytes (particularly potassium due to the risk of hyperkalaemia).
a) ARB (already on, now increased)
Continue candesartan, now increased to 16 mg daily (target 32 mg daily).
b) Beta-blocker
Start bisoprolol 1.25 mg with planned uptitration (target 10 mg daily).
c) Mineralocorticoid receptor antagonist (MRA)
Add spironolactone 25 mg once daily.
d) SGLT2 inhibitor for heart failure
Start empagliflozin 10 mg daily (to reduce total number of pills, a combination of empagliflozin and metformin (Jardiamet) is used)4,5.
Cardiovascular risk reduction
Increase atorvastatin to 40 mg – indicated given diabetes and established cardiovascular disease.
Hemi meets criteria for empagliflozin via Special Authority for HFrEF without requiring a confirmed echocardiogram1:
- Diagnosed with heart failure based on history, examination, and markedly raised BNP.
- NYHA functional class II–IV. Hemi has dyspnoea on exertion and when lying flat (class II–III).
- Echocardiogram is not reasonably practicable in a timely manner; in the treating practitioner's opinion, the patient would benefit from treatment.
- Receiving concomitant optimal standard funded heart failure treatment — furosemide and ARB.
The SGLT2 inhibitor: Empagliflozin for HFrEF
From 1 December 2024, empagliflozin was funded in New Zealand specifically for chronic HFrEF under Special Authority criteria, separate from the diabetes indication1.
SGLT2 inhibitors were originally developed as glucose-lowering agents but have demonstrated profound cardiovascular and renal benefits independent of glycaemic effect4,5,13.
Key trial evidence
- EMPA-REG OUTCOME (empagliflozin in T2DM + established CVD): 38% reduction in cardiovascular death; 35% reduction in heart failure hospitalisation13.
- EMPEROR-Reduced (empagliflozin in HFrEF, LVEF ≤40%, with and without diabetes): 25% reduction in the composite of cardiovascular death or HF hospitalisation (HR 0.75; 95% CI 0.65–0.86); benefit seen regardless of diabetes status; reduction in annual eGFR decline (0.55 vs 2.28 mL/min/1.73 m²/year)5.
- EMPEROR-Preserved (empagliflozin in HFpEF, LVEF >40%, with and without diabetes): 21% reduction in the composite of cardiovascular death or HF hospitalisation (HR 0.79; 95% CI 0.69–0.90); benefit driven primarily by a 29% reduction in HF hospitalisations; effect seen regardless of diabetes status and across a wide range of LVEF up to 65%7.
Practical monitoring
- Check eGFR before starting; expect a small early dip, which is expected and reversible.
- Monitor for volume depletion and hypotension; particularly important as Hemi is also on furosemide.
- Educate on genital hygiene to prevent mycotic infections (can be common with high glucose levels) and to stop empagliflozin when unwell to prevent euglycaemic ketoacidosis (rare).
- Hold empagliflozin 3 days before any elective procedure (sick day rules).
Blood pressure
Hypertension combined with HFrEF accelerates cardiac remodelling and renal decline. Uptitrating the four pillars of GDMT also supports BP optimisation, with a target of ≤130/80 mmHg in line with the New Zealand Heart Foundation CVD Consensus Statement6.
Lipid management
The New Zealand Heart Foundation/CSANZ CVD Risk Consensus Statement recommends an LDL-C target of ≤1.8 mmol/L for high-risk individuals, including those with heart failure, diabetes, or a 5-year CVD risk ≥15%6. The NZSSD recommend a target LDL cholesterol (LDLc) <1.4 mmol/L8.
For patients with HFrEF, T2D, significant albuminuria, and hypertension, high-intensity statin therapy is strongly indicated:
- Atorvastatin 40–80 mg or rosuvastatin 20-40 mg; ezetimibe may be required to reach LDL-C target6,8.
Māori and Pacific peoples are significantly less likely to be maintained on statin therapy following cardiovascular events compared with NZ Europeans6.
Active follow-up, adherence support, and ensuring access to funded options are essential equity considerations.
Three months later, the echocardiogram result is in your inbox: LVEF 33% – consistent with HFrEF. The clinical suspicion was correct, and therapy has been appropriately targeted.
Updated results at 3 months
- HbA1c: 70 mmol/mol
- eGFR: 40 mL/min/1.73 m²
Because Hemi has diabetic kidney disease and persistent hyperglycaemia, an additional glucose-lowering agent is appropriate. Special Authority is applied for dulaglutide (GLP-1 RA)10:
- Type 2 diabetes with suboptimal glycaemic control.
- Established cardiovascular disease (HFrEF).
- Diabetic kidney disease.
Hemi's eGFR is 40 mL/min/1.73 m². Metformin should be reduced to a total dose of 1 g/day (Jardiamet to 500 mg/5 mg twice daily) and closely monitored at this level; it should be withheld if eGFR falls below 15 mL/min/1.73 m²,12.
Diabetes management beyond empagliflozin: GLP1RAs
Why Dulaglutide?
- Major adverse cardiovascular events (MACE) reduction benefit in T2D with established CV risk factors (REWIND trial)14.
- Modest weight loss, which is beneficial in the context of reducing MACE.
- Once-weekly dosing, which significantly reduces the daily medication burden, supports adherence.
- Does not require dose adjustment for eGFR down to 15 mL/min.
Combination of SGLT2 inhibitor + GLP1RA: Recent meta-analyses confirm that combining SGLT2 inhibitors with GLP1RAs produces additive cardiovascular and renal protection beyond either agent alone in T2D with high CV risk5,10.
GLP1RA and HFrEF: The REWIND post-hoc analysis showed that dulaglutide did not reduce heart failure events (HR 0.93; 95% CI 0.77–1.12), though it has strong evidence for glycaemia and MACE reduction14. In contrast, semaglutide improved outcomes in heart failure: the SELECT trial showed reduced MACE, heart failure hospitalisation, and cardiovascular death in patients with HF11.
Metformin in HFrEF and CKD
Metformin is generally safe in stable, compensated HFrEF and should be continued where renal function permits12.
When to withhold metformin
- Acute HF decompensation (haemodynamic instability)
- eGFR <15 mL/min (risk of lactic acidosis)
- Contrast media procedures
- eGFR <30 mL/min: reduce dose and monitor closely.
Medication to avoid/caution in HFrEF
| Agent | Reason to avoid |
| Thiazolidinediones (e.g., pioglitazone) | Cause sodium and water retention; directly worsens HFrEF. |
| NSAIDs | Sodium retention, reduced renal perfusion, worsening of both HF and CKD. |
| Agent | Reason to avoid |
| DPP-4 inhibitors (e.g. vildagliptin) | Some DPP‑4 inhibitors have shown equivocal signals for increased HF hospitalisation in trials. This signal has not been observed with vildagliptin to date. |
| Sulfonylureas (e.g. gliclazide, glipizide) | Hypoglycaemia risk amplified in HFrEF (reduced appetite, frailty, impaired renal clearance). |
About six months after initial presentation, Hemi's wife is seen for a routine consult. She is concerned that Hemi has not been taking his medicines consistently.
When spoken with shortly after, Hemi explains:
- Night shifts and work pressure make routines difficult.
- He is overwhelmed by the number of tablets (now 6–8 medicines).
- He is worried about exercising with heart failure.
- He is uncertain which medicines matter most.
- Whānau responsibilities (including caring for his mokopuna) limit time and energy for self-management.
Adherence, work and whānau
The conversation shifts from simply prescribing more medicines to:
- Simplifying treatment where possible.
- Explaining the purpose of each medicine clearly.
- Using blister packs or a medication organiser.
- Involving whānau in planning.
- Supporting realistic, sustainable self-management.
Addressing medication burden, fears about exercise, and broader social context is as important as prescribing the right drugs.
Strategies for support:
- Referral to cardiac rehabilitation or a community heart failure programme.
- Access to Care Plus or similar chronic disease support.
- Pharmacy support for medication review and adherence strategies.
- Culturally appropriate education resources for HFrEF and diabetes, including resources developed with and for Māori communities.
Exercise: Safe and recommended
Physical activity is not only safe but recommended in stable HFrEF. Supervised exercise and cardiac rehabilitation improve functional capacity, quality of life, and reduce hospitalisation2,3.
Start with gentle walking, 20-30 minutes most days of the week, at a pace at which your patient can still hold a conversation.
Progress gradually; help patients learn to distinguish expected exertional dyspnoea from decompensation symptoms (sudden weight gain, worsening oedema, marked dyspnoea at rest).
Daily weight monitoring is a key self-management tool: weight gain of >2 kg in 2 days warrants urgent contact with the practice.
Key Points
- NSAIDs are contraindicated in suspected or confirmed heart failure, particularly in the context of diabetes and CKD.
- Heart failure can be diagnosed clinically in primary care without waiting for echocardiography when the clinical picture is convincing, and BNP is markedly elevated.
- New Zealand heart failure care emphasises early use of all four pillars of GDMT for HFrEF: ARNI/ACEi/ARB, a cardioselective beta-blocker, a mineralocorticoid receptor antagonist (MRA), and an SGLT2 inhibitor.
- From 1 December 2024, empagliflozin was funded under PHARMAC Special Authority specifically for chronic HFrEF – a separate pathway from the diabetes indication.
- Metformin is safe in stable, compensated HFrEF but should be dose-reduced when eGFR falls below 45 mL/min and withheld below 15 mL/min.
- Diabetic kidney disease should prompt consideration of an SGLT2 inhibitor and/or GLP-1 RA for cardiovascular and renal protection.
- GLP-1 RAs (e.g., dulaglutide) reduce MACE and glucose levels in T2DM with CVD, but should not prevent using SGLT2 inhibitors, which are the cornerstone of HFrEF and HFpEF pharmacotherapy.
- Non-adherence and treatment burden are common in complex chronic disease; a person-centred, whānau-aware approach is essential.
This MedCase was written by Dr Anthony Dewan MBChB, FRNZCGP, with expert review by Dr Ryan Paul, Endocrinologist and Diabetologist.
References
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