Vitamin D and Heart Failure
Heart failure patients have very high rates of vitamin D deficiency — often 70%+. The VINDICATE trial showed cholecalciferol supplementation improved left ventricular function in HFrEF patients. Correction is standard supportive care alongside guideline-directed HF therapy.
Deficiency prevalence in HF
Multiple observational studies find 70-90% of HF patients have 25(OH)D < 30 ng/mL and 30-50% < 20 ng/mL. Reasons include reduced sun exposure from mobility limitation, altered kidney function affecting activation, and loop-diuretic-related changes.
VINDICATE trial
Witte 2016 randomised 229 HFrEF patients with 25(OH)D < 20 ng/mL to 4,000 IU/day vitamin D vs placebo for 1 year. Vitamin D arm showed:
- ~6.7% absolute increase in LV ejection fraction.
- Improvement in LV end-diastolic and end-systolic volumes.
- No improvement in 6-minute walk distance primary endpoint.
- Modest quality-of-life improvement.
Loop diuretics and thiamine — separate but important
Furosemide, torsemide, and bumetanide (all loop diuretics) increase urinary thiamine losses. Chronic HF patients on loop diuretics develop thiamine deficiency at up to 33% prevalence. This is not a vitamin D issue but is worth screening — thiamine deficiency worsens HF, causes Wernicke's, and is easily correctable. See our thiamine page.
HFpEF (preserved ejection fraction)
HFpEF is increasingly recognised as a distinct syndrome — heart failure with normal ejection fraction, driven by diastolic dysfunction, hypertension, obesity, and diabetes. Vitamin D evidence in HFpEF is thinner than HFrEF; correcting deficiency is reasonable for general health but disease-specific benefit is unproven.
Practical guide
- All HF patients: test 25(OH)D annually.
- Correct deficiency: 2,000-4,000 IU/day cholecalciferol.
- On chronic loop diuretic: consider thiamine 100 mg/day, especially in older patients or malnourished.
- Guideline-directed HF therapy (ARNI/ACE-i, beta-blocker, MRA, SGLT2i) remains the priority.
- Monitor calcium and creatinine — HF patients on ACE-i/ARB and MRAs can develop hyperkalaemia; vitamin D-driven calcium changes deserve attention.