Secondary hyperparathyroidism in heart failure is a consequence of renin-angiotensin-aldosterone activation, chronic hyperaldosteronism, and loop diuretic usage, resulting in calcium excretion. The result is an inflammatory state with adverse effects on myocardial remodeling and systemic complications. Recent literature has suggested that elevated parathyroid hormone predicts adverse outcomes in patients with heart failure independent of serum calcium and phosphate, vitamin D deficiency, and renal insufficiency. Parathyroid hormone has been correlated with elevated brain natriuretic peptide levels, an established biomarker of heart failure severity. There are several limitations to the utilization of parathyroid hormone as a biomarker for heart failure, and further prospective studies need to be conducted to assess the value of multiple parathyroid hormone measurements over time and elucidate the role of parathyroid hormone in diastolic dysfunction. Pending further validation, there is promise for parathyroid hormone as a complementary biomarker in heart failure.