Key result
Calcium and vitamin D supplementation linked to ~104 msec QTc reduction in HF with hypoparathyroidism.
Why the study?
Persistent QTc prolongation due to hypocalcemia from hypoparathyroidism in heart failure patients requires early identification and management to prevent arrhythmias and sudden cardiac death.
Case Report (n=1)
This case highlights the importance of early identification and management of secondary causes of QTc prolongation, such as hypocalcemia, in patients with heart failure.
Hypocalcemia should be excluded in persistent QTc prolongation with HFrEF; single case leaves open targeted post-thyroidectomy screening.
The QT interval on an electrocardiogram reflects ventricular depolarization and repolarization, with prolonged QTc indicating a defect in myocardial repolarization. This condition increases the risk of arrhythmias, torsade’s de pointes, and sudden cardiac death. We present the case of a 40-year-old female with heart failure and reduced ejection fraction who exhibited persistent QTc prolongation due to hypocalcemia resulting from hypoparathyroidism secondary to a thyroidectomy performed 15 years prior. Management included standard heart failure treatment alongside active vitamin D and calcium supplementation, leading to clinical improvement. This case underscores the importance of early identification and management of secondary causes of QTc prolongation in heart failure patients.
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Khalid et al. (2025) conducted a case report in Heart failure with reduced ejection fraction, hypocalcemia, QTc prolongation (n=1). Calcium and active vitamin D supplementation was evaluated on QTc interval and serum calcium levels. Management with calcium and active vitamin D supplementation in a heart failure patient with hypoparathyroidism improved serum calcium levels and reduced QTc prolongation from 643 msec to 539 msec.
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