Unveiling the Hidden Stroke Threat in Patients With Atrial Fibrillation and Primary Hyperparathyroidism

Georges Khattar1, Samer Asmar1, Elie Bou Sanayeh1

  • 1Department of Internal Medicine, Staten Island University Hospital/Northwell Health, Staten Island, New York.

Insights

Primary hyperparathyroidism (PHPT) significantly increases ischemic stroke risk in atrial fibrillation (AF) patients. This finding is independent of the CHA₂DS₂-VASc score, suggesting PHPT is a crucial factor in stroke risk assessment.

Area of Science:

  • Cardiology
  • Endocrinology
  • Neurology

Background:

  • Current guidelines recommend considering stroke risk factors in atrial fibrillation (AF) patients.
  • Nontraditional risk factors for stroke in AF, such as primary hyperparathyroidism (PHPT), are not well-explored.

Purpose of the Study:

  • To investigate the association between PHPT and the risk of ischemic stroke in patients with AF.
  • To determine if PHPT is an independent risk factor for ischemic stroke in AF patients.

Main Methods:

  • Retrospective cohort study using the Nationwide Inpatient Sample Database.
  • Propensity score matching was used to control for over 20 confounding variables, including CHA₂DS₂-VASc score components.
  • Multivariate logistic regression analysis assessed the independent impact of PHPT on ischemic stroke risk.

Main Results:

  • Patients with AF and PHPT had higher rates of ischemic stroke (6.0% vs 4.4%) and mortality (6.3% vs 4.9%) compared to those without PHPT.
  • PHPT was associated with a 1.4-fold increased risk of ischemic stroke and a 1.32-fold increased risk of mortality, independent of CHA₂DS₂-VASc score.
  • Subgroup analysis indicated higher mortality in men with high CHA₂DS₂-VASc scores and PHPT.

Conclusions:

  • Primary hyperparathyroidism is significantly associated with an increased risk of ischemic stroke in patients with atrial fibrillation.
  • PHPT should be considered in the thromboembolic risk assessment for AF patients, beyond traditional risk scores.
  • Potential mechanisms include vascular changes, cardiac dysfunction, and coagulation alterations.

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