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Published on: May 10, 2021
A Case of Transient Hypercalcemia Following Fistulization of a Calcified Mitral Annulus
Kobi Jacob Perl1, Michal Julius1, Dror Cantrell1
1Department "C" of Internal Medicine, Shamir Medical Center, Sackler Medical School Tel Aviv University, Tzrifin 70300, Israel.
Insights
A calcified mitral annulus (CMAC) fistulization caused severe hypercalcemia and embolic strokes. This rare cardiac event highlights CMAC risks and a unique cause of transient hypercalcemia.
Area of Science:
- Cardiology
- Internal Medicine
- Pathology
Background:
- Severe symptomatic hypercalcemia can present with diverse etiologies.
- Calcified mitral annulus (CMAC) is a degenerative cardiac condition.
- The association between CMAC and systemic complications is not well-established.
Observation:
- A patient presented with severe hypercalcemia, successfully treated with fluids and furosemide.
- The patient later returned with multiple embolic strokes of unknown origin.
- Cardiac imaging revealed a disappearing calcified mitral annulus (CMAC) cavity, suggesting fistulization into the left ventricle.
Findings:
- The fistulization of the CMAC likely released caseous material into the bloodstream, causing transient hypercalcemia.
- The same event is proposed as the source of the embolic strokes.
- This case demonstrates a direct link between CMAC fistulization and both hypercalcemia and embolic events.
Implications:
- This case highlights a rare but serious mechanism for transient hypercalcemia.
- It underscores the potential embolic risks associated with calcified mitral annulus pathology.
- Early recognition of CMAC fistulization may prevent severe systemic complications.
Abstract:
We report a case of severe symptomatic hypercalcemia that resolved after a short course of therapy of exclusively fluids and furosemide. An extensive workup for metabolic, neoplastic, and drug-induced causes did not provide a possible etiology of the hypercalcemia. After calcium level returned to baseline, the patient was discharged, only to return a week later with multiple embolic strokes of unknown source. The comparison of cardiac imaging obtained during the hospitalization periods established a possible mechanism for both phenomena; the interior caseous cavity of a calcified mitral annulus (CMAC), which was demonstrated on echocardiography during the first hospitalization, disappeared in a subsequent study in the second hospitalization, probably reflecting a fistulization of the structure into the left ventricle. The spill of contents into the bloodstream, over several days presumably, explains the transient increase in calcium, and the embolic events that followed. We hereby demonstrate a clear relationship between the fistulization of a CMAC and hypercalcemia, emphasizing the risks of this valvular pathology, and introducing a rare mechanism for transient and potentially severe hypercalcemia.
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