Thorac Cardiovasc Surg 2007; 55 - V_132
DOI: 10.1055/s-2007-967490

Low serum calcium is associated and inverse related to hydroxyapatite deposits in native aortic valves of male patients with severe aortic stenosis

G Langebartels 1, JR Ortlepp 2, G Dohmen 1, R Autschbach 1
  • 1Universitätsklinikum der RWTH Aachen, Klinik für Thorax-, Herz- und Gefäßchirurgie, Aachen, Germany
  • 2Universitätsklinikum der RWTH Aachen, Abteilung für Intermediate Care, Aachen, Germany

Aims: The study evaluated the relationship between serum calcium levels and the degree of calcification found in stenotic aortich valves.

Methods: Using atomic absorption spectroscopy the hydroxyapatite content of 228 excised human stenotic aortic valves was determined and expressed as percent of mass. Left heart catheterization preceded valve replacement. In addition the levels of both calcium and creatinine were determined before excising the native calcific aortic valves.

Results: Valves taken from male patients contained more hydroxyapatite (mass %) than those derived from female patients (26.0±8.8 vs. 21.6±9.0, p<0.001) Patients presenting with lower serum calcium levels showed a slight trend towards higher levels of valve calcification. Ths association only appeared within the subgroup of male patients. Male patients with the lowest level s of serum calcium displayed the highest amounts of avlvular hydroxyapatite (1st calcium tertiary: 29.5±8.9% vs. 2cond calcium tertiary 26.4±7.8% mass vs. third calcium tertiary 21.4±8.9 mass%; n=122; p=0.001; linear regression R=–0.25; p=0.006). In male patients with normal serum creatinine levels assoiation was even more distinct. Furthermore serum calcium was inversely and significantly associated with serum C reactive protein in male patients.

Conclusions: Serum calcium level appears to be inversely related to valve calcification in severe aortic stenosis. This indicates the importance of systemic calcium metabolism or renal function. Iterestingly this association was evident in male patients, only suggesting a gender dependent pathogenesis.