Publications by authors named "M Pillich"

Calcific aortic valve stenosis, the most frequent heart valve disorder in developed countries, is an actively regulated process with similarities to bone formation. Fetuin-A has recently been identified as a potent circulating inhibitor of calcification. While several studies involving patients with end-stage renal disease have shown an association between low serum fetuin-A and cardiovascular calcification, nothing is known about fetuin-A serum levels in non-renal patients with calcific aortic valve stenosis.

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Background And Aim Of The Study: The study aim was to evaluate the relationship between serum calcium levels and the degree of calcification found in stenotic aortic valves.

Methods: Using atomic absorption spectroscopy, the hydroxyapatite content of 228 excised human stenotic aortic valves was determined and expressed as a percentage of valve mass. Left heart catheterization preceded valve replacement.

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Article Synopsis
  • The study aimed to explore the coexistence of atherosclerotic changes in patients with non-rheumatic calcific aortic valve stenosis (AS), highlighting the shared risk factors between these conditions.
  • In a sample of 282 patients undergoing aortic valve replacement due to severe calcific stenosis, researchers assessed the prevalence of atherosclerosis using coronary angiography and Doppler sonography.
  • Findings revealed a significant association between coronary and extracranial cerebral artery atherosclerosis, with high prevalence rates, especially in older patients, suggesting the need for routine screenings for atherosclerosis in those with calcific AS.
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Article Synopsis
  • The study aimed to explore the relationship between APOE gene variants and aortic stenosis (AS) using a large sample of patients with AS and healthy controls.
  • Patients were assessed for heart disease symptoms and risk factors, while their APOE alleles were analyzed through genetic testing.
  • The findings indicated that the presence of the APOE e4 allele does not have a significant association with AS, suggesting that the genetic influences on coronary artery disease (CAD) and AS may differ.
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