Hippokratia 2004, 8(4):166-169
D Yonova, M Geogiev, S Antonov, Z Kirijakov
Clinic of Nephrology, Medical University Hospital “Alexandrovsca”, Sofia, Bulgaria
Background: The damage of arteries and heart structures are a major contributory factor to the high cardiovascular morbidity and mortality of patients with chronic renal failure on dialysis. The aim of the study was to find some risk factors for development of cardiac valve calcifications and their relations to myocardial function in patients on hemodialysis treatment.
Material and methods: Conventional M-mode and B-mode echocardiography (Echo) and Pulse-doppler were made, accounting myocardial function and aorta valve calcifications (Ca-Ao), mitral valve calcifications (Ca-M) and total valve calcifications score (Cardiac Ca) of 37 patient with mean age 54.7±14.5 years and mean duration of hemodialysis treatment 82.05±27.35 months. Arterial blood pressure (ABP) and pulse rate were also registered. Tests of serum levels of Ca++, P, alkaline phosphatase (AP), parathormone (PTH), C -reactive protein (CRP), homocysteine and in 20 patients – fetuin-A and serum Mg were correlated to some myocardial functions (ejection fraction-EF; endsystolic stress – ESS; VpE / VpA), muscle mass index (MMI) and valve calcifications rate.
Results: Some significant correlations were found as follows: Ca++ / Cardiac Ca r:0.46, p < 0.01, PTH / Cardiac Ca r: 0.43, p < 0.01, EF / ESS r: 0.81, p < 0.01, EF / Cardiac Ca r: -0.38, p < 0.05, CRP / EF r: -0.4, p < 0.01, MMI / MAP r: 0.52, p < 0.01, VpE / VpA: Cardiac Ca r: -0.38, p < 0.05, Age / Cardiac Ca r: 0.4, p < 0.01, Dur.HD / Cardiac Ca r: 0.28, p < 0.05, PTH / EF r: -0.22, n.s., Fetuin A / PTH r : -0.33 p < 0.05, Fetuin A / CRP r: -0.43, p < 0.001, Fetuin A / Cardiac Ca r: -0.71, p < 0.001
Conclusion: The results prove the negative influence of increased myocardial burden (ESS, ABP) on the left ventricular function and on MMI. Close relations of disturbed mineral metabolism, PTH, inflammatory status (CRP), fetuin A, age and duration of HD with the rate of valve calcifications show that cardiac calcium deposits have multifactorial origin. The study also suggests that valve calcifications are involved in the complex of risk factors, causing damage of the valve structures and left ventricular dysfunction in HD patients.