Cardiovascular calcification is both a risk factor and contributor to morbidity and mortality in many patient populations. Patients at all stages of chronic kidney disease (CKD), but especially those with end-stage renal disease (CKD-5) are considered to be at the highest risk for cardiovascular disease. Atrial fibrillation and severe chronic kidney disease are frequently coexistent. Patients with both diseases have a higher risk for stroke and bleeding. Although warfarin, a vitamin K antagonist, has been considered the anticoagulant of choice for reducing the risk of thromboembolic stroke in patients with atrial fibrillation, there is growing evidence that warfarin enhances cardiovascular calcification in patients with CKD which may impair outcome. The uncertainty regarding whether warfarin provides similar protection to reduce the risk for thromboembolic stroke in patients with atrial fibrilation suffering from severe chronic kidney disease has aroused our scientific interest.
Using noninvasive techniques as pulse wave velocity, which is used to evaluate vascular stiffness, we aim to estimate the cardiovascular risk of these patients. Vascular stiffness translates into higher conduction velocity of an impulse along the vessel length. Decreased elasticity is the result of many contributing factors, such as atherosclerosis, vascular wall calcification, and changes in collagen and elastin content in the vessel wall. Applying transthoracic echocardiography we assess the systolic and diastolic function, the cardiac output and any valve calcifications. Furthermore, by analysis of key calcification regulators (Fetuin-A and Matrix-Gla-Protein) as well as the functional calcium-phosphate precipitation in serum we dissect the pathomechanisms for the increased vascular calcification.