Cardiac Disease in the Dialysis Patient: Good, Better, Best Clinical Practice

Abstract

Proven strategies to reduce cardiovascular events and cardiac mortality in hemodialysis patients are given on the basis of pathophysiology. This is an overview of our clinical know-how acquired during the last 30 years. We try to answer the following questions: (1) how to reduce cardiovascular events and cardiac mortality in hemodialysis patients; (2) how to achieve regression of left ventricular hypertrophy, the most important predictor of sudden cardiac death; (3) how to manage iron status during full correction of renal anemia to prevent iron deficiency-induced reactive thrombocytosis, which is recognized to cause fatal stroke and cardiovascular thrombosis; (4) how to maintain responsiveness to erythropoiesis-stimulating agents during correction of renal anemia, thereby avoiding unnecessarily high doses and so reaching ultimate cost-effectiveness. Conclusion: Normalization of renal anemia is not responsible for increased risk of cardiovascular events/cardiac mortality. The inability to adequately address iron status in hemoglobin normalization studies and the underprescription of effective cardiac/antihypertensive medication might explain the adverse outcome. Effective cardiac/antihypertensive medication, intensive iron therapy during normalization of hemoglobin, optimized correction of metabolic acidosis and supplementation of vitamins which are involved in the energy metabolism should be considered to significantly improve the outcome of hemodialysis patients.

Intensified home haemodialysis for managing severe cardiac failure

“…LV dilatation and systolic and diastolic dysfunction are common and independently associated with mortality [3,4]. These changes are postulated to result from chronic volume overload (due to salt and water retention, chronic anaemia and arteriovenous fistulae), pressure overload (due to hypertension, atherosclerosis, vascular and cardiac valvular calcification), metabolic (acidosis, malnutrition, inflammation and oxidative stress) and neuroendocrine (renin-angiotensin-aldosterone and sympathetic activation) factors and ischaemia [5,6].…”

Diagnostics and therapy of left ventricular hypertrophy in haemodialysis patients

“…Every-day short-term haemodialysis (6 times weekly, 3h) for 12 months decreases left ventricle hypertrophy by 30%, as compared to conventional haemodialysis (3 times weekly, 4h) [24]. Clinical trial results show that night-time haemodialysis (3 times weekly, 6-8h) during the six-month period significantly reduces left ventricle hypertrophy compared to conventional haemodialysis (3 times weekly, 4h) [25].…”

“…Well-timed risk factor detection and adequate therapy help regression of left ventricle hypertrophy in haemodialysis patients [22][23][24][25]. Results of large, well-controlled clinical trials stress that the management of anaemia and blood pressure control, the correction of metabolic disorders of calcium, phosphate, vitamin D and parathormone (parathyroid hormone), as well as the individualisation of treatment of haemodialysis as the most important factors in the successful management of left ventricle hypertrophy [22][23][24][25].…”

Effects of hemodialysis on ventricular activation time in children with end‐stage renal disease

“…These conditions are consequences not only of increasing uremic toxemia but also of fluid overload, malnutrition, insulin resistance, as well as of erythropoietin administration. Many authors suggest that cardiovascular abnormalities in patients with ESRD are extremely detrimental and lead to a considerable percentage of fatal outcomes …”

“…Many authors suggest that cardiovascular abnormalities in patients with ESRD are extremely detrimental and lead to a considerable percentage of fatal outcomes. [1][2][3] The most common clinical presentation of cardiac impairments in the course of ESRD is probably the left ventricle hypertrophy. 4,5 The recent reports, concerning dialyzed children, have revealed that systolic function of the left ventricle keeps intact only if there is no concomitant arterial hypertension, anemia, or heart failure.…”