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Atherogenesis and cardiac death: are they related to dialysis procedure and biocompatibility?
1Department Internal Medicine and Immunology Ruperto Carola University Heidelberg, Germany.
Insights
Cardiac events are a leading cause of death in dialysis patients, often due to atherosclerotic coronary heart disease acquired before dialysis. Intradialytic hypotension is a significant risk factor, alongside hypertension and dyslipidemia.
Area of Science:
- Nephrology
- Cardiology
- Pathophysiology
Background:
- Cardiac events are a major cause of mortality in dialysis patients.
- Atherosclerotic coronary heart disease is highly prevalent, with lesions often developing before dialysis.
- Factors like microvascular abnormalities and disturbed cardiac metabolism increase heart susceptibility to ischemia.
Purpose of the Study:
- To explore the multifactorial nature of cardiac events in dialysis patients.
- To identify risk factors and potential protective mechanisms influencing atherogenesis in this population.
Main Methods:
- Review of existing literature on cardiac events in chronic renal failure and dialysis.
- Analysis of factors modulating cardiac susceptibility to ischemia.
- Examination of proatherogenic and antiatherogenic mechanisms in dialysis patients.
Main Results:
- Intradialytic hypotension is an independent risk factor for cardiac events.
- Hypertension and dyslipidemia are potent risk factors for atherosclerosis in dialysis patients.
- Dialysis procedures may influence atherogenesis through various pathways, including lipid oxidation and inflammation.
Conclusions:
- Cardiac mortality in dialysis patients is complex, influenced by pre-dialysis lesion development and intradialytic factors.
- Understanding proatherogenic and protective mechanisms is crucial for managing cardiovascular risk in dialysis patients.
Abstract:
Cardiac events are a major cause of death in dialysed patients. This is due, at least in part, to the high prevalence of atherosclerotic coronary heart disease. To a large extent, however, coronary lesions are acquired in the predialytic phase of chronic renal failure. The susceptibility of the heart to ischaemia is modulated by a number of factors, e.g. microvascular abnormalities, increased cardiac pulsatile workload, disturbed cardiac glucose metabolism, imbalanced autonomic innervation. The paradoxical result of there being no relationship of cardiac death in dialysis patients to blood pressure may be explained by confounding factors. Intradialytic hypotension appears to be an independent risk factor. The dialysis patient is exposed to hypertension and dyslipidaemia, two potent risk factors of atherosclerosis. Although no definite information is available, it is conceivable that factors related to dialysis procedures may also influence early or late events in atherogenesis. Such potential factors include oxidative modification of lipids, modulation of insulin resistance or glucose metabolism by non-insulin-dependent pathways, expression of adhesion molecules and activation of potential effector cells in atherogenesis, particularly monocytes and platelets, changes of synthesis and/or response to endothelin and nitroxide (EDRF), and possibly also accelerated formation of advanced plaques by hyperphosphataemia and/or hyperparathyroidism. Such proatherogenic mechanisms must be balanced against factors potentially protecting against atherogenesis; these comprise altered arachidonic acid metabolism (increased prostacyclin and decreased thromboxane synthesis), impaired platelet aggregation, antiatherosclerotic effects of heparin, and diminished concentrations of 1,25(OH)2D3, i.e. of a proatherogenic compound.