English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Cardiovascular disease is a major cause of renal insufficiency, but conversely, renal insufficiency itself contributes to cardiac pathology in several ways. At least half of all the patients starting dialysis therapy have overt cardiovascular disease [1]. Chronic pressure and volume overload lead to left ventricular (LV) remodelling, with the development of a concentric or eccentric LV geometry and LV hypertrophy. The prevalence of LV hypertrophy increases with progressive renal insufficiency [2] to about 75% in dialysis patients [3,4]. Amplifying factors include hyperparathyroidism, hyperphosphataemia, angiotensin II, aldosterone, endothelin and plasma catecholamines [5–7]. In uraemia, LV hypertrophy is characterized by cardiomyocyte dropout, with diffuse interstitial fibrosis and hypertrophy of the remaining myocytes and microvascular disease [8]. These structural changes are associated with impaired LV perfusion and function. Decrease in myocardial capillary density and increase in myocyte size adversely affect myocardial oxygen supply and flow reserve [9]. Epicardial coronary artery disease is common in uraemic patients, and may lead to an acute coronary syndrome. LV dysfunction, however, seems to be related to microvascular disease [10]. LV function is also impaired by cardiomyocytes being replaced by fibrosis, leading to decreased contractile capacity and compliance. LV pressure–volume measurements have shown the steep relationship between end-diastolic pressure and volume in dialysis patients [11]. As LV remodelling is common in dialysis patients, a high prevalence of LV dysfunction is expected. However, cardiac function assessment in dialysis patients is fraught with pitfalls. The changing circulatory pressure–volume relations not only affect LV structure and function, contributing to cardiac morbidity, but also hamper LV function assessment. In this review, we will briefly discuss LV physiology in relation to the changing volume status in dialysis patients, explain the principles of conventional and newer LV function tests, and provide recommendations to optimize the evaluation of cardiac function in the dialysis patient.

Evaluation of cardiac function in the dialysis patient—a primer for the non-expert