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Left ventricular alterations and end-stage renal disease
1Centre Hospitalier FH MANHES, Fleury-Mérogis, France. glondon@club-internet.fr
Insights
Left ventricular hypertrophy (LVH) is common in end-stage renal disease (ESRD) due to factors like anemia and hypertension. Addressing these causes is crucial for improving patient outcomes.
Area of Science:
- Nephrology
- Cardiology
- Internal Medicine
Background:
- Left ventricular (LV) changes, particularly LV hypertrophy (LVH), are highly prevalent in patients with chronic kidney disease and end-stage renal disease (ESRD).
- LV enlargement in ESRD is often linked to increased stroke and cardiac index, typically with preserved systolic function.
- The primary drivers are chronic volume/flow overload from factors like anemia, arteriovenous shunts, and fluid retention.
Purpose of the Study:
- To elucidate the multifactorial causes of left ventricular hypertrophy (LVH) in end-stage renal disease (ESRD) patients.
- To highlight the contribution of both hemodynamic and non-hemodynamic factors to cardiac structural changes in ESRD.
- To emphasize the importance of managing contributing factors for improved clinical outcomes.
Main Methods:
- Review of existing literature on cardiovascular changes in ESRD.
- Analysis of etiological factors contributing to LVH in the ESRD population.
- Identification of hemodynamic and non-hemodynamic pathways involved in cardiac remodeling.
Main Results:
- High prevalence of LVH in ESRD patients, often associated with volume/flow overload.
- Hypertension identified as a major contributor to LVH in ESRD.
- Non-hemodynamic factors including angiotensin II, parathyroid hormone, and catecholamines also implicated in LVH and fibrosis.
Conclusions:
- Preventing LVH and its complications in ESRD requires addressing underlying causes of flow and pressure overload.
- Correction of anemia is essential for mitigating LVH in ESRD patients.
- A comprehensive approach targeting multiple contributing factors is necessary to improve cardiovascular outcomes in ESRD.
Abstract:
The prevalence of left ventricular (LV) changes, especially LV hypertrophy (LVH), is high among patients with chronic kidney disease and end-stage renal disease (ESRD). Ventricular enlargement usually is associated with normal systolic function and increased stroke and cardiac index. In the absence of intrinsic heart disease, LV enlargement is most probably attributable to chronic volume/flow overload associated with anaemia, the presence of arteriovenous shunts, and sodium and water retention. In ESRD patients, hypertension is also a leading cause of LVH, but structural LV changes and myocardial fibrosis may also be due to non-haemodynamic factors such as angiotensin II, parathyroid hormone, endothelin, aldosterone, increased sympathetic nerve discharge and increased plasma catecholamines. To improve the clinical outcomes in ESRD, it is essential to prevent LVH and its complications by correcting the factors that contribute to flow and pressure overload, including anaemia.