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Cardiac and arterial interactions in end-stage renal disease
G M London1, A P Guerin, S J Marchais
1Service de Néphrologie-Hémodialyse, Hôpital Manhes, Fleury-Mérogis, France.
Insights
End-stage renal disease (ESRD) patients exhibit parallel cardiac and arterial changes. Large artery alterations in ESRD contribute to left ventricular hypertrophy and functional changes, independent of other risk factors.
Area of Science:
- Cardiovascular Medicine
- Nephrology
- Vascular Biology
Background:
- Cardiac hypertrophy is a common complication in end-stage renal disease (ESRD).
- The relationship between arterial changes and cardiac hypertrophy in ESRD patients is not well understood.
- Large artery geometry and function in ESRD patients require further investigation.
Purpose of the Study:
- To investigate large arterial geometry and function in ESRD patients.
- To determine the relationship between arterial changes and cardiac hypertrophy in ESRD.
- To explore the contribution of arterial alterations to cardiac complications in ESRD.
Main Methods:
- Ultrasound imaging was used to assess common carotid artery (CCA) intima-media thickness, diameter, and left ventricular geometry and function in 70 ESRD patients and 50 controls.
- Applanation tonometry and carotid-femoral pulse wave velocity measurements were employed to determine arterial distensibility, compliance, and wave reflections.
- Multivariate analysis was performed to assess the independence of observed relationships.
Main Results:
- ESRD patients showed increased left ventricular mass, CCA diameter, intima-media thickness, and cross-sectional area compared to controls.
- Arterial hypertrophy in ESRD was associated with decreased distensibility and compliance, accelerated pulse wave velocity, and increased wave reflections.
- These arterial changes led to increased pulsatile pressure load and decreased subendocardial viability.
- CCA diameter and wall thickness correlated significantly with left ventricular dimensions and mass, independent of age, sex, blood pressure, and body surface area.
Conclusions:
- ESRD patients exhibit parallel cardiac and large artery adaptations.
- Structural and functional alterations in large arteries may contribute to the pathogenesis of left ventricular hypertrophy in ESRD.
- These findings highlight the interconnectedness of cardiovascular and renal health in ESRD.
Abstract:
Although cardiac hypertrophy is a frequent complication of end-stage renal disease (ESRD), relatively little is known about large arterial geometry and function in vivo in these patients, and the relationship between arterial changes and cardiac hypertrophy is unknown. Common carotid artery (CCA) intima-media thickness and internal diameter and left ventricular geometry and function were determined by ultrasound imaging in 70 uncomplicated ESRD patients and in 50 age-, sex-, and blood pressure-matched controls. Arterial distensibility and compliance were determined from simultaneously recorded CCA diameter and stroke changes in diameter and CCA pressure waveforms, obtained by applanation tonometry, and also by the measurement of carotid-femoral pulse wave velocity. Compared with control subjects, ESRD patients had greater left ventricular diameter (P < 0.01), wall thicknesses and mass (P < 0.001), increased CCA diameter (6.25 +/- 0.87 vs. 5.55 +/- 0.65 mm; P < 0.001), larger CCA intima-media thickness (777 +/- 115 vs. 678 +/- 105 microns; P < 0.001) and intima-media cross-sectional area (17.5 +/- 4.5 vs. 13.4 +/- 3.3 mm2; P < 0.001). In uremic patients, arterial hypertrophy was associated with decreased CCA distensibility (17.8 +/- 8.8 vs. 24.0 +/- 12.7 kPa-1.10(-3); P < 0.001) and compliance (5.15 +/- 2 vs. 6.0 +/- 2.5 m2.kPa-1.10(-7); P < 0.05), accelerated carotid-femoral pulse wave velocity (1055 +/- 290 vs. 957 +/- 180 cm/seconds; P < 0.001), early return and increased effect of arterial wave reflections (20.5 +/- 15.4 vs. 9.2 +/- 18.4%; P < 0.001). The latter phenomenons were responsible for increased pulsatile pressure load in CCA (58.3 +/- 21 vs. 48 +/- 17 mm Hg; P < 0.01) and were associated with a decreased subendocardial viability index (157 +/- 31 vs. 173 +/- 30%; P < 0.001). The CCA diameter was correlated with the left ventricular diameter (P < 0.01), and a significant correlations existed between CCA wall thickness or CCA intima-media cross-sectional area and left ventricular wall thicknesses and/or left ventricular mass (P < 0.01). In multivariate analysis, these relationships were independent regarding age, sex, blood pressure and body surface area. The present study documents parallel cardiac and vascular adaptation in ESRD, and demonstrates the potential contribution of structural and functional large artery alterations to the pathogenesis of left ventricular hypertrophy and functional alterations.