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Published on: June 2, 2022
Vascular calcification is associated with impaired microcirculatory function in chronic haemodialysis patients
Mhairi K Sigrist1, Christopher W McIntyre
1Division of Vascular Medicine, The University of Nottingham, Nottingham, UK.
Insights
Vascular calcification (VC) in dialysis patients is linked to heart issues. This study reveals impaired microcirculation in patients with VC, suggesting a key role in cardiovascular complications.
Area of Science:
- Nephrology
- Cardiology
- Vascular Biology
Background:
- Vascular calcification (VC) in dialysis patients correlates with increased cardiovascular events.
- The underlying pathophysiology of VC and its complications remains unclear.
- Microcirculatory dysfunction may contribute to myocardial ischemia in dialysis patients.
Purpose of the Study:
- To investigate cutaneous microcirculatory function in hemodialysis (HD) patients with and without large-vessel VC.
- To compare microcirculatory responses between HD patients with and without VC, and healthy controls.
Main Methods:
- Studied 37 non-diabetic subjects (20 HD patients, 17 healthy controls).
- Assessed VC using CT scanning of the superficial femoral artery.
- Utilized Laser Doppler imaging for cutaneous microcirculation at rest and during vasodilator challenge (ACh and SNP).
Main Results:
- No significant difference in baseline perfusion between VC+ HD patients, VC- HD patients, and controls.
- HD patients exhibited a reduced maximum vasodilatory response to ACh and SNP compared to controls.
- HD patients showed delayed vasodilation compared to controls.
- VC+ patients had lower maximum vasodilation and slower response times than VC- patients.
Conclusions:
- Demonstrated impaired and dysregulated microcirculatory function in dialysis patients with VC.
- This microcirculatory dysfunction may be crucial in understanding the pathophysiology of VC-related complications and cardiovascular events.
Abstract:
Although vascular calcification (VC) in dialysis patients is associated with increased cardiovascular events, the pathophysiology is still largely obscure. Microcirculatory dysfunction may contribute to demand myocardial ischaemia. We have studied cutaneous microcirculatory function in haemodialysis (HD) patients with and without large-vessel VC. 37 non-diabetic subjects (20 HD and 17 healthy controls) were studied. VC was assessed using CT scanning of a standardised segment of superficial femoral artery (11 VC+, 9 VC-). Laser Doppler imaging was undertaken using a Periscan PIM II(R) at rest and under vasodilator challenge. Baseline perfusion was not statistically different in VC+ patients than VC- patients or controls (1.03 +/- 0.2, 1.08 +/- 0.2, 0.93 +/- 0.3 PU respectively). Overall, the maximum vasodilatory response to both ACh (p < 0.001) and SNP (p = 0.004) was lower in the HD than the control group. In addition, the HD patients took longer to reach a maximum vasodilatation than the controls (p = 0.008 for ACh, n.s. for SNP). Further, the maximum vasodilatory response in the VC+ patients was lower and patients took longer to reach maximum vasodilatation than the VC- group. We have demonstrated, for the first time, impaired and dysregulated microcirculatory function in patients with VC. This may be important in understanding the pathophysiology of the complications and cardiovascular consequences of VC.
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