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Coronary endothelial function in cardiac transplant recipients with accelerated coronary disease
S S Kushwaha1, M Bustami, D A Lythall
1Department of Cardiology, Harefield Hospital, Middlesex, UK.
Insights
Endothelial function is impaired in cardiac transplant recipients with accelerated coronary artery disease. This dysfunction in coronary arteries may increase vasoconstrictor tone, impacting transplant outcomes.
Area of Science:
- Cardiology
- Transplant Medicine
- Vascular Biology
Background:
- Endothelium-dependent vasodilation with substance P is preserved in cardiac transplant recipients with normal coronary arteries.
- Endothelial dysfunction is recognized in cardiac transplant recipients with accelerated coronary disease, but its extent is unclear.
- This study investigates endothelial function in accelerated coronary disease post-cardiac transplantation.
Purpose of the Study:
- To assess endothelial function in cardiac transplant recipients experiencing accelerated coronary artery disease.
- To quantify the impact of substance P on coronary artery vasodilation in this patient group.
Main Methods:
- Thirteen cardiac transplant recipients with epicardial coronary disease received substance P infusions.
- Coronary artery vasodilation response to incremental substance P doses was measured.
- Isosorbide dinitrate infusion served as a comparator.
Main Results:
- Substance P induced less vasodilation at lower concentrations in patients with coronary disease.
- A higher substance P dose was needed for half-maximal dilation compared to controls.
- Maximal dilation with substance P was comparable to isosorbide dinitrate and controls without coronary disease.
Conclusions:
- Coronary endothelium functional vasodilatory capacity is impaired in cardiac transplant recipients with accelerated coronary disease.
- Impaired vasodilation occurs even in apparently unaffected epicardial artery segments.
- This dysfunction may elevate resting vasoconstrictor tone, with significant clinical implications.
Background:
Previous studies with the endothelium-dependent vasodilator substance P have shown a preserved vasodilator response in cardiac transplant recipients with angiographically normal coronary arteries. Although endothelial dysfunction is known to occur in cardiac transplant recipients with accelerated coronary disease, the degree to which the endothelium is affected is not known precisely. The aim of the present study was to examine endothelial function in accelerated coronary disease following cardiac transplantation.
Methods:
Thirteen cardiac transplant recipients with epicardial coronary disease underwent substance P infusion. The response to incremental doses of substance P was measured in smooth segments of affected coronary arteries. Substance P was infused over 2 min with a starting dose of 1.4 pmol/min and a maximum of 22.4 pmol/min, reached by doubling the dose in steps, followed by an infusion of 2 mg isosorbide dinitrate over 2 min.
Results:
Substance P caused less vasodilation at lower concentrations, with a significantly higher dose required to achieve half maximal dilation compared with cardiac transplant recipients with no coronary disease. The mean maximal dilatation achieved with substance P was 22.98 +/- 4.62% compared to 21.95 +/- 4.9% with isosorbide dinitrate; the latter value was not significantly different from the maximal dilation achieved in cardiac transplant recipients without coronary disease.
Conclusions:
In cardiac transplant recipients with accelerated coronary disease the functional vasodilatory ability of the coronary endothelium is impaired in segments of apparently unaffected epicardial arteries, which may lead to an increase in the resting vasoconstrictor tone and have important functional and therapeutic implications.