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Metabolic risk factors for atherosclerosis in heart transplant recipients
M S Kemna1, H A Valantine, S A Hunt
1Veterans Administration Medical Center, Stanford, Calif.
Insights
Heart transplant recipients show increased risks for coronary artery disease (CAD) due to metabolic changes. Immunosuppression contributes to dyslipidemia and glucose intolerance, impacting long-term survival.
Area of Science:
- Cardiology
- Metabolic Syndrome
- Transplantation
Background:
- Coronary artery disease (CAD) in cardiac allografts is a major cause of mortality post-heart transplantation.
- Previous research on CAD in transplant patients primarily focused on lipoprotein metabolism, neglecting glucose and insulin regulation.
- Metabolic dysregulation, including dyslipidemia and impaired glucose metabolism, significantly elevates CAD risk.
Purpose of the Study:
- To investigate glucose and insulin metabolism alongside lipid profiles in heart transplant recipients.
- To compare metabolic profiles between patients with pre-existing ischemic heart disease (IHD) and idiopathic cardiomyopathy (ICM) against healthy controls.
- To elucidate the role of immunosuppression in the development of CAD risk factors.
Main Methods:
- Cross-sectional study involving male cardiac transplant recipients (IHD: n=28, ICM: n=24) and healthy volunteers (n=40).
- Oral glucose tolerance tests were performed to assess plasma glucose and insulin responses.
- Fasting lipid and lipoprotein concentrations (triglycerides, cholesterol, LDL-C, HDL-C) were measured.
Main Results:
- Cardiac transplant recipients exhibited significantly higher plasma glucose and insulin levels post-glucose load compared to controls.
- Patients with pre-transplant IHD showed elevated fasting triglycerides, cholesterol, and LDL-C, with lower HDL-C and higher cholesterol/HDL-C ratio.
- Recipients with ICM had intermediate values, differing significantly from both IHD and control groups for most variables.
Conclusions:
- Male heart transplant recipients commonly present with dyslipidemia, relative glucose intolerance, and hyperinsulinemia.
- These metabolic alterations are present in recipients regardless of pre-transplant diagnosis (IHD or ICM).
- Immunosuppressive therapy plays a critical role in fostering metabolic risk factors for CAD in cardiac allograft recipients.
Abstract:
Development of coronary artery disease (CAD) in the cardiac allograft limits long-term survival after heart transplantation. Previous studies, focusing on lipoprotein metabolism, have paid little attention to changes in glucose and insulin metabolism that increase the risk of CAD in these patients. To address this issue, plasma glucose and insulin responses to an oral glucose load and lipid and lipoprotein concentrations were measured in male normal volunteers (n = 40) and cardiac transplant recipients with pretransplant diagnoses of either idiopathic cardiomyopathy (n = 24) or ischemic heart disease (n = 28), matched for age and body mass index. Patients with a pretransplant diagnosis of ischemic heart disease had higher plasma glucose and insulin concentrations in response to oral glucose as well as higher fasting plasma triglyceride, cholesterol, and low-density lipoprotein cholesterol concentrations than did the control group (p < 0.005 to p < 0.001). In addition, high-density lipoprotein cholesterol concentrations were lower and the ratio of cholesterol to high-density lipoprotein cholesterol higher than control values in those with a pretransplant diagnosis of ischemic heart disease (p < 0.001). Values for almost all variables were intermediate in patients with a pretransplant diagnosis of idiopathic cardiomyopathy and in most instances were significantly different from both. Thus, male cardiac transplant recipients are dyslipidemic, relatively glucose intolerant, and hyperinsulinemic compared to normal volunteers. These changes, observed in patients with a pretransplant diagnosis of either ischemic heart disease or idiopathic cardiomyopathy, emphasize the important role of immunosuppression in the development of metabolic risk factors for CAD in these individuals.