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Published on: October 12, 2017
Lipoprotein(a) levels and heart transplantation atherosclerosis
1Cardiovascular Division, Department of Medicine, University of Pennsylvania Health System, Philadelphia 19104-4024, USA.
Insights
Elevated lipoprotein(a) [Lp(a)] is linked to coronary issues, but this study found no association with accelerated cardiac allograft vasculopathy (ACAV) in heart transplant patients. Donor age, not Lp(a) levels, predicted ACAV development.
Area of Science:
- Cardiology
- Transplantation Immunology
- Biomarkers
Background:
- Elevated serum lipoprotein(a) [Lp(a)] is a known risk factor for native coronary atherosclerosis.
- The role of Lp(a) in accelerated cardiac allograft vasculopathy (ACAV) post-heart transplantation remains unclear.
Purpose of the Study:
- To investigate the association between serum Lp(a) levels and the presence of ACAV in heart transplant recipients.
- To identify predictors of ACAV one year after orthotopic heart transplantation.
Main Methods:
- A cohort of 74 heart transplant recipients with at least one year survival was analyzed.
- ACAV was diagnosed via angiography, defined as >=30% stenosis in epicardial arteries.
- Recipient and donor parameters, including serum Lp(a) and triglycerides, were collected and analyzed.
Main Results:
- ACAV was present in 35% of patients one year post-transplantation.
- Higher mean donor age and elevated serum triglyceride levels at 6 months were significant univariate predictors of ACAV.
- No significant difference in mean serum Lp(a) levels was found between patients with and without ACAV.
Conclusions:
- Serum Lp(a) does not appear to be a risk factor for developing ACAV one year after heart transplantation.
- Donor age emerged as the strongest independent predictor of ACAV.
- Further research is warranted to fully elucidate the impact of Lp(a) on cardiovascular disease after heart transplantation.
Background:
Elevated serum lipoprotein(a) [Lp(a)] levels are associated with the development of native coronary atherosclerosis. The association between increased levels of Lp(a) and the development of accelerated cardiac allograft vasculopathy (ACAV) in patients who have undergone orthotopic heart transplantation has not been firmly established.
Methods And Results:
We studied 74 consecutive heart transplant recipients with at least 1 year survival to determine the relation between Lp(a) and the presence of ACAV. Recipient and donor clinical and laboratory parameters, including mean serum Lp(a) levels, were obtained. ACAV was defined angiographically as > or =30% stenosis in one or more epicardial arteries. ACAV 1 year after heart transplantation was angiographically present in 26 (35%) patients. Mean donor age (36 +/- 13 years [ACAV (+)] vs 28 +/- 10 years, [ACAV (-)]; p = 0.004) and mean serum triglyceride levels 6 months after transplantation (286 +/- 275 mg/dl [ACAV (+)] vs 169 +/- 85 mg/dl [ACAV (-)]; p = 0.025) were univariate predictors of ACAV. No significant difference in mean serum Lp(a) levels was observed (20 +/- 19 mg/dl [ACAV (+)] vs 30 +/- 30 mg/dl [ACAV (-)]; p = NS). Donor age was the single greatest independent predictor of ACAV by multivariate logistic regression (p = 0.02).
Conclusions:
Lp(a) does not appear to be a risk factor for the development of ACAV 1 year after heart transplantation. Further studies are needed to define the influence of serum Lp(a) on the development of cardiovascular disease after orthotopic heart transplantation.
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