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Homocysteine‐Lowering Therapy and Early Progression of Transplant Vasculopathy: A Prospective, Randomized, IVUS‐Based Study
Author(s) -
Potena Luciano,
Grigioni Francesco,
Magnani Gaia,
Ortolani Paolo,
Coccolo Fabio,
Sassi Simonetta,
Koessels Koen,
Marrozzini Cinzia,
Marzocchi Antonio,
Carigi Samuela,
Musuraca Anna C.,
Russo Antonio,
Magelli Carlo,
Branzi Angelo
Publication year - 2005
Publication title -
american journal of transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.89
H-Index - 188
eISSN - 1600-6143
pISSN - 1600-6135
DOI - 10.1111/j.1600-6143.2005.01015.x
Subject(s) - medicine , homocysteine , randomized controlled trial , cardiology , oncology
Although observational studies suggest that hyperhomocysteinemia may be a risk factor for coronary allograft vasculopathy (CAV), prospective data on homocysteine‐lowering interventions and CAV development are lacking. We, therefore, randomized 44 de novo heart transplant (HT) recipients to 15 mg/day of 5‐methyl‐tetrahydrofolate (n = 22), or standard therapy (control group, n = 22) to investigate the effect of homocysteine lowering on the change in coronary intimal hyperplasia during the first 12 months after transplant, as detected by intra‐vascular ultrasound (IVUS). Although 12 months after HT, homocysteinemia was lower in folate‐treated patients (p < 0.001), coronary intimal area increased similarly in the two groups (p > 0.4). Conversely, hypercholesterolemia and cytomegalovirus infection were both associated with increased intimal hyperplasia (p < 0.04), independently from folate intake. Sub‐group analysis revealed that folate therapy reduced intimal hyperplasia in patients with hyperhomocysteinemia before randomization (n = 19; p = 0.02), but increased intimal hyperplasia in patients with normal homocysteine plasma concentrations (p = 0.02). This bimodal effect of folate therapy persisted significantly after adjusting for cytomegalovirus infection and hypercholesterolemia.Despite effective in prevent hyperhomocysteinemia after heart transplantation, folate therapy does not seem to affect early CAV onset. However, sub‐group analysis suggests that folate therapy may delay CAV development only in patients with baseline hyperhomocysteinemia, while may favor CAV progression in recipients with normal baseline homocysteinemia.