Does Cytomegalovirus Truly Increase Cardiac Allograft Vasculopathy via First-Year Intravascular Ultrasound after Heart Transplant in the Tacrolimus Era?

Abstract

Purpose Cytomegalovirus (CMV) has been documented as a risk factor for the development of cardiac allograft vasculopathy (CAV) after heart transplantation (HTx). It has not been firmly established whether CMV would cause an increase in first-year intimal thickening via intravascular ultrasound (IVUS) in the current tacrolimus era. First-year maximal intimal thickening (MIT) ≥0.5mm has been found to be predictive of poor outcome (worse survival, CAV) at 5-years post-transplant. In addition, there has not been a differentiation between CMV infection, CMV syndrome, and CMV disease as it applies to IVUS intimal thickening. CMV infection is noted by positive IgG CMV serology only; CMV syndrome refers to patients with documented CMV virus along with a clinical presentation; CMV disease is defined as organ-specific CMV infection i.e. CMV pneumonitis, CMV colitis etc. Therefore, we sought to use first-year IVUS to determine whether CMV infection, syndrome, or disease would lead to more first-year MIT ≥0.5mm. Methods Between 2010 and 2017, 294 heart transplant patients underwent baseline and 1-year IVUS. These patients were then divided into 4 groups: (Group A - no CMV infection (n=108); Group B - CMV infection (n=173); Group C - CMV syndrome (n=9); and Group D - CMV disease (n=3)). Diagnosis of CAV was based on a ≥ 0.5 mm increase in maximal intimal thickness (MIT) from baseline. Results Baseline MIT was similar among all study groups. The percent of patients with first-year MIT ≥0.5mm was also similar among all patient groups. Conclusion The development of CMV infection, syndrome and disease, does not appear to increase CAV risk by first-year MIT obtained by IVUS in the current tacrolimus era. Larger number of patients with longer follow-up studies are warranted to confirm these findings.