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Attenuated-signal plaque progression predicts long-term mortality after heart transplantation
In patients who had heart transplantation, attenuated-signal plaque progression may be an independent predictor of long-term mortality, researchers reported in the Journal of the American College of Cardiology.
According to the study background, previous research on coronary atherosclerosis found associations between attenuated-signal plaque, plaque instability and adverse events.
Kozo Okada, MD, from the division of cardiovascular medicine, Stanford Cardiovascular Institute, Stanford University School of Medicine, and colleagues enrolled 105 patients who had survived at least 1 year after heart transplantation and had preserved renal function between 2002 and 2013.
All patients underwent IVUS at baseline and at 1 year to determine attenuated-signal plaque progression. The primary endpoint was all-cause death or retransplantation.
During a median follow-up of 4.6 years, 19 patients died and one patient had to be retransplanted. Of the 19 deaths, 12 were cardiac-related and one was due to acute cellular rejection. Twenty-seven percent of all the patients experienced one or more episodes of significant acute cellular rejection during the first year.
IVUS changes
Patients who experienced all-cause death or retransplantation had greater loss of vessel (P < .05 for interaction) and lumen volume (P < .01 for interaction) than those who did not experience all-cause death or retransplantation.
Overall, 10.5% of patients had attenuated-signal plaque progression 1 year after transplant, and compared with those who did not have it, they were more likely to have acute cellular rejection at 1 year (63.6% vs. 22.3%; P = .006) and had greater intimal growth as measured by percent intimal volume (9.2% vs. 4.4%; P = .07), according to the researchers.
In addition, patients with significant acute cellular rejection at 1 year had greater increases in intimal volume (P = .008), maximal intimal thickness (P = .048) and percent intimal volume (7.3 compared with patients who did not experience acute cellular rejection.
Okada and colleagues reported that 16 patients had attenuated-signal plaque progression at baseline and six new patients developed it by 1-year follow-up. Patients with newly developed attenuated-signal plaque progression all died after follow-up IVUS. Those with attenuated-signal plaque progression at 1 year were at greatly elevated risk for death or retransplantation during the study period (HR = 4.64; 95% CI, 1.72-11.64), the researchers found.
“Serial IVUS assessment of plaque instability in [cardiac allograft vasculopathy] early after transplantation may add incremental prognostic value to the standard assessment of intimal thickening and pathological arterial remodeling, enhancing the identification of high-risk patients who may benefit from closer follow-up and targeted medical therapies,” Okada and colleagues wrote.
Future research
According to Ahmed Tawakol, MD, from Massachusetts General Hospital and Harvard Medical School, and Jean-Claude Tardif, MD, from Montréal Heart Institute, University of Montréal, because the findings are based on a small retrospective study, larger prospective studies that include additional measures like LDL are needed.
“The findings of Okada [and colleagues] provided important new data strongly suggesting that IVUS assessment of [attenuated-signal plaque progression] allows the identification of high-risk [cardiac allograft vasculopathy] and the prediction of long-term mortality or retransplantation. Once this observation is replicated in a larger multicenter setting, the logical next step will be to assess whether early detection of echo-attenuated plaques and [cardiac allograft vasculopathy] will trigger changes in treatment that result in improved clinical outcomes,” Tawakol and Tardif wrote in a related editorial. – by Tracey Romero
Disclosure: Okada reports no relevant financial disclosures. Please see full study for a list of all other authors’ relevant financial disclosures. Tawakol reports receiving funding from Actelion, Amgen, Genentech and Takeda. Tardif reports receiving funding from Amarin, AstraZeneca, Cymabay, DalCor, MedImmune, Merck, Pfizer, Roche, Sanofi and Servier; receiving honoraria from DalCor, Pfizer, Roche, Sanofi and Servier; and holding an endowed research chair sponsored by Pfizer.