Individual coronary plaque changes on serial CT angiography: Within-patient heterogeneity, natural history, and statin effects in HIV.

Background: It is not known how the volume and composition of individual coronary plaques change over time in HIV-infected people and whether statins influence these changes.

Methods: We included forty adults with HIV and subclinical coronary atherosclerosis who participated in a randomized controlled trial of placebo vs. atorvastatin. All participants underwent serial coronary computed tomography angiography at baseline and after one year. Individual coronary plaques were measured to assess the within-patient variability of plaque volume and composition changes. Left-main, proximal-right, proximal-left-anterior descending, and proximal-circumflex coronary segments were considered proximal. Plaque voxels with attenuation ≤130 Hounsfield Units (HU) were defined as noncalcified and further divided into fatty (<40HU) and fibrotic (40-130HU) components.

Results: In 37 patients who completed the trial, there were 92 coronary plaques. Individual plaque changes varied highly, with some plaques increasing while others decreased in the same patient. Overall, 77% vs. 51% of individual plaques progressed, while 24% vs. 49% regressed in placebo and statin, respectively (p = 0.016). Substantial increases in proximal plaques drove the progression in placebo. Statins suppressed these large increases, resulting in a 3-fold lower variance in plaque volume change compared to placebo (p = 0.025). Statins suppressed progression of fibrotic (p = 0.015) plaque, with a trend towards reducing fatty (p = 0.075) plaque and no significant effect on the calcified portion (p = 0.203).

Conclusion: In persons with HIV, a population with increased atherosclerosis burden and cardiovascular risk, individual coronary plaque changes vary within a given individual. Large increases in proximal plaques characterize progression, and statins act in part by stabilizing progressing plaques by reducing fatty and fibrotic plaque components, without influencing the calcified portion.