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Measuring Frailty in HIV-infected Individuals. Identification of Frail Patients is the First Step to Amelioration and Reversal of Frailty
Published on: July 24, 2013
Individual coronary plaque changes on serial CT angiography: Within-patient heterogeneity, natural history, and
Borek Foldyna1, Janet Lo2, Thomas Mayrhofer3
1Cardiovascular Imaging Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Clinic for Radiology, Cardiovascular Center, Bad Neustadt an der Saale, Germany.
Insights
In people with HIV, coronary plaque volume and composition changes significantly vary within individuals. Statins stabilize progressing plaques by reducing fatty and fibrotic components, lowering overall plaque volume variance.
Area of Science:
- Cardiovascular Imaging
- HIV Medicine
- Pharmacology
Background:
- HIV-infected individuals face heightened atherosclerosis and cardiovascular risk.
- Longitudinal changes in coronary plaque volume and composition in HIV are not well understood.
- The impact of statins on these plaque dynamics in HIV is unknown.
Purpose of the Study:
- To investigate the within-patient variability of coronary plaque volume and composition over time in adults with HIV.
- To determine if atorvastatin influences these plaque changes compared to placebo.
Main Methods:
- Serial coronary computed tomography angiography was performed at baseline and one year in 40 adults with HIV and subclinical atherosclerosis.
- Individual coronary plaques were analyzed for changes in volume and composition (noncalcified, fatty, fibrotic).
- Plaque voxels with attenuation ≤130 Hounsfield Units (HU) were defined as noncalcified, with fatty (<40HU) and fibrotic (40-130HU) subcomponents.
Main Results:
- Among 37 completers, 92 plaques showed high variability in individual changes; some progressed, others regressed within the same patient.
- Plaque progression was observed in 77% (placebo) vs. 51% (statin), with regression in 24% (placebo) vs. 49% (statin) (p=0.016).
- Statins significantly reduced plaque volume variance (p=0.025), suppressed fibrotic plaque progression (p=0.015), and showed a trend for reducing fatty plaque (p=0.075), without affecting calcified plaque (p=0.203).
Conclusions:
- Coronary plaque progression in HIV is characterized by significant within-individual variability, particularly large increases in proximal plaques.
- Atorvastatin stabilizes progressing plaques in HIV patients by reducing fatty and fibrotic components.
- Statins mitigate atherosclerosis progression in HIV by stabilizing plaque, not by affecting the calcified portion.
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.
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