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Taylor.aeha cac imt progression talk.1


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Taylor.aeha cac imt progression talk.1

  1. 1. Monitoring CAC and IMT: A useful clinical tool? Cardiology Service Walter Reed Army Medical Center Walter Reed Army Health Care System Allen J. Taylor MD COL, Medical Corps Professor of Medicine, USUHS Chief of Cardiology
  2. 2. How do we monitor successful control of cardiovascular risk? •Attainment of risk factor targets •BP, LDL-C, HDL-C •Use of specific medication classes •Compliance with therapeutic lifestyle changes •Tobacco, physical activity and diet •Inference: Control of risk factors equates to control of the target disease… Atherosclerosis
  3. 3. Is the answer within a “global risk” assessment? •Multi-variable risk indices are generally not validated for demonstrating the control of cardiovascular risk •Due to •Concept of exposure duration •Measurement error •High lifetime risk even in the setting of low near term risk Lloyd-Jones. AJC 2004;94:20-24
  4. 4. Is monitoring atherosclerosis the answer? •Serial angiographic study in 335 pts, mean age 51, f/u 44 months Waters et al. Circulation 1993;87:1067- •QCA progression •>15% increase in diameter stenosis •42% •50% increase in adjusted risk for cardiac death/MI P < .001
  5. 5. Coronary Atherosclerosis Progression A marker of increased risk for events •CLAS: secondary prevention, men, colestipol + niacin vs. placebo Azen et al. Circulation 1996;93:34-41 •CAD progression •Common (49%) •Associated with significantly higher risk for future events 1 1.7 2.3 0 0.5 1 1.5 2 2.5 Regression Stabilized Progression P = .03
  6. 6. IVUS progression predicts clinical events •Essen University: Serial IVUS study of the left main coronary artery in 56 pts undergoing left coronary PCI Erbel and colleagues. Circulation 2004;110:1579 •Change in plaque area related to clinical risk factors •Most events occurred in those with the greatest progression •P+M 25% vs. 6%
  7. 7. IMT Progression Rate A marker of increased risk for events •CLAS: secondary prevention, men, colestipol/niacin vs. placebo Hodis. Ann Intern Med 1998;128:262 P < .001 1 1.6 2.3 2.8 0 0.5 1 1.5 2 2.5 3 RR for MI/Death <.011 mm/y .011-.017 mm/y .018-.033 mm/y >.033 mm/y • Rate of progression is associated with significantly higher risk for future events • Predictive power superior to coronary artery progression
  8. 8. Therapeutics shown to slow progression of CIMT •Lifestyle interventions- exercise •Lipid modifying agents- •Binding resins, niacin, STATINS, new agents •Anti-hypertensives •CCB’s, β blockers, ACEI •Anti-diabetic agents •Metformin, TZD’s •Hormonal therapy: HRT
  9. 9. Could IMT be used to monitor a patients atherosclerosis extent? •Tension between expected IMT progression vs. test reproducibility •Annual CIMT progression: .01-.015 mm/y •Reproducibility •± .02-.04 mm •Most reproducible in common carotid > bulb/internal carotid •Extended time-horizon should improve ability to discriminate signal from noise
  10. 10. Methods to Improve CIMT Reproducibility •Common carotid vs. other segments •Collect/analyze images in duplicate •Consistent technology, sonographers and readers •High frequency imaging •Standardization of methods needed
  11. 11. Higher Frequency Imaging 7 MHz: 19958 MHz: 199910 MHz: 1999 13 MHz: 2005
  12. 12. • Common carotid artery advantageous: obtainable in virtually all • Far wall measurements • Minimum 7MHz probes • Minimum 10 mm length of IMT from well-visualized segment
  13. 13. CAC score progression Raggi et al. ATVB. 2004;24(7):1272-7 ∀↑ progression in individuals with events •Open issues: •Calculation? •%/year •Volume •Determinants uncertain Raggi et al. AJC. 2003;92:827
  14. 14. Statin/CAC Paradox: BELLES Raggi et al. Circulation 2005;112:563 •LDL control vs. CAC progression over 12 months •RCT, n = 615 •Atorva 80 vs. prava 40 •LDL 92 vs. 129 •No difference in CVS •~15%/yr
  15. 15. Statin/CAC Paradox: St. Francis Arad et al. J Am Coll Cardiol 2005;46:166 – •Atorva vs. placebo •RCT, n = 1005 •With CAC>80th percentile •4 year CAC progression •No difference despite strong trend for event reduction •CAC progression: •Slightly greater in those with events •44% vs. 33% •Unrelated to events
  16. 16. ATVB 2005;25:592 •In vitro study of statins on AVMF and osteoblasts “Statins inhibit calcification in AVMFs by inhibiting the cholesterol biosynthetic pathway, independent of protein prenylation, but paradoxically stimulate bone cell calcification. “
  17. 17. Conclusions •Individuals with atherosclerosis progression is associated with heightened risk for cardiovascular events •Invasive and noninvasive assessments •CIMT: Accurate detection of risk will require that the IMT measurement be reproducible enough and time horizon be long enough to accurately discriminate true progression •Progression of CAC >15% per year has been associated with increased risk of CHD events •Overlap, determinants, and statin paradox complicate this assessment •More study needed