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Aortic and Carotid Magnetic Resonance Image (MRI) Imaging

Aortic and Carotid MRI imaging can identify plaque components and provide accurate measurements of plaque size changes. It is non-invasive, radiation-free, and involves computerized morphometric analysis. Challenges include motion artifacts and small vessel size.

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Aortic and Carotid Magnetic Resonance Image (MRI) Imaging

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  1. Aortic and Carotid Magnetic Resonance Image (MRI) Imaging • Can identify plaque components such as fibrous cap, lipid core, calcium, hemorrhage, and thrombosis (vunerable plaques have thin fibrous cap and large lipid core) • Non-invasive and no radiation • Computerized morphometric analysis involves following edge of significant contrast, providing measures of total vascular and lumen area, the difference being the vessel wall area (Image Pro-Plus, Media Cybernetics). • Image-specific error of 2.6% for aortic and 3.5% for carotid plaques allows accurate measurement of changes in plaque size of >5.2% for aortic lesions and >7% for carotid lesions (Corti et al., 2001)

  2. MRI Assessment of Thoracic Aorta Plaque • Challenges include obtaining sufficient sensitivity for sub-mm imaging and exclusion of artifacts from respiratory motion and blood flow. • Multicontrast approaches include performing T1-,PD-, and T2-weighted images with high resolution “black blood” spin used to visualize adjacent vessel wall. • Matched MRI and TEE cross-sectional aortic images show strong correlation for plaque composition and maximum plaque thickness.

  3. In Vivo MRI imaging of Coronary Artery Plaque • Difficulties include cardiac and respiratory motion, nonlinear course of coronary arteries, and small size and location of coronary arteries. • Inter- and intraobserver variability assessed by intraclass correlation ranged from 0.96-0.99. • Wall thickness in human coronaries can be differentiated between normal and >40% stenosis; breathholding can minimize respiratory motion. • Fayad and Fuster, Am J Cardiol 2001; 88 (suppl): 42E-45E.

  4. Lipid-Lowering by Simvastatin and Reduction in MRI Vessel Wall Area • 18 asymptomatic hypercholesterolemic patients studied, with a total of 35 aortic and 25 carotid plaques measured • Serial black-blood MRI of aorta and carotid artery performed at baseline, 6, and 12 months • At 12 months (but not 6 months), significant reductions in vessel wall thickness and area (8% reduction in aorta and 15% reduction in carotid artery vessel wall area), without lumen area changes, were observed.

  5. MRI Serial T2-Weighted Images During Simvastatin Treatment: Coronary vessels (top) and descending aorta (bottom)(Corti et al., Circulation 2001; 104: 249-52)

  6. Changes in MRI vessel wall and lumen area and wall thickness after 6 and 12 months of simvastatin treatment Click for larger picture

  7. High-frequency Brachial Ultrasonography • The endothelium regulates vascular tone through release of vasodilators and vasoconstrictors. • Brachial artery flow-mediated vasodilation (FMD) is assessed by high-frequency ultrasound assessment of changes in brachial artery diameter after 5-minute blood pressure cuff arterial occlusion. • Endothelial dysfunction demonstrated as reduced FMD, and associated with coronary risk factors. • Brachial artery FMD correlates with coronary artery FMD.

  8. Brachial Ultrasonography (cont.) • Brachial or coronary artery flow mediated vasodilation (FMD) predict long-term cardiovascular events. • Clinical applicability not well-established, but measures frequently used to measure endothelial function. • FMD decreases after age 40 in men and 50 in women, reduced at SBP>100 mmHg, LDL > 75 mg/dl, and in diabetics • Cholesterol reduction rapidly improves FMD.

  9. Brachial Artery Images Pre-Post Pressure Cuff Occlusion Click for larger picture

  10. Intravascular Ultrasound (IVUS) Assessment of Atherosclerosis • Detects plaque changes resulting from compensatory expansion that remodels the external elastic membrane; lumen not often narrowed until late in the process • Invasive, expensive, normally reserved for persons with established coronary disease • Volume of plaque obtained by measuring external elastic membrane, lumen area, and plaque and repeating every mm for at least 25-50 mm of artery.

  11. IVUS: Clinical studies involving progression/regression of plaque • 25 patients randomized to 10 mg pravastatin vs. placebo for 3 years showed a 41% increase in atheroma volume in the placebo patients vs. a 7% decrease in the pravastatin patients (p=0.0005) • REVERSAL prospective, randomized, double-blind multicenter trial will examine changes in volume of plaque in patients treated with either 80 mg atorvastatin or 40 mg pravastatin; • Nissen S, Am J Cardiol 2001; 87 (suppl): 15A-20A

  12. Atheroma “regression” (reverse remodeling maintaining similar lumen area) seen by IVUS

  13. Multivariate Relative Risks of CHD/Mortality Associated with Composite *Subclinical Disease

  14. Use of Surrogate Endpoints: Considerations in Drug Development • Burden of sponsor is to provide evidence that the drug is safe and effective, and often studies to achieve clinical endpoints take longer. • Surrogate endpoint studies can change labeling and indications depending on results. • But surrogate endpoints are sometimes a “leap of faith” and an endpoint study is often still required to validate assumptions made regarding clinical benefit. Hard endpoint studies may not always parallel results of surrogate endpoint studies.

  15. LDL Goal(mg/dL) LDL Level at Which to Initiate Therapeutic Lifestyle Changes (TLC) (mg/dL) LDL Level at Which to ConsiderDrug Therapy (mg/dL) Risk Category <100 100 130 (100–129: drug optional) CHD or CHD Risk Equivalents(10-year risk >20%) 10-year risk 10–20%: 130 10-year risk <10%: 160 2+ Risk Factors (10-year risk 20%) <130 130 0–1 Risk Factor <160 160 190 (160–189: LDL-lowering drug optional) LDL Cholesterol Goals and Cutpoints for Therapeutic Lifestyle Changes (TLC)and Drug Therapy in Different Risk Categories

  16. CHD Risk Equivalents • Other clinical forms of atherosclerotic disease (peripheral arterial disease, abdominal aortic aneurysm, and symptomatic carotid artery disease) • Diabetes • Multiple risk factors that confer a 10-year risk for CHD >20%

  17. LDL Level at Which to Initiate Therapeutic Lifestyle Changes (TLC) LDL Level at Which to Consider Drug Therapy LDL Goal 130 mg/dL (100–129 mg/dL:drug optional) <100 mg/dL 100 mg/dL LDL Cholesterol Goal and Cutpoints for Therapeutic Lifestyle Changes (TLC) and Drug Therapy in Patients with CHD and CHD Risk Equivalents (10-Year Risk >20%)

  18. LDL-Lowering Therapy in Patients With CHD and CHD Risk Equivalents Baseline LDL Cholesterol: 130 mg/dL • Intensive lifestyle therapies • Maximal control of other risk factors • Consider starting LDL-lowering drugs simultaneously with lifestyle therapies

  19. LDL-Lowering Therapy in Patients With CHD and CHD Risk Equivalents Baseline (or On-Treatment) LDL-C: 100–129 mg/dL • LDL-lowering therapy • Initiate or intensify lifestyle therapies • Initiate or intensify LDL-lowering drugs • Treatment of metabolic syndrome • Emphasize weight reduction and physical activity • Drug therapy for other lipid risk factors • For high triglycerides/low HDL cholesterol • Fibrates or nicotinic acid

  20. Implications for Cardiovascular Risk Stratification and Treatment: NCEP III • Should we add to this high-risk group requiring more intensive LDL-C initiation levels and goals, the following? • Persons with significant carotid disease (e.g., at or above 5th quintile of combined IMT) • Persons with “significant” coronary calcium (e.g., those above 75th %tile seen to be at 4-6-fold or greater risk of events) • Persons with significant LV mass or LVH

  21. Implications on Cardiovascular Risk Stratification and Treatment: JNC-VI • JNC-VI currently recommends initiating drug treatment without delay for hypertension in persons with known CVD or diabetes at 130/85 mmHg or higher, and in those with at least 1 risk factor when BP is at 140/90 mmHg or higher. • Should the presence of significant carotid disease, CT coronary calcium, or other evidence warrant treatment at the more aggressive, lower cut-point?

  22. Conclusions • Mounting data show surrogate measures of atherosclerosis predict CHD risk and are sensitive to monitoring effects of therapeutic interventions. • Noninvasive methods to measure subclinical atherosclerosis and its progression provide an opportunity to enhance primary prevention efforts • Noninvasive identification of the vulnerable plaque (e.g., using MRI) may help identify those at highest risk. • Patient compliance to risk-reduction may be enhanced by knowledge of disease (e.g., CAC)

  23. Conclusions (cont.) • Identification of those with the greatest amount of subclinical atherosclerosis may provide a better rationale for aggressive treatment (lipids, HTN) of those with borderline levels, allowing us to better target limited resources. • Surrogate measures of atherosclerosis can also allow: • 1) testing of epidemiologic hypotheses related to CHD • 2) designing clinical trials testing efficacy of therapies • 3) monitoring preventive therapies to reduce risk of clinical events

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