Fondazione C.N.R./Regione Toscana G. Monasterio Pisa - Italy massimo lombardi Imaging: tool or toy? Aortic Compliance 2011 ESC Paris
Disclosure: Cardiovascular MR Unit is receiving research fundings from Chiesi, Apotex Pharma, Novartis, GEHC, Guerbet,
Aortic (arterial) compliance Who is? How to measure it? Where to measure it? Why to measure it? When to measure it?
Who is? Stress is defined as the force applied/area to a particular object ( F/A). It can be applied in any direction: at radial, circumferential, and longitudinal components. Circumferential wall stress, defined by Laplace s law, is directly proportional to the vessel pressure and radius and inversely proportional to its thickness. Strain is the resulting deformation (percentage change in length) of an object/material subjected to a stress force. It is dimensionless (no units) and is defined as: strain=l-l0 L0 where L is the final length and L0 is the initial length. JL Cavalcante (J Am Coll Cardiol 2011;57:1511 22
Who is? The elastic modulus (E), is the stress/strain ratio. Incremental modulus or Young s modulus (which necessitates the evaluation of the arterial wall thickness) or the Elastic modulus (Peterson) Elastic modulus is linearly related to Young s modulus by the radius-wall thickness ratio, which varies with age and pressure. In most biologic materials, this relation is nonlinear, and the slope defines the intrinsic elastic properties of the wall material. E is expressed by the formula: E =(stress/strain) / C where C is the arterial compliance. Stiffness should be understood as the resistance to deformation. JL Cavalcante (J Am Coll Cardiol 2011;57:1511 22
How to measure it? Arterial compliance (C) is the absolute change in area (or change in diameter (D)) for a given pressure step (P) at a fixed vessel length. It is the reciprocal of stiffness and is defined as: C = ΔD / ΔP Distensibility, by contrast, is defined as the relative compliance or relative change in diameter/area/pressure step increase. It is the inverse of the elastic modulus (E). Dist = (ΔD/D) / ΔP
JL Cavalcante (J Am Coll Cardiol 2011;57:1511 22
The reduction in aortic compliance seen with aging and observed in hypertensive patients during the development of atherosclerosis, in diabetes mellitus, in chronic kidney disease, etc., is the likely result of progressive deposition of collagen fibers in the interstitium of the vessel wall and fragmentation of elastic fibers, deposition of calcium, etc.
In the long term, pulsatility causes stretching of the load-bearing elastic lamellae and mechanical stress on the wall contributing to structural changes and stiffening. Over time, all these factors contribute to increased large-artery stiffness which worsens with aging. Genetics seems to also play a role in the development of AS. Polymorphisms of the matrix metalloprotein-9 gene were independent predictors of increased aortic Stiffness.
JL Cavalcante (J Am Coll Cardiol 2011;57:1511 22
JL Cavalcante (J Am Coll Cardiol 2011;57:1511 22
Pulse Wave Velocity is the most validated method to noninvasively quantify arterial stiffness. It is considered the gold standard index of AS, given its simplicity, accuracy, reproducibility, and strong prediction of adverse outcomes. PWV can be determined by measuring the pulse transit time from the pressure waveforms at the 2 sites along a vascular segment. The distance (L) is divided by the wave foot-to-foot time (T) it takes for that forward wave to reach the end measuring point (PWV) (Fig. 4). Pulse wave velocity is inversely related to vascular compliance. Hence, a stiffer vessel will conduct the pulse wave faster than a more distensible and compliant vessel. PWV is a regional functional measurement of arterial stiffness over a certain arterial length, whereas strain, compliance, and distensibility are local markers of arterial elasticity.
Aortic Distensibility (in cm 2 dyne -1 10-6 ) = 2(systolic diameter - diastolic diameter) / (diastolic diameter)(brachial pulse pressure)
Ultrasonic echo-tracking Time resolution: 1.15 msec. Smallest detectable movement :8 μm. Wilson KA J Vasc Surg 2000;31:507-13.
Lang RM et Al. Circulation. 1994;90:1875-1882.
Lang RM et Al. Circulation. 1994;90:1875-1882.
Applanation Tonometry pro: Cons: easy to perform, validated, portability, relativelly inexpensive lack of accuracy due to the impossiblity to calculate lumen lenght between the two recording sites (obese patients!!). Global distensibility. Echocardiography: pro: Cons: availability, easy to perform, validated, portability, relativelly inexpensive. Evaluation of LV function. Tissue Doppler and strain imaging are adding new insight acoustic window limitations, operator dependency, etc
Ibrahim et al. Journal of Cardiovascular Magnetic Resonance 2010, 12:26
Suever JD Int J Cardiov. Imaging 2011
Measurement of AS by MRI. Unlike Carotid Femoral PWV, which is an average measure of overall arterial stiffness, MRI enables the detection of more subtle changes in regional stiffness. MRI has several advantages over ultrasound in that full 3-dimensional visualization of the vessel is possible, enabling the imaging plane to be placed perpendicular to the vessel in a reproducible location. This is an obvious advantage for the measurement of distensibility measured in MRI as a change in 2-dimensional vessel perimeter or area instead of 1-dimensional vessel diameter. Furthermore, velocity data can be acquired simultaneously within 1 acquisition plane in 2 aortic locations, and the path length (distance between the 2 aortic locations) can be measured precisely. Aortic Distensibility (in cm 2 dyne -1 10 6 ) = maximum area -minimum area /minimum area x ΔP x1,000
Asc. Aorta Magnitude Desc. Aorta Magnitude Asc Desc Phase Phase Maximum Rate Sistolic Distenction (MRSD) Maximum Rate Diastoic Recoil (MRDR) GD Aquaro et Al. AJC, 2011
Control A) B) C) Frame 1 Frame 20 % of maximal area 110 105 100 95 90 85 80 75 MRSD MRDR 70 65 60 1 5 9 13 17 21 25 29 33 37 41 45 49 Time (10-3 sec) BAV 110 D) E) F) Frame 1 Frame 13 105 100 95 90 85 80 75 70 65 60 1 5 9 13 17 21 25 29 33 37 41 45 49 % of maximal area MRSD MRDR Time (10-3 sec)
MRSD 14 12 9.1±2.1 MRSD in BAV and Controls 10 8 * * * 4.37±1.1 4.5±1.1 4.3±1.0 6.6 6 4 2 Controls BAV Dilated-BAV Non-Dilated BAV GD Aquaro et Al. AJC, 2011
MRDR 0 MRDR in BAV and Controls -2-4 -6-8 -4±1.2-3.9±1.3-4.1±1.2 * * * -10-12 -7.6±2.7-14 Controls BAV Dilated-BAV Non-Dilated BAV GD Aquaro et Al. AJC, 2011
1) Distensibility of ascending aorta 2) Flow Velocity Propagation 16 4,0 14 3,5 12 3,0 10 2,5 8 1.29±0.4 2,0 6 4 2 0 8.7±3.4 Controls 6.4±3.0 BAV Controls 2.37±1.9 BAV 1,5 1,0 0,5 0,0 Conclusion: MRSD and MRDR were slower in the patients with BAV than in the controls, regardless of the dimensions of the ascending aorta. GD Aquaro et Al. AJC, 2011
Vel_max sistole - vel sistole II obs Interobserver variability 2,0 1,5 1,0 +1.96 SD 1,54 0,5 0,0-0,5 Mean -0,13-1,0-1,5-2,0 2 4 6 8 10 12 14 16 AVERAGE of Vel_max sistole and vel sistole II obs -1.96 SD -1,79 GD Aquaro et Al. AJC, 2011
MIP (maximum intensity projection) Volume rendering
Why to measure it? Carotid-femoral PWV, a global measure of AS, has been shown to be an independent predictor of CAD and stroke in healthy subjects and an independent predictor of mortality in the general population. CF PWV is also a predictor of future changes in systolic blood pressure (SBP) and future development of hypertension in healthy volunteers (risk of development of hypertension). Increased arterial stiffness has been associated with increased morbidity and both all-cause and cardiovascular (CV) mortality in hypertensive patients. a multiethnic population of patients with impaired glucose tolerance and/or diabetes, has been showed that higher aortic PWV was able to independently predict all-cause and CV mortality, more so than SBP. A meta-analysis including more than 15,000 subjects confirmed that CFPWV is an independent predictor of adverse CV events and all-cause mortality. An increase of aortic PWV of 1 m/s raises CV risk by more than 10%. The 2007 European guidelines for the management of hypertension and guidelines for CVD prevention in clinical practice recommend, given all the aforementioned, aortic PWV as a test to assess target organ damage.
When to measure it?
When to measure it? Chronic kidney disease and end-stage renal disease Diabetes mellitus. Aortic regurgitation. Congenital heart disease (BAV and tetralogy of Fallot). Connective tissue disorders (Marfan and Ehlers-Danlos syndrome). After aortic coarctation repair. Hypertrophic cardiomyopathy. Association with calcifications and Atherosclerosis
Pharmacological Angiotensin-converting enzyme inhibitors. Angiotensin-2 receptor blockers. Beta-blockers. (nebivolol,..etc) Calcium-channel blockers. Statins. Cross-link breakers. Non pharmacological Continuous positive airway pressure (CPAP) (a combination of enhanced endothelial function and reduction in sympathetic Tone). Aerobic exercise training.
Conclusions: Aortic compliance and distensibility would have to be measured sistematically Pulse Wave Velocity is the most validate tech. but has several limitations Imaging techniques (Echo and MRI) have the capability to make it easy. Therapeutical improvement is necessary.