Renovascular Hypertension and Renal Artery Ultrasounds Amajd AlMahameed, MD, MPH Division of...

Renovascular Hypertension and Renal

Artery Ultrasounds

Amajd AlMahameed, MD, MPHDivision of Cardiology

Beth Israel Deaconess Medical Center

Boston

Moderate RAS: visually estimated 50-69% w 10 mm Hg mean or 20 mm Hg systolic translesional gradient

Severe RAS: visually estimated diameter stenosis of > 70%

(Rundback et al Circulation 2002;106:1572–1585)Necropsy Studies: Luminal stenosis > 50% was found: Overall 27-53% of autopsiesAge > 70 y/o: 74%

(Holley et al Am J Med. 1964;37:14 –22)(Schwartz et al BMJ. 1964;5422:1415 –1421)

CHS: significant RAS (>60%) in 6.8%, M:F ratio 2:1, W = B

(Hansen et al J Vasc Surg 2002;36:443-51)

Patients with PAD: Significant RAS in 22% to 59%

(Olin et al Am J Med. 1990;88:46N–51N, Valentine et al Ann Vasc Surg. 1993;7:220 –224.)

Patients with proven history of MI: 12% had RAS > 75%

(Uzu et al Am J Kidney Dis 1997;29:733-8)

Bilateral RAS: is not uncommon, found in 44% of RAS patients

(Rimmer et al Ann Intern Med 1993;118:712-9)

Patients with 1 or more clinical clues to the presence of RAS, significant RAS can be found in up to 70%

(Olin et al Am J Med. 1990;88:46N–51N)

How Common is Renal Artery Stenosis

White CJ. Circulation. 2006;113:1464-1473. Hirsch AT et al. Circulation 2006;113;463-654

Incidence of Renal Artery Stenosis at Cardiac Catheterization

White CJ. Circulation. 2006;113:1464-1473.

Clues to RAS: Must Evaluate Such Patients

White CJ. Circulation. 2006;113:1464-1473.

29% of patients progressed, 11% developed total occlusion (mean f/u of 28 months)

(Dean et al Arch Surg 1981;116:1408-15)48% progressed from < 60% to > 60% stenosis (within 3 years)

(Zierler Am J Hypertens 1996;9:1055-61)

Progression occurred at an average rate of approximately 7% per year

(Zierler Am J Hypertens 1996;9:1055-61)

Disease progression, based on sonographic determination, was 35% at 3 years and 51% at 5 yearsCaps et al Circulation 1998;98:2866-72

Randomized trial, med Rx vs. PTA for RAS, over a 1-year, progression to RA occlusion occurred in 16% of the med Rx group compared with none in the angioplasty group

(van Jaarsveld et al N Engl J Med. 2000;342:1007–1014)Progressive worsening of RAS occurs despite medical therapy that effectively controls blood pressure

(Crowley et al Am Heart J. 1998;136:913–918, Dean et al Arch Surg. 1981;116:1408 –1415)

RAS is the cause of ESRD in 15% of patients over age 50 beginning dialysis each year(Rimmer Ann Intern Med. 1993;118:712–719, Scoble et al Clin Nephrol. 1989;31:119 –122)

Renal Artery Stenosis is a PROGRESSIVE Disease

White CJ. Circulation. 2006;113:1464-1473. Hirsch AT et al. Circulation 2006;113;463-654

RAS: An Ominous Diagnosis to Make

• RAS (50%): Stronger independent predictor of 4-yr all-cause mortality (RR 2.9) than CHF (RR 2.3), dec LVEF (RR 1.7), or dec renal function (RR 1.3)

Conlon et al J Am Soc Nephrol. 1998;9:252–256

• mild-to-moderate (50%) RAS was associated with a 30% 4-year mortality rate, which almost doubled (52%) with severe (95%) RAS (incremental effect)

Conlon Kidney Int. 2001;60:1490 –

1497.

• independent predictor of death regardless of the presence, severity, or method of revascularization of coronary artery disease

Kennedy et al Am J Kidney Dis. 2003;42:926 –935, Conlon et al J Am Soc Nephrol. 1998;9:252–256, Conlon Kidney Int. 2001;60:1490 –1497.

White CJ. Circulation. 2006;113:1464-1473. Hirsch AT et al. Circulation 2006;113;463-654

Indications for Revascularization

• Hemodynamically significant renal artery stenosis associated with:

- HTN (accelerated, resistant, malignant, with a unilaterally small kidney, and/or with

intolerance to medication)

- Renal insufficiency

- Recurrent CHF or “flash” pulmonary edema, refractory heart failure, or refractory angina pectoris●

White CJ. Circulation. 2006;113:1464-1473. Hirsch AT et al. Circulation 2006;113;463-654

Patient Selection for Renal Revascularization: Prediction of

Success

• Fractional flow reserve

• BNP

• Resistive Index

White CJ. Circulation. 2006;113:1464-1473. Hirsch AT et al. Circulation 2006;113;463-654

• Duplex scanning was introduced in 1974

• First applied to the carotid arteries

• Major advances since included:

◘ Improved B-mode imaging

◘ Better low-frequency transducers (deeper penetration)

◘ Improved microprocessor software, and

◘ The addition of color to B-mode image.

The History of Peripheral US

Principles of Peripheral US

Provides information Provides information about native anatomy and about native anatomy and

graftsgrafts

Localizes and measures Localizes and measures stenosesstenoses

Peripheral US

Identifies occlusion with reconstitutionIdentifies occlusion with reconstitution

Peripheral US

• Flow in a cylinder with concentric layers

• Friction created between layers

• Velocity is slowest near the walls and fastest in the center

Laminar Flow

• A product of FFT analysis (displays all velocities within the Doppler signal)

• Spectral broadening is the term used to describe turbulent flow filling the Doppler spectral window

Turbulent Flow

• Chaotic blood flow with different directions and speeds within the signal

• Identified after an area of disruption of flow (severe stenosis)

Turbulent Flow

Turbulant flow has a shape similar to Bart Simpson’s hair!

Aliasing

Aliasing corrected by dropping the baseline or increasing the scale

True Aliasing secondary to very high velocities “wrap around”

Velocity Criteria in Peripheral Ultrasounography

Proximal Lesions

Low Cardiac Output

Cardiac Arrhythmia

Compensatory Flow

Long Lesions

Tortuosity

Necessary for Standardization

Same Criteria for Stents

Several Limitations/Pitfalls

Doppler Angle

Hints to Proximal Stenotic Lesions

– Delayed acceleration time to peak systole

– Velocities alone not reliable as they may be normal, slightly elevated, or even low

– Turbulence should be documented distal to the lesion

– Occasionally, collateral vessels may be identified by abnormal flow patterns (retrograde)

Normal Doppler signal

Abnormal Doppler signal (turbulant)

High Resistive Low Resistive

Renal Artery US as the diagnostic test of choice for RAS

The Normal Anatomy of the Renal Arteries.

Direct Assessment of RAS

Velocity Criteria (+ Turbulance) Renal/Aortic Ratio

Supportive findings

White CJ. Circulation. 2006;113:1464-1473. Hirsch AT et al. Circulation 2006;113;463-654

• 0-59% stenosis (No clinically significant stenosis)– PSV<200cm/sec.

• 60-99% stenosis (Clinically significant stenosis)– PSV>200cm/sec– Post-stenotic turbulence present

• Occlusion– Artery visualized without flow

Velocity Criteria for RAS

White CJ. Circulation. 2006;113:1464-1473. Hirsch AT et al. Circulation 2006;113;463-654

• RAR < 3.5: Non-significant stenosis (0-59%)

• RAR > 3.5: Significant stenosis (60-99%) (Sensitivity 84-88%, Specificity 97-99%, PPV 94-98%)

• EDV > 150 cm/sec may indicate > 80% stenosis

• Aorta velocities must be between 40 and 100cm/sec for above criteria! If not go back to PSV > 200cm/sec (and the presence of post-stenotic turbulance).

Renal/Aortic Ratio

Normal Renal Artery: RAR < 3.5 and PSV < 200<60% stenosis: PSV > 200 but RAR < 3.5

(Note, AO PSV should be 40-100)60-99% stenosis: RAR > 3.5, regardless of PSV

White CJ. Circulation. 2006;113:1464-1473. Hirsch AT et al. Circulation 2006;113;463-654

• Resistive Index – Normal: 0.53 to 0 .70– > 0.70: suggests intrinsic kidney disease– < 0.53: suggests renal artery stenosis

• Acceleration time– Normal < 100m/sec

• Tardus/parvus waveform (delayed upstroke)

• Small kidney (< 8 cm in length or > 1.5 cm discrepancy from other kidney)

PSV-EDV

PSV

Supportive Data (Indirect Assessment)

White CJ. Circulation. 2006;113:1464-1473. Hirsch AT et al. Circulation 2006;113;463-654

RA US showing the whole course of the R renal artery

Aorta

R K

idne

y

RRA stenosis at origin. Note turbulent flow And increased velocities

Normal flow at RRA origin

Normal flow at RRA proximal segment

Increased velocities at mid renal artery segment: Typical of non-atherosclerotic RAS (such as FMD)

RA US can evaluate the parenchymal flow as well

RI 0.53AT 140 m/s

RA US can evaluate the parenchymal flow as wellNote increased acceleration time (AT) and borderline

resistive index (RI)

Another example of the common form of RAS (atherosclerotic)

Lesion is typically at the origin of the vessel

RI 1.00

Example of increased resistive index (indicativeOf intrinsic kidney disease)

US can also detect renal stents

Documentation of floe within the renal vein is part of RA US exam

Prediction of Clinical Response to Revascularization: RFFR

• The renal fractional flow reserve (FFR) is an assessment of the severity of the RAS by using maximal vasodilation with papaverine

• Patients with an abnormal baseline renal FFR (0.8) had a higher rate of blood pressure improvement (86%) compared with only 30% in those with a normal baseline FFR

White CJ. Circulation. 2006;113:1464-1473.Mitchell J, et al. Catheter Cardiovasc Interv. 2005;65:135. Abstract.

Prediction of Clinical Response to Revascularization: BNP

• Hemodynamically significant RAS activates renin-angiotensin system, leading to increased levels of angiotensin II.

• In animal experiments, angiotensin II induces synthesis and release of BNP, and the BNP mRNA is upregulated in the setting of RAS.

• BNP is increased in patients with refractory hypertension and renal artery stenosis

• An elevated baseline BNP 80 pg/mL strongly correlated with hypertension improvement after 3.5 months of follow-up.

White CJ. Circulation. 2006;113:1464-1473.Silva JA et al. Circulation. 2005;111:328 –333.

Prediction of Clinical Response to Revascularization: BNP

• Mean (±SE) Changes in Creatinine Clearance post PTA, According to the Resistive-Index Value before Revascularization

• Asterisks indicate a

significant difference (P<0.05) between the two groups with use of an unpaired t-test with Bonferroni's adjustment.

Radermacher et al. NEJM;344 (6): 410

Mean BP in patients without nephrosclerosis (RI <0.7), with mild nephrosclerosis (RI, 0.7 to 0.8), and with severe

nephrosclerosis (RI >0.8)

P >0.0001

P >0.0001P >0.05

RI < 0.7 RI 0.7- 0.8 RI > 0.8

Baseline One Year

Mea

n B

P

8488

92

96

100

104

108

White CJ. Circulation. 2006;113:1464-1473.

Zelelr T et al. Circulation. 2003;108:2244 –2249.

Serum Cr in patients without nephrosclerosis (RI <0.7), mild nephrosclerosis (RI, 0.7 to 0.8), and severe nephrosclerosis (RI

>0.8)

P = NS

P < 0.05

P < 0.05One YearBaseline

Se

rum

Cr

RI < 0.7 RI 0.7-0.8 RI > 0.8

White CJ. Circulation. 2006;113:1464-1473.

Zelelr T et al. Circulation. 2003;108:2244 –2249.