ESC Guidelines on the diagnosis and treatment of peripheral artery ...

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Recommendations for the management of mesenteric
artery disease
Recommendations Class a Level b Ref c
Mesenteric revascularization
should be considered in
patients with symptomatic
mesenteric artery disease.
In the case of revascularization,
endovascular treatment should
be considered as the first-line
strategy.
a Class of recommendation.
b Level of evidence.
c References.
4.4 Renal artery disease
IIa B
120,
143–150
IIa C -
Renal artery disease is increasingly related to atherosclerosis with
advancing age and prevalent hypertension, diabetes mellitus, renal
disease, aortoiliac occlusive disease, and CAD. 151 In the elderly
population, atherosclerosis accounts for ≏90% of cases and
usually involves the ostium and proximal third of the main renal
artery and the perirenal aorta. Less frequent causes are fibromuscular
dysplasia and arteritis. Screening angiography in potential
kidney donors indicates that RAS can be asymptomatic and may
be present in up to 3–6% of normotensive individuals. 152
4.4.1 Clinical presentation
Major clinical signs of RAS include refractory hypertension, unexplained
renal failure, and flash pulmonary oedema (Table 4). RAS
may cause or deteriorate arterial hypertension and/or renal
failure. Hypoperfusion of the kidney activates the renin–angiotensin–aldosterone
system (RAAS), causing classic renovascular
hypertension, primarily in young patients with fibromuscular dysplasia.
151,153 However, in patients with atherosclerosis, RAS may
induce an acute or subacute acceleration of a pre-existing essential
hypertension including flash pulmonary oedema usually in bilateral
kidney disease. 151 The association between RAS severity and
ischaemic nephropathy 154,155 has recently been challenged. 156
The loss of filtration capacity of the kidney in RAS may be due
not only to hypoperfusion, but also to recurrent microembolism.
Renal failure may occur with severe bilateral RAS or unilateral
stenosis in a single functional kidney.
Kidney disease and renovascular disease promote CVD and
hypertension. Increased risk of CVD in atherosclerotic RAS
patients may result from activation of the RAAS and sympathetic
nervous systems, decreased GFR, or concomitant atherosclerosis
in other vascular beds. 157 – 159 The prevalence of left ventricular
hypertrophy with RAS is 79% vs. 46% in patients with essential
hypertension, with a substantial impact on morbidity and
160 – 162
mortality.
4.4.2 Natural history
Data on progression of atherosclerotic RAS are inconsistent. More
recent studies show significant disease progression to high-grade
stenosis or occlusion in only 1.3–11.1% of patients, whereas
Table 4 Clinical situations where the diagnosis of RAS
should be considered
Clinical presentation
• Onset of hypertension before the age of 30 years and after 55 years
• Hypertension with hypokalemia, in particular when receiving thiazide
diuretics
• Hypertension and abdominal bruit
• Accelerated hypertension (sudden and persistent worsening of
previously controlled hypertension)
• Resistant hypertension (failure of blood-pressure control despite full
doses of an appropriate three-drug regimen including a diuretic)
• Malignant hypertension (hypertension with coexistent end-organ
damage, i.e. acute renal failure, flash pulmonary oedema, hypertensive
left ventricular failure, aortic dissection, new visual or neurological
disturbance, and/or advanced retinopathy)
• New azotemia or worsening renal function after the administration
of an angiotensin-converting enzyme inhibitor or an angiotensin II
receptor blocker
• Unexplained hypotrophic kidney
• Unexplained renal failure
RAS ¼ renal artery stenosis.
<strong>ESC</strong> <strong>Guidelines</strong>
older studies documented occlusion rates up to 18% over 5
years. 163 – 166 After 2 years, 3, 18, and 55% of the kidneys had
lost their function in the case of unilateral stenosis, bilateral stenosis,
and contralateral occlusion, respectively. 167
4.4.3 Diagnostic strategy
Baseline diagnostic evaluation includes physical examination, exclusion
of other potential causes of secondary hypertension, and
ambulatory blood pressure measurement. In clinical situations in
which RAS is suspected, such as those listed in Table 4, renal
artery imaging should be considered.
DUS is the first-line screening modality for atherosclerotic RAS.
It can be applied serially to assess the degree of stenosis and physiological
patterns, such as flow velocities and vascular resistance.
Increased peak systolic velocity in the main renal artery associated
with post-stenotic turbulence is most frequently used to determine
relevant RAS, and corresponds to ≥60% angiographic RAS
with a sensitivity and specificity of 71–98% and 62–98%, respectively.
168 – 170 Several duplex criteria should be used to identify significant
(.60%) stenosis. These include imaging of intrarenal
interlobar or segmental arteries, including calculation of the sidedifference
of the intrarenal resistance index, missing early systolic
peak, retarded acceleration, and increased acceleration time,
which are less specific and should be used to support the diagnosis
171 – 173
based on peak systolic velocity.
Common pitfalls of DUS include failure to visualize the entire
renal artery and missing the highest peak systolic velocity during
spectral Doppler tracing. Accessory renal arteries are generally
not adequately examined or identified. The accuracy of DUS is
operator dependent.