michigan hypertension core curriculum - State of Michigan
michigan hypertension core curriculum - State of Michigan
michigan hypertension core curriculum - State of Michigan
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trial, angioplasty resulted in significant reduction in BP and antihypertensive medications in patients<br />
with bilateral ARAS. 61 In a third, 28 % <strong>of</strong> medical patients crossed over to angioplasty. A contemporary<br />
review <strong>of</strong> 2 randomized trials, 8 comparative studies, and 34 cohort studies concluded that angioplasty<br />
leads to greater reduction <strong>of</strong> BP than medical therapy, particularly in patients with bilateral RAS. 63<br />
Several prospective studies and meta analysis documented reduction in BP after renal stenting<br />
16,51,64-72 In the only prospective randomized trial <strong>of</strong> angioplasty versus stenting in 85 patients, 19<br />
revascularization resulted in significant reduction <strong>of</strong> systolic (19 mmHg) and diastolic (12 mmHg)<br />
BP. There may be a relationship between renin-angiotensin activation and renal production <strong>of</strong> brain<br />
natriuretic peptide (BNP), and BNP may predict the <strong>hypertension</strong> response to renal stenting. 73,74<br />
After ARAS revascularization, <strong>hypertension</strong> cure (normal BP no medication) is observed in < 10 % <strong>of</strong><br />
patients, regardless <strong>of</strong> revascularization techniques.<br />
RAS and malignant <strong>hypertension</strong>. The augmented renin and angiotensin II levels in some patients<br />
with stenosis <strong>of</strong> a solitary kidney or that may occasionally occur in patients with bilateral ARAS may<br />
promote acute volume loading and vasoconstriction, flash pulmonary edema, and other manifestations<br />
<strong>of</strong> malignant <strong>hypertension</strong>. 6,75-79 Prevention <strong>of</strong> recurrent pulmonary edema is a Class I recommendation<br />
for renal revascularization 6 , based on several small studies. 77,79,80,27<br />
Failure <strong>of</strong> renal revascularization to cure <strong>hypertension</strong>. The explanations for why renal<br />
revascularization does not cure <strong>hypertension</strong> are somewhat speculative (Table 8). There is a persistent<br />
misperception that ARAS patients have renovascular <strong>hypertension</strong>, and contemporary reviews continue<br />
to use this terminology. 2,20 While the experimental Goldblatt models are compelling demonstrations<br />
<strong>of</strong> renin-angiotensin activation due to RAS 81 , the mechanisms <strong>of</strong> <strong>hypertension</strong> in humans with and<br />
without RAS are far more complex, and include sympathetic and cerebral nervous system activation,<br />
vasoactive oxygen species, abnormalities in endothelial dependent relaxation, and ischemic and<br />
hypertensive intra-renal injury. 82-86 Patients with ARAS do not have renovascular <strong>hypertension</strong>, as<br />
evidenced by similarities in the extent <strong>of</strong> renin activation compared to hypertensive patients without<br />
RAS 87,88 and the low cure rate <strong>of</strong> <strong>hypertension</strong> after successful revascularization. Although lumen<br />
enlargement after balloon angioplasty for ARAS is clearly suboptimal, observational studies do not<br />
suggest different cure rates after renal artery bypass or stenting. 89-100 The most likely explanations<br />
are that patients with ARAS have essential <strong>hypertension</strong>, many do not have renal ischemia, and<br />
unrecognized hypertensive nephropathy leads to self-perpetuating <strong>hypertension</strong>.<br />
NKFM & MDCH 113