Improvement in blood pressure after renal artery revascularization

A morbidly obese 74-year-old white woman was referred for assessment of difficult-to-control hypertension. She had undergone successful percutaneous coronary intervention (PCI) 1 year before her visit. Her chief symptom was occasional headaches in the occipital area, occurring two to three times a week. She had previously had angina pectoris, but it completely subsided following the PCI. In addition to aspirin and an HMG-CoA reductase inhibitor, she was taking four antihypertensive medications, including labetalol (Trandate), amlodipine (Norvasc), lisinopril (Prinivil, Zestril), and hydrochlorothiazide (Aquazide H, Hydrodiuril, Microzide).

The patient’s resting supine blood pressure was 176/94 mm Hg, and her pulse was 58 beats/min. Results of the physical examination were normal except for an S4 gallop. The electrocardiogram showed left atrial enlargement with nonspecific T-wave changes. An echocardiogram showed normal segmental wall motion and a normal left ventricular ejection fraction.

A magnetic resonance angiogram (MRA) was obtained to rule out atherosclerotic renovascular hypertension in this patient with established atherosclerotic coronary artery disease and refractory hypertension, despite her taking four antihypertensive medications. The MRA was obtained instead of a less expensive renal duplex study because of the patient’s morbid obesity. The MRA showed a significant stenosis of the left renal artery, for which angiography and possible intervention were scheduled.

The patient’s creatinine level was 1.2 mg/dL, and the rest of the electrolyte and glucose studies were normal. Her brain natriuretic peptide (BNP) level was increased, at 386 pg/mL. A repeated BNP test 2 hours prior to renal angiography was 304 pg/mL.

Selective renal angiography confirmed the presence of a moderate (50%—70%) ostial, left renal artery stenosis. A No. 4 French catheter placed across the lesion measured a 30-mm Hg translesional pressure gradient, indicating that the moderate stenosis was indeed obstructive. The patient was successfully revascularized with stent placement, and her blood pressure medications were withheld.

The patient’s blood pressure the morning after the procedure was 112/64 mm Hg, her creatinine level was 1.1 mg/dL, and her BNP level was 92 pg/mL. Her antihypertensive medications were withheld at discharge. Two weeks following the procedure, her blood pressure was 136/88 mm Hg, her creatinine level was 1.2 mg/dL, and her BNP level was 56 pg/mL. Her angiotensin-converting enzyme (ACE) inhibitor was restarted. After 3 months of follow-up, her blood pressure remained well controlled, at 128/82 mm Hg on the ACE inhibitor alone.

This patient, who had known atherosclerosis, refractory hypertension, and normal left ventricular systolic function, was at increased risk for renovascular hypertension. The next step, a noninvasive screening study (ultrasonography, computed tomographic angiography, or MRA), confirmed the clinical suspicion. She had an increased BNP level without an obvious cause. When the moderate angiographic stenosis was found, the lesion’s severity was assessed by measuring a translesional pressure gradient. Successful renal intervention was accomplished. The blood pressure significantly decreased after intervention, as well as the patient’s BNP level, which is consistent with the results of our study (see “Brain natriuretic peptide and blood pressure response in patients with renal artery stenosis”) showing that BNP is increased in patients with hemodynamically significant renal ar-

tery stenosis and that it declines following successful intervention.

Although technical success rates for renal artery stent placement continue to improve, in many cases approaching 100%, the percentage of patients with improvement in blood pressure lags behind, at 60% to 70%. A better tool to separate patients with renovascular hypertension from those with renal artery stenosis and hypertension would allow more targeted therapy. Other methods to discriminate between blood pressure responders and nonresponders, such as renal vein or plasma renin measurements, radionuclide scintigraphy, angiographic lesion severity, resistance indices, and translesional pressure gradients, have failed to accurately separate patients with renovascular hypertension from those with renal artery stenosis and hypertension.

Although the results of our study require confirmation in a larger cohort of patients, it appears that an increased BNP level may help to stratify which hypertensive patients with renal artery stenosis will have improved blood pressure after revascularization. In this particular patient, with moderate angiographic stenosis, the increased BNP level predicted that the hypertension would improve after revascularization.