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The DRASTIC Trial Dutch Renal Artery Stenosis Intervention Cooperative

The DRASTIC Trial Dutch Renal Artery Stenosis Intervention Cooperative. Reference van Jaarsveld BC, Krijnen P, Derkx FHM, et al . Resistance to antihypertensive medication as predictor of renal artery stenosis: comparison of two drug regimens. J Hum Hypertension . 2001;15:669–676. Background

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The DRASTIC Trial Dutch Renal Artery Stenosis Intervention Cooperative

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  1. The DRASTIC Trial Dutch Renal Artery Stenosis Intervention Cooperative Reference van Jaarsveld BC, Krijnen P, Derkx FHM, et al. Resistance to antihypertensive medication as predictor of renal artery stenosis: comparison of two drug regimens. J Hum Hypertension. 2001;15:669–676.

  2. Background Renal artery stenosis is among the most common curable causes of hypertension. The definitive diagnosis is made by renal angiography, an invasive and costly procedure. The prevalence of renal artery stenosis is less than 1% in non-selected hypertensive patients but is higher when hypertension is resistant to drugs.

  3. Aim To study the usefulness of standardized two drug regimens for identifying drug-resistant hypertension as a predictor of renal artery stenosis.

  4. Methods

  5. Summary of Key Results Of the 1106 patients with complete follow-up, 1022 had been assigned to either the amlodipine- or enalapril-based regimens, 772 by randomization. • Drug-resistant hypertension identified in 41% of the patients while 20% had renal artery stenosis. • Renal function impairment was observed in 8% of the patients on ACE inhibitor, and this was associated with a 46% prevalence of renal artery stenosis.

  6. • In the randomized patients, the prevalence of renal artery stenosis did not differ between the amlodipine- and enalapril-based regimens.

  7. Follow-up • Blood pressure at entry was higher among drug-resistant patients, and they used more medication. • In the drug-resistant group, blood pressure during follow-up was 170±22 mm Hg systolic and 105±9 mm Hg diastolic (average of the three follow-up visits). In patients who completed follow-up, 8% of them on ACE inhibitor showed a rise. • Creatinine at entry was higher in these patients than in those with stable creatinine levels (98, 59–199 _mol/L vs 83, 40–197 _mol/L [1.11, 0.67–2.25 mg/dL vs 0.94, 0.45–2.23 mg/dL], median and range, P=0.002). • In the randomized patients, a larger proportion remained hypertensive during En(+Th) treatment than during Am(+At) treatment. • Prevalence of drug-resistant hypertension was higher in the combined non-randomized groups than in the combined randomized groups (51% vs 37%, P<0.001). The non-randomized groups also showed a higher incidence of renal function impairment after ACE inhibitor treatment (7% vs 2%, P<0.001).

  8. Conclusion The use of these two drug combinations is a rational first step in the diagnostic workup for renovascular hypertension. By taking into consideration some other well-known clinical characteristics, the risk estimation can be narrowed down to the individual patient. Use of standardized two drug regimens to identify drug-resistant hypertension is sufficient to increase the average a priori chance of renal artery stenosis to 20% or more. Combination of amlodipine (10 mg) and atenolol (50 mg) appears at least as effective as the combination enalapril (20 mg) and hydrochlorothiazide (25 mg). Use of these two-drug combinations is a rational first step in the diagnostic workup for renovascular hypertension.

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