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22 NEW GOALS IN SYSTOLIC HYPERTENSION THERAPY ARE REVEALED BY VASCULAR COLLAGEN.
  1. R. Barndt,
  2. N. Mina,
  3. A. Y. Cho,
  4. S. Jagtap,
  5. A. Stavrakis
  1. Bethel Public Service Clinic, Downey, CA; Detroit, MI; Drexel University College of Medicine, Philadelphia, PA; Los Angeles, CA.

Abstract

Ultrasonic measurement (UM) of % aortic collagen (AC) and % coronary stenosis (CS) reveals that systolic hypertension (SH) begins at systolic blood pressure (SBP) of 121 mm Hg by group analysis (mean 126 ± 6). Our pilot studies (PSs) show that UM of AC is predictive of AC assay in separate in vitro tissue studies (r = .97, p < .001). AC predicts average SBP (ASBP), pulse pressure (PP), aortic stiffness (AS), and maximum %CS in coronary arteries (%SCA in left anterior discending [LAD]), all at r = .97, p < .001 in PS. UM of %SCA predicted %SCA by angiography in clinical PS and separate postmortem angiographic studies, all at r = .97, p < .001. In PS, PP at normal systemic vascular resistance (SVR) predicted % AC (r = .97, p < .001). Normal SVR was predicted by a rise in PP < 11 mm Hg during sustained isometric handgrip (RPPHG = 5 psi for 3 minutes) with 0 to 20 mg hydralazine (p < .01 by t-test). Prospective patients (ProsGroup [G]) were randomly selected and grouped by PS %AC levels (mean AC ± range values) to predict different hypertension (H) levels: control (C) G = 16 ± 2, mild (M) = 24 ± 3, moderate (Md) = 32 ± 4, and Md severe (MdS) = 45 ± 8. Labile hypertension (LH) Gs (L1 and L2) were randomly selected and had AC at 16 ± 2 with significant RPPHG (RPPHG > 15 mm Hg). All groups were matched by age (mean 50), sex (M/F = 1/1), and race. Exclusions: Smoking, diastolic H (> 85 mm Hg), LVH, diabetes, hyperlipidemia, and chronic diseases. Serial measurements were made of AC, AS (PP/aortic diameter distention in mm), %SCA, PP, ASBP by AC, and baseline cuff SBP at normal SVR. Data were analyzed by blind matrix. BP was regulated every 6 weeks for 10 years in all with AC > 21 or RPPHG > 10 mm Hg. All groups except for C and L1 were treated with Tenormin (12-100 mg/d) and Cardura (1-16 mg/d) (Rx) to maintain SBP < 121 and RPPHG < 11 mm Hg. ProsG results: G means at start/end (1/2). See Table. Where * = significant (Sig*) difference from CG at p < .01 by t-test. This study shows that Sig* SH begins at ASBP 121 mm Hg, AC 21%, and AS 11, causing Sig* %SCA (maximum SCA in LAD). Regression analysis revealed PS formulas predict ProsG: AS, PP, ASBP, and %SCA by AC (all at r = .96, p < .001). Sig* AC and %SCA regression occurred with Rx at SBP < 121 and RPPHG < 11, without sig* changes in serum lipids. Sig* regression of AC correlated with functional improvement of the aorta (AS, p < .01 by t-test). Rx of LH in G L2 prevented progression of AC and SCA that was seen in matched G L1. There were no adverse vascular events. This prospective study shows that AC and SCA can be reversed by Rx of SBP to C levels. Thus, UM of AC and SCA proves that SH begins to cause vascular damage at SBP > 120 mm Hg and RPPHG > 10 mm Hg and should be treated to reduce vascular risk.

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