Article Text

  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.


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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