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23 CALCIUM THERAPY CAUSES PROGRESSION OF CORONARY STENOSIS IN TYPE A WOMEN.
  1. R. Barndt,
  2. S. Jagtap,
  3. N. Mina,
  4. A. Stavrakis,
  5. A. Y. Cho,
  6. M. Castandi
  1. Bethel Public Service Clinic, Downey, CA; Drexel University College of Medicine, Philadelphia, PA; Detroit, MI; Los Angeles, CA.

Abstract

Our pilot study (PS) shows calcium therapy (Rx) causes systolic hypertension (SBP > 120 mm Hg) and coronary stenosis (CS) in type A women (TA) on calcium hormonal replacement therapy (CHRRx). Low systolic time intervals (STI < 40) and TA behavior were predicted in general population screening by a significant (Sig* at p < .01 by t-test = TT) rise in pulse pressure (PP) to handgrip (RPPHG > 15 mm Hg at 5 PSI, 3 minutes). Both identify high adrenergic neurovascular tone (ANVT with STI = PEP/LVET × 100%). STI predicted TA behavior test results (r = .98, p < .001). In prospective studies, normal TA women were randomized into two groups (G1, G2) with type B (TB) women as controls (C). G1, G2, and C had normal systolic blood pressures (SBP = 110 ± 10), with no significant coronary stenosis by ultrasonography using methods previously reported by our clinic (see Table below) at time 1 (T1 = start). General population screening revealed 40% of the population (500/1250) on CHRRx had systolic hypertension and Sig* PP increase predictive of Sig* %CS by previous PS equations. G3 was randomly selected (200 of 500) TA women on CHRRx for 10 years versus TB behavioral C, also on therapy for 10 years. All study patients were age 55 ± 5 years old and had LDL < 130, HbA1c < 6.1, Hgb > 13, normal serum tryglycerides (< 145 mg%), and normal C-reactive protein levels and were nonsmokers. All Gs were treated each day (qd) with 1,500 mg calcium, 0.625 mg estrogen, and 2.5 mg progesterone with informed consent. G2 and G3 also had Rx (Rx2) qd of amitriptyline 10 to 50 mg, Tenormin 13 to 100 mg, and diltiazem CD 240 to 360 mg to reduce ANVT, SBP, STI, and systemic vascular resistance (SVR) to CG levels. Serial measurements were made at T1 and T2 (1/2) (T2 = 6 years) in all Gs (G3 = 10 years). Serial measurements were made of SBP, PP, RPPHG, STI, SVR, AS (aortic stiffness), AC (aortic collagen = %AC/area), and maximum %CS with ultrasonic measurements by methods previously reported by our clinic in standard units. In PS, the greatest degree of stenosis and change was found in the left anterior descending (LAD). Quality of life (QL 1-100) was assessed. Data were placed into a blind matrix for analysis later. Prospective results by G analysis: G means shown. See Table. Where * = Sig difference from CG at p < .01. ** = Sig change from T1 to T2 at p < .02 both by TT. G1 reveals **Sig progression of AC and maximum %CS in the LAD. Multiple regression analysis revealed SBP and SVR (reflected by STI) as the Sig** risk factors predictive of CS (mR = 0.97, p < .001 in G1 at T2 and G3 at T1). G2 (a matched G to G1) on Rx2 demonstrates *Sig prevention of progression of AC and %CS compared with G1. G3 at T2 shows Sig** regression of AC and %CS due to SBP, SVR, and STI reduction to C levels. This study demonstrates that systolic hypertension (SBP > 120) and high SVR are significant vascular risk factors during CHRRx in TA women. Thus, control of SBP (< 121 mm Hg), SVR (< 1,600 standard units), and STI (> 45) is necessary for the prevention or regression of AC and %CS during calcium Rx.

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