Our pilot study (PS) shows calcium (Cal) therapy (RX) causes systolic hypertension (SH, SBP≥125 mmHg) and coronary stenosis (CS) in normal type A women (TAW) on Cal hormonal replacement therapy (Cal-HRRx). In TA screening a significant (Sig* at P≤0.01 by T test = TT) rise in pulse pressure (PP) to handgrip (RPPHg≥15 mmHg at 5 PSI, 3 min.) predicts both low systolic time intervals (STI≤40) and TA behavior (TAB). Both identify high adrenergic neurovascular tone (NVT with STI=PEP/LVET X100%). STI predicted TAB test results (R=0.98, P≤0.001). In prospective studies TAW were randomized into group (G) 1 and G2 with type B controls (C1). G3 were randomly selected TAW on Cal-HRRx for 10 yrs vs. TB C (C3). All groups at time (T) 0 were: normal, on 500 mg dietary Cal/day (d), maintaince vitamins/d, age 55+/-5 yrs, SBP 110+/-10 (orthostatic), LDL≤130, HgA1c ≤6.1, normal serum Cal and phosphorus. Each G received additional Rx/d: 1500 mg Cal, 0.625 mg estrogen and 2.5mg progesterone. G 2 and 3 also had Rx (Rx2)/d: elavil 10-50 mg, atenolol 13-100 mg, and diltiazem CD 240-360 mg to reduce NVT, SBP and systemic vascular resistance (SVR) to CG levels. Serial measurements (SM) were made at T1 (start) and T2 (6 yrs) in all G (G3 at 10 yrs). SM were: BP, PP, RPPHg, SVR, AS (aortic stiffness), AC (aortic collagen) and %CS with ultrasonic measurements (UM) by methods previously reported by our clinic. Quality of life (QL 1-100) reflected NV symptom levels (migraine, chest pressure, paresthesias, etc.). All data was placed into a blind matrix for analysis later. Results: Screening revealed 38% of the population (475/1250) on Cal-HRRx had SBP ≥125, with a Sig* PP level (6 yrs) predictive of Sig** %CS change by PS equations (PSE). The Sig** PP change predicted Sig** %CS increases in G1 (6 yrs) and in G3 at 10 yrs (R=0.97, P≤0.001). G analysis: G means shown. (Table)
Where: *=Sig difference from CG at P≤0.01 and **=Sig change from time 1 at P≤0.02 both by TT. Rx2 resulted in prevention of AC and %CS change in G2 with QL≥G1 and Sig** regression in G3 without lipid therapy. Cal-HRRx has vascular risk that can be prevented and regressed by prospective therapy.