Article Text

  1. P. P. Gupta,
  2. R. Barndt
  1. Bethel Public Service Clinic, Los Angeles, CA


Our pilot studies (PS) show that systolic hypertension (SH) is due to high adrenergic neurovascular tone (ANVT) and is associated with a low central blood volume (CBV) in a significant (sig) number of patients. This complicates treatment (Rx) since sig postural hypotension (PH) occurs with low CBV when systolic blood pressure (SBP) is reduced by Rx of systemic vascular resistance (SVR) alone (Rx1 = atenolol 13-100 mg/day). These patients can be identified in the PS by the abnormal rise of pulse pressure (RPP) > 25 mm Hg, during sustained isometric handgrip (5 psi - 3 min) and by low systolic time intervals (STI) < 31% and low cardiac output (CO) < 3.5 L/min. These PS criteria were used in a prospective study (ProsS) predicting Group (G) 1 patients. G2 patients had RPP < 25 and > 11 mm Hg and STI > 31%. G1 and G2 were selected with SBP > 135 mm Hg, diastolic BP 80 ± 5 all Caucasian, female-male ratio 2/1, mean age 57 (range 50-65), HgA1C < 6.1, nonsmokers. The control (C) G had a SBP < 126 mm Hg, RPP < 11 mm Hg and STI > 50% and were age/sex matched to G1 and 2. STI is a measure of ANVT (STI = PEP/LVET × 100). G1 and G2 had Rx1 and Rx2 (diltiazem CD 240-360 mg/day followed by atenolol 13-100 mg/day) in a double-blind crossover design. Serial measurements were made at time (T) 1-6 as shown in the table below. Measurements of CO and systemic vascular resistance (SVR) were made by ultrasonic methods. All data were placed into a blind matrix for later correlation. Prospective results: group means are shown.

Where *Sig difference from GC at p < .01; **Sig change from T3 to T4 at p < .01, both by t-tests. SBP at 1 = initial sitting, 2 = initial standing, 3 = on Rx1 sitting, 4 = standing on Rx1, 5 = sitting on Rx2, 6 = standing on Rx2. SVR = standard units. The increased SVR in G1 is found to mask the low CO and low CBV (-28%) in 29% of the hypertensive general population. Prospective G1 and G2 predictions were both accurate at 50/50. In G1 SBP was reduced by Rx2, increasing the CBV before reducing SBP without PH. Hematocrit dilution proved the low CBV with additional confirmation by Rx1 results. G2 was found as predicted to have normal CBV and to respond to Rx1. Thus, Rx2 adequately controlled SH by maintaining normal CO during reduction of SVR, where needed, avoiding the complications of postural hypotension.

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