James S. Lieberman

Estrogen replacement, vascular distensibility, and blood pressures in postmenopausal women.

The pathogenesis of blood pressure (BP) rise in aging women remains unexplained, and one of the many incriminating factors may include abnormalities in arteriolar resistance vessels. The aim of this study was to determine the effects of unopposed estrogen on arteriolar distensibility, baroreceptor sensitivity (BRS), BP changes, and rate-pressure product (RPP). We tested the hypotheses that estrogen replacement therapy (ERT) enhances arteriolar distensibility and ameliorates BRS, which leads to decreases in BP and RPP. Postmenopausal women participated in a single-blind crossover study; the participants of this study, after baseline measurements, were randomly assigned to receive estrogen (ERT) or a drug-free treatment with a 6-wk washout period between treatments. The single-blind design was instituted because subjects become unblinded due to physiological changes (i.e., fluid shifts, weight gain, and secretory changes) associated with estrogen intake. However, investigators and technicians involved in data collection and analyses remained blind. After each treatment, subjects performed identical autonomic tests, during which electrocardiograms, beat-by-beat BPs, and respiration were recorded. The area under the dicrotic notch of the BP wave was used as an index of arteriolar distensibility. The magnitude of the reflex bradycardia after a precipitous rise in BP was used to determine BRS. Power spectral analysis of heart rate variability was used to assess autonomic activity. BPs were recorded from resistance vessels in the finger using a beat-by-beat photoplethysmographic device. RPP, a noninvasive marker of myocardial oxygen consumption, was calculated. Repeated-measures analyses of variance revealed a significantly enhanced arteriolar distensibility and BRS after ERT (P < 0.05). A trend of a lower sympathovagal balance at rest was observed after ERT, however, this trend did not reach statistical significance (P = 0.061) compared with the other treatments. The above autonomic changes produced significantly lower systolic and diastolic BP changes and RPPs (P < 0.05) at rest and during isometric exercise. We conclude that short-term unopposed ERT favorably enhances arteriolar distensibility, BRS, and hemodynamic parameters in postmenopausal women. These findings have clinical implications in the goals for treating cardiovascular risk factors in aging women.The pathogenesis of blood pressure (BP) rise in aging women remains unexplained, and one of the many incriminating factors may include abnormalities in arteriolar resistance vessels. The aim of this study was to determine the effects of unopposed estrogen on arteriolar distensibility, baroreceptor sensitivity (BRS), BP changes, and rate-pressure product (RPP). We tested the hypotheses that estrogen replacement therapy (ERT) enhances arteriolar distensibility and ameliorates BRS, which leads to decreases in BP and RPP. Postmenopausal women participated in a single-blind crossover study; the participants of this study, after baseline measurements, were randomly assigned to receive estrogen (ERT) or a drug-free treatment with a 6-wk washout period between treatments. The single-blind design was instituted because subjects become unblinded due to physiological changes (i.e., fluid shifts, weight gain, and secretory changes) associated with estrogen intake. However, investigators and technicians involved in data collection and analyses remained blind. After each treatment, subjects performed identical autonomic tests, during which electrocardiograms, beat-by-beat BPs, and respiration were recorded. The area under the dicrotic notch of the BP wave was used as an index of arteriolar distensibility. The magnitude of the reflex bradycardia after a precipitous rise in BP was used to determine BRS. Power spectral analysis of heart rate variability was used to assess autonomic activity. BPs were recorded from resistance vessels in the finger using a beat-by-beat photoplethysmographic device. RPP, a noninvasive marker of myocardial oxygen consumption, was calculated. Repeated-measures analyses of variance revealed a significantly enhanced arteriolar distensibility and BRS after ERT ( P < 0.05). A trend of a lower sympathovagal balance at rest was observed after ERT; however, this trend did not reach statistical significance ( P = 0.061) compared with the other treatments. The above autonomic changes produced significantly lower systolic and diastolic BP changes and RPPs ( P < 0.05) at rest and during isometric exercise. We conclude that short-term unopposed ERT favorably enhances arteriolar distensibility, BRS, and hemodynamic parameters in postmenopausal women. These findings have clinical implications in the goals for treating cardiovascular risk factors in aging women.

Mechanoreceptors and autonomic responses to movement in humans.

Mechanoreceptor contribution to efferent autonomic outflow is incompletely understood. To determine the effects of mechanorceptor stimulation on autonomic reflexes, we compared autonomic responses in 34 subjects using a cross-over, counterbalanced design, in which hemodynamic, electromyographic, metabolic, and autonomic data were gathered during rest, passive, and active movement protocols. Because metaboreceptors and ventilatory responses influence autonomic outflow we verified and controlled for these influences during all protocols through comparisons of breath-by-breath gas exchange measurements. Verification of active and passive movements was made via electromyographic recordings of the moving legs. Spectral analysis of R-R variability was used to assess autonomic activity, and low to high frequency ratios were considered representative of sympathovagal balance. A repeated measures analysis of variance revealed significant modulating effects of mechanoreceptor stimulation on sympathovagal balance during passive movement upon efferent autonomic outflow (p<0.01) independent of central command, chemoreceptor, and metaboreceptor stimulation. Furthermore, breathing frequency and volume were identical for both movement protocols. Therefore, findings in this investigation suggest that modulating influences are being exerted by mechanoreceptor stimulation on autonomic outflow to the heart.

Präder-Willi syndrome fails to alter cardiac autonomic modulation

Twenty-six healthy subjects with a diagnosis of Präder-Willi syndrome were compared with 26 age-, gender-, and body mass index-matched controls for autonomic modulation and baroreflex sensitivity. Electrocardiograms, beat-to-beat finger blood pressures, and respiration were recorded for several minutes in the following sequence: (1) supine, (2) after transition from supine to standing, (3) sitting, (4) during a Valsalva maneuver, (5) while performing moderate exercise, and (6) during recovery from exercise while seated. All recordings were channeled and stored in a computer; analyses were carried out at a later date. Power spectral analysis (fast-Fourier transform) of heart period variability was used to assess cardiac autonomic modulation. The slope of the regression equation between heart period and blood pressure rise after the Valsalva maneuver was used as an index of baroreflex sensitivity. Analysis of variance failed to reveal significant differences in any of the autonomic and baroreflex sensitivity variables between the two groups. Because breathing patterns entrain autonomic modulation, we verified respiration and found no differences between the two groups. Therefore, findings in the current investigation indicate that cardiac autonomic modulation in patients with Präder-Willi syndrome does not differ from age-and body mass index-matched subjects.

Acetylsalicylic acid and autonomic modulation.

Loss of autonomic balance characterized by increased sympathetic activity and decreased vagal activity has been implicated as a major cardiovascular risk factor. Aspirins cardioprotective abilities involve a multitude of physiologic processes. However, the effects of aspirin on cardiac autonomic activity are unknown. In a double-blind crossover study, 22 subjects randomly received either aspirin or placebo in the amounts of 325 mg with each meal (three times per day) over a 2.5-day period. The total amount of aspirin ingested was 2,275 mg, which resulted in plasma levels of 3.3 mg/dl. At the conclusion of each treatment, subjects were evaluated for autonomic physiology activity using standard autonomic tests. Power spectral analyses of the electrocardiograms were used to delineate autonomic function. A 2×4 repeated measures analysis of variance revealed significant and favorable changes in autonomic activity after the use of aspirin. Specifically, at rest high-frequency (HF) power was significantly higher (mean, 1,090±1,463.5 msec2) compared with the placebo (mean, 692±742 msec2) (p<0.05). Low-frequency (LF) power was significantly reduced (mean, 963±745 msec2) after aspirin compared with placebo (mean, 1,100±906 msec2). After the aspirin treatment, a significantly lower LF-to-HF power ratio (mean, 1.7±2 msec2) was noted at rest when compared with the placebo (mean, 2.5±2.7 msec2) (p<0.05). Similar significant trends were seen during the sustained isometric contraction after aspirin therapy for HF power (mean 210±2.15 msec2) compared with placebo (mean, 213±184 msec2) (p<0.05). Accordingly, the LF-to-HF power ratio was lower as well when compared to placebo treatment (mean, 2.3±3.5 msec2) (mean, 5.3±8.4 msec2) (p<0.05). No differences were found in breathing rates for hemodynamic variables between any of the protocols. The significant reduction of LF-to-HF ratio, a marker of sympathovagal balance, for both protocols appeared to be largely due to a withdrawal of LF modulation and concomitant but lesser increase in HF modulation. Favorable alterations in autonomic outflow through prostaglandin inhibition may be one of the mechanisms by which low therapeutic amounts of aspirin provide prophylactic cardioprotection.

Lateral plantar nerve entrapment: Foot pain in a power lifter

Entrapment neuropathies of the lateral plantar nerve, medial plantar nerve, calcaneal nerve, or posterior tibial nerve are causes of heel and foot pain.2.3,5.9 Nerve conduction studies assist in the verification of diagnosis and the evaluation of effectiveness of treatment in those patients who present with foot pain produced by entrapment neuropathies.4.8,l1 This paper relates a case of lateral plantar nerve entrapment producing foot pain in a power lifter. The pain was relieved by the use of rigid foot orthoses. Lateral plantar