Neurohormonal and hemodynamic changes in severe cases of the ovarian hyperstimulation syndrome.
OBJECTIVE
To evaluate systemic hemodynamics, endogenous vasoactive neurohormonal factors (renin-angiotensin and sympathetic nervous systems, antidiuretic hormone, atrial natriuretic factor, and renal prostaglandins), and renal function in the severe ovarian hyperstimulation syndrome.


METHODS
Prospective longitudinal study.


METHODS
Assisted-reproduction unit of a tertiary care hospital in Barcelona, Spain.


METHODS
31 consecutive patients having in vitro fertilization with development of ascites because of severe ovarian hyperstimulation syndrome.


METHODS
Mean arterial pressure; cardiac output; peripheral vascular resistance; hematocrit concentration; renal function; plasma renin activity; plasma aldosterone, norepinephrine, antidiuretic hormone, and atrial natriuretic peptide determinations; and urinary excretion of prostaglandin E2 and 6-keto-prostaglandin-F1 were measured during the syndrome and 4 to 5 weeks after recovery (baseline).


RESULTS
During the syndrome, patients showed increased hematocrits (mean of the paired difference, 0.047; 95% CI, 0.029 to 0.064), decreased mean arterial pressure (-16.6 mm Hg; CI, -19.8 to -13.6), increased cardiac output (2.6 L/min; CI, 2.13 to 3.17), and reduced peripheral vascular resistance (-709 dyne/s.cm-5;CI, -792 to -627). This was accompanied by marked increases of plasma renin (14.4 ng/L.s; CI, 9.87 to 18.90), norepinephrine (1.857 nmol/L; CI, 0.533 to 3.161), antidiuretic hormone (3.3 pg/mL; CI, 1.89 to 4.71), and atrial natriuretic peptide levels (9.7 fmol/mL; CI, 6.1 to 13.2). Hemoconcentration developed in 16 patients (mean of the paired difference in hematocrit concentration, 0.082; CI, 0.063 to 0.101) but not in 15 others (0.009; CI, 0.003 to 0.021). Both groups showed similar values for arterial pressure, cardiac output, and peripheral vascular resistance, but patients with hemoconcentration had higher (P < 0.05) levels of renin (mean, 20.97 ng/L.s[CI, 13.3 to 28.63] compared with 7.83 ng/L.s[CI, 4.08 to 11.58]), norepinephrine (3.907 nmol/L [CI, 3.057 to 4.757] compared with 2.417 [CI, 2.035 to 2.799]), and antidiuretic hormone (6.0 pg/mL [CI, 4.1 to 7.9] compared with 2.4 [CI, 1.7 to 3.03]).


CONCLUSIONS
In addition to increased capillary permeability, severe ovarian hyperstimulation syndrome is consistently associated with arteriolar vasodilation. The simultaneous occurrence of these disorders leads to hyperdynamic circulatory dysfunction with marked stimulation of the sympathetic nervous system, renin-angiotensin system, and antidiuretic hormone.
Balasch
J
J
Department of Obstetrics and Gynecology, Hospital Clínic i Provincial, Barcelona, Spain.
Arroyo
V
V
Fábregues
F
F
Saló
J
J
Jiménez
W
W
Paré
J C
JC
Vanrell
J A
JA
D000328:Adult; D009320:Atrial Natriuretic Factor / Q000097:blood; D005260:Female; D006439:Hemodynamics / Q000502:physiology*; D006728:Hormones / Q000378:metabolism*; D006801:Humans; D007668:Kidney / Q000378:metabolism / Q000503:physiopathology; D008137:Longitudinal Studies; D009638:Norepinephrine / Q000097:blood; D016471:Ovarian Hyperstimulation Syndrome / Q000378:metabolism / Q000503:physiopathology*; D011446:Prospective Studies; D011453:Prostaglandins / Q000652:urine; D012084:Renin-Angiotensin System / Q000502:physiology; D014667:Vasopressins / Q000097:blood
D006728:Hormones; D011453:Prostaglandins; D014667:Vasopressins; D009320:Atrial Natriuretic Factor; D009638:Norepinephrine