Discussion
Coronary spasm is defined as a transient abnormal contraction of the
coronary arteries. Factors known to contribute to the onset of the
disease include smoking, alcohol consumption, abnormal lipid and sugar
metabolism, stress and hyperventilation, genetic factors, and female
hormone deficiency1). The female hormone estrogen is
known to have cardioprotective effects2). The
mechanism is thought to be vasodilation via estrogen receptors in
vascular endothelial cells, vascular smooth muscle cells, and the heart,
suppression of neointimal proliferation, and suppression of angiotensin
1 receptor expression, which has a myocardial hypertrophic
effect3-5). Premenopausal women have a late luteal to
menstrual phase when blood estrogen levels are low, and a follicular and
ovulatory phase, and early luteal phase when estrogen levels are high.
For this reason, it has been noted that coronary spasms and acute
coronary syndromes are more common during the late luteal phase and
menstrual phase, when estrogen levels are low6). In
the present patient, life-threatening arrhythmias due to coronary spasm
occurred during the luteal phase to the menstrual phase.
The frequency of coronary spasm attacks and anginal symptoms improved
after treatment with estrogen (Duphaston®) and progesterone (Premarin®)
was started. Sugiura et al. reported that oral contraceptives and
low-dose estrogen/progesterone products, regardless of their type, are
associated with a significant increase in deep vein
thrombosis7). In the perioperative period, it is
recommended that medication be withdrawn 4 weeks prior to surgery for
surgeries lasting longer than 45 minutes, and postoperatively until
immobility is resolved8). In the present case, both
drugs were withdrawn 30 days prior to surgery. Considering that the
scheduled surgery time for this case was 30 minutes, and the patient was
scheduled to be discharged the day after surgery, there may have been no
need for drug withdrawal. The timing of the surgery was appropriate
because it was scheduled around the time of ovulation, 2 weeks after the
last menstrual period. Problems with estrogen/progesterone therapy
include an increased risk of breast cancer owing to high progesterone
levels9), increased incidence of coronary vascular
disease, and abnormal vaginal bleeding. However, it has been pointed out
that estrogen monotherapy increases the risk of developing endometrial
hyperplasia and endometrial cancer. The frequency of endometrial
hyperplasia coexisting with or progressing to cancer is reported to be
about 1% to 30%10), and if the patient is required
to take oral contraceptive pills from a young age, as in this patient,
the risk of developing cancer in the future may be high. In the present
patient, intravenous diltiazem hydrochloride and nicorandil were started
at the time of induction of anesthesia for the prevention of coronary
spasms, and was continued during and after surgery, until just before
discharge. According to the Guidelines for the Diagnosis and Treatment
of Coronary Angina Pectoris, the Ca2+ antagonist
diltiazem hydrochloride is extremely effective in preventing coronary
spasms, and is recommended as class I drug. Nicorandil has selective
coronary vasodilation and anticoronary spasm effects, and is classified
as a class II drug that is recommended with a high likelihood of
efficacy when used in combination with a Ca2+antagonist for seizures that are difficult to control with the
antagonist alone.11)
There have been no reports on the anesthesia of patients with
menstrual-associated coronary angina pectoris. The present patient
required an endometrial ablation, and the attending physician,
cardiologist, and anesthesiologist discussed whether the procedure
should be performed under general anesthesia or spinal anesthesia.
Anesthesia management with spinal anesthesia was initially considered,
but there were concerns regarding side effects from the use of various
drugs, and the risk of suppression of cardiac function. However, there
have been many previous reports of coronary spasms induced by relative
parasympathetic dominance due to sympathetic blockade by epidural or
spinal anesthesia12)13).Therefore, in this case, the
patient was managed under general anesthesia, considering the
possibility that coronary spasms might occur due to sympathetic blockade
by spinal anesthesia.