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 In the perioperative period, it is recommended that medication be withdrawn 4 weeks prior to surgery for surgeries lasting longer than 45 minutes, and postoperatively until immobility is resolved8). In the present case, both drugs were withdrawn 30 days prior to surgery.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.