CORONARY artery spasm (CAS) can induce angina in patients with or without a history of coronary artery disease. CAS is presumably the underlying cause of unstable or Prinzmetal angina, which if left untreated, can result in myocardial infarction and death. 1Perioperative CAS with characteristic changes on electrocardiogram has been reported in patients with 1–7or without 8,9a history of coronary artery disease undergoing general or regional anesthesia. We describe a patient who experienced angina and electrocardiographic changes during initiation of epidural anesthesia. This case is unique in that the events occurred before surgical stimulation in a patient without coronary artery disease. These findings strongly support the idea that epidural anesthesia can contribute to CAS in the absence of preexisting coronary artery disease.
A 60-yr-old, 72-kg, 132-cm woman was scheduled for an exploratory laparotomy and total abdominal hysterectomy secondary to a cystic adnexal mass. Her medical history was significant for remote tobacco use (35 yr previously), childbirth, Crohn disease, and a recent diagnosis of borderline hypertension. Her surgical history was significant for proctectomy, colectomy, ileostomy, and caesarian section. She had no history of allergies or cardiovascular symptoms. Physical examination and laboratory data were unremarkable. Chest radiography and electrocardiography were unremarkable.
On the day of surgery, her vital signs were as follows: heart rate of 66 beats/min, respiratory rate of 16 breaths/min, temperature of 36.7°C, and 100% oxygen saturation measured by pulse oximetry on room air. A blood pressure measurement of 184/95 mmHg was obtained, with a repeat reading of 127/65 mmHg. Preoperative fasting status was verified, and consent was obtained for placement of an epidural catheter. The epidural catheter was placed in the holding area per institutional routine. The patient was sitting with pulse oximetry, five-lead electrocardiography, and blood pressure monitoring. Her back was prepared with iodine, and her skin was anesthetized with 3 ml 1% lidocaine; a 17-gauge Tuohy needle was inserted by the loss of resistance technique at the T11–T12 interspace. A 20-gauge single orifice catheter was threaded 5 cm into the epidural space. After a negative aspiration test, 3 ml 2% lidocaine with 1:200,000 epinephrine was injected with no changes in heart rate or sensory block.
In the operating room, she was transferred to the operating table, placed on monitors, provided oxygen by facemask (8 l/min), and administered 1 mg midazolam intravenously for sedation. Initial vital signs were heart rate of 82 beats/min and blood pressure of 135/79 mmHg. Once the patient was supine, 5 ml 0.75% bupivacaine with 1:200,000 epinephrine was administered incrementally through the epidural catheter. Fifteen minutes after completion of dosing (total of 18 ml), the patient began complaining of left-sided jaw pain and a 2.7-mm ST segment depression was noted in leads II and V5 (fig. 1). The sensory block was T6. Blood pressure (120/60 mmHg) and heart rate (80 beats/min) were stable during this time. The surgeon was notified and the procedure cancelled. Pain subsided with administration of intravenous morphine (1 mg). A 12-lead electrocardiogram, obtained in the postanesthesia care unit, showed sinus rhythm and ST segment depression in leads II, III, AVF, and V5. Sensory level peaked by pinprick at T2. The patient chewed a 325-mg aspirin tablet, and nitroglycerin was infused intravenously at 0.25 μg−1· kg−1· min−1. After 15 min, blood pressure was 95/50 mmHg and phenylephrine was started intravenously at 0.5 μg−1· kg−1· min−1. The blood pressure returned to the baseline value (122/55 mmHg). ST segment changes resolved with the aforementioned therapy after 30 min (fig. 1). Sensory block regressed over 2 h, and the catheter was removed.
The patient was transferred to the cardiac care unit. Laboratory data after the event were as follows: troponin I, 10.48 ng/ml (reference range, 0.03–0.15 ng/ml); MB (isoenzyme of creatine kinase [CK] containing M and B subunits) fraction 33 μg/l (reference range, 0–7 μg/l); and CK-MB/total CK index, 11% (reference range, 0–3%). After 8 h, enzyme levels were obtained: troponin I, 0.24 ng/ml; MB fraction, 19 μg/l; and CK-MB/total CK index, 7%. Based on electrocardiographic changes, troponin levels, and CK-MB fractions, the patient was diagnosed with a non–Q-wave myocardial infarction. Coronary angiography on the following day was unremarkable, and a presumptive diagnosis of CAS was made. The ECG tracing normalized, except for inverted T waves in the lateral leads, and the patient was discharged from the hospital with a prescription for 30 mg oral nifedipine per day. One week later, the patient underwent surgery under general anesthesia without problems. The patient was monitored in the intensive care unit for 24 h. Her hospital course to time of discharge was uneventful.
Coronary artery spasm can cause angina and myocardial ischemia in the absence or presence of fixed coronary artery disease, and it is a rare complication of general and regional anesthesia. The first reports in the anesthesia literature concerning unstable angina involved patients with coronary artery disease emerging from general anesthesia. 6,10Additional reports 1,2,4,5,7–9followed in patients with coronary artery disease undergoing cardiac or noncardiac procedures. Krantz et al. 9first reported CAS in the setting of regional anesthesia. However, the contribution of the epidural anesthetic to the onset of CAS was difficult to interpret because of ongoing surgical stimulation and fixed coronary stenosis. Thus, it is possible that regional anesthesia played a limited role in early reports and that catecholamine surges during or after surgery may have produced myocardial ischemia by vasoconstricting areas around a preexisting stenosis.
Other reports of CAS during regional anesthesia have suggested that sympathetic nerve blockade and parasympathetic dominance may be one mechanism for myocardial ischemia. A case report similar to ours described CAS at the initiation of regional anesthesia. Hako et al. 11described a patient with a history of unstable angina and multiple risk factors for coronary artery endothelial dysfunction, who experienced chest pain and electrocardiographic changes with initiation of lumbar epidural anesthesia. Symptoms began when the anesthetic level reached T4 and the patient experienced a decrease in systolic blood pressure from 110 to 86 mmHg. Therapy with nitroglycerin infusion and diltiazem was initiated 20 min after the onset of symptoms. The chest discomfort resolved. The authors postulated that the sympathetic blockade in an already susceptible patient permitted parasympathetic hyperactivity, CAS, and myocardial ischemia. Their hypothesis was supported by Yasue et al. , 12who studied parasympathetic activity as a trigger for CAS in patients diagnosed with unstable angina. They induced CAS by intracoronary injection of acetylcholine, the neurotransmitter of the parasympathetic system. In contrast to the report by Hako et al. , the contribution of epidural anesthesia to the initiation of CAS is more evident in our patient, because no hemodynamic changes preceded the jaw pain or electrocardiographic changes. In addition, our patient had no history of angina, and subsequent coronary angiography showed healthy coronary arteries and normal myocardial perfusion.
An alternate mechanism of epidural anesthesia-associated CAS may be compensatory sympathetic excitation above the level of partial or complete sympathetic blockade. Baron et al. 13evaluated forearm vascular tone and reactivity in patients during lumbar epidural anesthesia. They found increased reactivity and vasoconstriction in sympathetically intact areas. During lumbar epidural anesthesia, increased sympathetic activity above the level of sympathetic block would include the cardiac sympathetic nerves. This increase in sympathetically mediated norepinephrine may be sufficient to stimulate CAS. 14In contrast, a total sympathectomy, including cardiac sympathetic blockade, should limit the likelihood of CAS. However, other authors have suggested that susceptible patients with higher resting coronary tone in this setting may have an exaggerated response to a vasoconstricting stimuli (i.e. , hypotension), resulting in CAS. 15,16
Outside the perioperative period, many physicians prefer to treat unstable angina with calcium channel blockers. Nifedipine is often chosen, but nicardipine, diltiazem, and verapamil may also be effective. 2,12Calcium antagonists prevent calcium flux, thereby relaxing the coronary vessels and preventing a response to vasoconstrictive stimuli. 4In our case, the use of calcium channel blockers in the setting of acute myocardial infarction is controversial. Although CAS was considered, we opted for conventional treatment of the symptoms with rate control, aspirin, and nitroglycerin. Once stable, the cardiologist and anesthesiologist agreed that initiating and maintaining nifedipine therapy through the perioperative period would be prudent, with subsequent weaning of the calcium channel blocker over 1 or 2 weeks. The period of delay for subsequent surgery is unknown.
In summary, we present a case of variant angina at the initiation of epidural anesthesia. Our patient developed transient jaw pain, ST segment increase, increased cardiac enzymes, and non–Q-wave myocardial infarction. She did not experience chest pain, perhaps because the sensory block was effective. She subsequently was treated with nifedipine and underwent a successful operation under general anesthesia with no further episodes of CAS. This case reinforces the need for close monitoring during the initiation and regression of regional anesthesia for signs and symptoms of sensory and neurologic changes, rhythm disturbances, and myocardial ischemia, even in patients without fixed coronary artery disease.