Cardio Case Challenge: Syncope in a 53-Year-Old Woman With Dyspnea and Morning Chest Pain

Maria Cristina Bravi, MD, PhD


April 18, 2022

Intravenous or sublingual nitrate therapy is the initial medical treatment, whereas long-acting nitrates and calcium channel blockers are used to reduce the frequency of recurrent episodes of chest pain.[10] The amino acid L-arginine, which is converted by the body into the vasodilator nitric oxide, may also be prescribed for chest pain. Magnesium deficiency may contribute to CAS; therefore, oral supplementation of magnesium should be considered.[11] Statins in combination with calcium channel antagonists have beneficial effects on endothelial function. Yasue and colleagues demonstrated that the addition of a statin (fluvastatin) to conventional calcium channel blocker therapy is able to suppress acetylcholine-induced CAS.[12]

Beta-blockers can be beneficial in patients with atherosclerotic coronary lesions, and when used in conjunction with calcium channel blockers and nitrates, they can aid in symptom control in Prinzmetal angina. Nevertheless, because of their effect on beta-2 receptors, which physiologically mediate vasodilatation, nonselective beta-blockers may induce coronary spasm, worsening vasospastic angina. Beta blockade may also place the patient at risk for unopposed alpha activity in the setting of cocaine-induced vasospasm.[10] Cardioselective beta blockers have a stronger affinity for beta-1 than for beta-2 receptors, but at higher dosages they lose their selectivity and so can also induce CAS. Therefore, many clinicians avoid using even cardioselective beta-blockers in patients with Prinzmetal angina.

Very high dosages of aspirin (325 mg tablets taken 4-8 times daily) should also be avoided in Prinzmetal angina, since, by inhibiting the function of cyclo-oxygenase (COX), they suppress prostaglandin synthesis, aggravating CAS.[13]

Myocardial infarction is a potential complication of CAS, and its incidence and prognosis depend on the extent and severity of underlying atherosclerotic coronary stenosis. Even if patients with CAS are considered to be "at high cardiovascular risk," overall mortality is low.

A poorer prognosis is related to intolerance of calcium channel antagonists, concurrent coronary atherosclerosis, and smoking. The risk for sudden death is about 2%. If life-threatening arrhythmias are documented, defibrillator implantation may be considered.[14] Patients with CAS should receive appropriate medical and lifestyle interventions to prevent atherosclerotic lesions, as atherosclerosis is common in patients with vasospastic angina.

The patient in this case was discharged from the hospital several days after her angiography with recommendations to quit smoking, pursue a moderate daily exercise program, and follow a low-calorie and low-fat diet. She was discharged with prescriptions for a calcium channel blocker and long-acting nitrate therapy in addition to her home ACE inhibitor and statin regimen. The patient was offered an implantable cardioverter-defibrillator (ICD) for secondary prevention of sudden cardiac death, but she refused. For the first month after discharge, the patient was monitored by outpatient telemetry for rhythm disturbances and episodes of myocardial ischemia. She remained symptom-free without recurrence of dysrhythmia or cardiac syncope during the first year of monitoring following her cardiac arrest. At the time of this report, the patient is in good health and is followed regularly by her cardiologist.


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