Does a Negative Ergonovine Provocation Test Truly Predict Freedom from Variant Angina?
A 49-year-old-man visited our outpatient clinic on October 1, 2007 with atypical chest pain that had started 2 months before. He complained of crushing chest pain that lasted for 5 to 10 seconds. The pain usually occurred early in the morning and was not related to exercise. The pain would disappear without any specific treatment. ECG showed no definite ST-segment changes. Echocardiography also showed normal left ventricular systolic function and there were no regional wall motion abnormalities. He was not taking any medication except for a budesonide inhaler and mometasone (topical corticosteroid) for treatment of asthma.\nThe patient underwent coronary angiography and ergonovine provocation test. Ergonovine 0.2 mg was injected twice intravenously at a 5-minute interval. We achieved cineangiogram at 90 seconds after each ergonovine injection. Coronary angiography showed no significant lesions in the coronary arteries and the intravenous ergonovine provocation test was negative (). There was no chest pain, ST-segment changes, or coronary artery vasospasm noted during the ergonovine provocation test. We did not prescribe any antianginal medication such as nitroglycerine before the ergonovine provocation test, which would have affected the results of the test. Esophagogastroduodenoscopy showed hemorrhagic gastritis and erosive duodenitis. The gastrointestinal tract was thought to be the source of the pain and he was prescribed a proton pump inhibitor and prokinetics for pain relief.\nAfter 5 years, on January 15, 2012, he visited the ER with sudden onset of chest pain while sleeping. The characteristics of the chest pain were very similar to the pain that occurred in 2007. In the ER, the chest pain was relieved by sublingual nitroglycerin and he was admitted to the coronary care unit. After several hours, the chest pain recurred and the patient complained of dizziness, nausea, and vomiting. His blood pressure dropped to 76/41 mm Hg, and he had symptomatic sinus bradycardia. ECG showed no definite ST-segment changes (), but troponin I was elevated to 90.3 ng/mL. Suspicious of non ST-segment elevation myocardial infarction combined with cardiogenic shock, we performed coronary angiography. Coronary angiography showed no significant stenosis of the left main, left anterior descending, or left circumflex coronary arteries (), but total occlusion with distal Thrombolysis in Myocardial Infarction flow grade 2 in the distal right coronary artery, posterior descending artery, and posterolateral branch bifurcation segment was observed (). After intra-coronary nitroglycerin injection, the occluded segment was dilated () and chest pain was slowly relieved. Blood pressure and heart rate were also stabilized. Echocardiography showed akinesia of the apical anterior, septal, and inferior walls. Chest pain did not recur after taking diltiazem and nicorandil. The patient is now under outpatient clinic follow up without any further event.