A 56 year-old male without known cardiac risk factors presented to the emergency room complaining of retrosternal chest pain radiating to his back with excessive sweating, vertigo and mild dyspnea for about 30 minutes. Physical examination revealed scattered wheezing and a little shortness of breath. The first electrocardiogram (ECG) (18:18) demonstrated ST segment elevation of 2 mm in leads I, aVL, and ST depression in leads II, III and aVF (Fig. 1). The second ECG at 18:32 indicated that all ST segments recovered to baseline. 2 hours later, the chest pain relapsed, ECG showed ST segment elevation of 3-4mm in leads II, III, aVF, V3R~V5R (Fig. 2). Emergency coronary angiography revealed 50% stenosis in the middle segment of left anterior descending(LAD), 50% stenosis in the proximal segment of LCX, 90% stenosis in the middle and subocclusion in the distal segment of right coronary artery (RCA) all the stenosis disappeared after 200μg intracoronary nitroglycerin (Fig. 3). He was diagnosed as coronary vasospasm and given oral isosorbidemononitrate and diltiazem as well as atrovastatin and double anti-platelet therapy (DAPT), chest pain seemed to be controlled. 11 days later, severe substernal chest pain attacked again at 2:40 during sleep, ECG showed ST segment elevation of 4mm in leads V1~V4 and ST depression of 3mm in leads V5 and V6 (Fig. 4). The frequent onset of chest pain was not controlled by doubled anti-vasospasm drugs during hospitalization.

The frequent onset of ischemic chest pain pushed us to probe into the inducer of coronary vasospasm, and detailed medical history enquiry provided new information pointing to anaphylaxis: the patient had experienced bronchial asthma for 6 months. Seven days before the first attack of cardiac event, he was given Chinese traditional decoction called “Ma-Xing shi gan tang”, which was boiled with Ephedra (Ma-Huang), earthworm (Di-Long) and other herbs. He suffered skin allergy with flushing, itching, erythematous rashes and urticaria on the exact day taking the decoction and experienced several episodes of mild chest pain. Therefore, discontinuation of the traditional herbs therapy (which was the suspicious sensitizer of coronary vasospasm) accompanied by oral loratadine were performed to cure anaphylaxis, this treatment strategy seemed to be effective because the onset of chest pain turned rare and mild in the following 1 month, and the patient kept symptomless for the next 2 months. However, he then attempted to resume the herbs and suffered the 3^rd cardiac event, presenting extremely strong chest pain, tall and peaked T waves in leads V3~V6 in ECG (Fig. 5) and obvious elevation of blood eosinophil of 23.4%. This time he completely discarded the herbs and complied to anti-vasospasm therapy for 6 months, he felt no more attacks and discontinued the anti-vasospasm drugs. During the 3 years’ follow-up, he kept free of ischemic chest pain without any anti-vasospasm drugs, although wheezing still relapsed intermittently.

A 57 year-old male suffered anaphylactic shock and loss of consciousness when Given Intravenous administration of cervus and cucumis polypeptide for treatment of low back pain in a local hospital. His vital signs recovered in 30 minutes after successful salvage, but then he developed tightening central chest pain and dyspnea, the ECG showed ST segment elevation of 0.5 mm in leads II, III and avF (Fig. 6). He was suspected acute myocardial infarction and sent to our hospital. He had no cardiac risk factors and history of cardiovascular disease (CVD). On admission, his symptom had partly relieved, ECG showed ST segment recovered and Q wave in leads III (Fig. 7). Emergency coronary angiography (5 hours after the event) showed 50% stenosis in the proximal and middle segments of LAD, 25–50% stenosis in the middle segment of LCX and 25–50% stenosis in the middle segment of Without evidence of thrombosis or trace of dissolved thrombosis in the coronary arteries. Chest pain did not relapse during hospitalization, T waves inversion persisted in leads II, III and Q wave in leads III in subsequent ECGs (Fig. 8). His troponin I was 2.27ng/mL on the 5^th hour of onset and reached to the peak of 3.0 ng/mL on the 18th hour, and blood eosinophil was 15.5% on arrival. Echocardiography showed regional wall motion abnormality in the inferior left ventricular wall. The patient was diagnosed as acute ST-segment elevation myocardial infarction due to allergic coronary vasospasm, the allergen was recognized as injection cervus and cucumis polypeptide. He had neither injected cervus and cucumis polypeptide nor suffer any attack of chest pain during the 1-year follow-up.

A 68 year-old male without known cardiac risk factors had suffered bronchial asthma for 2 years, aggregating for 3 months with the suspected allergen of detergent and pesticide sprays since he moved from south China to Beijing, accompanied by recurrent precordial squeezing pain, dyspnea and excessive sweating several hours after the episodes of wheezing and spontaneously resolved in 10~15 minutes. After admitted to the cardiology unit, he complained allergy to the smell of pesticide sprays and suffered chest pain for several times at 1:00~3:00 in the morning which was relieved by intravenous administration of nitroglycerin. ECG showed ST segments depression of 0.2-0.3 mv in leads V1-V6 on attack and resolution of ST segments when symptom was resolved, Holter showed non-sustained ventricular tachycardia at the time he felt dyspnea, while repeated tests of troponin I were negative. Coronary angiography was performed on the third day after admission, revealing a 90% stenosis in the proximal segment of LAD, a 75% stenosis in the middle segment of LAD and a 50% stenosis in the proximal segment of LCX respectively, and all stenosis disappeared after 200ug intracoronary administration of nitroglycerin. The patient was diagnosed as coronary vasospasm and was given oral isosorbidemononitrate and diltiazem for long-term therapy. The attacks of chest pain developed less frequently but still relapsed after wheezing, he could predict the mid-night chest pain by the preceding contact of allergen and wheezing, and experimentally taking loratadine (which is a non-sedating anti-histamine drug that inhibit the release of histamine from mast cells) could effectively prevent or alleviate the episodes of chest pain.

A 42 year-old female without history of atopy and cardiovascular risks received surgical abortion under intravenous anesthesia of Propofol in February, 2013. At 7:00 on the 7^th morning of the surgery, she suffered a sudden severe pressure-like pain of 10 minutes in the left subclavian and retrosternal area when she was lying in bed. After that, such pain recurrently occurred in the midnight and early morning. She was diagnosed as angina pectoris in the local hospital and given aspirin, clopidogrel, atorvastatin and nitrates, but chest pain still relapsed. After a serious attack of 15 minutes with heavy sweating at 2:00, she was sent to our hospital. On admission, her blood pressure was 150/100 mmHg, heart rate was 76 beat per minute, physical examination revealed no abnormalities. ECG on admission was normal (Fig. 9), troponin I was negative and the rate of eosinophil was 2.5%, coronary angiography revealed a plaque in the proximal segment of LAD without stenosis and other coronary arteries were normal. She was suspected as coronary vasospasm and was given mononitrate, nifedipine, aspirin, clopidogrel and atrovastatin. However, ischemic chest pain continued attacking in the morning during hospitalization. On the 3^rd morning after angiography, she suffer a 5-minute episode, ECG showed downsloping ST segments depression of 1~3mm in leads I, aVL, II, III, aVF and V2-V6 (Fig. 10), the symptom was relieved by one dose (0.5 mg) of sublingual nitroglycerin and ST segments recovered, whereas another two attacks occurred 2 hours and 4 hours later, respectively, with the same ECG presentation. After continuous 48-hour intravenous administration of nitroglycerin, as well as added dose of mononitrate and nifedipine before night sleep, chest pain seemed to calm down, she kept symptomless for 5 days and discharged. She occasionally suffered early morning chest pain for 5-10 minutes in the first 4 months though adhering to drugs. Interestingly, the episodes suddenly stopped when her menopause recovered in August, 2013, and her chest pain never relapsed during the 4 years follow-up.

A 45 year-old male developed flushing and urticaria 15 minutes after eating pineapple, then he felt precordial squeezing pain radiating to the left shoulder, lasting for several minutes, accompanied by palpitation and excessive sweating. He is a smoker with no other cardiac risk factors and no history of CVD, he was allergic to pineapple before but only manifested as slight itching and skin rashes which spontaneously disappeared in hours. Before this onset, he had been working day and night for 1 month with doubled tabacco smoking, though he did not smoke after eating pineapple. The patient was sent to the emergency room, on arriving, his symptoms had been relieved by sublingual nitroglycerin, his blood pressure was 120/70mmHg, pulse rate was 80 beat per minute, and ECG revealed no abnormalities while the symptom had relieved. 24h Holter (Figs. 11, 12 and 13) revealed ST segment elevation for 2~3 mm in leads II, III, aVF, V5, V6 at 13:40-13:42 (when he felt malaise, chest pain and palpitation at rest) and 20:20-20:22 (when he was driving, he felt chest pain and left arm numb), as well as ventricular bigeminy and nonsustained ventricular tachycardia at 13:20 and 13:42. He was admitted to cardiology department, blood test showed normal troponin I level and elevated eosinophil of 7.6% on the first day of admission. Coronary angiography showed subocclusion in the proximal segment of LCX with TIMI grade 3 flow, which was relieved by 3 times of 200μg intracoronary nitroglycerin. He was diagnosed as coronary vasospasm on the basis of anaphylaxis to pineapple, and received anti-vasospasm therapy of mononitrate and nifedipine as well as antiallergic agent, the eosinophil rate declined to 6.1% on the 7^thday, chest pain didn’t relapse during hospitalization. After 12 months of mononitrate and nifedipine medication, anti-vasospasm therapy was discontinued. During 3 years follow-up, he kept free of cardiac events.