Kounis syndrome:a clinical entity penetrating from pediatrics to geriatrics

1 Introduction Kounis syndrome constitutes a coronary hypersensitivity disorder defined by the association of an anaphylactoid,anaphylactic,allergic or hypersensitivity reaction with an acute coronary syndrome,in a physiopathological context involving various interrelated and interacting inflammatory cells,such as mast-cells,eosinophils and platelets.[1,2]Similar entities to Kounis syndrome might involve cerebral and mesenteric arteries.

Acute myocardial infarction due to Kounis syndrome:A case report

BACKGROUND Acute myocardial infarction(AMI)can be induced by several factors.However,AMI induced by Kounis syndrome(an allergic reaction)is extremely rare and is highly susceptible to misdiagnosis.CASE SUMMARY A 70-year-old man presented after suffering an allergic reaction that caused chest pain triggered upon eating ice cream.Troponin I was found to be elevated,and an electrocardiogram showed ST-segment elevation.The diagnosis was AMI.He underwent two coronary angiographies,with one intravascular ultrasound during hospitalization showing no evidence of atherosclerotic coronary artery disease.The final diagnosis was vasospastic myocardial infarction due to Kounis syndrome.The patient was then treated with hydrocortisone and intravenous antihistamines,and his chest pain symptoms resolved.CONCLUSION Allergic reactions(such as Kounis syndrome)can cause serious damage to the heart.Physicians should be alert to the consequences and avoid misdiagnosis.

Kounis syndrome： allergic acute coronary syndrome

Kounis syndrome is defined as a group of acute coronary syndromes that manifests as unstable vasospasticor nonvasospastc angina, and even as acute myocarda! infarction triggered by the release of inflammatory mediators following an allergic insult.1 Kounis syndrome is a rare and complex syndrome. Instant treatment decisions need to be made once it happens. Here, we defined a case of severe Kounis syndrome, culminating in acute coronary syndrome, as a result of an acute allergic reaction, which was likely related to iodinated contrast media or dextran-40 use. A 71-year-old male patient, with a history of hypertension, no history of coronary heart disease and diabetes, was admitted to our hospital because of intermittent claudication for one year. On admission, his temperature was 36.4℃, pulse was 80 beats/min, respiratory rate was 18 beats/rain and blood pressure was 105/80 mmHg （1 mmHg=0.133 kPa）. Physical examination did not show any sign of heart disease, but the lower extremity arterial pulsation was weak. His artery angiography of abdominal aorta and lower limbs showed that the left iliac artery was completely obstructed. A total of 400 U iodinated contrast media was used during the operation. The patient was back to ward safely. Ten minutes after taking the dextran-40 as a postoperative treatment, he began to present sudden hyperspasmia, transient unconsciousness, skin flushes, excessive sweating and sinus tachycardia （approximately 140 beats/min）. At the same time, his skin temperature decreased and his blood pressure collapsed quickly. He accepted oxygen therapy, fluid replacement, dexamethasone and dopamine immediately. After that the ECG revealed ST elevation of 0.3-0.7 mV in leads II, III, avF, V3.6, and frequent premature ventricular （Figure 1A）. Following the therapy of promethazine, glycerin trinitrate and lidocaine, the shock symptoms was gradually relieved： consciousness was recovered, ST segment gradually went back to normal in half an hour （Figure 1 B） and blood pressure increased to 50/40 mmHg. However, the skin appeared in pattern and urticaria. The patient was transferred to CCU ward for observation, with dopamine used constantly for a few hours. The patient＇s general state was stable after a few hours. His skin rash vanished gradually and his blood pressure was back to 90/60 mmHg. The ECG had no specific changes in the next day. The infarction graphics had only a one- time change, so we did not take further examinations forcardiac markers because it disappeared quickly. The patient accepted a short-term anti-platelet aggregation therapy after he was stable. He was discharged from the hospital after he successfully accepted femoral artery endarterectomy in half month. The discharge diagnosis was left lower extremity arteriosclerosis obliterans. The patient was followed up for several years after discharge. He did not complain any symptoms of angina pectoris or heart failure. The most common symptoms of Kounis syndrome, include fainting, dyspnea, palpitation, serious weakness, nausea, vomiting, urticaria, itching, profuse sweating, paleness, hypotonia and sometimes arrhythmia. The patient described here developed signs of anaphylaxis in an hour after using iodinated contrast media and dextran-40. The diagnosis of this case mainly relies on the patient＇s typical symptoms and ECG （ischemic ST-T changes）. The symptoms of hypotension caused by the release of vascular active substances expand capillaries widely in allergic reactions. During the reaction, peripheral resistance decreases as vascular permeability and capillary capacity increase, so blood pressure dropped rapidly. Furthermore, hypotension can aggravate the myocardial hypoperfusion. After taking the H1 blocker, corticosteroids, rehydration, and so on, the

Hypersensitivity to drug-eluting stent and stent thrombosis- Kounis or not Kounis syndrome？

With the utilization of coronary-stents, coronary remodeling and restenosis were reduced compared with balloon angioplasty alone,t However, the risk of restenosis is still in the range of 15% to 20%. Drug-eluting stents （DES）, which could release antiproliferative pharmacological agents after deployment, were designed to inhibit the response to injury reaction after hare-metal stent （BMS） implantation.

Acute coronary artery stent thrombosis caused by a spasm:A case report

BACKGROUND Acute stent thrombosis(AST)is a serious complication of percutaneous coronary intervention(PCI).The causes of AST include the use of stents of inappropriate diameters,multiple overlapping stents,or excessively long stents;incomplete stent expansion;poor stent adhesion;incomplete coverage of dissection;formation of thrombosis or intramural hematomas;vascular injury secondary to intraoperative mechanical manipulation;insufficient dose administration of postoperative antiplatelet medications;and resistance to antiplatelet drugs.Cases of AST secondary to coronary artery spasms are rare,with only a few reports in the literature.CASE SUMMARY A 55-year-old man was admitted to the hospital with a chief complaint of back pain for 2 d.He was diagnosed with coronary heart disease and acute myocardial infarction(AMI)based on electrocardiography results and creatinine kinase myocardial band,troponin I,and troponin T levels.A 2.5 mm×33.0 mm drugeluting stent was inserted into the occluded portion of the right coronary artery.Aspirin,clopidogrel,and atorvastatin were started.Six days later,the patient developed AST after taking a bath in the morning.Repeat coronary angiography showed occlusion of the proximal stent,and intravascular ultrasound showed severe coronary artery spasms.The patient’s AST was thought to be caused by coronary artery spasms and treated with percutaneous transluminal coronary angioplasty.Postoperatively,he was administered diltiazem to inhibit coronary artery spasms and prevent future episodes of AST.He survived and reported no discomfort at the 2-mo follow-up after the operation and initiation of drug treatment.CONCLUSION Coronary spasms can cause both AMI and AST.For patients who exhibit coronary spasms during PCI,diltiazem administration could reduce spasms and prevent future AST.