Coronary vasospasm:A narrative review

Coronary artery vasospasm(CAVS)plays an important role in acute chest pain syndrome caused by transient and partial or complete occlusion of the coronary arteries.Pathophysiology of the disease remains incompletely understood,with autonomic and endothelial dysfunction thought to play an important role.Due to the dynamic nature of the disease,its exact prevalence is not entirely clear but is found to be more prevalent in East Asian and female population.Cigarette smoking remains a prominent risk factor,although CAVS does not follow traditional coronary artery disease risk factors.Many triggers continue to be identified,with recent findings identifying chemotherapeutics,allergens,and inflammatory mediators as playing some role in the exacerbation of CAVS.Provocative testing with direct visualization is currently the gold-standard for diagnosis,but non-invasive tests,including the use of biomarkers,are being increasingly studied to aid in the diagnosis.Treatment of the CAVS is an area of active research.Apart from risk factor modification,calcium channel blockers are currently the first line treatment,with nitrates playing an important adjunct role.High-risk patients with life-threatening complications should be considered for implantable cardioverter defibrillator(ICD),although timing criteria for escalated therapy require further investigation.The role of pharmaceuticals targeting oxidative stress remains incompletely understood.

Acute right ventricular myocardial injury and sudden cardiac arrest in a patient with persistent spontaneous coronary vasospasm

Coronary vasospasm is a rare diagnosis resulting in sudden arrhythmic cardiac arrest. We report a case of a healthy,non-smoking elderly woman resuscitated from arrhythmic cardiac arrest. She had persistent spontaneous coronaxy vasospasm, leading to right ventricular myocardial injury and failure, and shock. She responded quickly to intravenous normal saline bolus infusion, but had irreversible neurological sequelae. Additionally, she had atrial fibrillation preceding ischemic ventricular fibrillation, a rare finding in coronary vasospasm-related cardiac arrest. We suggest immediate coronary angiography of patients in sudden arrhythmic cardiac arrest with acute right ventricular failure for a prompt,accurate diagnosis and appropriate management of the coronary vasospasm.

Diffuse coronary artery vasospasm in a patient with subarachnoid hemorrhage: A case report

BACKGROUND Coronary artery vasospasm(CAV)is a reversible,transient form of vasoconstriction with clinical manifestations ranging from stable angina to acute coronary syndromes(ACS).Vasospasm of epicardial coronary arteries or associated micro-vasculature can lead to total or subtotal occlusion and has been demonstrated in nearly 50%of patients undergoing angiography for suspected ACS.The mechanism for CAV has been described in literature,but in a subgroup of patients presenting with intracranial hemorrhage,it appears to be multifactorial.These patients tend to have electrocardiographic changes,elevation of cardiac biomarkers of injury and neurogenic stress cardiomyopathy.CASE SUMMARY A 44-year-old woman presented with severe headaches and tonic-clonic seizures.She was found to have diffuse subarachnoid hemorrhage(SAH)requiring ventricular drain placement,coil embolization and induced hypertension.She subsequently developed chest pain with ST elevations in anterior precordial leads,elevated cardiac enzymes and apical ballooning with left ventricular ejection fraction of 35%on transthoracic echocardiogram.Coronary angiogram revealed severe diffuse triple vessel stenoses secondary to CAV seen distally.Subsequent cardiac MRI notable for apical non-viability and scar formation.CONCLUSION This case highlights a unique etiology of acute myocardial infarction in a patient with SAH leading to ST elevations,diffuse triple vessel CAV and apical scar.

Reversible ischemia on treadmill exercise in left main coronary artery vasospasm

Coronary vasospasm of the left main coronary artery （LMCA） is a rare condition with potentially devastating consequences. We present 2 patients with LMCA vasospasm-related angina, the first being a 46-year-old woman and the second a 51-year-old woman. Both of them developed ST-segment ischemic changes on treadmill exercise tests. Coronary angiography showed spontaneous LMCA vasospasm in one patient and methylergonovine-induced LMCA vasospasm in the other patient. Follow-up treadmill exercise tests revealed no exercise-induced ischemia after calcium antagonist monotherapy. These cases demonstrate the importance of identifying LMCA vasospasm, as the treatment of choice varies in patients with angina pectoris. Reversible myocardial ischemia caused by LMCA vasospastic angina can be controlled by calcium antagonist monotherapy and detected by repeat non-invasive stress testing.

Smoking and hyperlipidemia are important risk factors for coronary artery spasm

To investigate the role of coronary artery spasm in the etiology of chest pain lacking significant coronary stenosis and to identify the clinical risk factors related to coronary artery spasm Methods Two hundred and seventy five patients with chest pain, but without significant coronary artery stenosis underwent the intracoronary acetylcholine test Coronary artery spasm was diagnosed while coronary artery stenosis increased to 90% and was accompanied by the usual chest pain with or without ischemic changes on electrocardiogram Logistic regression was employed to investigate the relationships between coronary artery spasm and sex, age, hypertension, diabetes mellitus, smoking, hyperlipidemia and results of electrocardiographic treadmill stress te st Left ventricular ejection fraction and end diastolic pressure were compared between spasm group and non-spasm group Results Coronary artery spasm was detected in 103 out of 271 patients, a rate of 38% Logistic regression analysis showed that smoking and hyperlipidemia increased the relative risk of coronary artery spasm 4 2 times and 2 3 times, respectively There was a significantly negative relationship between diabetes mellitus and coronary artery spasm Furthermore, there was no coronary artery spasm detected in left ventricular ejection fraction and end diastolic pressure Conclusions Coronary artery spasm was one of the important etiological factors for patients with chest pain but no coronary artery stenosis Smoking and hyperlipidemia were the main clinical risk factors for coronary artery spasm

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

Acute myocardial infarction after capecitabine treatment： not always vasospasm is responsible

Capecitabine is an orally available chemotherapeutic agent that is converted to 5-fluorouracil （5-FU） after absorbtion. Capecitabine and its active metabolite, 5-FU, have cardiotoxic effects with reported instances of acute coronary syndromes caused due to coronary vasospasm. However, these agents exert toxic effects on cardiovascular system and beyond vasospasm provacation. We report a 46-year-old patient diagnosed as acute inferior infarction who is treated with capecitabine for 3 months due to metastatic breast carcinoma, in whom thrombotic coronary occlusion was observed in angiography. This case demonstrates that apart from vasospasm, coronary thrombosis could be observed after capecitabine treatment, with a possible direct effect of this drug.