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Vasospastic angina is extremely uncommon for adolescents to experience chest discomfort, which is defined by transitory ST segment elevation or depression and angina symptoms that occur while at rest. It may result in potentially fatal conditions like myocardial infarction, ventricular fibrillation, or even sudden cardiac arrest. To aim of this article is to report a very rare case of a 17-year-old male Afghan refugee who was diagnosed with vasospastic angina after presenting with chest pain, and after receiving calcium channel blocker and nitrates for medical therapy, there were no angina attacks. Our case underlines the value of a thorough evaluation of adolescent's chest pain, the need to diagnose based on the symptoms, and the necessity of performing coronary angiography to rule out coronary causes when there is a high suspicion to a cardiac cause.

Acute vasospastic angina, formerly known as Prinzmetal angina, is characterized by transient electrocardiographic changes that are not related to exertion. Its atypical presentation makes it difficult to establish the diagnosis, so it is probably underrecognized and therefore mismanaged. We treated a 49-year-old woman who presented with a 2-day history of chest pain associated with palpitations. Abnormal radionuclide stress test results prompted diagnostic coronary angiography, during which the patient reported chest pain and became hemodynamically unstable. Active coronary vasospasm at multiple sites was treated with intracoronary nitroglycerin and nicardipine, leading to immediate recovery. Our case highlights the importance of accurate, timely diagnosis of vasospastic angina, and of early recognition and management of spontaneous coronary spasm during angiography., (© 2022 by the Texas Heart® Institute, Houston.)

Background: Vasospastic angina (VSA) reportedly accounts for one form of sudden cardiac arrest (SCA). Intracoronary acetylcholine (ACh) testing is useful for diagnosing VSA although invasive provocation testing after SCA is a clinical challenge. In addition, even if the ACh test is positive, any causal relationship between VSA and SCA is often unclear because patients with VSA may have other underlying cardiac disorders., Methods: A total of 20 patients without overt structural heart disease who had been fully resuscitated from SCA were included. All patients underwent the ACh provocation test and scrutiny such as cardiac computed tomography or magnetic resonance imaging. Patients were followed up for all-cause death or recurrent SCA including appropriate implantable cardioverter defibrillator therapy., Results: An ACh provocation test was performed 20 ± 17 days after cardiac arrest. Fifteen out of 20 (75.0%) patients had a positive ACh test and 2 (10.0%) had adverse events such as ventricular tachycardia and transient cardiogenic shock during the test. In patients with a positive ACh test, 6 of 15 (40.0%) patients had other overlapping cardiac disorders such as long QT syndrome, Brugada syndrome, cardiac sarcoidosis, myocarditis, or cardiomyopathy. Long-term prognosis was not different regardless of a positive ACh test or the presence of other cardiac disorders overlapping with VSA., Conclusions: Three-quarters of the patients who had been resuscitated from SCA had a positive ACh test. Further examinations revealed other overlapping cardiac disorders in addition to VSA in 40% of patients with a positive ACh test.

Competing Interests: Competing interests: None declared.

We report the case of a 63-year-old woman who presented with typical angina (crushing chest pain) and recurrent frank syncope two years after her heart transplant. She was observed to have transient ST-elevations on continuous ST-segment monitoring that correlated with her symptoms, and coronary angiography revealed severe and transient spasm of the right coronary artery concurrent with her symptoms and ST-segment changes. The observed spasm completely resolved following administration of intracoronary nitroglycerin in the cardiac cathetherization laboratory. Although rare (occurring in ~5% of patients following cardiac transplantation), coronary artery spasm can occur in post-transplanted hearts and is occasionally diagnosed by coronary angiography., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Variant angina is caused by coronary artery spasm (CAS) with ST-segment elevation. We herein report a case of recurrent CAS during 2 operations in the same patient. An 80-year-old woman was scheduled to undergo tracheostomy, submandibular dissection, left partial maxillectomy, and coronoidectomy. We administered ephedrine and phenylephrine to manage hypotension during general anesthesia. Immediately after the administration of these drugs, the ST segment elevated. We decided to cease the operation and transport the patient to the department of cardiology. Computed tomography angiography revealed pneumomediastinum. The cardiologists considered that the electrocardiography findings had changed secondary to pneumomediastinum. About 6 weeks later, a second operation was scheduled. We administered ephedrine and phenylephrine to manage hypotension during general anesthesia. Immediately after the administration of these drugs, ST-segment elevation occurred. We discontinued use of these drugs, and the ST-segment elevation did not recur. We considered that the cause of the ST-segment elevation was vasopressor-induced CAS because the vasopressors were administered immediately before the occurrence of CAS. Vasopressors such as ephedrine or phenylephrine are frequently used to manage hypotension during general anesthesia. Therefore, anesthesiologists should consider the occurrence of CAS before using vasopressors and know how to manage CAS well.

Vasospastic angina is a diagnosis of exclusion that manifests with signs and symptoms, which overlap with obstructive coronary artery disease, most often ST-segment elevation myocardial infarction. The pharmacotherapy that is available to treat vasospastic angina can help ameliorate angina symptoms. However, the etiology of vasospastic angina is ill-defined, making targeted pharmacotherapy difficult. Most patients receive pharmacotherapy that includes calcium channel blockers and/or long-acting nitrates. This article reviews the efficacy and safety of the pharmacotherapy used to treat vasospastic angina. High-dose calcium channel blockers possess the most evidence, with respect to decreasing angina incidence, frequency, and duration. However, not all patients respond to calcium channel blockers. Nitrates and/or alpha1-adrenergic receptor antagonists can be used in patients who respond poorly to calcium channel blockers. Albeit, evidence for use of nitrates and alpha1-adrenergic receptor antagonists in vasospastic angina is not as robust as calcium channel blockers and can exacerbate adverse effects when added to calcium channel blocker therapy. Despite having a clear benefit in patients with obstructive coronary artery disease, the benefit of beta-adrenergic receptor antagonists, statins, and aspirin remains unclear. More data are needed to elucidate whether or not these agents are beneficial or harmful to patients being treated for vasospastic angina. Overall, the use of pharmacotherapy for the treatment of vasospastic angina should be guided by patient-specific factors, such as tolerability, adverse effects, drug-drug, and drug-disease interactions., (© The Author(s) 2016.)

Background: Coronary artery spasm (CAS) is a well-known endothelial dysfunction, and a major cause of vasospastic angina (VSA). The renin-angiotensin system (RAS) is known to be closely associated with endothelial function. However, there are only a few studies that investigated the impact of RAS inhibitor on long-term clinical outcomes in VSA patients., Methods and Results: A total of 3349 patients with no significant coronary artery disease, diagnosed with CAS by acetylcholine provocation test were enrolled for this study. Significant CAS was defined as having ≥70% narrowing of the artery after incremental injections of 20, 50, and 100 μg of acetylcholine into the left coronary artery. Patients were divided into 2 groups according to whether the prescription included RAS inhibitor or not (RAS inhibitor group: n=666, non-RAS inhibitor group; n=2683). To adjust for any potential confounders that could cause bias, propensity score matching (PSM) analysis was performed using a logistic regression model. After PSM analysis, 2 matched groups (524 pairs, n=1048 patients, C-statistic=0.845) were generated and their baseline characteristics were balanced. During the 5-year clinical follow-up, the RAS inhibitor group showed a lower incidence of recurrent angina (8.7% versus 14.1%, P=0.027), total death (0.0% versus 1.3%, P=0.045), and total major adverse cardiovascular events (1.0% versus 4.1%, P=0.026) than the non-RAS inhibitor group., Conclusions: Chronic RAS inhibitor therapy was associated with lower incidence of cardiovascular events in VSA patients in the 5-year clinical follow-up., (© 2016 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.)

Background: Statin therapy reduces the risk of cardiovascular events in patients with obstructive coronary artery disease. The aim of the present study was to determine the effects of statins on the prognosis of patients with coronary vasospastic angina (VSA) free of significant atherosclerotic stenosis., Methods and Results: After exclusion of 475 from 1877 consecutive patients who underwent an acetylcholine-provocation test between January 1991 and December 2010, data of 640 VSA patients without significant organic stenosis of the remaining 1402 were analyzed retrospectively. Propensity score matching was performed to reduce the effect of treatment-selection bias and possible confounders. The primary endpoint was major adverse cardiac events (MACE), including cardiac death, nonfatal myocardial infarction, and unstable angina. Among the study population, dyslipidemia on admission was identified in 160 of 168 (95.2%) patients of the statin group compared with only 125 of 472 (26.5%) of the no-statin group. Of the 640 patients, 24 (3.8%) developed MACE. Multivariate Cox hazard regression analysis identified statin therapy as a significant negative predictor of MACE (hazard ratio, 0.11; 95% CI, 0.02-0.84; P=0.033). In the propensity-score matched cohorts (n=128 each), Kaplan-Meier survival curve showed a better 5-year MACE-free survival rate for patients of the statin group compared to the no-statin group (100% vs 91.7%, respectively; P=0.002)., Conclusions: Statin therapy correlated with a lower rate of cardiovascular events in VSA patients free of significant organic stenosis. Statins seems to improve the prognosis of VSA patients free of significant organic stenosis., (© 2016 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.)

Introduction: Moyamoya disease is characterized by progressive steno-occlusive changes of the distal internal carotid and developed collateral vasculature, so called 'moyamoya' vessels at the base of the brain. Variant angina is a rare occurrence in patients with moyamoya disease., Case Presentation: Here we report the case of a 41-year-old Korean woman who developed chest pain after indirect revascularization surgery of moyamoya disease. A treadmill test and an exercise stress echocardiograph showed positive results, but there was no significant major coronary arteries stenosis. Suspicious of vasospasm, we conducted an ergonovine spasm stimulation test, which demonstrated tight stenosis of her proximal left anterior descending artery. At the site of spasm, intravascular ultrasound virtual histology showed intraluminal fibrous plaque., Conclusion: Physicians who follow up patients with moyamoya disease would need to be aware of the possibility of cardiac ischemia as well as neurological manifestations.

Introduction: The adverse effects of synthetic cannabinoids are not well-described nor have they been thoroughly studied., Case Report: A 16-year-old male with a past medical history of asthma and attention deficit hyperactivity disorder (ADHD) presented to the emergency department (ED) complaining of 24 h of substernal pressure associated with dyspnea, nausea, and vomiting. He reported smoking tobacco cigarettes daily and occasional marijuana use but denied recent use of marijuana. The initial electrocardiogram (EKG) revealed ST-segment elevations in leads II, III, AVF, and V4-V6. The initial troponin level was reported as 1.47 ng/mL, and the initial creatine kinase MB (CKMB) level was 17.5 ng/mL. The patient admitted to smoking "K2" 60-90 min prior to the onset of symptoms. The patient manifested persistent ST elevations with a peak troponin of 8.29 ng/mL. The urine drug immunoassay was positive for benzodiazepines and opiates. Cardiac catheterization revealed normal coronary arteries, no wall motion abnormalities, and normal systolic function., Discussion: Synthetic cannabinoids may have significant potential adverse effects. Chest pain due to myocardial ischemia is rare in adolescents. When evaluating patients with chest pain, it is important to elicit a detailed drug history, specifically inquiring about synthetic cannabinoid use. Urine drug immunoassays may be unreliable and in this case did not detect synthetic cannabinoids.

Background: Hyperglycemia on admission is associated with increased mortality rates in patients with ST-elevation myocardial infarction (STEMI) who are treated with either fibrinolytic therapy (FT) or primary percutaneous coronary intervention (PCI). However, data regarding the relationship between hyperglycemia and the success of FT are lacking. The aim of this study was to investigate the value of admission blood glucose for the prediction of failed reperfusion following FT., Methods and Results: This is a retrospective study of 304 STEMI patients who received FT and whose admission glucose levels were recorded. The main outcome measure was ST segment resolution≥50%. The median (interquartile range [IQR]) blood glucose level in the entire study group was 112 (95-153). In 92 (30.2%) patients, FT was unsuccessful and rescue PCI was performed. Admission glucose (126 [99-192] vs. 110 [94-144] mg/dL, p<0.001), time from symptom onset to FT (180 [120-270] vs. 150 [120-180] min, p=0.009), and maximum ST elevation amplitude (3 [2-7] vs. 3 [2-6] mm, p=0.05) were higher in the failed reperfusion group than in the reperfusion group. Admission hyperglycemia was an independent predictive factor for failed reperfusion (hazard ratio 4.79 [1.80-12.76], p=0.002), along with time from symptom onset to fibrinolysis and anterior wall myocardial infarction., Conclusions: In patients with STEMI who undergo FT, admission hyperglycemia is an independent predictor of the failure of fibrinolysis.

Background: Variant angina, or vasospastic angina, is a form of angina caused by vasospasm of the coronary arteries, probably caused by endothelial dysfunction. This form of angina is provoked by non-classical risk factors such as stress, alcohol use, use of sympathomimetics and low environmental temperatures, but also by smoking. Treatment is based on elimination of risk factors and vasodilator therapy with nitrates and long-acting calcium antagonists., Case Description: We present a 68-year-old woman with recurring thoracalgia at rest and during exercise, suggestive of severe variant angina in more than one coronary artery. Despite elimination of risk factors and administration of vasodilatory therapy the treatment was initially insufficient. It eventually emerged that the probable cause was frequent use of a vasoconstrictive nasal spray, although this was not described in literature, and not originally mentioned by the patient., Conclusion: A thorough case history is of vital importance in a patient presenting with a history suggestive of variant angina. Even undescribed and apparently less important risk factors can be responsible for persistence of symptoms, and can lead to an applied treatment not producing the desired result.

Objectives: In this study, we assessed whether any abnormalities in coronary microvascular and peripheral vasodilator functions are present in patients with variant angina (VA) caused by epicardial coronary artery spasm (CAS)., Methods: We studied 23 patients with VA (i.e. angina at rest, ST-segment elevation during angina attacks and documented occlusive CAS at angiography) and 18 matched healthy controls. Endothelium-dependent and -independent coronary microvascular function was assessed by measuring coronary blood flow (CBF) response to adenosine and the cold pressor test (CPT) in the left anterior descending artery by transthoracic Doppler echocardiography. Systemic endothelium-dependent and -independent arterial dilator function was assessed by measuring brachial flow-mediated dilation (FMD) and nitrate-mediated dilation (NMD), respectively., Results: In VA patients, CBF responses to both adenosine (1.71 ± 0.25 vs. 2.97 ± 0.80, p < 0.01) and CPT (1.68 ± 0.23 vs. 2.58 ± 0.60, p < 0.01) were reduced compared to controls. Brachial FMD was also lower (3.87 ± 2.06 vs. 8.51 ± 2.95%, p < 0.01), but NMD was higher (16.7 ± 1.8 vs. 11.9 ± 1.4%, p < 0.01) in patients compared to controls. Differences were independent of the presence of coronary atherosclerotic lesions at angiography., Conclusions: Our data show that patients with VA have a generalized vascular dysfunction that involves both peripheral artery vessels and coronary microcirculation., (© 2014 S. Karger AG, Basel.)

We present the case of a 46-year-old woman with Prinzmetal's angina and syncope due to severe bradyarrhythmias. Dynamic electrical changes were documented on 12-lead 24-hour electrocardiographic (ECG) monitoring. We highlight the importance of continuous ECG monitoring in making the diagnosis and the indication for permanent cardiac pacing in this case.

Approximately 20% of patients undergoing diagnostic angiography for the evaluation of chest pain are found to have a normal coronary angiogram. Although this finding is generally associated with a low risk of cardiac events, approximately half will continue to experience chest pain over the next 12 months. Therefore, the finding of normal angiography warrants further evaluation of the potential causes for the presenting chest pain if we are to improve the disability suffered by these patients. In this review, the potential non-cardiac and cardiac causes for the chest pain in patients with normal angiography are briefly discussed with an in-depth focus on coronary vasomotor disorders including coronary artery spasm (variant angina) and microvascular disorders such as syndrome X, microvascular angina, the coronary slow flow phenomenon and microvascular spasm., (© 2013 The Authors. International Journal of Evidence-Based Healthcare © 2013 The Joanna Briggs Institute.)

Objectives: It is well known that myocardial bridge (MB) is a risk factor of vasospastic angina. However, clinical and angiographic characteristics according to different acetylcholine (ACh) dose in patients with MB are not clarified yet., Methods: A total 483 consecutive patients who had angiographically proven MB underwent the intracoronary ACh provocation test. ACh was injected by incremental doses of 20, 50 and 100 μg into the left coronary artery. We evaluated the clinical and angiographic characteristics of patients with MB according to 3 different ACh doses., Results: The baseline clinical and procedural characteristics are well balanced among the three groups. The MB patients who responded to the lower ACh dose (20 μg) had higher incidence of baseline spasm, severe vasospasm and diffuse long spasms (>30 mm) than those who responded to the higher doses (50 and 100 μg). The incidence of 12-month mortality and recurrent chest pain was higher in the lower ACh dose group (20 μg)., Conclusion: The patients with MB significantly reacting at the low ACh dose had more pronounced baseline spasm, severe and diffuse long coronary artery spasm, higher 12-month mortality and recurrent chest pain than those reacting with the higher ACh doses, suggesting that more intensive medical therapy will be required., (Copyright © 2013 S. Karger AG, Basel.)

Objective: To investigate the efficacy of coronary stenting in patients with variant angina refractory to medical treatment., Subjects and Methods: Variant angina was diagnosed in 81 patients admitted to the Department of Cardiology between January 2003 and June 2011. However, coronary stenting was performed in 21 patients refractory to medical treatment, but coronary angiography and intravascular ultrasound were performed in all patients, and acetylcholine provocative test was performed in 11 of the 21 patients refractory to medical treatment. Coronary angiography was repeated after 9-12 months in the 21 patients with coronary stents. Clinical follow-up time was 2.5 ± 3.1 years (range 1-8)., Results: Of the 81 patients, coronary angiography and intravascular ultrasound did not reveal significant stenosis in 13 (16.0%), but revealed 20-75% fixed stenosis in the remaining 68 (84.0%) patients. The acetylcholine provocative test was positive in the 11 patients. Of the 21 patients with coronary stents, the spasm site was located in the right coronary artery in 16 (76.2%) and in the left anterior descending artery in the remaining 5 (23.8%) patients. During the 1- to 8-year follow-up period, 1 of the 21 patients with stents developed recurrent episodes of variant angina, 5 patients had occasional chest pain, and the other 15 were asymptomatic. Coronary angiography at 9-12 months after initial evaluation demonstrated no stenosis in 3 patients, 20-40% in-stent mild intimal hyperplasia in 15 patients, and 50-80% in-stent restenosis in 3 patients. Coronary stenting was performed again in 2 patients., Conclusions: The present study showed that coronary stenting for severe refractory coronary vasospasm was effective and without serious complications. It can be an alternative and viable option for some patients who are refractory to medical therapy and at a high risk of acute coronary syndrome recurrence., (© 2013 S. Karger AG, Basel.)

Objectives: The present study was performed to investigate the clinical implications of an implantable cardioverter-defibrillator (ICD) in patients with vasospastic angina (VSA) resuscitated from lethal ventricular arrhythmia., Background: The prognosis of VSA is known to be good with medication; however, ventricular arrhythmia and cardiopulmonary arrest are rare but life-threatening complications of this disease. The ICD is a proven modality for patients with ventricular arrhythmia, but the clinical implications in this population remain to be elucidated., Methods: We conducted a retrospective, observational, multicenter study involving patients with an ICD due to documented ventricular arrhythmia and VSA diagnosed by acetylcholine provocation test. All patients were followed up for appropriate ICD therapy, sudden cardiac arrest, or death from all causes., Results: Twenty-three patients were included in the present study and completely followed up. All patients are still alive. During a follow-up of 2.9 years (median 2.1 years), 4 ventricular fibrillations and 1 episode of pulseless electrical activity occurred in 5 patients (21.7%). There were no statistically significant differences in patient characteristics between the recurrence and nonrecurrence groups, including medication, smoking status, and whether the patient was or was not free of symptoms after ICD implantation., Conclusions: Patients with VSA and lethal ventricular arrhythmia are a population at high risk for recurrence of cardiopulmonary arrest, and there is no reliable indicator for predicting recurrence of ventricular arrhythmia. Insertion of an ICD with medication for VSA is appropriate for this high-risk population., (Copyright © 2012 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Antiphospholipid syndrome (APS) is an acquired hypercoagulable disease that is associated with both arterial and venous thrombosis. It is known to cause a spectrum of cardiovascular manifestations including myocardial infarction, stroke, valvular abnormalities, as well as vascular and intracardiac thrombosis. The pathogenesis of myocardial infarction and angina due to APS is thought to be due to coronary thrombosis. Coronary vasospasm without thrombosis can produce myocardial ischemia and chest pain, this is known as Prinzmetal's angina. To our knowledge, Prinzmetal's angina is not known to be associated with APS. In our clinical practice, we came across two cases of APS in which the patients presented with angina and were found to have coronary vasospasm without thrombosis. The finding of these two uncommon diagnoses in multiple individuals raises the possibility that these disorders are associated., (© 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins)

Spastic angina is considered rare but its prevalence is probably underestimated especially in case of atherosclerotic coronary lesions. Its diagnosis remains important due to its poor prognosis and therapeutic characteristics. We report three clinical cases illustrating two different clinical presentations and the problem of diagnosis of spastic angina. We performed a review of the literature essentially concerning commonly used diagnosis means and especially provocative testing for coronary spasm. This test needs to be adapted to the evolution of techniques and uses of coronary angiography in 2011, particularly the wide spread use of radial approach. Therefore new recommendations are needed, specifying the terms of provocative testing and establishing clear diagnosis criteria including clinical, electrocardiographic and angiographic data. Such guidelines would probably help to better diagnose and treat these patients in our practice., (Copyright © 2011 Elsevier Masson SAS. All rights reserved.)

We report a case of recurrent variant angina pectoris which occurred even while receiving antispastic treatment. Coronary angiography revealed no obvious lesion. Behçet's syndrome was diagnosed based on recurrent oral aphthous and genital ulcer as well as skin manifestation. After treatment with immunosuppressant, neither angina nor oral ulcer relapsed. We strongly believe that the variant angina is due to coronary vasospasm induced by Behçet's syndrome in this patient.

Wellens syndrome is characterised by negative or biphasic T waves in V2-V4 leads and critical stenosis of proximal part of the left descending coronary artery. These ECG changes without atherosclerotic changes in coronary angiography, i.e. coronary artery spasm are called pseudo-Wellens syndrome. We describe a patient with acute coronary syndrome and pseudo-Wellens syndrome as a cause of vasospastic angina. These ECG abnormalities need differentiation with acute pulmonary embolism.

Formally described by Prinzmetal and colleagues in 1959, variant angina represents a syndrome of resting angina that results from severe coronary artery vasospasm associated with ST elevation. The majority of patients respond to nitrates or calcium channel blockers. However, medical treatment-resistant vasospasm can occur in up to 20% of cases, thus requiring further interventions. We present a rare instance of coronary vasospasm associated with complete heart block resistant to medical therapy that was successfully treated with stenting. This case example is followed by a detailed review of the literature with regard to percutaneous or surgical coronary revascularization of patients with medically resistant vasospasm.

Variant angina is caused by focal spasm of the epicardial coronary arteries and is variably associated with atherosclerotic coronary disease. We present the clinical course of profound coronary spasm in a woman which resulted in life-threatening symptoms. Although not previously reported, administration of the endothelin antagonist bosentan resulted in complete resolution of her symptoms which were refractory to commonly used anti-anginals, and these symptoms recurred when the drug was inadvertently withdrawn, confirming efficacy of the agent. The details of her clinical outcome and a review of the role of endothelin and its antagonists in coronary vasospasm are discussed., (Copyright (c) 2010 S. Karger AG, Basel.)

A patient with Prinzmetal's variant angina (PVA) developed a cardiac arrest due to coronary vasospasm and subsequent myocardial infarction. After resuscitation postanoxic brain injury was diagnosed. After an initial improvement of consciousness he deteriorated rapidly on the seventh day after admission due to severe brain ischaemia apparently caused by cerebral vasospasm, until ultimately brain death was diagnosed. To our knowledge, the association between PVA and cerebral vasospasm has never been described. The combination suggests that this patient had a generalized vasospastic disorder.

Prinzmetal's variant angina (VA) and cardiac syndrome X (CSX) are two distinct, usually easily recognizable, forms of angina syndromes, caused by epicardial spasm, usually responsible for transient transmural myocardial ischemia at rest and by coronary microvascular dysfunction (CMVD), usually responsible for effort induced subendocardial ischemia, respectively. In this article we report clinical evidence in three patients of the simultaneous occurrence of angina episodes typical of both VA and CSX, suggesting that common pathogenetic factors may be responsible for clinical manifestations both of functional macrovascular and microvascular coronary artery abnormalities in some angina patients.

A 65-years-old female presented with features suggesting acute coronary syndrome, initially as non STEMI and later as classical Prinzmetal's angina. While being treated she also had recurrent episodes of dizziness and cardiac arrest due to complete heart block and asystole. These episodes occurred while on nitroglycerine infusion and were not accompanied by chest pain or ST-T segment changes. Coronary angiography revealed evidence of reversible multi-vessel coronary spasm. Electrophysiological studies were normal. She was treated with nitrates and calcium blockers and a permanent pacemaker implantation.

A coronary arteriovenous (AV) fistula consists of a communication between a coronary artery and a cardiac chamber, a great artery or the vena cava. It is the most common anomaly that can affect coronary perfusion. Yet bilateral involvement of a coronary fistula, constitutes an uncommon subgroup of coronary AV fistulas. We herein report on a case of bilateral coronary AV fistula that was coexistent with variant angina originating from the distal right ventricular branch of the right coronary artery and the distal septal branch of the left anterior descending artery, and the latter drained into the right ventricle.

Sirolimus-eluting stents (SES) prevent neointimal proliferation and have been widely used to treat stenotic lesions in coronary arteries because of a significant reduction of restenosis in comparison with bare-metal stents. Sirolimus, however, may cause endothelial dysfunction by damage to vascular endothelium or impairing vascular repair. Recent studies report the occurrence of exercise- or acetylcholine-induced coronary vasoconstriction in the vessel segments adjacent to the SES. We report here a clinical case of intractable Prinzmetal's angina 3 months after SES implantation and recommend extended, thorough follow up of patients who have undergone SES implantation.

A case of multivessel variant angina after an open radical nephrectomy operation (RNO) is presented. A 52-year-old man was admitted to the coronary care unit with recurrent chest pain and dynamic ST-T wave changes on electrocardiogram early after an RNO. The first diagnosis of the clinical condition was non-ST segment elevation acute coronary syndrome. However, recurrent angina with ST segment elevation occurred after the standard medical therapy, which included beta-blockers. Emergency coronary angiography showed diffuse and multiple narrowing of all the three major coronary arteries during the chest pain, which was relieved by intracoronary nitroglycerine injection. Variant angina was suspected, and beta-blocker therapy was replaced with calcium channel blocker treatment. No angina attacks were observed during the clinical follow-up. Although a direct relationship between the type of surgery and variant angina was not established, coronary vasospasm after an RNO should be kept in mind, especially in the differential diagnosis of a patient with recurrent angina and dynamic ST-T changes on electrocardiogram. Although beta-blocker therapy is a first-line treatment for all acute coronary syndromes, it can be harmful in patients with variant angina and should be stopped immediately after verification of diagnosis.

A 49-year-old man with chest pain and syncope presented saddleback or occasionally coved type ST elevation in V1-V3. Coronary spasm in the left anterior descending artery was induced by acetylcholine injection and ST elevation changed from saddleback to coved type in V2-V3 together with ST depression in V4-V5, whereas acetylcholine injection into the right coronary artery did not provoke spasm, but induced augmented and coved type ST elevation in V2 without ST-T changes in V4-V5. These electrocardiographic changes in response to acetylcholine administration into each coronary artery are compatible with pathogenesis of vasospastic angina and Brugada syndrome, respectively.