Search

Coronary spasm in carcinoid heart disease has an incidence of 10%, but is rare in patients with neuroendocrine tumours without carcinoid heart disease. We present a rare case of right coronary artery spasm and ST elevations secondary to a neuroendocrine carcinoma of the lung, uniquely provoked by positional changes. Our patient is a 55-year-old man with recurrent ST-elevation myocardial infarction secondary to coronary vasospasm that was diagnosed with neuroendocrine carcinoma of the lung. We believe his positional coronary spasm episodes were likely due to intermittent tumour compression from changes in body position. Our case highlights positional coronary spasm as a previously unreported and potentially early manifestation of neuroendocrine carcinoma of the lung.

A 39-year-old woman with gastro-oesophageal reflux disease, tobacco abuse and family history of premature coronary artery disease (CAD) presented to the hospital reporting of new onset substernal chest pain for 4 days prior to admission. She experienced multiple episodes of chest pain at rest and

Trastuzumab-induced cardiomyopathy is a known complication of its use in breast cancer treatment. However, cardiac complications of trastuzumab without left ventricular systolic dysfunction have been rarely reported. These include left bundle branch block, sinus node dysfunction, and ventricular tachycardia. We herein report a case of a 47-year-old female with human epidermal growth factor receptor 2-positive, stage IV breast cancer without a history of cardiovascular disease. During treatment with trastuzumab emtansine (T-DM1), she presented with out-of-hospital cardiac arrest and was resuscitated by automated cardioverter defibrillator (AED). Emergent cardiac catheterization revealed no organic obstruction and coronary vasospasm in her coronary arteries, and no left ventricular systolic dysfunction. Ventricular fibrillation (VF) was documented by an event memory of AED. T-DM1 was withdrawn and implantable cardioverter defibrillator was implanted. Thereafter, VF or life-threatening arrhythmia were not documented for 36 months until her death by breast cancer. We concluded that the etiology of her VF event was T-DM1-induced cardiotoxicity. We believe this is the first report of life-threatening VF event without cardiomyopathy induced by T-DM1.

Purpose Catheter ablation (CA) is an established treatment for atrial fibrillation (AF). Although coronary artery spasms (CAS) during or after ablation procedures have been described as a rare complication in some case reports, the incidence and characteristics of this complication have not been fully elucidated. The present observational study aimed to clarify the CAS in a large number of patients experiencing AF ablation. Methods A total of 2913 consecutive patients (male: 78%, mean 66 ± 10 years) who underwent catheter ablation of AF were enrolled. Results Nine patients (0.31%, mean 66 ± 10 years, 7 males) had transient ST-T elevation (STE). Eight out of the 9 patients had STE in the inferior leads. STE occurred after the transseptal puncture in 7 patients, after the sheath was pulled out of the left atrium in 1, and 2 h after the ablation procedure in 1. Six patients had definite angiographic CAS without any sign of an air embolization on the emergent coronary angiography. In the3 other patients, the STE improved either directly after an infusion of nitroglycerin or spontaneously before the CAG. The patients with CAS had a higher frequency of a smoking habit (89% vs. 53%; P = .04), smaller left atrial diameter (36 ± 6 vs. 40 ± 7; P = .07), and lower CHADS2 score (0.6 ± 0.5 vs. 1.3 ± 1.1; P = .004) than those without. Conclusions Although the incidence was rare (0.31%), CAS should be kept in mind as a potentially life-threatening complication throughout an AF ablation procedure especially performed under conscious sedation.

Background Renal denervation (RDN) is an invasive intervention to treat drug-resistant arterial hypertension. Its therapeutic value is contentious. Here we examined the effects of RDN on inflammatory and infectious kidney disease models in mice. Methods Mice were unilaterally or bilaterally denervated, or sham operated, then three disease models were induced: nephrotoxic nephritis (NTN, a model for crescentic GN), pyelonephritis, and acute endotoxemic kidney injury (as a model for septic kidney injury). Analytical methods included measurement of renal glomerular filtration, proteinuria, flow cytometry of renal immune cells, immunofluorescence microscopy, and three-dimensional imaging of optically cleared kidney tissue by light-sheet fluorescence microscopy followed by algorithmic analysis. Results Unilateral RDN increased glomerular filtration in denervated kidneys, but decreased it in the contralateral kidneys. In the NTN model, more nephritogenic antibodies were deposited in glomeruli of denervated kidneys, resulting in stronger inflammation and injury in denervated compared with contralateral nondenervated kidneys. Also, intravenously injected LPS increased neutrophil influx and inflammation in the denervated kidneys, both after unilateral and bilateral RDN. When we induced pyelonephritis in bilaterally denervated mice, both kidneys contained less bacteria and neutrophils. In unilaterally denervated mice, pyelonephritis was attenuated and intrarenal neutrophil numbers were lower in the denervated kidneys. The nondenervated contralateral kidneys harbored more bacteria, even compared with sham-operated mice, and showed the strongest influx of neutrophils. Conclusions Our data suggest that the increased perfusion and filtration in denervated kidneys can profoundly influence concomitant inflammatory diseases. Renal deposition of circulating nephritic material is higher, and hence antibody- and endotoxin-induced kidney injury was aggravated in mice. Pyelonephritis was attenuated in denervated murine kidneys, because the higher glomerular filtration facilitated better flushing of bacteria with the urine, at the expense of contralateral, nondenervated kidneys after unilateral denervation.

Myocardial infarction with non-obstructive coronary arteries (MINOCA) as a relatively new disease entity distinguished from the group of acute coronary syndromes (ACS) is not a rare clinical problem and it requires in-depth diagnostics. MINOCA accounts for 5–10% of all ACS cases. MINOCA is most common between the ages of 50–60 and predominates in females. Coronary microvascular dysfunction and coronary vasospasm are among the potential mechanisms. The latest guidelines for the treatment of ACS in patients presenting without persistent ST-segment elevation emphasize the importance of searching for the causes of angina in patients with insignificant lesions in the coronary arteries by extending invasive diagnostics (e.g., acetylcholine provocation test) and using noninvasive diagnostics (e.g., CMR or SPECT). In the context of MINOCA, among the typical risk factors for coronary artery disease, arterial hypertension (HTN) seems to be the most important by inducing coronary microcirculation remodeling (mostly hypertrophy) and hence the narrowing of the lumen. Studies comparing patients with MINOCA and obstructive coronary artery disease (MI-CAD) in the context of risk factors, in particular HTN, were analyzed. In five out of nine analyzed studies, HTN occurred significantly more often in patients with MINOCA compared to patients with MI-CAD. The current pharmacotherapy recommendations focus on slowing the progression of coronary microvascular dysfunction (CMD), i.e., adequate treatment of risk factors and comorbidities, such as HTN. Therefore, it seems reasonable to conduct studies directly analyzing the relationship between HTN and MINOCA in order to improve diagnostics and establish appropriate pharmacotherapy that will improve prognosis.

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.

Kounis syndrome is an anaphylactic reaction leading to acute coronary syndrome. The acute treatment of anaphylaxis is epinephrine; however, epinephrine may cause coronary vasoconstriction, reduce coronary blood flow, increase myocardial oxygen demand, and worsen myocardial ischemia. On the other hand, coronary vasodilation, a treatment for acute coronary syndrome, can aggravate hypotension in patients with anaphylaxis. Herein, the authors report a case of type II Kounis syndrome, with vasospasm in a patient with coronary disease, requiring the administration of epinephrine and a coronary vasodilator for resuscitation. The authors administered intravenous epinephrine continuously from lower dosages and performed delicate titration. The coronary vasodilator nicorandil, which has little effect on hemodynamics, also was administered. These treatments improved hemodynamics without complications. Circulatory management that considers both anaphylaxis and coronary lesions is crucial to improve prognosis in this syndrome.

Coronary artery spasm-induced acute myocardial infarction (CASIAMI) is one of the etiologies of myocardial infarction with non-obstructive coronary arteries (MINOCA). We retrospectively analyzed the incidence and clinical characteristics of Japanese patients with CASIAMI and non-obstructive coronary arteries. We experienced 62 patients with MINOCA (10 thrombosis, 7 unknown causes, and 45 CASIAMI) among 991 patients with suspected AMI. Pharmacological spasm provocation testing was performed in 37 patients. CASIAMI without obstructive coronary arteries was found in 4.5% of patients with suspected AMI and was observed in 73% of patients with MINOCA. Patients with CASIAMI were frequently males and had relatively small AMIs. Spontaneous spasm was recognized in 8 patients. We could reproduce provoked spasm in 37 patients with MINOCA, including 23 patients with multiple spasm. No patients died during the follow-up period. The clinical outcomes in patients with CASIAMI under optimal coronary vasodilators were satisfactory.

The occurrence of acute coronary syndrome (ACS) following a scorpion sting has been very rarely reported in literature, and most of the cases presented had a normal coronary angiogram. The possible pathogenetic mechanisms include imbalance in blood pressure and coronary spasm caused by a combination of sympathetic excitation with subsequent thrombosis of coronary vessels developed after the release of vasoactive, inflammatory, and thrombogenic substances contained in the scorpion venom. In this report, we present a case of a scorpion sting complicated by ACS, called Kounis syndrome (KS). His coronary angiogram revealed the presence of significant stenosis of the left anterior descending artery. He was treated successfully with percutaneous transluminal coronary angioplasty, antivenom serum, and supportive therapy.

Background: Vasospastic angina (VA), or Prinzmetal’s angina, is characterized by symptoms of coronary angina caused by coronary vasospasm, usually in the absence of atherosclerotic changes. It typically presents with chest pain, which can be accompanied by transient electrocardiographic changes, if visualized during the attack. It can also rarely present with severe manifestations of acute myocardial angina, ventricular fibrillation, or cardiac arrest. Case presentation: We present a case of a 50-year-old Caucasian male who initially presented to the hospital with chest pain and was diagnosed with VA. Later, he was brought to the hospital by emergency medical services later with ventricular fibrillation, despite normal coronary anatomy on angiogram. He was managed with placement of an intra–cardiac defibrillator (ICD) for secondary prevention. The patient continued to have recurrent episodes of ventricular fibrillation with associated ICD shocks, and had multiple admissions to the hospital with similar presentations. Symptoms and arrhythmia improved after optimizing antianginal therapy. Conclusions: Ventricular fibrillation can be an uncommon but severe manifestation during VA crises. In cases with normal coronary vasculature, it is important to recognize VA as a cause of recurrent ventricular fibrillation in order to optimize medical management for prevention of fatal arrhythmias.

A 47-y-old man was bitten by a hump-nosed viper (Hypnale zara) and gradually developed retrosternal chest pain associated with ST segment elevation on electrocardiogram. He had normal troponin I levels and no evidence of coagulopathy. Initially, he was managed as having anterior ST elevation myocardial infarction with thrombolysis. Later, because troponin levels were normal, he was suggested to have the type I variant of Kounis syndrome (allergic coronary artery spasm). This was supported by high eosinophil counts in peripheral blood. He was successfully managed with supportive treatment and discharged 6 d after the snakebite. Cardiac complications are rarely reported after hump-nosed viper bites, and clinical reports of coronary vasospasm after snakebites are extremely rare in the literature. This is the first known report of Kounis syndrome after a hump-nosed viper bite.

Kounis syndrome is one of the rare variants of acute coronary syndrome that occurs as a result of an allergic reaction. Its main pathophysiological mechanism is coronary vasospasm. Clinically, Kounis syndrome is manifested by symptoms of both an allergic reaction and an acute coronary syndrome, and its treatment is not an easy task, since both cardiac and allergic manifestations must be treated at the same time. In the given article we describe a clinical case of diagnosis and successful treatment of Kounis syndrome caused by cold urticaria in a 58-year-old patient who was hospitalized to the Grodno Regional Clinical Cardiology Center.

Coronary intraluminal white clot formation, apparently in response to acetylcholine testing, may explain a woman’s long-term history of daily chest pain and multiple myocardial infarctions. Acetylcholine testing reproduced chest pain and revealed luminal filling defects in multiple vessels; imaging showed fresh white platelet clots. Antiplatelet prasugrel has substantially suppressed her symptoms. (Level of Difficulty: Advanced.), Central Illustration

In vasospastic angina (VSA), coronary vasomotion abnormalities could develop not only in epicardial coronary arteries but also in coronary microvessels, where calcium channel blockers (CCBs) have limited efficacy. However, efficacy of exercise training for VSA remains to be elucidated. We thus aimed to examine whether vasodilator capacity of coronary microvessels is impaired in VSA patients, and if so, whether exercise exerts beneficial effects on the top of CCBs.We performed 2 clinical protocols. In the protocol 1, we measured myocardial blood flow (MBF) using adenosine-stress dynamic computed tomography perfusion (CTP) in 38 consecutive VSA patients and 17 non-VSA controls. In the protocol 2, we conducted randomized controlled trial, where 20 VSA patients were randomly assigned to either 3-month exercise training group (Exercise group) or Non-Exercise group (n= 10 each).In the protocol 1, MBF on CTP was significantly decreased in the VSA group compared with the Non-VSA group (138 ± 6 vs 166 ± 10 ml/100 g/min, P = 0.02). In the protocol 2, exercise capacity was significantly increased in the Exercise group than in the Non-Exercise group (11.5 ± 0.5 to 15.4 ± 1.8 vs 12.6 ± 0.7 to 14.0 ± 0.8 ml/min/kg, P 0.01). MBF was also significantly improved after 3 months only in the Exercise group (Exercise group, 145 ± 12 to 172 ± 8 ml/100 g/min, P 0.04; Non-Exercise group, 143 ± 14 to 167 ± 8 ml/100 g/min, P = 0.11), although there were no significant between-group differences.These results provide the first evidence that, in VSA patients, exercise training on the top of CCBs treatment may be useful to improve physical performance, although its effect on MBF may be minimal.

Moyamoya disease (MMD) is characterized by progressive steno-occlusive lesions of the distal or proximal branch of the internal carotid arteries, and cerebrovascular symptoms are its major complications. Extracranial vascular involvement including the coronary artery has been reported, and some case reports have described variant angina or myocardial infarction. However, no report has yet described a case of myocardial infarction after coronary artery bypass grafting (CABG). Here, we present a patient with MMD who suffered cardiac arrest caused by myocardial infarction due to a coronary spasm after off-pump CABG and who was discharged successfully after treatment with a veno-arterial extracorporeal membrane oxygenator and percutaneous coronary intervention.

Coronary artery spasm (CAS) plays an important role in the pathogenesis of ischemic heart disease. The clinical manifestations of CAS include variant angina, myocardial infarction and sudden death. Although endothelial dysfunction and hyperreactivity of vascular smooth muscle cells have been associated with CAS, the underlying mechanisms remain unclear. Thus, there is a long way to go to truly understand the pathogenesis of CAS to formulate effective treatments. This article discusses the pathophysiological mechanisms as well as downstream molecular pathways of CAS, with a focus on potential therapeutic targets.

Background Coronary vasospasm is a recognized side effect of 5-fluorouracil (5-FU). There are limited and conflicting data on the incidence, risk factors, and prognostic effect of 5-FU–associated vasospasm. Objectives This study sought to assess the incidence, risk factors, and prognostic implications of 5-FU coronary vasospasm among patients receiving 5-FU regimens at a single tertiary care center. Methods The study conducted a retrospective analysis of all patients who received 5-FU at a single academic center from January 2009 to July 2019. Vasospasm was defined as the occurrence of a typical chest pain syndrome in the presence of 5-FU. The presence of associated electrocardiogram changes or elevated biomarkers was used to further confirm the diagnosis. Patients with vasospasm were compared with patients treated with 5-FU without vasospasm in a 1:2 ratio. Data regarding demographics, medical history, and follow-up were collected by manual chart review. Results From approximately 4,019 individual patients who received 5-FU from 2009 to 2019 at a single center, 87 (2.16%) developed vasospasm. Patients who developed vasospasm were younger (age 58 ± 13 years vs. 64 ± 13 years; p = 0.001) and were less likely to have any cardiovascular risk factors (70.1% vs. 84.5%; p = 0.007). Patients with vasospasm and patients without vasospasm were otherwise similar in terms of types of cancer, stage of cancer, sex, and race. There was no significant difference in progression-free survival, overall mortality or cancer specific mortality between patients who developed vasospasm versus those who did not. Conclusions In a large, single-center report of 5-FU–associated vasospasm, patients who developed vasospasm were younger, had lower rates of traditional cardiovascular risk factors, and had no significant difference in progression-free or overall survival compared with those who did not develop vasospasm.

Objectives Whether there are prognostic links between coronary morphologies and coronary functional abnormalities was examined in ischemia and nonobstructive coronary artery disease (INOCA) patients. Background Although INOCA has attracted much attention, little is known about the prognostic impact of coronary morphologies in this disorder. Methods A total of 329 consecutive INOCA patients were enrolled and underwent spasm provocation testing combined with lactate sampling for diagnosis of epicardial and microvascular spasm (MVS). On the basis of the functional tests, the patients were classified into 4 groups: a control group without epicardial spasm or MVS (n = 32), MVS alone (n = 51), diffuse spasm in ≥2 coronary segments (n = 204), and focal spasm in 1 segment (n = 42). In this population, optical coherence tomography imaging of the left anterior descending coronary artery was performed for evaluation of adventitial vasa vasorum (AVV) and intraplaque neovessels (IPN). Index of microcirculatory resistance was also measured. Results MVS frequently coexisted with diffuse (70%) and focal spasm (68%) with a good correlation between AVV and index of microcirculatory resistance (R = 0.353; p = 0.022). For a median follow-up of 1,043 days, focal spasm showed the worst prognosis (log rank p = 0.005), for which IPN was a significant prognostic factor. By contrast, diffuse spasm showed the greatest AVV with an intermediate prognosis. The prognostic value of INOCA was significantly enhanced by adding AVV and IPN to the physiological indices (area under the curve = 0.88 vs. 0.76; p = 0.048). Conclusions These results provide the first evidence that there are important prognostic links between coronary morphologies (evaluated by optical coherence tomography) and coronary functional abnormalities in patients with INOCA, indicating the importance of both evaluations in this population.

Background Kounis syndrome is an acute coronary syndrome that appears in the setting of anaphylactic reaction or hypersensitivity. Many drugs and environmental exposures have been identified as potential offenders, and diagnosis and treatment can be challenging. Case presentation A 62-year-old man with recurrent bladder cancer underwent an intra-iliac artery epirubicin injection. After the injection, he developed chest pain and a systemic allergic reaction, with electrocardiographic alterations and elevated troponin-I levels. Emergent coronary angiography showed right coronary artery spasm and no stenosis of the other coronary arteries. This reaction was considered compatible with an allergic coronary vasospasm. A diagnosis of Kounis syndrome was made. Conclusions Kounis syndrome is common, but a prompt diagnosis is often not possible. This case is the first to suggest that an intraarterial epirubicin injection could potentially be one of its triggers. All physicians should be aware of the pathophysiology of this condition to better recognize it and start appropriate treatment; this will prevent aggravation of the vasospastic cardiac attacks and yield a better outcome.

Hypokalemia is a common electrolyte disturbance and is related to poor prognosis in patients with cardiovascular disease. However, the role of hypokalemia in patients with vasospastic angina (VSA) has not yet been studied. The present study enrolled 1454 patients diagnosed with VSA according to ergonovine provocation test results and available admission serum potassium data. The primary outcome was a composite of cardiac death, acute coronary syndrome, and new-onset life-threatening arrhythmia. Based on a hypokalemia definition as serum potassium concentration ≤ 3.5 mEq/L, the hypokalaemia group included 70 patients (4.8%). The median potassium levels were 3.4 mEq/L [interquartile range (IQR) 3.3–3.5] in the hypokalemia group and 4.1 mEq/L (IQR 3.9–4.3) in the no-hypokalemia group. The median follow-up duration was 764 days. Primary outcomes occurred in seven patients (10.0%) in the hypokalemia group and 51 patients (3.7%) in the no-hypokalemia group. The Kaplan–Meier analysis showed a higher cumulative incidence of primary outcomes in the hypokalemia group compared to that in the no-hypokalemia group (log-rank P = 0.014). Multivariate Cox regression analysis also showed that hypokalemia was an independent predictor of primary outcomes. In conclusion, hypokalemia at admission was associated with adverse clinical outcomes in VSA.

Cocaine use accounts for 40% of the annual drug use related emergency department visits in the United States. Cocaine use is hence recognized as a major health problem. Cocaine blocks the presynaptic reuptake of norepinephrine and dopamine. The resulting increased adrenergic activity leads to vasoconstriction. Additionally, via various mechanisms, cocaine leads to a prothrombotic state and increases myocardial demand. Cocaine can cause coronary vasospasm and is therefore, associated with acute myocardial injury even in the absence of pre-existing atherosclerotic coronary artery disease. Nitroglycerin has a class 1C indication by the ACCF/AHA guidelines for patients with ST-segment elevation or depression that accompanies ischemic chest discomfort in the setting of cocaine use. It has been shown to reverse cocaine-induced coronary vasospasm and chest pain. In this case report, for the first time, we discuss how intravenous administration of high dose nitroglycerin to a patient in pulseless ventricular tachycardia with angiographically confirmed vasospasm induced by cocaine resulted in return of spontaneous circulation.

Background Hyperkalemia and acute coronary syndrome are not only all responsible for syncope related to complete atrioventricular block, but also share parts of electrocardiogram manifestations. Additionally, they influence each other. Case presentation A 32-year-old Chinese man presented with severe hypokalemia (1.63 mmol/l) at midnight in the emergency room. He developed unexpected rebound hyperkalemia (7.76 mmol/l) after 18 hours of oral and intravenous potassium chloride supplementation at a concentration of about 10 g/day and a rate of 10 mmol/hour. Subsequently, the patient complained of chest discomfort and dyspnea, followed by syncope for several minutes, approximately 2 hours after potassium reduction treatment had been started. The instant electrocardiogram showed complete atrioventricular block and elevated ST segment in the inferolateral leads, which resolved 15 minutes later, before hyperkalemia was corrected. Combined with mild coronary stenosis and negative myocardial injury markers, transient complete atrioventricular block induced by coronary vasospasm due to iatrogenic hyperkalemia was diagnosed. Normal urine potassium excretion, acid–base state, and other examinations made the diagnosis of hypokalemic periodic paralysis possible. Conclusions Hyperkalemia may provoke acute coronary syndrome, and early coronary angiography is an effective strategy for identifying the direct cause of acute complete atrioventricular block.

Objective A pathological acetylcholine (ACh) test was observed at lower ACh doses in females compared with males in European populations. We retrospectively analyzed the sex-related differences in Japanese patients with provoked positive spasm by ACh spasm provocation testing. Methods We performed the ACh spasm provocation tests in 1,854 patients from Jan 1991 until Mar 2019. ACh was injected in incremental doses of 20/50/100/200 μg into the left coronary artery and 20/50/80 μg into the right coronary artery. Positive spasm was defined as >90% stenosis and usual chest pain or ischemic ECG changes. We compared the clinical characteristics, angiographical findings during ACh testing, and clinical outcomes between female and male patients with and without provoked positive spasm. Results Positive provoked spasm was diagnosed in 917 patients including 737 (80.4%) males and 180 (19.6%) females. The incidence of provoked positive spasm in females was significantly lower than that in males (33.5% vs. 56.0%, p

A 46-year-old man complained of chest pain at rest for the past three months. His symptoms gradually exacerbated and were suspected of being due to unstable angina. A coronary angiogram revealed focal tight stenosis at the proximal left anterior descending coronary artery with gross spastic coronary findings. Optical coherence tomography (OCT) revealed layered low-intensity structures with microvessels and the accumulation of macrophages, which indicated progressive stenosis with multiple-layered organized thrombus caused by coronary erosion. We treated the stenosis using a drug-coated balloon instead of drug-eluting stents. There was no restenosis, and OCT revealed good plaque healing at follow-up. This case suggests that the pre-interventional OCT plaque morphology can have a positive impact on the revascularization strategy.

A 19-year-old-man was admitted to our hospital with intermittent chest pain. The day before admission, he had been diagnosed with enteritis and prescribed clarithromycin. He had experienced severe chest pain three times after taking clarithromycin; thus, acute coronary syndrome (ACS) was suspected. Emergent coronary angiography showed normal coronary arteries; however, the result of a subsequent acetylcholine provocation test was positive. We diagnosed him to have ACS caused by coronary vasospasms and suspected clarithromycin-induced Kounis syndrome. Although more common in older patients, Kounis syndrome must be suspected and a thorough medication history should be taken whenever a patient complains of chest pain.

Background: Non-diabetic coronary artery spasm (CAS) without obstructive coronary artery disease increases insulin resistance. We investigated the risk of incident type 2 diabetes (diabetes) associated with CAS. Methods: Patient records were retrospectively collected from the Taiwan National Health Insurance Research Database during the period 2000-2012. The matched cohorts consisted of 12,413 patients with CAS and 94,721 patients in the control group. Results: During the entire follow-up, the incidence of newly-diagnosed diabetes was 22.2 events per 1000 person-years in the CAS group and 13.9 events per 1000 person-years in the control group. The increased risk of CAS-related incident diabetes was observed regardless of sex and length of follow-up. The median time to incident diabetes was 2.9 and 3.5 years in the CAS and the control group (P

Background/Aims: Calcium channel blockers (CCBs) are the most widely pre scribed medication for patients with vasospastic angina (VA). However, few studies have compared the prognosis of VA patients who are prescribed different CCBs. Methods: We enrolled 2,960 patients who received provocation test prospectively in 11 university hospitals in Korea. We divided 1,586 patients received four major CCBs into two groups: a first generation CCB (diltiazem and nifedipine) group and a second generation CCB (amlodipine and benidipine) group. Primary out come was time to events of composite of death from any cause, acute coronary syndrome (ACS) and symptomatic arrhythmia during 3-year follow-up. We also compared the effect of each CCB on the control of angina symptoms. Results: There was no difference of the primary outcome among the two groups with a cumulative incidence rate of 5.4%, 2.9%, and a person-month incidence rate of 2.33 and 1.26, respectively (hazard ratio [HR], 0.54; 95% confidence interval [CI], 0.25 to 1.17; p = 0.120, as reference with the 1st generation CCBs). The incidence of ACS was significantly lower in 2nd generation CCBs group with a person-month incidence rate of 1.66 vs. 0.35 (HR, 0.22; 95% CI, 0.05 to 0.89; p = 0.034). Use of benidipine showed a significant better control of angina symptom compared with diltiazem for 3 years (odds ratio, 0.17; 95% CI, 0.09 to 0.32; p < 0.0001 at 3rd year). Conclusions: The first and second generation CCB groups did not differ in terms of composite outcome occurrence. However, the ACS incidence rate was signifi cantly lower in the users of the 2nd generation CCBs.

Background: Endothelial dysfunction is a predictor of atherosclerotic cardiovascular disease (ASCVD) and plays an important role in vasospastic angina (VA). Objectives: This study evaluated whether flow-mediated dilation (FMD) is also a good marker of 10-year ASCVD risk (10Y-ASCVDR) in patients with VA. Methods: Based on their clinical history and coronary artery diameter stenosis (DS), patients were retrospectively enrolled into VA (DS Results: Each group contained 50 patients. The 10Y-ASCVDR was significantly higher in the sCAD group than in the VA and mCAD groups (10.86 ± 7.30, 4.71 ± 4.04, and 4.77 ± 4.30, respectively, p < 0.001). The FMD was significantly higher in the mCAD group than in the VA and sCAD groups (6.37 ± 4.25, 3.10 ± 2.23, and 3.07 ± 1.89, respectively, p < 0.001). A significant correlation was found between the FMD and 10Y-ASCVD in the mCAD group (r = −0.622, p < 0.001) and the sCAD group (r = −0.557, p < 0.001) but not in the VA group (r = −0.193, p = 0.179). After adjusting for potential confounders such as BMI, C-reactive protein, maximal coronary stenosis, and brachial-ankle pulse wave velocity, multivariate analysis showed that FMD was independently associated with 10Y-ASCVDR in all patients. However, when looking only at the VA group, FMD did not correlate independently with 10Y-ASCVDR. Conclusions: Unlike mCAD and sCAD, we found no correlation between 10Y-ASCVDR and endothelial function in VA. Thus, our results support that FMD is not a good marker of atherosclerotic cardiovascular risk in VA.

Background and aim We report a case of a 39-year-old lady presenting with worsening angina. Materials and methods This is a case report study. Clinical case data was retrieved from hospital paper and electronic records. Results Invasive coronary angiography revealed disease in the left main stem, proximal left anterior descending (LAD) artery and circumflex artery. The patient proceeded to on-pump coronary artery bypass grafting. Intraoperatively, there were multiple unsuccessful attempts to wean off cardiopulmonary bypass. An on-table angiogram-which initially triggered asystole requiring internal cardiac massage and institution of venoarterial extracorporeal membrane oxygenation (ECMO)- showed no native coronary artery disease. Instead, this angiogram revealed severe vasospasm with narrowing in the grafts and distal LAD. The patient received calcium channel blockers and bilateral thoracic sympathectomies to suppress any further coronary vasospasm. She was subsequently successfully weaned off ECMO. Discussion and conclusion This case reveals the life-threatening nature and diagnostic dilemma posed by severe multivessel coronary vasospasm. We also highlight the novel role of thoracic sympathectomy for definitive management of refractory vasospastic angina.

Kounis syndrome is a rare type of acute coronary syndrome caused by coronary spasm with or without atherosclerotic plaque erosion or rupture due to inflammatory factors released by allergic reactions. Due to a lack of awareness, Kounis syndrome is often underdiagnosed. Here, we for the first time report a case of Kounis syndrome induced by anisodamine. A 48-year-old woman presented with upper abdominal pain and vomiting after eating. She was diagnosed with gastrointestinal spasm and intramuscularly injected with 10 mg anisodamine. The patient subsequently developed chest pain and hypotension with erythematous rash. A systemic allergic reaction was diagnosed. Saline solution, promethazine and dexamethasone were administered immediately. A 12-lead electrocardiogram indicated ST-segment elevation in II, III and aVF leads. Emergent coronary angiography was recommended. According to a preoperative electrocardiogram, the ST-segment elevation in the II, III and aVF leads had disappeared. Coronary angiograph revealed no significant coronary stenosis. The patient was diagnosed with Kounis syndrome induced by anisodamine, showing acute ST-segment elevation myocardial infarction due to allergic coronary vasospasm. During the 9-month follow-up, the patient did not receive further anisodamine injections and remained free of chest pain. In conclusion, it is essential for clinicians to be aware of Kounis syndrome because of the wide range of triggers and its potentially fatal evolution if not identified in time.

Coronary artery vasospasms have been known to cause episodic angina pectoris, along with ST-T wave changes. In addition, vasospasm if prolonged can cause myocardial ischemia leading to malignant arrhythmias such as ventricular fibrillation and ventricular tachycardia resulting in sudden cardiac death (SCD). Treatment for this disorder can be challenging. Current data is lacking on the management of patients receiving appropriate vasodilator medications who present with Ventricular Fibrillation (VFib) as a consequence of coronary artery vasospasms. We present a case of a 71-year-old man who was hospitalized due to recurrent episodes of coronary vasospasms leading to acute decompensation and VFib with subsequent resuscitation while undergoing cardiac catheterization. We also provide review of the literature and updates on the current guidelines from the American Heart Association on this potentially life-threatening disorder.

BACKGROUND An association between early repolarization and ventricular fibrillation has recently been reported in patients with vasospastic angina (VSA). However, no studies have clarified whether the presence of early repolarization can predict VSA. METHODS Participants comprised 286 patients (136 males) with clinically suspected VSA who underwent intracoronary provocation tests using acetylcholine or ergonovine. Patients were divided into a VSA group [n = 94, positive provocation test as induction of coronary arterial spasm (>90% stenosis)] and a non-VSA group (n = 192). Detailed early repolarization data were compared between groups. RESULTS The VSA group showed a higher frequency of smokers (28.7%) than the non-VSA group (17.2%; P = 0.02). On baseline 12-lead ECG, early repolarization (defined as a J-point elevation ≥0.1 mV from baseline in both or either of inferolateral leads) was found in 39 patients (inferior leads, n = 27; inferolateral leads, n = 12). Early repolarization was found more frequently in the VSA group (28.7%) than in the non-VSA group (6.2%, P

Background Thyroid storm is a rare condition with well-known cardiovascular manifestations including tachycardia, atrial fibrillation, heart failure, and myocardial infarction (MI). Several uncommon conditions that can mimic MI are associated with thyrotoxicosis and discussed in this case. Case summary A 23-year-old previously healthy male presented after the onset of generalized weakness and inability to rise from bed in the setting of 35 kg of unintentional weight loss, and was found to have profound hypokalaemia, elevated thyroid hormone, and suppressed thyroid-stimulating hormone consistent with thyrotoxicosis secondary to Grave’s disease. Following hospital admission, he developed worsening tachycardia with dynamic anteroseptal ST-segment elevations and elevated cardiac biomarkers concerning for MI. He was treated with aspirin, ticagrelor, and a heparin infusion, but was unable to tolerate beta-blockade acutely due to hypotension. Echocardiography demonstrated a severely dilated left ventricle (left ventricular end-diastolic volume index 114 mL/m2) and severely reduced systolic function (ejection fraction 23%) with global hypokinesis. Following initiation of propylthiouracil, iodine solution, and stress-dosed steroids his tachycardia and ST-elevations resolved. Computed tomography (CT) coronary angiography demonstrated no evidence of coronary stenosis. He was discharged on methimazole, metoprolol, and lisinopril and found to have recovered left ventricular systolic function at 2-month follow-up. Discussion Thyrotoxicosis can rarely cause coronary vasospasm, stress cardiomyopathy, and autoimmune myocarditis. These conditions should be suspected in hyperthyroid patients with features of MI and normal coronary arteries. Workup should include laboratory evaluation, electrocardiography (ECG), echocardiography, and non-invasive or invasive ischaemic evaluation.

Hypoxic coronary vasospasm may lead to myocardial ischaemia and cardiac dysfunction. Inosine 3′,5′‐cyclic monophosphate (cIMP) is a putative second messenger to mediate this pathological process. Nevertheless, it remains unclear as to whether levels of cIMP can be regulated in living tissue such as coronary artery and if so, what is the consequence of this regulation on hypoxia‐induced vasoconstriction. In the present study, we found that cIMP was a key determinant of hypoxia‐induced constriction but not that of the subsequent relaxation response in porcine coronary arteries. Subsequently, coronary arteries were treated with various phosphodiesterase (PDE) inhibitors to identify PDE types that are capable of regulating cIMP levels. We found that inhibition of PDE1 and PDE5 substantially elevated cIMP content in endothelium‐denuded coronary artery supplemented with exogenous purified cIMP. However, cGMP levels were far lower than their levels in intact coronary arteries and lower than cIMP levels measured in endothelium‐denuded coronary arteries supplemented with exogenous cIMP. The increased cIMP levels induced by PDE1 or PDE5 inhibition further led to augmented hypoxic constriction without apparently affecting the relaxation response. In intact coronary artery, PDE1 or PDE5 inhibition up‐regulated cIMP levels under hypoxic condition. Concomitantly, cGMP level increased to a comparable level. Nevertheless, the hypoxia‐mediated constriction was enhanced in this situation that was largely compromised by an even stronger inhibition of PDEs. Taken together, these data suggest that cIMP levels in coronary arteries are regulated by PDE1 and PDE5, whose inhibition at a certain level leads to increased cIMP content and enhanced hypoxic constriction.

Background Coronary vasospasm is primarily characterized by transient and reversible vasoconstriction causing myocardial ischaemia and can manifest with various clinical features, including syncope. Case summary A 50-year-old man presented with recurrent episodes of syncope for 3 days. The last syncope history occurred during an early morning walk, accompanied by dizziness and loss of consciousness. There was no clear history of chest pain at the time. He smoked one pack of cigarettes daily and frequently consume alcohol. Approximately 3 h after admission, echocardiography initially revealed normal systolic function; however, during the examination, the patient suddenly complained of dizziness and regional wall motion abnormalities (RWMA) of the left anterior descending artery (LAD) territory were observed. Both RWMA and dizziness spontaneously improved within a few minutes. Emergency coronary angiography (CAG) was performed to confirm vasospasm. Coronary angiography revealed mild atherosclerosis of proximal LAD. After 3 min, he complained of dizziness and vague chest discomfort, and electrocardiogram revealed ST-segment elevation. We immediately performed angiography of the left coronary artery, and CAG revealed total occlusion of the proximal LAD without any provocation. After administration of intracoronary nitroglycerine, coronary flow was restored completely and ST-segment deviation normalized along with relief in chest discomfort. The patient’s symptoms have not recurred for 3 months while being on calcium channel blocker and long-acting nitrates. Discussion Coronary vasospasm can present as transient and dynamic myocardial ischaemia along with angina. Coronary vasospasm should always be considered in the differential diagnosis for syncope.

Coronary angiography (CAG) sometimes shows nonobstructive coronary arteries in patients with suspected angina or acute coronary syndrome (ACS). The high prevalence of nonobstructive coronary artery disease (CAD) in those patients has recently been reported not only in Japan but also in Western countries, and is clinically attracting attention. Coronary spasm is considered to be one of the leading causes of both suspected stable angina and ACS with nonobstructive coronary arteries. Coronary spasm could also be associated with left ventricular dysfunction leading to heart failure, which could be improved following the administration of calcium channel blockers. Because we rarely capture spontaneous attacks of coronary spasm with electrocardiograms or Holter recordings, an invasive diagnostic modality, acetylcholine (ACh) provocation test, can be useful in detecting coronary spasm during CAG. Furthermore, we can use the ACh-provocation test to identify high-risk patients with coronary spasm complicated with organic coronary stenosis, and then treat with intensive care. Nonobstructive CAD includes not only epicardial coronary spasm but also microvascular spasm or dysfunction that can be associated with recurrent anginal attacks and poor quality of life. ACh-provocation test could also be helpful for the assessment of microvascular spasm or dysfunction. We hope that cardiologists will increasingly perform ACh-provocation test to assess the pathophysiology of nonobstructive CAD.

Coronary spasm is an established cause for angina pectoris. Ethnic differences have been suggested among Asian compared to Caucasian patients regarding prevalence, gender distribution, and angiographic patterns of coronary spasm. The aim of this study was to compare contemporary German and Japanese patients with coronary spasm. Between 2011 and 2015, 149 patients with resting angina and unobstructed coronary arteries with acetylcholine-induced epicardial spasm were enrolled in Stuttgart, Germany (n = 69) and Sendai, Japan (n = 80). All patients underwent intracoronary acetylcholine testing according to a standardized protocol. Comprehensive analysis included type of spasm (focal/diffuse), dose of acetylcholine leading to spasm, and frequency of multivessel spasm. Patients in this study were 61 ± 11 years old, predominantly female (54%), and had normal left ventricular ejection fraction (73 ± 9%). Diffuse spasm was the most prevalent type of spasm (85%) whereas focal spasm was found in the remaining 15% of patients. 31% of patients had multivessel spasm. Comparing the German with the Japanese patients, distribution of spasm type (focal/diffuse, p = 0.19) and frequency of multivessel spasm (p = 0.22) were comparable. Moreover, when Japanese patients were compared with German patients and diffuse spasm with focal spasm patients, respectively, no significant differences were observed regarding the acetylcholine dose required to induce spasm (p = 0.078 and p = 0.46, respectively). In conclusion, diffuse epicardial coronary spasm is the most frequent finding among German and Japanese patients with resting angina, unobstructed coronary arteries, and epicardial spasm on acetylcholine testing. Japanese and German patients share several similarities including comparable types of spasm and frequency of multivessel spasm.

Autonomic nerve system and endothelial function play important roles in vasospastic angina. Elevated heart rate (HR), blood pressure (BP), and double product (DP) can increase endothelial-dependent coronary artery dilation and blood flow. However, the impact of HR, BP, and DP on occurrence and severity of VSA in the clinical setting is unclear.A total of 170 patients undergoing intracoronary acetylcholine (ACh) provocation test during hospitalisation was included. Resting HR, BP, and DP were measured at least four times, and their variabilities were evaluated by standard deviations (SD) and coefficient of variations (CVs). Angiographic coronary artery vasospasm was defined as total or subtotal occlusion induced by ACh provocation.Mean±SD HR (65.7±9.1 vs 69.6±7.9 beats per minute; p=0.003), systolic BP (122.3±13.4 vs 127.7±14.6 mmHg; p=0.01), and DP (8,001±1,229 vs 8,903±1,495; p0.001) were significantly lower in patients with a positive ACh test than the counterpart, whereas SD and CV of both HR and systolic BP were not significantly different between the two groups. Mean HR, BP, and DP progressively decreased with increase in the number of vessels with angiographic vasospasm. Multivariate analysis showed current smoking and lower DP as independent predictors of the greater number of vessels with provoked angiographic vasospasm.Resting HR, BP, and DP were lower in patients with vasospastic angina, especially in those with severe vasospasm.

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. 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. 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. 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.

This study sought to obtain large-scale evidence supporting the clinical usefulness of ergonovine echocardiography.The role of noninvasive ergonovine provocation testing with echocardiographic monitoring of ventricular wall motion (ergonovine echocardiography) needs to be defined.Clinical data of patients who underwent ergonovine echocardiography in 3 tertiary referral hospitals in South Korea were analyzed.Ergonovine echocardiography was performed in 14,012 patients (mean age 52.8 ± 11.1 years; 6,213 [44.3%] women) after exclusion of significant coronary arterial stenosis by functional (treadmill or perfusion scan, n = 9,824) or anatomic test (invasive or computerized tomographic coronary angiography, n = 4,188). Premature termination developed in 0.4% (n = 51), and a positive result was observed in 2,144 patients (15.3%), with variable frequencies according to the diagnosis (acute coronary syndrome [38.2%], variant angina [31.8%], effort angina [14.9%], aborted sudden cardiac death [17.6%], syncope [9.9%]). There was no mortality or development of myocardial infarction during the test. During median follow-up of 11.4 (interquartile range: 7.2 to 15.8) years, death of any cause and cardiovascular death occurred in 494 and 143 patients, respectively. The 10-year overall (96.7 ± 0.2% vs. 91.5 ± 0.6%; p 0.0001) and cardiovascular mortality-free (99.2 ± 0.1% vs. 96.7 ± 0.4%; p 0.0001) survival rates were lower in patients with positive ergonovine echocardiography. Regarding patients with positive test results, the functional test group and the anatomic test group did not show a significant difference in the survival rates. After adjustment of age and male sex, a positive test was an independent risk factor associated with all-cause mortality (hazard ratio: 1.879, 95% confidence interval: 1.548 to 2.280; p 0.001) and cardiovascular death (hazard ratio: 2.903, 95% confidence interval: 2.061 to 4.089; p 0.001).Ergonovine echocardiography for coronary vasospasm diagnosis could be safely performed even without angiographic documentation of fixed coronary stenosis depending on the clinical presentation, and provided important prognostic implication. Ergonovine echocardiography can replace the invasive spasm provocation testing, which has been overlooked unfairly.

A 75-year-old man was admitted for repeat ablation of atrial fibrillation. At 30 min after infusion of 3.5 ml of ethanol into the vein of Marshall, inferior ST-segment elevation with coronary arterial vasospasm was observed. This is the first report of coronary vasospasm after chemical ablation of the vein of Marshall. (Level of Difficulty: Intermediate.), Graphical abstract, A 75-year-old man was admitted for repeat ablation of atrial fibrillation. At 30 min after infusion of 3.5 ml of ethanol into the vein of Marshall, inferior…

Marijuana is the most widely used recreational drug across the United States. Ongoing efforts to legalize marijuana, as well as the drug's increasing popularity contribute to the marijuana's reputation as having a low risk profile. Marijuana's association with adverse cardiovascular events, such as arrhythmia and vasospasm is well-documented. We synthesized what is known about how marijuana use pertains to and is implicated endothelial cell damage and its effects on microcirculation. THC exerts effects through the cannabinoid receptors, CB1 and CB2. The downstream effects of CB1 activation point to a role for this receptor in atherogenesis and vasospasm, likely by precipitating oxidative stress. Endothelial cells, when exposed to reactive oxygen species, provide a stimulus for vasoconstriction with a diminished ability for vasodilation. This phenomenon has manifested itself in cases of coronary vasospastic angina, and coronary slow and no flow that have resulted from marijuana use, as confirmed by cardiac catheterization reports that showed no evidence of obstructive lesions that could otherwise be responsible for the patients' symptoms. Marijuana users suffer from acute ischemic stroke at higher rates than non-users. Several theories have been proposed to support this observation, namely marijuana induced reversible cerebral vasoconstriction syndrome, and mitochondrial damage caused by oxidative stress that disproportionately affects cerebral vasculature. As marijuana use continues to grow, so does the important of elucidating the drug's effect on endothelial cells and microcirculation. Further studies should investigate the temporal association between marijuana and endothelial damage, as well as the possibility of recovery from such injury, and whether there is therapeutic potential in cannabinoid receptors.

With the rise of the number of states fully legalizing marijuana, the use of this substance in the United States is at an all-time high. This increasing legalization gives the impression that marijuana is rather safe. However, multiple reports by our groups and others documented serious cardiovascular complications associated with marijuana use ranging from life threatening arrhythmia to myocarditis and myocardial infarction. In this report, we present a case of a 61 year old man presented with left sided typical chest pain shortly after marijuana consumption with the diagnosis of non ST-elevation myocardial infarction (NSTEMI) established based on clinical, EKG and troponin values with eventual cardiac catheterization documenting non-occlusive coronary artery disease with 30% obstruction of the proximal first obtuse marginal artery. We also review the putative pathophysiologic mechanisms of marijuana induced coronary vasospasms, highlighting the implications of these findings in the evaluation and management of cardiac chest pain in marijuana users.

Objectives The aim of this study was to investigate the prognosis of a large cohort of patients with stable angina and unobstructed coronaries undergoing acetylcholine spasm testing. Background Coronary artery spasm can be found in up to 60% of patients with symptoms of myocardial ischemia despite unobstructed coronary arteries. Methods Consecutive symptomatic patients with unobstructed coronary arteries undergoing acetylcholine testing to detect epicardial or microvascular coronary spasm were prospectively enrolled. After a median follow-up period of 7.2 years (6.5 to 7.9 years), data regarding mortality, nonfatal myocardial infarction, stroke, repeat coronary angiography, recurrent symptoms, and quality of life were obtained in 736 patients (57% women, mean age 62 ± 12 years). Results In total, 55 deaths (7.5%), 8 nonfatal myocardial infarctions (1.4%), and 12 strokes (2.2%) occurred during the follow-up period. Recurrent symptoms were reported by 64% of patients, and repeat coronary angiography was performed in 12% of cases. Multivariate analysis revealed epicardial spasm as a predictor of nonfatal myocardial infarction (hazard ratio: 14.469; 95% confidence interval: 1.735 to 120.646) and repeat angiography (hazard ratio: 1.703; 95% confidence interval: 1.062 to 2.732), whereas patients with microvascular spasm more often had recurrent angina at follow-up (hazard ratio: 1.311; 95% confidence interval: 1.013 to 1.697). Conclusions In this long-term follow-up study, the overall prognosis of patients with coronary spasm was favorable. Patients with epicardial spasm were at increased risk for myocardial infarction and repeat angiography, while microvascular spasm was associated with recurrent angina. Acetylcholine testing may help identify patients at increased risk for adverse cardiac events among this overall low-risk population.

5-Fluorouracil (5-FU) is a chemotherapeutic agent frequently used for the treatment of solid tumors. In a few cases, 5-FU can be associated with coronary vasospasm, cardiac ischemia, or life-threatening arrhythmias. Recognition of 5-FU cardiotoxicity is clinically important as after the rapid sensation of therapy, cardiotoxicity can be completely reversible, and on the other hand, readministration may lead to serious damage of the heart and even death. A 70-year-old male came to the emergency department (ED) with chest pain which started while receiving an infusion of 5-FU. The patient did not have a personal history or risk factors of coronary artery disease and his electrocardiogram (ECG) before starting chemotherapy was completely normal. In the ED, his ECG had ischemic changes, troponin was elevated, and echocardiogram showed anterior wall hypokinesis. However, emergent coronary angiogram did not reveal any acute coronary occlusion. 5-FU-induced cardiotoxicity was suspected; the patient was admitted to a progressive care unit for close monitoring and infusion of calcium channel blockers was initiated. The patient’s symptoms and ECG findings gradually resolved, and two days later on discharge, patient was chest pain free and ECG was normal. This case supports the vasospastic hypothesis of 5-FU cardiac toxicity, describes its clinical course, and emphasizes the importance of better awareness and early recognition of the rare side effect as it may allow physicians to reduce the risk of life-threatening complications.