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The implantable loop recorder (ILR) is a small device used to monitor the electrical activity of the heart by recording a single‑lead bipolar electrocardiograph signal over a long period of time. The ILR is a valid diagnostic tool but has been vastly underused. In addition to arrhythmia, the ILR may be a useful tool for the detection of repolarization disorders in patients with myocardial ischemia.

In a patient with variant angina of the proximal left anterior descending coronary artery, myocardial ischemia changed the QRS-ST-T configurations without J-waves into those resembling “lambda” waves at maximal ST-segment elevation, and couplets or triplets of supraventricular extrasystole (SVE) changed the ischemia-induced “lambda” waves into QRS-ST-T configurations resembling a “tombstone” morphology or “monophasic QRS-ST complex.” At the resolution phase of coronary spasm, the QRS-ST-T configurations returned to those without J-waves and were changed by SVE into “lambda” waves. Interestingly, neither ischemia- nor SVE-induced “lambda” waves or SVE-induced “tombstone” morphology or “monophasic QRS-ST complex” were complicated by ventricular tachyarrhythmia.

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.

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

We report on an interesting case of resuscitated sudden cardiac death (SDC) in a 51-year-old with hypertension and positive family history for SDC. The patient was resuscitated and an emergency angiogram ruled out coronary artery disease. Cardio-MRT ruled structural disease or infection. Holter and telemetry monitoring revealed premature ventricular complexes and transient ST-changes followed by anginaepisodes in correlation with the use of the nicotine-replacement-spray. The patient was urged to quit smoking and smoking-substitutes. Medical therapy with calcium-channelblocker and a long acting nitrate was administered. One-month follow up reported no arrhythmic or angina events.

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.

Objective Although the importance of evidence-based optimal medical therapy (OMT) after acute myocardial infarction (AMI) has been recognized, the prescription rate of OMT is not sufficiently high in real-word clinical settings. The purpose of this study was to identify the clinical characteristics of AMI patients who did not receive OMT. Methods The present study was a retrospective study. OMT was defined as the combination of antiplatelet therapy, angiotensin-converting enzyme (ACE) inhibitors/angiotensin II receptor blockers (ARBs), beta-blockers, and statins at the time of hospital discharge. Non-OMT was defined as the lack of either antiplatelet therapy, ACE inhibitors/ARBs, beta-blockers, or statins. Results A total of 457 AMI patients were included as the final study population, and 98 patients (22.4%) lacked at least 1 OMT medication. The prescription rates of antiplatelet therapy, ACE inhibitors/ARBs, beta-blockers, and statins were 98.7%, 87.5%, 90.4%, and 96.7%, respectively. In the multivariate logistic regression analysis, age [per 1-year increase: odds ratio (OR) 1.033, 95% confidence interval (CI) 1.007-1.059, p=0.014], hemodialysis (vs. no hemodialysis: OR 2.707, 95% CI 1.082-6.774, p=0.033), estimated glomerular filtration rate

Background Chronic vasodilator therapy with long‐acting nitrate is frequently used to treat vasospastic angina. However, the clinical benefits of this approach are controversial. We investigated the prognostic impact of vasodilator therapy in patients with vasospastic angina from the multicenter, prospective VA‐KOREA (Vasospastic Angina in KOREA) registry. Methods and Results We analyzed data from 1895 patients with positive intracoronary ergonovine provocation test results. The patients were divided into 4 groups: no vasodilator (n=359), nonnitrate vasodilator (n=1187), conventional nitrate (n=209), and a combination of conventional nitrate and other vasodilators (n=140). The primary end point was a composite of cardiac death, acute coronary syndrome, and new‐onset arrhythmia at 2 years. Secondary end points were the individual components of the primary end point, all‐cause death, and rehospitalization due to recurrent angina. The groups did not differ in terms of the risk of the primary end point. However, the acute coronary syndrome risk was significantly higher in the conventional nitrate (hazard ratio [HR], 2.49; 95% CI, 1.01–6.14; P =0.047) and combination groups (HR, 3.34; 95% CI, 1.15–9.75, P =0.027) compared with the no‐vasodilator group, as assessed using the inverse probability of treatment weights. Subgroup analyses revealed prominent adverse effects of nitrate in patients with an intermediate positive ergonovine provocation test result and in those with low Japanese Coronary Spasm Association scores. Conclusions Long‐acting nitrate‐based chronic vasodilator therapy was associated with an increased 2‐year risk of acute coronary syndrome in patients with vasospastic angina, especially in low‐risk patients.

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.

A 54-year-old Japanese woman was admitted to our ward because of recurrent chest pain at rest for 2 months. She had been treated with nivolumab, an immune checkpoint inhibitor for inoperable advanced hypopharyngeal cancer for 21 months. She had no chest pain after cessation of nivolumab treatment. Cardiac catheterization confirmed the presence of vasospastic angina. Benidipine 8 mg was started, and she had no chest pain even after resuming therapy with nivolumab. Vasospastic angina is an adverse effect of nivolumab.

Introduction Since Prinzmetal first described a "variant" form of angina pectoris, with predominantly resting episodes of pain and cyclic severity variations, it has gradually become apparent that this clinical presentation is caused by episodes of coronary artery spasm (CAS) involving focal or diffuse changes in large and/or small coronary arteries in the presence or absence of "fixed" coronary artery stenoses. However, most clinicians have only limited understanding of this group of disorders. Areas covered We examine the clinical presentation of CAS, associated pathologies outside the coronary vasculature, impediments to making the diagnosis, provocative diagnostic tests, available and emerging treatments, and the current understanding of pathogenesis. Expert opinion CAS remains a poorly understood, often debilitating and substantially under-diagnosed condition, which occurs more frequently in women than in men, and is poorly correlated with all conventional coronary risk factors except smoking. Many patients presenting with CAS crises have non-diagnostic ECGs and normal serum troponin concentrations, but CAS can be suspected on the basis of history and association with migraine, Raynaud's phenomenon and Kounis syndrome. Definitive diagnosis requires provocative testing at coronary angiography. Treatment still centres around the use of calcium antagonists, but with greater understanding of pathogenesis, new management options are emerging.

Background Vasospastic angina (VSA) is reportedly associated with several clinical characteristics such as smoking and high-density lipoprotein (HDL) cholesterol, in which gender differences are present. For instance, smoking rates among men are higher than those among women, and a normal range of HDL cholesterol differs across genders. However, their impact between men and women on VSA is unclear. Methods A total of 797 patients (427 men and 370 women) undergoing intracoronary acetylcholine (ACh) provocation test to diagnose VSA were included. The positive ACh provocation test was defined as angiographic vasospasm accompanied by chest pain and/or ischemic electrocardiographic changes. Factors contributing to VSA across genders were evaluated by multivariable analyses. Results Of 797 patients, 414 (51.9%) had positive ACh provocation test. The incidence of positive ACh test was higher in men than in women (56.9% vs. 46.2%, p = 0.003). In the entire study population, current smoking and a lower HDL cholesterol level were determined as factors associated with VSA. In both men and women, an HDL cholesterol level was identified as a factor contributing to positive ACh test. Conclusions Among patients suspected for VSA, men as compared with women were more likely to have positive ACh provocation test. While current smoking and an HDL cholesterol level were associated with VSA in the entire study population, a lower HDL cholesterol level was determined as the only factor contributing to positive ACh test across genders, suggesting that HDL cholesterol plays important roles in the mechanism of VSA.

Current problems of Prinzmetal angina (vasospastic angina, variant angina) considers in this review. Attention is drawn to early diagnosis, which should be comprehensive, taking into account possible atypical courses and the development of complications. The important role of electrocardiographic monitoring (including using implantable recorders) is highlighted. It is emphasized that patients with cardiac arrhythmias, syncope are at high risk of developing sudden cardiac death. In this category of patients, it is recommended to timely determine the indications for implantation of a cardioverter - defibrillator. Authors consider the prospects of using new methods of treatment of angina pectoris.В обзоре рассмотрены актуальные проблемы стенокардии Принцметала (вазоспастическая стенокардия, вариантная стенокардия). Обращается внимание на своевременную диагностику, которая должна быть комплексной с учетом возможного атипичного течения и развития осложнений. Освещается важная роль электрокардиографического мониторирования (в том числе с использованием имплантируемых рекодеров). Подчеркивается, что больные с нарушением ритма сердца, синкопой находятся в группе высокого риска развития внезапной сердечной смерти. Данной категории больных рекомендуется своевременно определять показания к имплантации кардиовертера - дефибриллятора. Авторы анализируют перспективы применения новых методов лечения вариантной стенокардии.

Anti-platelet agents are commonly used in vasospastic angina (VA) patients with comorbidity like coronary artery disease. However, long-term clinical outcomes in the use of aspirin, clopidogrel or the two agents together have rarely been investigated in VA patients. In a prospective study, we enrolled 2960 patients who received coronary angiography and ergonovine provocation test at 11 university hospitals in Korea. Among them, 1838 patients were diagnosed either with definite (n = 680) or intermediate (n = 1212) VA, using the criteria of chest pain, ECG changes and ergonovine provocation test results. They were analyzed according to their use of aspirin, clopidogrel or both, or no anti-platelet agent at all. The primary outcome was time to composite events of death from any cause, acute coronary syndrome (ACS) and symptomatic arrhythmia during a 3-year follow-up. A primary composite outcome was significantly more common in the aspirin plus clopidogrel group, at 10.8% (14/130), as compared with the non-antiplatelet group, at 4.4% (44/1011), (hazard ratio [HR] 2.41, 95% confidence interval [CI], 1.32–4.40, p = 0.004). With regard to the person-time event rate, similar results were shown, with the highest rate in the aspirin plus clopidogrel user at 4.72/1000 person months (95% CI, 2.79–7.96, log-rank test for primary outcome p = 0.016). The person-time event of the ACS rate was also highest in that group, at 2.81 (95% CI, 1.46–5.40, log-rank test for ACS p = 0.116). Kaplan-Meier survival analysis demonstrated poor prognosis in primary outcomes and ACS in aspirin plus clopidogrel users (log-rank test, p = 0.005 and p = 0.0392, respectively). Cox-proportional hazard regression analysis, adjusting for age, sex, history of coronary heart disease, hypertension, diabetes, presence or not of definite spasm, use of calcium channel blocker, demonstrated that the use of aspirin plus clopidogrel is an independent risk for the primary outcome (HR 2.01, CI: 1.07–3.81, p = 0.031). The aspirin-alone group had a similar primary and individual event rate compared to the no-antiplatelet agent group (HR 0.96, CI, 0.59–1.55, p = 0.872). Smokers using aspirin plus clopidogrel had poorer outcomes than non-smokers, with HR 6.36 (CI 2.31–17.54, p = 0.045 for interaction). In conclusion, among VA patients, aspirin plus clopidogrel use is associated with a poor clinical outcome at 3 years, especially in ACS. Aspirin alone appears to be safe for use in those patients.

Background Japanese Circulation Society (JCS) guidelines do not include adolescents with coronary artery spasm.Methods and Results:We recruited 18 adolescents less than 20 years old with vasospastic angina (VSA): 11 were Japanese and 3 had chest symptoms for >12 months before admission. ST-segment elevation was observed in 11 patients and none of the 18 patients had a fixed stenosis. Spasm provocation tests were performed in 9 patients and two-thirds had multiple spasms; 6 suffered from acute myocardial infarction and ventricular fibrillation occurred in 2 patients; 1 patient died and the remaining 17 patents survived. Conclusions Clinical status of adolescents with VSA was as severe as in adults with refractory VSA. Cardiologists should cooperate with pediatricians to diagnose and treat adolescents with VSA. There is a need to establish the additional issues for adolescents with coronary spasm in the JCS guidelines.

ST-segment elevation (STE) and an increased Tpeak-Tend interval (Tp-e) have prognostic value for malignant arrhythmia events (MAEs) in patients with ST-segment elevation myocardial infarction (STEMI) and Brugada syndrome. Whether STE could predict MAEs and has an electrophysiological relationship with Tp-e in electrocardiogram (ECG) of vasospastic angina (VA) patients needs to be elucidated.Sixty-five patients with VA and 23 patients with VA complicated by MAEs were enrolled. The relationship of ECG parameters and MAEs (defined as ventricular tachycardia/ventricular fibrillation (VT/VF), syncope, and aborted sudden death) was analyzed by t-test, regression and receiver operating characteristic (ROC) curve analyses.Patients with MAEs showed greater STE (P0.001) and corrected QT dispersion (cQTd) (P=0.021), a longer corrected Tp-e interval (cTp-e) (P0.001), and a larger Tp-e/QT ratio (P0.001) than those in non-MAE groups. Univariate analysis revealed that cQTd (odds ratio (OR)=1.065; P=0.020), cTp-e (OR=1.159; P=0.001), Tp-e/QT (OR=1.344, P=0.002), and STE (OR=5.655, P0.001) were significantly associated with MAEs. In the multivariate analysis, Tp-e/QT and STE remained predictors of MAEs. ROC curve analysis showed that the areas under curve (AUCs) for Tp-e/QT (AUC=0.944) and STE (AUC=0.974) were not significantly different (P0.05), but both were significantly different than AUCs for cQTd (AUC=0.724) and cTp-e (AUC=0.841) (all P0.05). STE was well fitted with the Tp-e/QT ratio in a multivariable linear regression model.STE and increased Tp-e/QT ratio had related electrophysiological properties and were independent prognostic indicators of MAEs in patients with VA.

Impaired glucose metabolism is associated with an increased risk of cardiovascular complications, and coronary artery spasm is thought to underlie the development of coronary artery disease. Intraday glucose variability (GV) accelerates oxidative stress and inflammatory cytokine release, but its impact on coronary artery spasm remains unclear. This study investigated the relationship between intraday GV and coronary artery spasm. The study included 50 patients with dysglycemia and suspected coronary spastic angina. GV was analyzed by 24-h monitoring of the blood glucose concentration using a flash glucose monitoring system. The mean amplitude of glycemic excursion (MAGE) was calculated as an index of GV. Coronary artery spasm was assessed using the intracoronary acetylcholine provocation test. Coronary spasm was defined as acetylcholine-induced total or subtotal coronary occlusion. Changes in vessel diameter in response to acetylcholine were evaluated with quantitative coronary angiography. Coronary artery spasms were observed in 21 patients (42%). MAGE was significantly higher in patients with spasms compared to those without spasms (127.5 ± 33.5 vs. 91.4 ± 37.6, p

Vasospastic angina (VSA) is a variant form of angina pectoris, in which angina occurs at rest, with transient electrocardiogram modifications and preserved exercise capacity. VSA can be involved in many clinical scenarios, such as stable angina, sudden cardiac death, acute coronary syndrome, arrhythmia or syncope. Coronary vasospasm is a heterogeneous phenomenon that can occur in patients with or without coronary atherosclerosis, can be focal or diffuse, and can affect epicardial or microvasculature coronary arteries. This disease remains underdiagnosed, and provocative tests are rarely performed. VSA diagnosis involves three considerations: classical clinical manifestations of VSA; documentation of myocardial ischaemia during spontaneous episodes; and demonstration of coronary artery spasm. The gold standard diagnostic approach uses invasive coronary angiography to directly image coronary spasm using acetylcholine, ergonovine or methylergonovine as the provocative stimulus. Lifestyle changes, avoidance of vasospastic agents and pharmacotherapy, such as calcium channel blockers, nitrates, statins, aspirin, alpha1-adrenergic receptor antagonists, rho-kinase inhibitors or nicorandil, could be proposed to patients with VSA. This review discusses the pathophysiology, clinical spectrum and management of VSA for clinicians, as well as diagnostic criteria and the provocative tests available for use by interventional cardiologists.

Background J waves may develop during coronary angiography (CAG). Patients and results Seven patients (61±6 years, 6 male) had vasospastic angina. ST-segment elevation and ventricular fibrillation were documented in all patients. CAG revealed normal arteries, but slurring or notching (J waves) with an amplitude of 0.20±0.06 mV appeared for the first time (n=6) or in an augmented manner (n=1) with distinct alterations in QRS morphology when contrast medium was injected into the right coronary artery. Conclusion In patients with vasospastic angina, J waves observed during CAG can be a manifestation of a local conduction delay caused by contrast medium-induced myocardial ischemia.

A 49-year-old man with a 25 pack-year history of tobacco abuse presented to our institution reported new onset severe left-sided chest pain. The patient experienced multiple episodes of chest pain which lasted for approximately 5 min each, radiating to left upper extremity. Symptoms occurred both

Coronary artery vasospasm, or Prinzmetal angina, remains a challenging diagnosis. Prinzmetal angina usually affects only one coronary vessel; however, in this case, it occurred simultaneously in three coronary arteries, and was totally relieved after nitrate administration.

We report the case of a 40-year-old man, transferred from another hospital to our ICU because of acute coronary syndrome. Coronarography did not show coronary stenosis. Twenty-four hours monitoring EKG allowed diagnosis of Prinzmetal angina and appropriate therapy was administered. Six months after discharge due recurrence of symptoms, ranolazine was added to therapy. After one year the patient is symptoms free.

Background: This study aimed to evaluate the effect of adenosine on epicardial coronary artery diameter during ergonovine provocation testing. Methods: A total of 158 patients who underwent an ergonovine provocation test with intracoronary adenosine injection between 2011 and 2014 were selected. Patients were divided into four groups based on the severity of percent diameter stenosis following intracoronary ergonovine administration: Group 1, induced spasm < 50%; Group 2, 50–89%; Group 3, 90–99%; and Group 4, total occlusion. Results: Spasm positivity was observed in 44 (27.8%) cases in the study population (mean age, 57.4 ± ± 10.7 years). Intracoronary adenosine increased the diameter of the ergonovine-induced epicardial artery by 0.51 ± 0.31 mm, 0.73 ± 0.39 mm, 0.44 ± 0.59 mm, and 0.01 ± 0.04 mm in Groups 1, 2, 3, and 4, respectively. Subsequent administration of nitroglycerin further increased vessel diameter by 0.49 ± 0.28 mm, 0.93 ± 0.68 mm, 2.11 ± 1.25 mm, and 2.23 ± 0.69 mm in Groups 1, 2, 3, and 4, respectively. The ratios of adenosine-induced diameter to reference diameter were significantly lower in patients with spasm positive results (0.68 [0.59–0.76] vs. 0.18 [0.00–0.41], p < 0.001 in the study population; 0.60 [0.54–0.67] vs. 0.40 [0.27–0.44], p < 0.001 in Group 2) with the best cut-off value of 0.505 (sensitivity 0.955, specificity 0.921). Conclusions: Intracoronary administration of adenosine dilated the ergonovine-induced vasoconstricted epicardial coronary artery. The ratio of adenosine-induced diameter to reference diameter was significantly lower in patients with spasm positive results.

We evaluated the effect of chronic exposure to air pollutants (APs) on coronary endothelial function and significant coronary artery spasm (CAS) as assessed by intracoronary acetylcholine (ACH) provocation test.A total of 6430 patients with typical or atypical chest pain who underwent intracoronary ACH provocation test were enrolled. We obtained data on APs from the Korean National Institute of Environmental Research (http://www.nier.go.kr/). APs are largely divided into two types: particulate matter with aerodynamic diameter of less than or equal to 10 µm in size (PM10) and gaseous pollutants such as nitrogen dioxide, sulfur dioxide, carbon monoxide, and ozone. The primary endpoint is the incidence of significant CAS and its associated parameters during ACH provocation test.The incidence of CAS was positively correlated with an exposure duration of PM10, whereas nitrogen dioxide, sulfur dioxide, carbon monoxide, and ozone were shown to be unrelated to CAS. During the ACH provocation test, as PM10 increased, the frequency of CAS was increased, and the incidence of transient ST-segment elevation was also increased. There was a trend toward higher incidence of spontaneous spasm as PM10 increased. The mean exposure level of PM10 was 51.3±25.4 µg/m. The CAS risk increased by 4% when the level of PM10 increased by 20 µg/m by an adjusted Cox regression analysis.CAS incidence is closely related to exposure to PMs but not to gaseous pollutants. Particularly, higher exposure concentrations and longer exposure duration of PM10 increased the risk of CAS. These important findings provide a plausible mechanism that links air pollution to vasospastic angina and provide new insights into environmental factors.

Background Variant angina (VA) is caused by reversible coronary artery spasm, which is characterized by chest pain with ST segment elevations on a standard 12-lead electrocardiogram (ECG) at rest. VA attack often causes lethal ventricular arrhythmia. The early repolarization (ER) pattern is associated with ventricular fibrillation (VF). However, whether the ER pattern is involved in VF in patients with VA is not known. We investigated the association between the ER pattern and VF in patients with VA. Methods Fifty patients underwent induction of ST elevation on 12-lead ECGs with total or nearly total occlusion by provocation test (VA patients). Twelve of these patients underwent induction of VF or had documented VF before hospital admission (VF occurrence group). The J-wave morphology was characterized as exhibiting notching or slurring. The amplitude of each J wave was measured manually with amplified waveforms. Results ER patterns were observed significantly more often in the VF occurrence group than in the non-VF occurrence group (P = 0.007). The J-wave amplitude was significantly higher in the VF occurrence group compared with the non-VF occurrence group (P = 0.02). Univariate analyses suggested that age, smoking, and ER patterns were associated with VF. Upon multivariate analyses, age (odds ratio [OR] = 0.880; 95% confidence interval [CI]: 0.794-0.975; P = 0.014) and ER patterns (OR = 8.937; 95% CI:1.661-48.06; P = 0.011) predicted VF independently. Conclusions These data suggest that an ER pattern in VA patients is a risk factor for VF. The ER pattern may be one of the useful factors for adaptation of implantation of implantable cardioverter-defibrillator in patients with coronary spasm-induced VF.

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.

Although coronary obstruction due to atherosclerosis is the most common cause of myocardial ischemia, a significant proportion of patients have myocardial ischemia in the absence of obstructive epicardial coronary artery disease (CAD). This finding is more common among women and alternative causes can mediate myocardial ischemia. Abnormalities in vascular structure, alterations in coronary vasomotion and dysfunction of the coronary microcirculation can all cause ischemia in the absence of obstructive CAD due to atherosclerosis. In this review, we provide an update on three alternative causes of myocardial ischemia: spontaneous coronary artery dissection (SCAD), vasospastic angina (VSA) and coronary microvascular dysfunction (CMVD). We review pathophysiology, clinical presentation, diagnosis, treatment and outcomes related to these important clinical entities. There is increasing interest in better defining this patient population with use of advanced imaging and testing tools. Despite the increased associated risk with future cardiac events, evidence-based treatments for these diagnoses remain under-studied and poorly defined. These alternative diagnoses should be kept in mind when evaluating women with myocardial ischemia without obstructive CAD due to atherosclerosis.

A 52-year-old man complaining of persistent recurring chest pain at night underwent coronary angiogram at another institution. Normal coronaries were observed and he was discharged with muscle spasmolytic prescription. Since symptoms had continued, 24-hour Holter monitoring was ordered at our facility and results revealed huge ST elevation and polymorphic ventricular tachycardia. Cold pressor test performed in catheterization laboratory also resulted in ventricular tachycardia. Nifedipine was prescribed and follow-up Holter monitoring revealed no further vasospastic episodes. Utility of 24-hour Holter rhythm monitoring and cold pressor test in patients with recurrent chest pain at night is demonstrated in this report.

Aims Coronary microvascular dysfunction and/or vasospasm are potential causes of ischaemia in patients with no obstructive coronary artery disease (INOCA). We tested the hypothesis that these patients also have functional abnormalities in peripheral small arteries. Methods and results Patients were prospectively enrolled and categorised as having microvascular angina (MVA), vasospastic angina (VSA) or normal control based on invasive coronary artery function tests incorporating probes of endothelial and endothelial-independent function (acetylcholine and adenosine). Gluteal biopsies of subcutaneous fat were performed in 81 subjects (62 years, 69% female, 59 MVA, 11 VSA, and 11 controls). Resistance arteries were dissected enabling study using wire myography. Maximum relaxation to ACh (endothelial function) was reduced in MVA vs. controls [median 77.6 vs. 98.7%; 95% confidence interval (CI) of difference 2.3–38%; P = 0.0047]. Endothelium-independent relaxation [sodium nitroprusside (SNP)] was similar between all groups. The maximum contractile response to endothelin-1 (ET-1) was greater in MVA (median 121%) vs. controls (100%; 95% CI of median difference 4.7–45%, P = 0.015). Response to the thromboxane agonist, U46619, was also greater in MVA (143%) vs. controls (109%; 95% CI of difference 13–57%, P = 0.003). Patients with VSA had similar abnormal patterns of peripheral vascular reactivity including reduced maximum relaxation to ACh (median 79.0% vs. 98.7%; P = 0.03) and increased response to constrictor agonists including ET-1 (median 125% vs. 100%; P = 0.02). In all groups, resistance arteries were ≈50-fold more sensitive to the constrictor effects of ET-1 compared with U46619. Conclusions Systemic microvascular abnormalities are common in patients with MVA and VSA. These mechanisms may involve ET-1 and were characterized by endothelial dysfunction and enhanced vasoconstriction. Clinical trial registration ClinicalTrials.gov registration is NCT03193294.

A 64-year-old man was resuscitated from out-of-hospital VF, and coronary spasm was provoked by ergonovine at catheterization. An ECG was analyzed before and after each intracoronary injection of drugs or contrast medium. The baseline ECG showed nondiagnostic J waves in leads II, III, and aVF, but administration of acetylcholine, contrast medium and nitroglycerin into the right coronary artery induced a distinct augmentation of J-wave amplitudes with changes in the QRS morphology. Transient ischemia induced by the intracoronary administration of these agents seemed to be the mechanism underlying the increase in J-wave amplitudes.

Prinzmetal’s angina occurs following spasms in a single or multiple vascular beds, resulting in a typical chest pain and an ST-segment elevation in electrocardiography (ECG). It can lead to life-threatening arrhythmias and sudden cardiac death. We describe a 37-year-old woman who was admitted with a typical chest pain and hypotension. Her initial ECG showed an ST-segment elevation in the inferior and precordial leads. She was transferred to the catheterization unit, where coronary angiography illustrated multivessel spasms. The spasms were relieved with a nitroglycerin injection. She was discharged with stable hemodynamics 7 days later, and at 1 month’s follow-up, no recurrent attack was detected.

Rationale: Carbon monoxide (CO) poisoning can cause severe damage to the nervous system, and can also cause serious damage to organs, such as the heart, kidneys, and lungs. CO damage to myocardial cells has been previously reported. This can lead to serious complications, such as myocardial infarction. Patient concerns: A 47-year-old female patient complained of sudden chest pain for 30 minutes. Before admission, the patient had non-radiating burning chest pain after inhalation of soot. Diagnosis: An electrocardiogram showed that myocardial ischemia was progressively aggravated, manifested by progressive ST-segment elevation, and accompanied by T wave inversion and other changes. No obvious coronary stenosis was observed in a coronary angiographic examination. Therefore, the patient was considered to have developed variant angina resulting from CO poisoning-induced coronary artery spasm. Interventions: The patient was treated with drugs for improving blood circulation and preventing thrombosis, and underwent hyperbaric oxygen therapy. Outcomes: Clinical symptoms relieved after the treatment. Lessons: Findings from this case suggest that CO can cause coronary artery spasm and it is one of the predisposing factors of variant angina. For these patients, hyperbaric oxygen therapy can improve blood circulation and prevent formation of thrombus and encephalopathy.

We report the case of a middle aged woman who was previously diagnosed with hypertension. She had been drinking a kelp concentrate solution daily for her hypertension instead of taking the prescribed medicine due to her personal beliefs about the kelp solution. As a consequence, she experienced vasospastic angina complicated by myocardial infarction and cardiogenic syncope resulting from iatrogenic thyrotoxicosis. Complementary medicine is widely used by the general population. However, there is still a lack of evidence regarding their efficacy and safety. This case shows that inadequate use of complementary medicine could have no effect and may even be harmful. In patients with chronic diseases such as hypertension, self-care in the form of life style modification, home blood pressure monitoring and medial adherence are important for disease management.

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 long-term prognosis of patients with variant angina presenting with aborted sudden cardiac death (ASCD) is unknown.The purpose of this study was to evaluate the long-term mortality and ventricular tachyarrhythmic events of variant angina with and without ASCD.Between March 1996 and September 2014, 188 patients with variant angina with ASCD and 1,844 patients with variant angina without ASCD were retrospectively enrolled from 13 heart centers in South Korea. The primary endpoint was cardiac death.Predictors of ASCD manifestation included age (odd ratio [OR]: 0.980 by 1 year increase; 95% confidence interval [CI]: 0.96 to 1.00; p = 0.013), hypertension (OR: 0.51; 95% CI: 0.37 to 0.70; p 0.001), hyperlipidemia (OR: 0.38; 95% CI: 0.25 to 0.58; p 0.001), family history of sudden cardiac death (OR: 3.67; 95% CI: 1.27 to 10.6; p = 0.016), multivessel spasm (OR: 2.06; 95% CI: 1.33 to 3.19; p = 0.001), and left anterior descending artery spasm (OR: 1.40; 95% CI: 1.02 to 1.92; p = 0.04). Over a median follow-up of 7.5 years, the incidence of cardiac death was significantly higher in ASCD patients (24.1 per 1,000 patient-years vs. 2.7 per 1,000 patient-years; adjusted hazard ratio [HR]: 7.26; 95% CI: 4.21 to 12.5; p 0.001). Death from any cause also occurred more frequently in ASCD patients (27.5 per 1,000 patient-years vs. 9.6 per 1,000 patient-years; adjusted HR: 3.00; 95% CI: 1.92 to 4.67; p 0.001). The incidence rate of recurrent ventricular tachyarrhythmia in ASCD patients was 32.4 per 1,000 patient-years, and the composite of cardiac death and ventricular tachyarrhythmia was 44.9 per 1,000 patient-years. A total of 24 ASCD patients received implantable cardioverter-defibrillators (ICDs). There was a nonsignificant trend of a lower rate of cardiac death in patients with ICDs than those without ICDs (p = 0.15).The prognosis of patients with variant angina with ASCD was worse than other patients with variant angina. In addition, our findings supported ICDs in these high-risk patients as a secondary prevention because current multiple vasodilator therapy appeared to be less optimal.