Acute coronary syndrome due to multi-vessel coronary artery spasm in an Afghan refugee adolescent mimicking recurrent myocarditis.

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

Spontaneous Multivessel Coronary Spasm During Diagnostic Coronary Angiography.

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.

Vasospastic angina and overlapping cardiac disorders in patients resuscitated from cardiac arrest.

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

Severe coronary artery spasm presenting as Prinzmetal's angina following cardiac transplantation.

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

Recurrent Coronary Artery Spasm Induced by Vasopressors During Two Operations in the Same Patient Under General Anesthesia.

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.

Impact of Renin-Angiotensin System Inhibitors on Long-Term Clinical Outcomes of Patients With Coronary Artery Spasm.

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

Impact of Statin Therapy on Clinical Outcome in Patients With Coronary Spasm.

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

Pharmacotherapy of Vasospastic Angina.

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.

[Many possible causes of variant angina]. / Veel mogelijke oorzaken voor vasospastische angina pectoris.

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

Variant angina in moyamoya disease--a correlative etiology and different presentation: a case report.

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

K2--not the spice of life; synthetic cannabinoids and ST elevation myocardial infarction: a case report.

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

Admission hyperglycemia is associated with failed reperfusion following fibrinolytic therapy in patients with STEMI: results of a retrospective study.

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