Vasospastic angina: a review on diagnostic approach and management.

Vasospastic angina (VSA) refers to chest pain experienced as a consequence of myocardial ischaemia caused by epicardial coronary spasm, a sudden narrowing of the vessels responsible for an inadequate supply of blood and oxygen. Coronary artery spasm is a heterogeneous phenomenon that can occur in patients with non-obstructive coronary arteries and obstructive coronary artery disease, with transient spasm causing chest pain and persistent spasm potentially leading to acute myocardial infarction (MI). VSA was originally described as Prinzmetal angina or variant angina, classically presenting at rest, unlike most cases of angina (though in some patients, vasospasm may be triggered by exertion, emotional, mental or physical stress), and associated with transient electrocardiographic changes (transient ST-segment elevation, depression and/or T-wave changes). Ischaemia with non-obstructive coronary arteries (INOCA) is not a benign condition, as patients are at elevated risk of cardiovascular events including acute coronary syndrome, hospitalization due to heart failure, stroke and repeat cardiovascular procedures. INOCA patients also experience impaired quality of life and associated increased healthcare costs. VSA, an endotype of INOCA, is associated with major adverse events, including sudden cardiac death, acute MI and syncope, necessitating the study of the most effective treatment options currently available. The present literature review aims to summarize current data relating to the diagnosis and management of VSA and provide details on the sequence that treatment should follow.

Diagnosis and treatment of epicardial coronary artery spasmVasospastic angina (VSA) refers to chest pain experienced as a consequence of a sudden narrowing of the epicardial coronary arteries. VSA can occur in patients with non-obstructive coronary arteries and obstructive coronary artery disease, with transient spasm causing chest pain and persistent spasm potentially leading to acute myocardial infarction. Reduced blood and oxygen supply in patients with non-obstructive coronary arteries is not a benign condition, as patients are at elevated risk of adverse cardiovascular events. These patients also experience impaired quality of life and associated increased healthcare costs. This review aims to summarise current data relating to the diagnosis of VSA and provides details on treatment strategies.

Angina due to coronary artery spasm (variant angina): diagnosis and intervention strategies.

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 is often debilitating and substantially under-diagnosed and occur mainly in women. 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 centers around the use of calcium antagonists, but with greater understanding of pathogenesis, new management options are emerging.

Síndrome de taquicardia postural ortostática y angina vasoespástica, una combinación de difícil abordaje terapéutico / Postural orthostatic tachycardia syndrome and vasospastic angina: therapeutic approach to a previously unreported association

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Vasospastic angina: A literature review of current evidence.

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.

Placement of a Continuous Stellate Ganglion Block for Treatment of Refractory Ventricular Fibrillation in the Setting of Known Prinzmetal Angina During Pregnancy: A Case Report.

A patient with a history of Prinzmetal angina, refractory ventricular fibrillation, cardiac arrest with an implantable cardioverter-defibrillator, and obesity presented to the emergency department at 17 weeks gestational age with a chief complaint of angina and multiple episodes of defibrillation. A T3/4 thoracic epidural was placed to assess the effectiveness of a partial chemical sympathectomy in alleviating symptoms of angina as well as decreasing the amount of defibrillation episodes. Once this proved to be beneficial in accomplishing both of these goals, a more specific approach was designed. A continuous stellate ganglion block was then placed controlling both her angina and preventing further episodes of defibrillation long enough for her pregnancy to progress beyond 24 weeks gestational age.

Stent and implantable cardioverter defibrillator implantation in medically resistant vasospastic angina patient.

Vasospastic angina, also known as Prinzmetal's angina, is thought to occur due to vascular hyper-reactivity to various stimuli. Response to medical therapy is usually good; however, 1 out of 5 patients has resistant symptoms. Rarely, potentially lethal arrhythmias can occur due to vasospasm, and those patients are reported to have a poorer prognosis. Presently described is a case of resistant vasospastic angina with persistent symptoms under calcium channel blocker and nitrate treatment. The patient presented with hemodynamically unstable rapid-rate ventricular tachycardia, which was quite resistant to recurrent cardioversion. She was treated with stent implantation for definite vasospastic segments of the coronaries, in combination with medical therapy. An implantable cardioverter defibrillator was also implanted for secondary prevention of ventricular arrhythmia, as vasospasm was considered to be a diffuse disease without a certain definitive treatment.

Alternative causes of myocardial ischemia in women: An update on spontaneous coronary artery dissection, vasospastic angina and coronary microvascular dysfunction.

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.

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.

Usefulness of the wearable cardioverter-defibrillator in patients at high risk for sudden cardiac death.

BACKGROUND: Wearable cardioverter-defibrillators (WCD) have been available in Japan since April 2014, but their application is still limited. METHODS AND RESULTS: We report 9 patients with a WCD applied between April and September 2014. All patients were at high risk of life-threatening ventricular arrhythmias. During WCD use, 1 patient had sustained ventricular tachycardia and successful shock delivery; 6 (67%) subsequently underwent implantable cardioverter-defibrillator (ICD) therapy, while 2 had no requirement because of reduced risk, and 1 died of heart failure during WCD use. CONCLUSIONS: WCD is useful during acute-phase care of high-risk patients, and may help to avoid unnecessary ICD implantation.

Rare giant T-wave inversions associated with myocardial stunning: report of 2 cases.

Prominent T-wave inversions are well recognized electrocardiographic signs that can occur in acute myocardial infarction (AMI). However, the giant negative T waves may be associated with myocardial stunning without AMI.This case report describes 2 patients without AMI who developed rare giant T-wave inversions measuring up to 35 mm in depth and QT prolongation after admission to hospital. While 1 patient presented with acute pulmonary edema, the other patient presented with severe chest pain at rest and transient ST elevation.The giant T-wave inversion with QT prolongation may be caused by myocardial stunning due to the triple vessel diseases and elevated wall stress, high-end diastolic pressure and decreased coronary arterial flow during pulmonary edema in the first patient. The giant T-wave inversion with QT prolongation in the second patient may be caused by myocardial stunning due to the left anterior descending artery spasm (transient ST elevation) leading to transient total occlusion of left anterior descending artery. Percutaneous coronary intervention was successfully undergone for both patients. The patients remained well.The electrophysiologic mechanism responsible for giant T-wave inversion with QT prolongation is presently unknown. The two cases demonstrate that the rare giant negative T waves may be associated with myocardial stunning without AMI.