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.

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.

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.

Bradyarrhythmic syncope in a patient with Prinzmetal's variant angina: a case report.

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

Clinical outcome of coronary stenting in patients with variant angina refractory to medical treatment: a consecutive single-center analysis.

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

Vasospastic angina with J-wave pattern and polymorphic ventricular tachycardia effectively treated with quinidine.

BACKGROUND: Myocardial ischemia during coronary spasm may generate malignant ventricular arrhythmias. The J-wave pattern was suggested to be a marker of a disorder associated with life-threatening arrhythmias. RESULTS: We report the case of a patient with vasospastic angina and J-wave pattern in inferior and lateral leads associated with polymorphic ventricular tachycardia which was effectively treated only with quinidine-vasodilating drugs were not able to prevent the arrhythmia although they were effective in preventing ischemic events. CONCLUSION: The J-wave pattern in inferolateral leads may be a sign of electrical vulnerability to lethal ventricular arrhythmia in patients suffering from vasospastic angina--quinidine can effectively prevent such arrhythmias in these patients.

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.

Prinzmetal's variant angina is effectively treated with enhanced external counterpulsation.

A 57-year-old woman suffering from severe Prinzmetal's angina was treated with a 7-week course of enhanced external counterpulsation (EECP). After completing EECP the angina intensity was reduced from CCS class IV to class I, quality of life was increased and medication was significantly reduced. The number of hospitalisations due to chest pain was reduced from 81 in the two years before EECP to 2 in the two years after EECP. To our knowledge, this is the first report demonstrating the effect of EECP on Printzmetal's angina.

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.

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.

[Malignant arrhythmia in a patient with variant (Prinzmetal's) angina pectoris]. / Maligní arytmie u pacienta s variantní (Prinzmetalovou) anginou pectoris.

Malignant arrhythmia is a frequent complication of myocardial ischemia due to the occurrence of coronary artery spasm. The paper describes a patient with variant angina pectoris with an ICD implant who was repeatedly resuscitated for circulatory arrest in malignant arrhythmia. During myocardial ischemia the ECG showed elevations in the ST segments in the region of the ventral cardiac wall, with the formation of permanent polymorphous chamber tachycardia. External defibrillation was necessary due to recurrent tachyarrhythmias. A spasm developed when the RIA (radio immuno assay) was introduced during coronarography. The spasm started in the periphery of the artery and extended as far as the area of bifurcation with RD, with transitory closure of the artery and the development of chamber tachycardia. The patient fully recovered after the addition of Ca-blocker, nitrate depot and the withdrawal of the beta-blocker.

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.

Coronary artery stent placement as a treatment of acute coronary syndrome in course of variant angina.

High doses of calcium antagonists and nitrates are the treatment of choice in vasospasm angina when no stenosis or mild stenosis is present. In ca. 5-30% patients this kind of treatment is not effective. We present five cases of variant angina with acute coronary syndrome in patients despite standard pharmacological treatment. These patients also did not respond for intracoronary nitroglycerine injection. They were successfully treated with stent implantation in place of vasospasm. Our observations indicate that early enough interventional treatment prevent myocardial infarction. In one case in which stent placement was performed 12 h after clinical manifestation myocardial infarction with Q waves and enzymes release occurred. In others, accurately treated with stent implantation, coronary spasm did not produce myocardial damage. We did not see any clinical and biochemical evidence of myocardial infarction.

Variations in presentation and various options in management of variant angina.

Patients with variant angina represent a diagnostic and therapeutic dilemma. Variant angina is a disease with various causes, variations in treatment guidelines and variable prognosis. In an era of robotic cardiac surgery and automatic cardioverter defibrillators, it is regrettable that we lack enough information on the optimal management of this entity. Lack of randomised trials and a tendency for spontaneous remissions makes interpretation of results difficult. We review the pathophysiology, presentation and recent developments in medical and surgical management of variant angina. Literature is full of conflicting data and it is difficult to make specific recommendations.

[Recurrent cardiac arrest due to electro-mechanical dissociation in a patient with variant angina -- a case report]. / Nawracajace zatrzymania krazenia w mechanizmie rozkojarzenia elektromechanicznego w przebiegu anginy Prinzmetala. Opis przypadku.

We present a case of a 44-year-old male with recurrent episodes of cardiac arrest in the course of Prinzmetal's angina. Episodes of variant angina can be life threatening due to episodes of advanced atrioventricular block, asystole, ventricular tachycardia or ventricular fibrillation. It has been suggested to implant an ICD in all patients with variant angina after cardiac arrest. This patient received an ICD, however, he died suddenly 6 months later. The possible mechanism of cardiac arrest was an electromechanical dissociation.

Comparative results of percutaneous transluminal coronary angioplasty in patients with dynamic versus fixed coronary stenosis.

This study compares the results of percutaneous transluminal coronary angioplasty in a group of 132 patients (group A) with fixed atherosclerotic narrowing (no spontaneous or ergonovine-provoked spasm) and in a group of 97 patients (group B) with dynamic coronary stenosis (spasm superimposed on the stenosis). All these patients underwent complete follow-up angiography. The rate of restenosis (defined as a loss of 50% of the initial gain) was significantly higher in patients in group B (dynamic coronary stenosis) than in group A (fixed narrowing) (35 versus 22%, p less than 0.05). Despite treatment with a calcium antagonist, coronary artery spasm persisted in 44% of the patients in group B and was detected for the first time in 15% of the patients in group A. Thus, in patients with dynamic coronary stenosis, the results of coronary angioplasty were less satisfactory than in patients with fixed narrowing, and in both groups coronary artery spasm was frequently (64%) superimposed on the restenosis.