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.

Prinzmetal angina in a child with actin gene ACTC1 mutation.

Prinzmetal angina is a rare cause of intermittent chest pain in paediatrics. Here, we report the case of a 2-year-old female who presented with episodic chest pain, malaise, diaphoresis, fatigue, and poor perfusion on exam. During her hospitalisation, these episodes were associated with significant low cardiac output as evidenced by lactic acidosis and low mixed venous oxygen saturations. Her workup revealed an actin alpha cardiac muscle 1 (ACTC1) gene mutation and associated left ventricular non-compaction with decreased systolic function. She was started on oral heart failure medications as well as a calcium channel blocker but continued to have episodes which were found to promptly resolve with nitroglycerine. She was ultimately listed for cardiac transplant given her perceived risk of sudden death.

Vasospastic Angina With ST-Segment Elevation Seen During Mobile Cardiac Outpatient Telemetry (MCOT) Monitoring.

A 54-year-old man presented with significant ST-segment elevations noted on both channels displayed on the mobile cardiac outpatient telemetry (MCOT). Pertinent cardiac history was remarkable for syncope and episodes of atypical chest pain. The latter were described as infrequent and not associated with exercise intolerance. His syncopal episodes were described as occurring mostly in the mornings after the use of the restroom. Episodes happen 1 or 2 times a year since 2015. Patient had undergone thorough investigation with no significant findings. An MCOT was prescribed since frequency of symptoms has recently increased. Significant ST-segment elevations were noted. The patient described atypical chest pain and a sensation of presyncope during these recordings. He was urgently admitted, and a coronary angiogram revealed no epicardial luminal stenosis. However, the presence of sluggish coronary flow was suggestive of possible vasospastic angina. No ST-segment changes were noted during his coronary angiogram. The remarkable element portrayed by this case hinges in showing the unique utility of MCOT, as the most uncharacteristic diagnostic tool, in identifying transient ST-segment elevations that finally led to the diagnosis.

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.

Variant Angina with Spontaneously Documented Ischemia- and Tachycardia-induced "Lambda" Waves.

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.

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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Variant angina induced by carbon monoxide poisoning: A CARE compliant case report.

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.

ST-segment elevation and the Tpeak-Tend/QT ratio predict the occurrence of malignant arrhythmia events in patients with vasospastic angina.

BACKGROUND: 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. METHODS: 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. RESULTS: Patients with MAEs showed greater STE (P<0.001) and corrected QT dispersion (cQTd) (P=0.021), a longer corrected Tp-e interval (cTp-e) (P<0.001), and a larger Tp-e/QT ratio (P<0.001) 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, P<0.001) 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 (P>0.05), but both were significantly different than AUCs for cQTd (AUC=0.724) and cTp-e (AUC=0.841) (all P<0.05). STE was well fitted with the Tp-e/QT ratio in a multivariable linear regression model. CONCLUSIONS: STE and increased Tp-e/QT ratio had related electrophysiological properties and were independent prognostic indicators of MAEs in patients with VA.

Ventricular Fibrillation Induced by Coronary Vasospasm in a Patient with Early Repolarization and Hyperthyroidism.

Vasospastic angina (VSA) has been recognized as a cause of ventricular fibrillation (VF) degenerating into sudden cardiac death. We experienced a case of VSA with hyperthyroidism in which VF was provoked with an augmented J-wave amplitude in the inferior leads. The patient underwent insertion of an implantable cardioverter-defibrillator for the secondary prevention of VF in addition to taking Ca-channel antagonists. He has shown no recurrence of fatal arrhythmia or anginal attack for a follow-up period of one year.

Early repolarization is involved in ventricular fibrillation in patients with variant angina.

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 and Aborted Sudden Cardiac Death.

PURPOSE OF REVIEW: Variant angina, which is characterized by recurrent chest pain and transient ECG changes along with angiographic evidence of coronary artery spasm, generally has a favorable prognosis. However, episodes of ischemia caused by vasospasm may lead to potentially life-threatening ventricular arrhythmias and cardiac arrest, even in patients with no history of prior cardiac disease. This review describes the epidemiology, pathogenesis, clinical spectrum, and management of variant angina, as well as outcomes in patients who present with aborted sudden cardiac death (ASCD). RECENT FINDINGS: Contrary to prior opinions, evidence from recent observational studies indicate that patients with variant angina presenting with ASCD face a worse prognosis than those without this type of presentation. Predictors of ASCD include age, hypertension, hyperlipidemia, family history of sudden cardiac death, multi-vessel spasm, and left anterior descending artery spasm. Medical therapy alone with calcium channel blockers and nitrates may not be sufficiently protective in these patients and there is lack of concrete data on the optimal management strategy. Current guidelines recommend implantable cardiac defibrillator (ICD) therapy in patients who are survivors of cardiac arrest caused by ventricular fibrillation or unstable ventricular tachycardia after reversible causes are excluded, and should strongly be considered in these patients. Although medical therapy is absolutely imperative for patients with variant angina and a history of ASCD, ICD therapy in these patients is justified. Further large-scale studies are required to determine whether ICD therapy can improve survival in this high-risk group of patients.

The association of chronic air pollutants with coronary artery spasm, vasospastic angina, and endothelial dysfunction.

BACKGROUND: 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. PATIENTS AND METHODS: 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. RESULTS: 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. CONCLUSION: 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.

Vasospastic Angina Presenting With Syncope and Chest Pain: A Case Report and Brief Literature Review.

A 65-year-old male presented to the hospital with chest pain associated with recurrent syncope. He had a history of coronary artery disease and a long-standing history of smoking. While he was hospitalized, he had an episode of chest pain during which he was found to have transient ST segment elevation in the inferior leads. He was also noted to have a brief cardiac tachyarrhythmia. Coronary arteriography revealed vasospasm of the left anterior descending artery and right coronary artery, which were relieved to a significant extent after administration of intracoronary nitroglycerin. Subsequent angiograms and fractional flow reserve studies, demonstrated underlying non-obstructive coronary artery disease at the sites of spasm. No percutaneous coronary intervention was pursued. The patient was started on a calcium channel blocker on dismissal from the hospital. Upon follow up several months later, he remained free of symptoms that brought him to the hospital.

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.