Coronary Artery Vasospasm

Coronary artery vasospasm (CVS) is an important mechanism of myocardial ischemia and produces any of the manifestations of coronary artery disease from silent myocardial ischemia, to effort-induced angina and variant angina, to acute coronary syndrome including myocardial infarction or sudden cardiac death. The pathogenesis, characteristic clinical features, diagnosis, and treatment of CVS are summarized. Emphasis is placed on correct diagnosis of CVS using pharmacological spasm provocation test, either during coronary angiography or with echocardiographic monitoring of ventricular wall motion. Current underutilization of pharmacologic provocative test at the time of coronary angiography cannot be justified, as there is no evidence supporting that the incidence of CVS is declining. Physicians' vigilance for objective documentation of CVS is necessary for appropriate management of patients with various clinical presentations of ischemic heart disease.

Spontaneous Partial Regression of Coronary Artery Fistula Following Optimal Medical Therapy in a Patient Who Had Combined Significant Coronary Artery Spasm

Coronary artery fistulas (CAFs) are one of the most rare cardiac anomalies. Some patients with CAF may suffer from ischemic chest pain that originates from combined significant coronary artery spasm (CAS). Spontaneous regression of CAF has been reported in a few cases, almost all of which were infants. We report an adult patient who presented with ischemic chest pain due to multiple coronary arteries to pulmonary artery fistulas and combined significant CAS induced by intracoronary acetylcholine provocation test. Spontaneous regression of one of the fistulas was observed at 2-year angiography follow-up.

A Case of Acute Myocardial Infarction With ST-Segment Elevation in a Lead Augmented Right Vector Caused by a Left Main Coronary Artery Vasospasm

Diagnosing and selecting an appropriate treatment strategy for left main coronary artery (LMCA) obstruction is very important. Although this disease is not frequently encountered, it can cause severe hemodynamic deterioration resulting in a less favorable prognosis without a suitable management approach. Another aspect of LMCA that we must not overlook is coronary artery spasm, which can be an infrequent but important cause of acute coronary syndrome. Although it is rare, LMCA can cause critical complications. In this study, we report the case of a 35-year-old female who was admitted to the hospital with a diagnosis of acute myocardial infarction with ST-segment elevation in the aVR lead caused by a left main coronary spasm that was examined on intravascular ultrasound.

Phantom Ischemia Mimicking ST Segment Elevation Myocardial Infarction in Fulminant Myocarditis / 이화의대지

A 30-year-old man visited the emergency room for chest pain, dyspnea and fever. Despite increased serum cardiac enzymes, ST segment elevation and inferior wall akinesis in electrocardiography and echocardiography, no atherosclerosis was evident in the coronary angiography. However, radionuclide myocardial perfusion image at day 2 showed a persistent perfusion defect in the left ventricular (LV) inferior wall. At day 3, prominent myocardial edema and severe LV systolic dysfunction developed with signs of heart failure. In this case, fulminant myocarditis seemed to originate from the right coronary artery territory and simulated a ST segment elevation myocardial infarction without coronary artery obstruction. The pathogenesis of the localized perfusion defect was unlcear.

Decrease in Plasma Adiponectin Concentrations in Patients with Vasospastic Angina

BACKGROUND AND OBJECTIVES: Plasma adiponectin, which decreases the progression of atherosclerosis and insulin resistance, as well as suppressing lipid accumulation in macrophages, is decreased in patients with acute myocardial infarction and unstable angina pectoris; however, the correlation between plasma adiponectin and vasospastic angina pectoris (VAP) remains to be verified. We compared the plasma adiponectin concentration between patients with VAP and other coronary artery diseases; moreover, we investigated the association between the plasma adiponectin concentration and VAP. SUBJECTS AND METHODS: Following coronary angiography for the evaluation of chest pain, 395 subjects (180 women and 215 men) were divided into 4 groups: acute coronary syndrome (ACS)(n=117), VAP (n=94), stable angina pectoris (SAP)(n=108) and angiographically normal coronary artery (n=76). The acetylcholine provocation test was used to confirm VAP, and plasma adiponectin concentrations were measured in all participants. RESULTS: The plasma adiponectin concentrations in patients with VAP and ACS were significantly lower than that of the normal coronary artery group (6.6+/-5.4 vs. 5.2+/-4.0 vs. 9.0+/-6.2 microgram/mL, p<0.001, respectively). A multivariate analysis indicated that plasma adiponectin [odd ratio (OR) 0.744, 95% confidence interval (CI) 0.645 to 0.858, p=0.001], smoking (OR 2.054, 95% CI 1.027 to 4.106, p=0.042) and age (OR 0.966, 95% CI 0.935 to 0.997, p=0.031) were independently correlated in patients diagnosed with VAP. CONCLUSION: Our results suggest that a decreased plasma adiponectin concentration may be associated with VAP.

Long-term Follow up in Patients with Vasospastic Angina in Relation to Medication Period and Disease Activity / 대한내과학회지

OBJECTIVES: Clinical course of vasospastic angina is variable : spontaneous remission, persistent angina and progression of disease or death. Several studies from western institutes have been performed on the clinical characteristics and long-term prognosis of patient with coronary vasospasm. In these reports, 53-82% of patients had spontaneous remission. These results may be assumed differ from that of Korean patients with vasospastic angina, but no detailed studies have been reported in Korea. Currently, in patients with vasospastic angina, treatment with calcium antagonists and/or nitrates are effective in reducing the frequency of anginal attacks. And, clinical course and outcome of vasospastic angina may be different from previous western reports thereafter. The purpose of this study is to describe the disease activities and the factors influencing the clinical course of vasospastic angina in relation to medication-period; age, sex, risk factors, extents of coronary vasospasm, initial ischemic events and significance of fixed lesion. Also we tried to determine if clinical or angiographic variables might be useful in predicting the possibility of spontaneous remission for an each patient. METHODS: Eighty-seven patients with vasospastic angina(M/F ; 58/29, mean age ; 53+/-9 years) were included and all documented coronary vasospasm on the coronary angiogram, spontaneous spasm in 35, positive ergonovine or acetylchoine provocation in 52. Coronary artery spasm was declined as more than 75% reduction in coronary luminal diameter and ST segment changes on electrocardiogram, or typical anginal symptoms together and then narrowed coronary arteries were recovered after intracoronary nitroglycerin. The patients were treated with calcium antagonists(nifedipine, diltiazem, amlodipine and felodipine) and nitrates single or both and were divided into 3 groups according to angina activity : group I, which anginal attacks less than one time monthly, group II, which anginal symptoms occurred in 24-48 hours after withdrawal of medication, group III, which symptoms recurred frequently with the incidence of over one time weekly. After discharge, each patient returned to a medical out-patient department at every 1-2 months. RESULTS: Age, gender, other coronary risk factors, disease activity of vasospastic angina, initial clinical presentation at admission, coronary angiographic findings, fixed lesion and alcohol-induced anginal attacks were not statistically different among the 3 groups. But admission frequency of group II and III, which had a high anginal activities, were more than that of group I significantly. CONCLUSION: In the present study, it is concluded that medical treatment in patients with vasospastic angina in Korea may be taken long duration during follow-up period if the patient of group II and III considered to persistent angina group. To assess the prevalence of spontaneous remission, we consider that systematic attempts to taper medication may be done for patient of group I(angina free-on treatment) after absence of anginal attacks for at least one year medication-period.