Myocardial Infarction with Nonobstructive Coronary Arteries.

Myocardial infarction with nonobstructive coronary arteries (MINOCA) is an important subtype of myocardial infarction (MI) that occurs in approximately 6-8% of patients with spontaneous MI who are referred for coronary angiography. MINOCA disproportionately affects women, but men are also affected. Pathogenesis is more variable than in MI with obstructive coronary artery disease (MI-CAD). Dominant mechanisms include atherosclerosis, thrombosis, and coronary artery spasm. Management of MINOCA varies based on the underlying mechanism of infarction. Therefore, systematic approaches to diagnosis are recommended. The combination of invasive coronary angiography, multivessel intracoronary imaging, provocative testing for coronary spasm, and cardiac magnetic resonance imaging provides the greatest diagnostic yield. Current clinical practice guidelines for the secondary prevention of MI are based largely on data from patients with MI-CAD. Thus, optimal medications after MINOCA are uncertain. Clinical trials focused on the treatment of patients with MINOCA are urgently needed to define optimal care.

Acute Coronary Spasm Following Pelvic Fracture, Bleeding, and Shock in a Trauma Patient.

We report a case of a patient with severe pelvic fracture who showed concurrent ST elevation on electrocardiogram. A 70-year-old man incurred an unstable pelvic fracture from a motorcycle accident. On admission, he was hemodynamically unstable, and massive transfusion and noradrenaline were administered immediately. Although ST elevation was present in leads II, III, aVF, V5, and V6, cardiac function was preserved; thus, trans-arterial embolization and external fixation for pelvic fracture were given priority. Four days after the injury, he suffered a cardiac arrest, and coronary angiography revealed that the cause of ST elevation and cardiac arrest was coronary vasospasm. Physicians should be aware that pain-related stress and platelet activation as well as use of noradrenaline in severe trauma cases can induce coronary vasospasm.

Pathophysiology of Coronary Microvascular Dysfunction.

Ischemic heart disease (IHD) is commonly recognized as the consequence of coronary atherosclerosis and obstructive coronary artery disease (CAD). However, a significant number of patients may present angina or myocardial infarction even in the absence of any significant coronary artery stenosis and impairment of the coronary microcirculation has been increasingly implicated as a relevant cause of IHD. The term "coronary microvascular dysfunction" (CMD) encompasses several pathogenic mechanisms resulting in functional and/or structural changes in the coronary microcirculation and determining angina and myocardial ischemia in patients with angina without obstructive CAD ("primary" microvascular angina), as well as in several other conditions, including obstructive CAD, cardiomyopathies, Takotsubo syndrome and heart failure, especially the phenotype with preserved ejection fraction. The pathogenesis of CMD is complex and involves the combination of functional and structural alterations leading to impaired coronary blood flow and resulting in myocardial ischemia. In the absence of therapies specifically targeting CMD, attention has been focused on the role of modifiable risk factors. Here, we provide updated evidence regarding the pathophysiological mechanisms underlying CMD, with a particular focus on the role of cardiovascular risk factors and comorbidities. Moreover, we discuss the specific pathogenic mechanisms of CMD across the different cardiovascular diseases, aiming to pave the way for further research and the development of novel strategies for a precision medicine approach.

Vascular Endothelial Dysfunction in Myeloproliferative Neoplasms and Gene Mutations.

Essential thrombocythemia (ET) and polycythemia vera (PV), are common Philadelphia-negative myeloproliferative neoplasms (MPN). Patients with MPN have a high rate of cardiovascular complications and often have acquired JAK2V617F and CALR genetic mutations. In this study, we aimed to analyze vascular endothelial function in patients with MPN.We evaluated 27 outpatients, including 10 patients diagnosed with MPN, flow-mediated dilatation (FMD), and nitroglycerin-mediated dilation (NMD), between September 2014 and August 2016. We measured serum adiponectin, which protects vascular endothelial function, and serum asymmetric dimethyl arginine (ADMA), which inhibits the production of adiponectin. The presence or absence of JAK2V617F and CALR mutations was evaluated in patients with MPN.Venous thrombosis was observed more frequently in patients with MPN than in those without. Seven MPN patients were diagnosed with PV, and 3 MPN patients were diagnosed with ET. JAK2V617F and CALR mutations were found in 5 and 3 MPN patients, respectively. FMD was significantly lower in JAK2V617F-positive MPN patients than in JAK2V617F-negative MPN patients, although NMD, adiponectin, and ADMA were similar in both groups. Adiponectin levels were higher and ADMA levels were lower in CALR-positive MPN patients than in CALR-negative MPN patients. There was no difference in FMD and NMD prevalence between the 2 groups. Furthermore, we had 3 representative MPN patients who were complicated with coronary spasm, possibly caused by MPN-related endothelial dysfunction.We found that patients with MPN presented with endothelial dysfunction, which was related to the presence of genetic mutations and was sometimes associated with cardiovascular disease.

Assessment of coronary vasomotor responses to acetylcholine in German and Japanese patients with epicardial coronary spasm-more similarities than differences?

Coronary spasm is an established cause for angina pectoris. Ethnic differences have been suggested among Asian compared to Caucasian patients regarding prevalence, gender distribution, and angiographic patterns of coronary spasm. The aim of this study was to compare contemporary German and Japanese patients with coronary spasm. Between 2011 and 2015, 149 patients with resting angina and unobstructed coronary arteries with acetylcholine-induced epicardial spasm were enrolled in Stuttgart, Germany (n = 69) and Sendai, Japan (n = 80). All patients underwent intracoronary acetylcholine testing according to a standardized protocol. Comprehensive analysis included type of spasm (focal/diffuse), dose of acetylcholine leading to spasm, and frequency of multivessel spasm. Patients in this study were 61 ± 11 years old, predominantly female (54%), and had normal left ventricular ejection fraction (73 ± 9%). Diffuse spasm was the most prevalent type of spasm (85%) whereas focal spasm was found in the remaining 15% of patients. 31% of patients had multivessel spasm. Comparing the German with the Japanese patients, distribution of spasm type (focal/diffuse, p = 0.19) and frequency of multivessel spasm (p = 0.22) were comparable. Moreover, when Japanese patients were compared with German patients and diffuse spasm with focal spasm patients, respectively, no significant differences were observed regarding the acetylcholine dose required to induce spasm (p = 0.078 and p = 0.46, respectively). In conclusion, diffuse epicardial coronary spasm is the most frequent finding among German and Japanese patients with resting angina, unobstructed coronary arteries, and epicardial spasm on acetylcholine testing. Japanese and German patients share several similarities including comparable types of spasm and frequency of multivessel spasm.

Cardiotoxicities of 5-Fluorouracil and Other Fluoropyrimidines.

OPINION STATEMENT: Fluoropyrimidine (FP) is used to treat a wide range of cancers; however, it is associated with drug-induced vascular toxicity, as well as angina pectoris and coronary spasm. FP has been administered for many years, although the incidence, mechanisms, and appropriate methods for managing its associated cardiovascular toxicities have not been clarified, and the management of these complications has not been standardized. This lack of evidence is not limited to FP. Many trials of anticancer agents have been conducted, excluding patients with heart diseases. Hence, there is a paucity of epidemiological data on cardiovascular adverse events caused by anticancer agents. There have been remarkable improvements in cancer treatment in recent years, with consequent improvements in prognosis. In this context, new cardiovascular toxicities related to new drugs have emerged. We are now compelled to respond to cardiovascular adverse events despite the lack of evidence regarding optimal management. The result has been establishment and rapid maturation of the new academic field of cardio-oncology. Despite the relative lack of evidence, we must review small pieces of evidence that have accumulated to date and make the utmost efforts to provide patients with effective evidence-based medical care. Simultaneously, we urgently need randomized clinical trials to build strong evidence.

Chest pain in Brugada syndrome: Prevalence, correlations, and prognosis role.

BACKGROUND: Brugada syndrome (BrS) is sometimes diagnosed because of chest pain. Prevalence and characteristics of such BrS patients are unknown. METHODS: A total of 200 BrS probands were retrospectively included. BrS diagnosis made because of chest pain (n = 34, 17%) was compared to the other ones. RESULTS: BrS probands with diagnosis because of chest pain had significantly more often smoker habits, increased body mass index, and familial history of coronary artery disease but less frequently previous resuscitated sudden death/syncope or atrial fibrillation. Presence of coronary spasm and familial coronary artery disease were independently associated with BrS diagnosed because of chest pain. They presented more often with spontaneous type 1 ST elevation (59% vs 26%, P = .0004) and higher ST elevation during the episode of chest pain compared to other patients or compared to baseline electrocardiogram after chest pain resumption. ST elevation during chest pain was lower compared to ajmaline test. A total of 20% of them had significant coronary artery disease and four (11%) had coronary spasm, and they experienced more often recurrent chest pain episodes (24% vs 5%, P = .0002). Presence of chest pain at BrS diagnosis was not correlated to future arrhythmic events in univariate analysis. Only previous sudden cardiac death (SD)/syncope and familial SD were still significantly associated with outcome in multivariate analysis. CONCLUSION: Chest pain is a common cause for BrS diagnosis, although major part is not apparently explained by ischemic heart disease. Mechanisms leading to chest main remain unknown in the other ones. ST elevation is higher in this situation but does not seem to carry poor prognosis.

Myocardial bridging is an independent predictor of positive spasm provocation testing by intracoronary ergonovine injections: a retrospective observational study.

The relationship between myocardial bridging (MB) and coronary spasms during spasm provocation testing (SPT) remains unclear. We aimed to investigate whether MB was correlated with the SPT by ergonovine (ER) injections in a retrospective observational study. Of the 3340 patients who underwent a first coronary angiography, 166 underwent SPT using ER injections and were divided into 2 groups: MB(+) (n = 23), and MB(-) (n = 143). MB was defined as an angiographic reduction in the diameter of the coronary artery during systole. The patients who had severe organic stenosis in the left anterior descending coronary artery were excluded. The MB(+) group more frequently had diabetes mellitus and chronic kidney disease, and a thicker interventricular septum thickness. The rate of SPT-positivity was higher in the MB(+) group than MB(-) group (56.5% vs. 22.4%, P = 0.001). A multivariate regression analysis showed that the presence of MB was independently associated with SPT-positivity (odds ratio 5.587, 95% confidence interval 2.061-15.149, P = 0.001). In conclusion, coronary spasms during provocation tests with ER independently correlated with the MB. MB may predict coronary spasms.

Questionnaire in patients with aborted sudden cardiac death due to coronary spasm in Japan.

OBJECTIVES: We investigated the medical or mechanical therapy, and the present knowledge of Japanese cardiologists about aborted sudden cardiac death (ASCD) due to coronary spasm. METHODS: A questionnaire was developed regarding the number of cases of ASCD, implantable cardioverter-defibrillator (ICD), and medical therapy in ASCD patients due to coronary spasm. The questionnaire was sent to the Japanese general institutions at random in 204 cardiology hospitals. RESULTS: The completed surveys were returned from 34 hospitals, giving a response rate of 16.7%. All SCD during the 5 years was observed in 5726 patients. SCD possibly due to coronary spasm was found in 808 patients (14.0%) and ASCD due to coronary spasm was observed in 169 patients (20.9%). In 169 patients with ASCD due to coronary spasm, one or two coronary vasodilators was administered in two-thirds of patients [113 patients (66.9%)], while more than 3 coronary vasodilators were found in 56 patients (33.1%). ICD was implanted in 117 patients with ASCD due to coronary spasm among these periods including 35 cases with subcutaneous ICD. Majority of cause of ASCD was ventricular fibrillation, whereas pulseless electrical activity was observed in 18 patients and complete atrioventricular block was recognized in 7 patients. Mean coronary vasodilator number in ASCD patients with ICD was significantly lower than that in those without ICD (2.1 ± 0.9 vs. 2.6 ± 1.0, p < 0.001). Although 16 institutions thought that the spasm provocation tests under the medications had some clinical usefulness of suppressing the next fatal arrhythmias, spasm provocation tests under the medication were performed in just 4 institutions. CONCLUSIONS: In the real world, there was no fundamental strategy for patients with ASCD due to coronary spasm. Each institution has each strategy for these patients. Cardiologists should have the same strategy and the same knowledge about ASCD patients due to coronary spasm in the future.

Mechanisms and diagnostic evaluation of persistent or recurrent angina following percutaneous coronary revascularization.

Persistence or recurrence of angina after a percutaneous coronary intervention (PCI) may affect about 20-40% of patients during short-medium-term follow-up. This appears to be true even when PCI is 'optimized' using physiology-guided approaches and drug-eluting stents. Importantly, persistent or recurrent angina post-PCI is associated with a significant economic burden. Healthcare costs may be almost two-fold higher among patients with persistent or recurrent angina post-PCI vs. those who become symptom-free. However, practice guideline recommendations regarding the management of patients with angina post-PCI are unclear. Gaps in evidence into the mechanisms of post-PCI angina are relevant, and more research seems warranted. The purpose of this document is to review potential mechanisms for the persistence or recurrence of angina post-PCI, propose a practical diagnostic algorithm, and summarize current knowledge gaps.

Extreme ST-segment elevations in seemingly no significant angiographic coronary artery abnormalities: a case report.

BACKGROUND: Obstructive coronary artery disease is found in approximately 97% of patients presenting with ST-elevation myocardial infarction and 92% of patients with non ST-elevation myocardial infarction (Bainey KR, Welsh RC, Alemayehu W, Westerhout CM, Traboulsi D, Anderson T, et al. Int J Cardiol 264: 12-17, 2018). Recent studies showed that myocardial infarction without obstructive coronary atherosclerosis (MINOCA) is also associated with a long-term risk of adverse events (Bainey KR, Welsh RC, Alemayehu W, Westerhout CM, Traboulsi D, Anderson T, et al. Int J Cardiol 264: 12-17, 2018).. The following case illustrates that MINOCA may also be associated with short term adverse events (depending on the underlying mechanism). CASE PRESENTATION: A 49-year old Caucasian male with no significant medical history was referred to our cardiac emergency department with acute chest pain. The ambulance ECG showed extreme ST-segment elevation anterolateral ('tombstone sign'), which had resolved completely at arrival in the hospital. Coronary angiography showed no obstructive coronary artery disease. Conservative (medical) therapy was started and patient was discharged. Two days later he presented with recurrent cardiac ischemia with ventricular fibrillation. Coronary angiography showed no changes compared with earlier presentation. During admission to the ICU his clinical condition gradually deteriorated, eventually leading to his death. Post-mortem studies showed no significant atherosclerotic lesions. Massive myocardial infarction was found, probably caused by temporary occlusion of the left main coronary artery. CONCLUSIONS: Several pathophysiological mechanisms are recognized in MINOCA, of which vasospasm is the most probable one in this case. MINOCA is associated with increased over-all mortality and risk of ventricular arrhythmias. Therefore, additional testing should be considered when there is no explanation for the mismatch between ST-elevations (STEMI) and (no significant) coronary abnormalities.

The impact of intraday glucose variability on coronary artery spasm in patients with dysglycemia.

Impaired glucose metabolism is associated with an increased risk of cardiovascular complications, and coronary artery spasm is thought to underlie the development of coronary artery disease. Intraday glucose variability (GV) accelerates oxidative stress and inflammatory cytokine release, but its impact on coronary artery spasm remains unclear. This study investigated the relationship between intraday GV and coronary artery spasm. The study included 50 patients with dysglycemia and suspected coronary spastic angina. GV was analyzed by 24-h monitoring of the blood glucose concentration using a flash glucose monitoring system. The mean amplitude of glycemic excursion (MAGE) was calculated as an index of GV. Coronary artery spasm was assessed using the intracoronary acetylcholine provocation test. Coronary spasm was defined as acetylcholine-induced total or subtotal coronary occlusion. Changes in vessel diameter in response to acetylcholine were evaluated with quantitative coronary angiography. Coronary artery spasms were observed in 21 patients (42%). MAGE was significantly higher in patients with spasms compared to those without spasms (127.5 ± 33.5 vs. 91.4 ± 37.6, p < 0.01). Regression analysis showed a positive correlation between MAGE levels and coronary diameter changes induced by acetylcholine (r = 0.47, p < 0.01). In multiple regression analysis, MAGE was independently associated with acetylcholine-induced coronary diameter change (ß = 0.47, p < 0.01). Intraday GV was associated with coronary artery spasm in patients with dysglycemia.

Association of East Asian Variant Aldehyde Dehydrogenase 2 Genotype (ALDH2*2*) with Coronary Spasm and Acute Myocardial Infarction.

Coronary spasm plays an important role in the pathogenesis of ischemic heart disease, including angina pectoris, acute myocardial infarction (AMI), silent myocardial ischemia, and sudden death. The prevalence of coronary spasm is higher among East Asians probably due to genetic as well as environmental factors. ALDH2 eliminates toxic aldehydes including 4-hydroxy-2-nonenal (4-HNE) derived from lipid peroxidation and acrolein in tobacco smoking as well as ethanol-derived acetaldehyde and thereby protects tissues and cells from oxidative damage. Deficient variant ALDH2*2 genotype is prevalent among East Asians and is a significant risk factor for both coronary spasm and AMI through accumulation of toxic aldehydes, thereby contributing to oxidative stress, endothelial damage, vasoconstriction, and thrombosis. Toxic aldehydes are thus identified as risk factors to be targeted for the treatment of coronary spasm and AMI.

[Prinzmetal angina. Questions of pathogenesis, clinic, diagnosis and treatment].

Current problems of Prinzmetal angina (vasospastic angina, variant angina) considers in this review. Attention is drawn to early diagnosis, which should be comprehensive, taking into account possible atypical courses and the development of complications. The important role of electrocardiographic monitoring (including using implantable recorders) is highlighted. It is emphasized that patients with cardiac arrhythmias, syncope are at high risk of developing sudden cardiac death. In this category of patients, it is recommended to timely determine the indications for implantation of a cardioverter - defibrillator. Authors consider the prospects of using new methods of treatment of angina pectoris.

[MINOCA-myocardial infarction with non-obstructive coronary arteries]. / MINOCA ­ Myokardinfarkt ohne obstruktive Koronarerkrankung.

In recent years it has been observed with increasing interest that there is a group of patients with electrocardiographic and laboratory features of myocardial infarction (MI) but no obstructive coronary artery disease (<50% diameter stenosis). For this entity the term myocardial infarction with non-obstructive coronary arteries (MINOCA) has been coined. The prevalence of MINOCA is estimated to be 6-9% among patients diagnosed with MI and it is more common in women than men as well as in patients presenting with NSTEMI than in those presenting with STEMI. The MINOCA is a working diagnosis that requires a further diagnostic work-up by invasive techniques, such as intravascular ultrasound (IVUS) and optical coherence tomography (OCT) or non-invasive imaging with cardiac magnetic resonance imaging (CMRI). When it is ascertained that obstructive coronary artery disease has not been inadvertently overlooked, other coronary disorders, such as plaque rupture or erosion, thrombosis, dissection, spasms or microvascular dysfunction should be evaluated. Furthermore, myocarditis or tako-tsubo cardiomyopathy should be excluded by CMRI as non-coronary causes. The further treatment and prognosis of patients with MINOCA depend on the underlying cause and the final diagnosis.

Unrecognized coronary vasospasm in patients referred for percutaneous coronary intervention: Intracoronary nitroglycerin, the forgotten stepchild of cardiovascular guidelines.

OBJECTIVE: The goal of this study was to demonstrate the importance of intracoronary nitroglycerin (IC NTG) administration during diagnostic coronary angiography and prior to percutaneous coronary intervention (PCI). BACKGROUND: PCI has been a mainstay treatment for patients with symptomatic coronary artery disease. While current guidelines emphasize the importance of periprocedural antithrombotic medications, they fail to mention the use of nitroglycerin prior to PCI. METHODS: Retrospective chart and angiographic review was performed to identify patients referred for PCI who had significant angiographic stenoses that resolved after administration of IC NTG. RESULTS: The study group consisted of 6 patients (3 men, 3 women) with mean age 52 ± 4years (range 46-57 years). All had anginal symptoms and significant (>70%) stenosis on diagnostic coronary angiography. None had documented ST segment elevation. The median interval between diagnostic and staged PCI procedures was 3 days. IC NTG was not administered to any of the patients at the time of diagnostic coronary angiography. In each case, repeat coronary angiography following administration of IC NTG (155 ± 46 mcg) before planned PCI demonstrated resolution of the target stenosis. PCI was deferred and all patients were successfully managed medically. CONCLUSION: Coronary artery spasm is an under-recognized cause of chest pain in patients with significant angiographic lesions. Coronary spasm should be suspected especially in younger patients (less than 60 years old) with apparent single vessel disease. IC NTG should be routinely administered during diagnostic angiography and before PCI to avert unnecessary coronary interventions. © 2017 Wiley Periodicals, Inc.

The real world in the clinic before and after the establishment of guidelines for coronary artery spasm: a questionnaire for members of the Japanese Cine-angio Association.

We investigated the clinical situations and the present knowledge of Japanese cardiologists about coronary artery spasm before and after the establishment of guidelines for this condition in the real world. A questionnaire was developed regarding the number of cases of coronary angiography, percutaneous coronary intervention, and invasive/non-invasive spasm provocation tests before (2008) and after (2014) the establishment of the Japanese Circulation Society (JCS) guidelines for coronary artery spasm and the status of spasm provocation tests. The questionnaire was sent to members of the Japanese Cine-angio Association in 81 cardiology hospitals in Japan. The completed surveys were returned from 20 hospitals, giving a response rate of 24.7%. Pharmacological spasm provocation tests increased in 2014 and vasospastic angina and variant angina also increased in 2014 compared with 2008, but the increase was not significant. Non-invasive spasm provocation tests such as hyperventilation tests and cold stress tests decreased remarkably in 2014. Spasm provocation tests were initially performed in the left coronary artery was employed in just 30% of the hospitals. The majority of institutions did not perform the spasm provocation testing in patients with unknown causes of heart failure or in survivors of ventricular fibrillation. Although 40% of the hospitals were not satisfied with standard spasm provocation tests, the majority of the hospitals agreed that spasm provocation tests will be necessary in the future. In general, the JCS guidelines contributed to the widespread use of provocative testing for coronary artery spasm in the real world. However, some issues about spasm still remained in the clinic.

Beneficial effects of long-acting nifedipine on coronary vasomotion abnormalities after drug-eluting stent implantation: The NOVEL study.

AIMS: It is widely known that drug-eluting stents (DES) induce coronary vasomotion abnormalities. We have previously demonstrated that chronic treatment with long-acting nifedipine suppresses coronary hyperconstricting responses induced by the first-generation DES (e.g. sirolimus- and pacritaxel-eluting stents) through inhibition of vascular inflammation in pigs. To examine whether this is also the case with the second-generation DES (everolimus-eluting stents, EES) in humans, the most widely used DES in the world, we conducted a prospective, randomized, multicentre trial, termed as the NOVEL Study. METHODS AND RESULTS: We evaluated 100 patients with stable angina pectoris who underwent scheduled implantation of EES in the left coronary arteries. They were randomly assigned to receive either conventional treatments alone or additionally long-acting nifedipine (10-60 mg/day) (n = 50 each). After 8-10 months, 37 patients in the control and 38 in the nifedipine group were examined for coronary vasoreactivity to intracoronary acetylcholine (ACh) by quantitative coronary angiography after 48-h withdrawal of nifedipine. Coronary vasoconstricting responses to ACh were significantly enhanced at the distal edge of EES compared with non-stented vessel (P = 0.0001) and were significantly suppressed in the nifedipine group compared with the control group (P = 0.0044). Furthermore, the inflammatory profiles were also improved only in the nifedipine group, which evaluated by serum levels of high-sensitivity CRP (P = 0.0001) and adiponectin (P = 0.0039). CONCLUSIONS: These results indicate that DES-induced coronary vasomotion abnormalities still remain an important clinical issue even with the second-generation DES, for which long-acting nifedipine exerts beneficial effects associated with its anti-inflammatory effects. TRIAL REGISTRATION: This study is registered at the UMIN Clinical Trial Registry (UMIN-CTR; ID=UMIN000015147).

Blocked Coronary Artery Due To Coronary Spasm Treated With Stent Insertion: A Sub-Optimal Result?

Myocardial infarction (MI) is an extremely common cause of chest pain. MI can be acute with ST elevation (STEMI) or non-STEMI (NSTEMI). Coronary artery spasm can be severe enough to cause occlusion of the coronary arteries particularly with an exaggerated response in regions of coronary atheroma and plaque ulceration. It is not uncommon for coronary spasm to be mistaken with acute thrombotic occlusion of the coronary artery. We describe a case of a 42-year old man with known cardiac risk factors presents with chest pain for few hours to a tertiary centre hospital. A coronary angiogram showed occlusion of the right epicardial coronary artery with a severe spasm at the level of the atheroma. The initial coronary stent which was deformed because of intense pressure of spasm required another stent to be placed within the first stent. Diltiazem and Nitrates were started as secondary prevention treatment to reduce effect of coronary spasm. The patient made an uneventful recovery and was discharged home with no sequelae over the next 3 years follow up.