Pericarditis as a trigger for Prinzmetal angina - a case report.

Prinzmetal angina is one of the causes of acute coronary syndromes, the exact etiology of which is still unknown. Here we introduce a 27-year-old man with no history of cardiovascular disease, with a history of hospitalization due to acute pericarditis in the previous month, who was discharged with a good response to ibuprofen treatment but had clinical and electrocardiographically recurrence of pericarditis with compressive retrosternal chest pain and electrocardiogram (ECG) changes in favor of acute infero-postero-right ventricular (RV) myocardial infarction (MI). Treatment with vasodilator improved compressive retrosternal chest pain and reversed acute myocardial infarction changes completely and left pleuritic chest pain and pericarditis changes in the ECG. Due to the typical chest pain, he was admitted to the emergency room; ECG revealed generalized ST-segment elevation with acute pericarditis pattern again. Acute infero-posterior and right ventricular acute myocardial infarction pattern was also evident. After treatment with nitroglycerin in the Critical Cardiac Unit (CCU), all ECG ischemic changes returned to baseline, and pericarditis remained in all leads. The patient was discharged with non-steroidal anti-inflammatory drugs (NSAIDs), calcium channel blockers, and a good general condition.

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.

Effect of intracoronary adenosine on ergonovine-induced vasoconstricted coronary arteries.

BACKGROUND: This study aimed to evaluate the effect of adenosine on epicardial coronary artery diameter during ergonovine provocation testing. METHODS: A total of 158 patients who underwent an ergonovine provocation test with intracoronary adenosine injection between 2011 and 2014 were selected. Patients were divided into four groups based on the severity of percent diameter stenosis following intracoronary ergonovine administration: Group 1, induced spasm < 50%; Group 2, 50-89%; Group 3, 90-99%; and Group 4, total occlusion. RESULTS: Spasm positivity was observed in 44 (27.8%) cases in the study population (mean age, 57.4 ± ± 10.7 years). Intracoronary adenosine increased the diameter of the ergonovine-induced epicardial artery by 0.51 ± 0.31 mm, 0.73 ± 0.39 mm, 0.44 ± 0.59 mm, and 0.01 ± 0.04 mm in Groups 1, 2, 3, and 4, respectively. Subsequent administration of nitroglycerin further increased vessel diameter by 0.49 ± 0.28 mm, 0.93 ± 0.68 mm, 2.11 ± 1.25 mm, and 2.23 ± 0.69 mm in Groups 1, 2, 3, and 4, respectively. The ratios of adenosine-induced diameter to reference diameter were significantly lower in patients with spasm positive results (0.68 [0.59-0.76] vs. 0.18 [0.00-0.41], p < 0.001 in the study population; 0.60 [0.54-0.67] vs. 0.40 [0.27-0.44], p < 0.001 in Group 2) with the best cut-off value of 0.505 (sensitivity 0.955, specificity 0.921). CONCLUSIONS: Intracoronary administration of adenosine dilated the ergonovine-induced vasoconstricted epicardial coronary artery. The ratio of adenosine-induced diameter to reference diameter was significantly lower in patients with spasm positive results.

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.

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.

Prinzmetals angina presenting with non critical lesion with normal FFR -to stent or not to stent.

Variant angina also called Prinzmetals angina is an enigma characterized by transient circadian symptoms of chest pain associated with ECG changes. The patient is symptom free with normal ECG and echo during symptom free periods. We present a case associated with transient ST-segment elevation with non critical lesion with normal FFR.

Differential incidence and type of spasm according to coronary arterial location.

BACKGROUND: We encounter a less provoked spasm in the left circumflex artery (LCX) by acetylcholine (ACh) testing compared with left anterior descending artery and right coronary artery (RCA) in the real world. OBJECTIVES: We investigated the clinical characteristics of provoked spasm in the LCX by ACh testing. METHODS: We retrospectively analyzed consecutive 1392 ACh testing over 20 years (1991-2011). The maximal ACh dose was 100 µg into the left coronary artery and 80 µg into the RCA. Positive spasm was defined as transient of more than or equal to 90% narrowing and usual chest symptoms or ischemic ECG changes. RESULTS: Positive provoked spasm was recognized in 622 patients (44.7%) including 456 RCA spasms, 448 left anterior descending artery spasms, and 176 LCX spasms. LCX-provoked spasm was significantly lower than other vessels (P<0.001). LCX-provoked spasm was observed in 176 patients, of whom 113 patients (64.2%) had triple-vessel spasm, 46 patients (26.1%) had double-vessel spasm, and 17 patients (9.7%) had single-vessel spasm. More than 90% patients with LCX-provoked spasm had multiple spasms. Of 17 patients with LCX single-vessel spasm, 15 patients (88.2%) had focal spasm. CONCLUSION: Under a maximal ACh dose of 100 µg into the left coronary artery, LCX-provoked spasm was significantly lower than other vessels and more than 90% of patients had multiple spasms.

A woman with recurrent chest pain and ST-segment elevation.

A 32-year-old female presents with recurrent episodes of unprovoked chest pain associated with inferior ST-segment elevation and reciprocal ST-segment depression. Coronary angiography during one of these episodes revealed coronary artery spasm that spontaneously resolved followed by resolution of these electrocardiographic changes. There was no atherosclerotic occlusive disease. Her cardiac markers were normal and echocardiogram showed no regional wall motion abnormalities. Electrocariogram and angiography findings are shown in Fig. 1.

Maximal acetylcholine dose of 200 µg into the left coronary artery as a spasm provocation test: comparison with 100 µg of acetylcholine.

As a spasm provocation test of acetylcholine (ACH), incremental dose up (20/50/100 µg) into the left coronary artery (LCA) is recommended in the guidelines established by Japanese Circulation Society. Recently, Ong et al. reported the ACOVA study which maximal ACH dose was 200 µg in the LCA. We compared the angiographic findings between ACH 100 µg and ACH 200 µg in the LCA and also examined the usefulness and safety of ACH 200 µg in Japanese patients without variant angina. As a spasm provocation test, we performed intracoronary injection of ACH 200 µg after ACH 100 µg in 88 patients (55 males, 68.4 ± 11.7 years old) including 59 ischemic heart disease (IHD) patients and 29 non-IHD patients. Positive spasm was defined as >99 % transient stenosis (focal spasm) or 90 % severe diffuse vasoconstriction (diffuse spasm). Positive spasm by ACH 200 µg was significantly higher than that by ACH 100 µg (36 pts: 40.9 % vs. 17 pts: 19.3 %, p < 0.01). Diffuse distal spasm on the left anterior descending artery was more recognized in ACH 200 µg than in ACH 100 µg (30.7 vs. 13.6 %, p < 0.01). In 29 rest angina patients, positive spasm by ACH 200 µg (19 pts) was significantly higher than that by ACH 100 µg (7 pts) (65.5 vs. 24.1 %, p < 0.01). No serious irreversible complications were found during ACH 200 µg. Administration of ACH 200 µg into the LCA was safe and useful. We may reexamine the maximal ACH dose into the LCA.

Three cases of vasospastic angina that developed following the initiation of corticosteroid therapy.

Three patients diagnosed as having remitting seronegative symmetrical synovitis with pitting edema syndrome, pemphigus erythematosus and idiopathic interstitial pneumonia were treated with oral prednisolone. Several weeks after starting the treatment, they experienced repeated chest pain attacks between midnight and early morning, although none of the patients had a past history of ischemic heart disease. One of the patients exhibited aggravation of symptoms soon after increasing the dose of prednisolone. A definitive diagnosis of vasospastic angina was made using electrocardiograms, coronary angiography and vasospasm provocation tests. These cases emphasize that clinicians should be aware of the possible occurrence of vasospastic angina following the initiation of corticosteroid therapy.

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.

Persistent coronary artery spasm documented by follow-up coronary angiography in patients with symptomatic remission of variant angina.

For patients with variant angina it is very important to start medical therapy using calcium-channel blockers. However, the decision of physicians regarding whether to decrease the dose of the drug or discontinue it is controversial. We investigated whether the nature of spasm is remissive and whether the termination of medications is safe. The subjects studied were included in the Vasospastic Angina in Catholic Medical Center Registry from March 2001 to December 2009. We analyzed 37 patients (62 lesions) with variant angina, diagnosed using coronary angiography (CAG) and he acetylcholine provocation test, without any organic coronary stenosis, whose symptoms were well controlled after medication. The follow-up CAG with provocation test was performed at a median interval of 44 months. The characteristics of spasm were analyzed on each pair of CAGs. The study group consisted of 23 men (62.2 %) and 14 women (37.8 %) with a mean age of 59 ± 11.1 years. The follow-up CAG with provocation test showed that the characteristics of the spasmodic nature were consistent with the first test in all patients. Although the patients with variant angina had no chest pain after medical treatment, the spasmodic nature of coronary arteries still remained. We may decrease the drug dosage after carefully checking the patient's symptoms but recommend not discontinuing therapy, even if the patient is asymptomatic.