Coronary Spastic Angina Research Articles

The Bezold-Jarisch Reflex in a Patient With Stanford Type A Acute Aortic Dissection

The Bezold-Jarisch reflex is a depressor reflex of the heart due to the preferential distribution of vagal nerves in the inferior wall of the left ventricle. We report a case of Stanford type A acute aortic dissection, in which coronary spastic angina caused the Bezold-Jarisch reflex in the acute phase. A 53-year-old man presented with left chest pain and cold sweating. An electrocardiogram was normal and the high-sensitivity cardiac troponin T level was negative. A diagnosis of Stanford type A acute aortic dissection was made based on computed tomography (CT); there was no evidence of ischemic heart disease on coronary CT angiogram obtained simultaneously. While waiting for emergency surgical repair, chest pain worsened, followed by bradycardia and hypotension, along with ST-segment elevations in the inferior leads, all of which were resolved by conservative treatment. During surgery, no evidence to suggest an extension of the dissection to the ostium of the right coronary artery was observed. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: The present case highlights the importance of recognizing the Bezold-Jarisch reflex because this depressor reflex may require different management than other conditions.

Coronary spastic angina after the administration of intravenous immunoglobulin in myasthenia gravis: a case report

BackgroundMyasthenia gravis (MG) is an autoimmune disease caused by antibodies that block or destroy nicotinic acetylcholine receptors at the neuromuscular junction. Most of MG patients need immunosuppression agents in addition to treatments that alleviate the symptoms. Intravenous immunoglobulin (IVIg) and plasma exchange are specific treatments given to patients with severe MG and myasthenia gravis crisis. IVIg therapy can cause an increase in serum viscosity; therefore, the risk for thromboembolic events, such as stroke, myocardial infarction, and pulmonary embolism, are reported after IVIg therapy.Case presentationAn MG patient was treated with pyridostigmine bromide and prednisolone. The patient’s symptoms worsened 26 days after the commencement of treatment and was presented with head drop and dyspnea. The patient was diagnosed with MG crisis and IVIg was initiated. However, the patient reported chest pain and dyspnea 3 days after IVIg had started. An electrocardiogram (ECG) revealed ST elevations in leads II, III, and aVF. A cardiac catheterization was performed and stenosis, obstruction, and sclerosis were ruled out. Glyceryl trinitrate relieved the patient’s symptoms, suggesting coronary spastic angina (CSA).ConclusionsWe report the first case of CSA after IVIg. Practitioners should be aware of the potential risks of CSA when administering IVIg for MG patients, in particular in old patients with vascular risk factors.

Mutational analysis of β-arrestin in Japanese patients with coronary spastic angina

Mutational analysis of β-arrestin in Japanese patients with coronary spastic angina

East Asians Variant Mitochondrial Aldehyde Dehydrogenase 2 Genotype Exacerbates Nitrate Tolerance in Patients With Coronary Spastic Angina.

Aldehyde dehydrogenase 2 (ALDH2) plays a central role in the biotransformation of glyceryl trinitrate (GTN) or nitroglycerin, which is widely used for the treatment of coronary artery disease (CAD). The deficient variant ALDH2 genotype (ALDH2*2) is prevalent among East Asians. This study examined whether there are differences in nitroglycerine-mediated dilation (NMD) and flow-mediated dilation (FMD) response between wildALDH2*1/*1and variantALDH2*2patients with CAD.Methods and Results:The study subjects comprised 55 coronary spastic angina (CSA) patients, confirmed by coronary angiography and intracoronary injection of acetylcholine (42 men and 13 women, mean age 68.0±9.0 years). They underwent NMD and FMD tests in the morning before and after continuous transdermal GTN administration for 48 h. NMD was lower at baseline inALDH2*2than in theALDH2*1/*1group (P=0.0499) and decreased significantly in both groups (P<0.0001 and P<0.0001, respectively) after GTN, with significantly lower levels in theALDH2*2group (P=0.0002). FMD decreased significantly in bothALDH2*1/*1andALDH2*2groups (P<0.0001and P=0.0002, respectively) after continuous GTN administration, with no significant differences between the 2 groups both before and after GTN. Continuous administration of GTN produced endothelial dysfunction as well as nitrate tolerance in bothALDH2*1/1andALDH2*2patients with CSA.ALDH2*2attenuated GTN response and exacerbated GTN tolerance, but not endothelial dysfunction, as compared toALDH2*1/*1in patients with CSA.

Gender Difference in Association between Coronary Spastic Angina and Polyunsaturated Fatty Acids

Gender Difference in Association between Coronary Spastic Angina and Polyunsaturated Fatty Acids

Intravascular ultrasound findings and stent implantation for a patient with coronary spastic angina at site of progressive atherosclerotic plaque and responded poorly to medical treatment: a case report

BackgroundMost coronary spastic angina patients are responsive to coronary vasodilators therapy, and stent implantation is not recommended for regular use. We reported the angiographic and intravascular ultrasound (IVUS) images of a rare case who responded poorly to medical treatment due to progressive atherosclerotic plaque at the spastic site.Case presentationA 60-year-old man complaining of 1-month history of episodic chest pain at rest was admitted to our hospital. The diagnosis of coronary spastic angina was made based on the angiographic evidence of vasospasm at the right coronary artery (RCA). The patient responded poorly to conventional medical treatment during the 1-year follow-up. The repeated angiography revealed totally occlusion of the proximal segment of the RCA at the same location as 1 year before, and IVUS demonstrated there was vulnerable plaque and thrombus at the site of spasm. Episodic chest pain ceased completely in the follow up period after stenting.ConclusionCoronary spasm might present at the vessel site with advanced atherosclerotic plaque. For patients with refractory vasospastic angina and significant occlusion, stenting might be a viable and valuable treatment strategy under the guidance of intracoronary imaging.

Clinical characteristics in patients with rest angina and hypoplastic right coronary artery.

Hypoplastic coronary artery disease is a rare congenital abnormality reported to be associated with myocardial infarction and sudden cardiac death. Provoked positive spasm in the left circumflex coronary artery (LCX) with pharmacological spasm provocation tests was remarkably lower than other coronary arteries. We sometimes encountered patients with rest angina and hypoplastic right coronary artery (H-RCA). Among 5953 patients with diagnostic and follow-up coronary arteriography, we found 93 patients (1.6%) with H-RCA. During the same period, we could perform spasm provocation tests in 564 patients with rest angina including 13 patients with H-RCA and 249 patients with effort angina including 10 patients with H-RCA. Pharmacological spasm provocation tests were performed in 51 of 93 patients including 34 patients with ischemic heart disease (IHD) and 17 patients with non-IHD. Provoked spasm incidence in patients with IHD was higher than in those with non-IHD but not significant (52.9% vs. 29.4%, p = 0.1114). Provoked positive spasm in the LCX in patients with rest angina and H-RCA was significantly higher than that in those without H-RCA (69.2% vs. 23.4%, p < 0.001). Provoked spasm on both left anterior descending artery and LCX in patients with rest angina and H-RCA was also remarkably higher than in those without H-RCA (53.8% vs. 3.1%, p < 0,001). There were no clinical differences between patients with and without H-RCA rest angina. Two-vessel spasm (61.5% vs. 0%, p < 0.01) and LCX-provoked spasm (69.2% vs. o%, p < 0.01) were significantly higher in patients with H-RCA and rest angina than that in those with H-RCA and effort angina. In patients with rest angina and H-RCA, LCX-positive spasm was significantly higher and these patients may have a potential of high disease activity in the clinic as a coronary spastic angina.

IQGAP1 activates PLC-δ1 by direct binding and moving along microtubule with DLC-1 to cell surface.

Phospholipase C (PLC)‐δ1, activated by p122RhoGTPase‐activating protein (GAP)/deleted in liver cancer‐1 (p122RhoGAP/DLC‐1), contributes to the coronary spastic angina (CSA) pathogenesis. The present study aims to further investigate the p122RhoGAP/DLC‐1 protein. We examined molecules assisting this protein and identified a scaffold protein—IQ motif‐containing GTPase‐activating protein 1 (IQGAP1). IQGAP1‐C binds to the steroidogenic acute regulatory‐related lipid transfer (START) domain of p122RhoGAP/DLC‐1, and PLC‐δ1 binds to IQGAP1‐N, forming a complex. In fluorescence microscopy, small dots of PLC‐δ1 created fine linear arrays like microtubules, and IQGAP1 and p122RhoGAP/DLC‐1 were colocated in the cytoplasm with PLC‐δ1. Ionomycin induced the raft recruitment of the PLC‐δ1, IQGAP1, and p122RhoGAP/DLC‐1 complex by translocation to the plasma membrane (PM), indicating the movement of this complex is along microtubules with the motor protein kinesin. Moreover, the IQGAP1 protein was elevated in skin fibroblasts obtained from patients with CSA, and it enhanced the PLC activity and peak intracellular calcium concentration in response to acetylcholine. IQGAP1, a novel stimulating protein, forms a complex with p122RhoGAP/DLC‐1 and PLC‐δ1 that moves along microtubules and enhances the PLC activity.

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 (β = 0.47, p < 0.01). Intraday GV was associated with coronary artery spasm in patients with dysglycemia.

Efficacy of alpha 1 adrenergic antagonist in patients with intractable coronary spastic angina

Efficacy of alpha 1 adrenergic antagonist in patients with intractable coronary spastic angina

Unexpectedly High Prevalence of Coronary Spastic Angina in Patients With Anderson-Fabry Disease.

Although we and others have reported cases of patients with Anderson-Fabry disease (AFD) complicated by coronary spastic angina (CSA), the prevalence of CSA in these patients remains unknown. Methods and Results: We performed the acetylcholine-induced provocation test, according to the Japanese guidelines for the diagnosis and treatment of patients with CSA, in 9 consecutive patients having 5 independent AFD pedigrees. Coronary spasms were provoked in conjunction with symptoms and ECG ischemic changes in 8 of 9 (89%) patients with AFD. We found an unexpectedly high prevalence of CSA in patients with AFD.

P3620Low value of brain natriuretic peptide correlates with the existence of coronary spastic angina diagnosed by ergonovine provocation test

P3620Low value of brain natriuretic peptide correlates with the existence of coronary spastic angina diagnosed by ergonovine provocation test

1347Unexpectedly high prevalence of coronary spastic angina in patients with Fabry disease

1347Unexpectedly high prevalence of coronary spastic angina in patients with Fabry disease

Optimal Medications and Appropriate Implantable Cardioverter-defibrillator Shocks in Aborted Sudden Cardiac Death Due to Coronary Spasm.

Objective Life-threatening ventricular arrhythmias are recognized in patients with coronary spastic angina. Implantable cardioverter-defibrillators (ICDs) are effective in patients with structural heart disease and ventricular fibrillation. However, the optimal medication for patients with aborted sudden cardiac death (SCD) due to coronary artery spasm after the implantation of ICD remains controversial. Methods We investigated the medications and the numbers of appropriate ICD shocks in 137 patients with a history of aborted SCD due to coronary spasm. Results Appropriate ICD shocks were observed in 24.1% (33/137) of patients with aborted SCD due to coronary spasm during 41 months of follow-up. Only 15 (15.6%) of the 96 patients with ICDs received aggressive medical therapy, including two or three calcium-channel antagonists. The rate of appropriate ICD shocks was significantly higher in Western countries than in Asian countries (42.9% vs. 19.3%, p<0.01), whereas the medications did not differ between the two regions. Appropriate ICD shocks successfully resuscitated 33 patients. Three patients died due to second serious fatal arrhythmias. Conclusion Appropriate ICD shocks were recognized in a quarter of patients with aborted SCD due to coronary spasm and ICD implantation was effective for suppressing the next serious fatal arrhythmia in these patients. We should reconsider prescribing more medications after ICD implantation in patients with aborted SCD due to coronary artery spasm.

Orofacial Pain Associated with Vasospastic Angina: A Case Report.

The primary symptom of ischemic heart disease is typically chest pain, but in some cases, this pain may radiate to the maxillofacial region. This article describes the case of a 44-year-old man with orofacial pain of cardiac origin. The patient was suspected to be suffering from cardiac disease by the oral and maxillofacial surgeon and was referred to a cardiologist, where he received a heart examination. The patient was diagnosed by means of cardiac catheterization as having coronary spastic angina. During catheterization, intracoronary ergonovine maleate induced orofacial pain that was almost the same in character and intensity as the patient's first episode. The orofacial pain was considered to be telalgia from coronary spastic angina. The patient started medication on the same day as the diagnosis. There was no recurrence of any symptoms. These findings indicate that in such cases, the dentist may contribute to identifying ischemic heart disease and should refer the patient to a cardiologist.

Impact of pharmacological spasm provocation test in patients with a history of syncope.

Coronary artery spasm is involved in the pathogenesis of various cardiac disorders. We investigated patients with a history of syncope who underwent elective coronary angiography. We retrospectively analyzed 5781 consecutive patients who had diagnostic or follow-up angiography during a 26-year period. During this period, we found 95 patients with a history of syncope before elective coronary angiography. Pharmacological spasm provocation testing was performed in 64 patients with a history of syncope (<1year). Positive pharmacological response was observed in 48 patients, while the remaining 16 patients had negative tests. Positive spasm was defined as a transient ≥90% narrowing with ischemic electrocardiographic changes. Among the 64 patients, definite coronary spastic angina (CSA) was found in 35 patients (54.7%) and suspected CSA was found in 13 patients (20.3%). Among the 35 patients with definite CSA, 22 patients (62.9%) had chest symptoms before syncope, but 13 (37.1%) had no chest symptom before syncope. No difference in clinical characteristics was observed between the two groups. Focal spasm during pharmacological spasm provocation tests was significantly higher in patients with chest symptoms than in those without chest symptoms before syncope (54.3 vs. 12.0%, p<0.002). CSA was observed in 75.0% of patients with a history of syncope (<1year). Thirteen patients with definite CSA had neither chest pain nor chest pressure before syncope. We should therefore investigate coronary artery spasm as a potential etiology in patients with a history of syncope.

Clinical roles of calcium channel blockers in ischemic heart diseases.

Calcium (Ca) channel blockers (CCBs) inhibit Ca2+ channels in the myocardium or vascular smooth muscle cells, inhibit myocardium contraction, inhibit the impulse conduction system (anti-arrhythmias) and cause vasodilation. New classifications based on subtypes of Ca channels and α1 subunits have been proposed. Moreover, CCBs have pleiotropic effects on coronary spastic angina (CSA), including variant angina, myocardial infarction (MI) and stent thrombosis (ST). Although the roles of CCBs in clinical situations remain unknown, further studies in this field are expected to broaden our understanding. In this article, we explain the clinical roles of CCBs in ischemic heart diseases, such as CSA, MI and ST, based on previous knowledge and as demonstrated in representative clinical trials.

Overview of the Non-Invasive Examinations in Patients with Coronary Spastic Angina

Exercise test, hyperventilation test or cold pressor test was employed to reproduce ST elevation in patients with variant angina. However, cardiologists could not get the high positive frequency from these tests in patients without high disease activity. Now a days, cardiologists can easily perform coronary angiography or coronary computed tomography. Cardiologists skipped the non-invasive spasm provocation tests such as hyperventilation test or cold pressor test to diagnose patients with coronary artery spasm. Approximately a half patient with coronary spasm had pathologic responses of exercise tests. More than a third patient with coronary spasm and without fixed stenosis had ischemic findings on exercise tests, whereas more than two-third patients with coronary spasm and with organic stenosis had pathologic responses on exercise testing. We should reconsider the usefulness of exercise tests to obtain the ischemic findings due to coronary artery spasm in the clinic before performing the cardiac catheterization.

Acetylcholine coronary spasm provocation testing: Revaluation in the real clinical practice

Background: Japanese Circulation Society guidelines for coronary spastic angina recommended the step-by-step bolus administration of acetylcholine (ACh) dose on both coronary arteries (left coronary artery (LCA): 20/50/100 µg, right coronary artery (RCA): 20/50 µg). Our routine practice employed the maximal 80 µg ACh into the RCA and 200 µg ACh into the LCA not to misdiagnose the patients with coronary spasm. At least from five to seven times procedures are necessary during ACh spasm provocation tests. Radiation exposure and the adverse effect of contrast medium is one of the problems. Objectives: We investigated the procedures of the ACh administration on both coronary arteries in the real clinical practice retrospectively. Methods: We analyzed the consecutive 150 patients who had maximal ACh dose of 200 µg into the LCA. We compared clinical issues with and without saving ACh dose. Positive spasm was defined as a transient >90% narrowing and usual chest symptom or ischemic ECG changes. Results: Among 150 patients, 63 patients (42.0%) had positive provoked spasm. Patients with step-by-step ACh dose into the LCA were significantly higher than those with step-by-step ACh dose into the RCA. Saving of ACh 20 µg, 50 µg, and 100 µg into the LCA was observed in 59 patients, 18 patients, and one patient, respectively. Saving of 20 µg ACh and 50 µg ACh into the RCA was found in 98 patients and 60 patients, respectively. Positive spasm frequency was not different between the patients with and without saving ACh procedures. Radiation exposure time/dose and total used amount of contrast medium in saving ACh tests were significantly lower than those in step-by-step ACh tests. No serious irreversible complications were found. Conclusions: We should reconsider the saving ACh spasm provocation tests in the real clinical practice.

A case of coronary spastic angina with exercised-induced ischemia that confirmed curative effect by exercise stress myocardial scintigram

A case of coronary spastic angina with exercised-induced ischemia that confirmed curative effect by exercise stress myocardial scintigram