Coronary Spasm In Patients Research Articles

Does the intracoronary pressure differ according to two types (diffuse or focal) of coronary spasm?

Several reports show that two types of coronary vasospasm (diffuse and focal spasm) are associated with the severity or prognosis of coronary spasm in patients with vasospastic angina (VSA). It is unclear whether intracoronary pressure differs between the two spasm types. To investigate such relationships using a pressure wire during the spasm provocation test (SPT) in patients with VSA. Eighty-seven patients with VSA (average age: 67 years; 50 men, 37 women) underwent SPT. During the SPT, a pressure wire was advanced into the distal portion of the right coronary artery and left anterior descending coronary artery, and the ratio of the intracoronary pressure to the aortic pressure (Pd/Pa) was continuously monitored. An SPT was performed using acetylcholine (ACh), and the presence of coronary spasm was defined as the presence of > 90% arterial narrowing in response to an ACh infusion, with the usual chest symptoms and/or ischemic ECG changes. Focal spasm was defined as total or subtotal spasm within one segment of the AHA classification, while diffuse spasm was defined as > 90% spasm with two or more segments. Among 87 patients, the frequencies of metabolic syndrome and having coronary atherosclerosis were higher in the focal group (n = 33) than in the diffuse spasm group (n = 54, P < 0.05). In the vessel analyses, in these 134 spastic segments, diffuse and focal spasms were detected in 100 and 34 vessels, respectively. The Pd/Pa at baseline was similar in both groups (diffuse: 0.96 ± 0.05, focal: 0.95 ± 0.05, P = 0.35); however, the Pd/Pa during coronary spasm was lower in focal spastic vessels (0.66 ± 0.20) than in diffuse spastic vessels (0.76 ± 0.11, P < 0.01), and the reduction in Pd/Pa during an SPT was also lower in focal spastic vessels (-0.29 ± 0.20) than in diffuse spastic vessels (-0.18 ± 0.11, P < 0.01). The presence of focal spasm was a significant factor responsible for reduction in Pd/Pa during SPT. These findings suggest that focal spasm may be more severe than diffuse spasm, judging from the intracoronary pressure during coronary spasm.

429 KOUNIS-ZAVRAS SYNDROME: UNDERREPRESENTED OR UNDERDIAGNOSED?

Abstract A 64-year-old man was admitted to the emergency department for a major allergic reaction to an insect bite. On physical examination, he presented with tachycardia, hypotension and diffuse pomphoid erythema requiring treatment with intravenous cortisone and antihistamines, with partial benefit. From his past medical history hypertension and previous percutaneous coronary intervention (PCI) with drug eluting stents (DES) on left anterior descendant (LAD) and circumflex coronary artery (Cx) for stable angina emerged. Almost 15 minutes after his admission he developed oppressive chest pain and dyspnea, so an electrocardiogram (EKG) was performed showing an ST segment elevation in inferior-posterior-lateral leads. Therefore, the patient was transferred to the Cath Lab to perform a coronary angiography study with finding of intrastent thrombosis (IST) of Cx and LAD and sub-occlusion of the posterior interventricular branch of the right coronary artery (RCA), not responsive to nitrates. PCI was performed with manual thrombus aspiration and high pressure non-compliant balloons of the IST and PCI with a single DES of the RCA lesion. The patient was then transferred to coronary intensive care unit. Echocardiography revealed a normal left ventricle ejection fraction without any wall motion abnormalities and the EKG showed a complete ST resolution. Laboratory exams showed increased troponin, typical of myocardial infarction, and an increase in IgE and serum tryptase, typical for an allergic reaction. Based on clinical, angiographic and biochemical data, diagnosis of type III Kounis-Zavras (KS) syndrome was made. KS is an acute coronary event in the setting of a hypersensitivity reaction which trigger the release of inflammatory mediators by activated mast cell leading to coronary artery spasm, atheromatous plaque rupture or stent thrombosis. Optimal medical therapy for both ischemic heart disease and allergic reaction was set, with ace inhibitor, high dose statin, non-dihydropyridine calcium channel blocker, dual antiplatelet therapy, antihistamines and cortisone with a decalage scheme. There is no consensus for KS management and the difficulty lies in the fact that treating one of the two concomitant conditions could worsen the other. Three variants of this syndrome have been described in the literature. Type I KS is characterized by coronary spasm in patients typically lacking cardiovascular risk factors and coronary arteries free from atheromatous lesions. Type II KS is characterized by instability of an already present coronary plaque. Type III KS is characterized by intrastent thrombosis in patients with previous coronary angioplasty. Several factors incriminated in KS syndrome have been described, including medications (such as antibiotics, analgesics and anti-inflammatories) and environmental factors (such as, bee sting, viper venom, wasp sting). The underlying pathophysiological process involves a series of mediators, such as histamine and tryptase, released by activated mast cells locally during an immunological reaction. KS syndrome is a real challenge since there is no definitive guidelines for diagnosis, management and treatment and the plethora of clinical presentation range from angina pectoris with mild atopic dermatitis to acute coronary syndrome with cardiogenic shock and anaphylaxis. This broad spectrum of clinical manifestations associated with the increasing new triggers (drugs, contrast dye, insects) often leads to a misdiagnosis with a delay of the proper administration of the effective therapy, sometimes resulting fatal.

Prevalence of Coronary Microvascular Disease and Coronary Vasospasm in Patients With Nonobstructive Coronary Artery Disease: Systematic Review and Meta-Analysis.

BackgroundA relevant proportion of patients with suspected coronary artery disease undergo invasive coronary angiography showing normal or nonobstructive coronary arteries. However, the prevalence of coronary microvascular disease (CMD) and coronary spasm in patients with nonobstructive coronary artery disease remains to be determined. The objective of this study was to determine the prevalence of coronary CMD and coronary vasospastic angina in patients with no obstructive coronary artery disease.Methods and ResultsA systematic review and meta‐analysis of studies assessing the prevalence of CMD and vasospastic angina in patients with no obstructive coronary artery disease was performed. Random‐effects models were used to determine the prevalence of these 2 disease entities. Fifty‐six studies comprising 14 427 patients were included. The pooled prevalence of CMD was 0.41 (95% CI, 0.36–0.47), epicardial vasospasm 0.40 (95% CI, 0.34–0.46) and microvascular spasm 24% (95% CI, 0.21–0.28). The prevalence of combined CMD and vasospastic angina was 0.23 (95% CI, 0.17–0.31). Female patients had a higher risk of presenting with CMD compared with male patients (risk ratio, 1.45 [95% CI, 1.11–1.90]). CMD prevalence was similar when assessed using noninvasive or invasive diagnostic methods.ConclusionsIn patients with no obstructive coronary artery disease, approximately half of the cases were reported to have CMD and/or coronary spasm. CMD was more prevalent among female patients. Greater awareness among physicians of ischemia with no obstructive coronary arteries is urgently needed for accurate diagnosis and patient‐tailored management.

Interplay Between Myocardial Bridging and Coronary Spasm in Patients With Myocardial Ischemia and Non-Obstructive Coronary Arteries: Pathogenic and Prognostic Implications.

BackgroundMyocardial bridging (MB) may represent a cause of myocardial ischemia in patients with non‐obstructive coronary artery disease (NOCAD). Herein, we assessed the interplay between MB and coronary vasomotor disorders, also evaluating their prognostic relevance in patients with myocardial infarction and non‐obstructive coronary arteries (MINOCA) or stable NOCAD.Methods and ResultsWe prospectively enrolled patients with NOCAD undergoing intracoronary acetylcholine provocative test. The incidence of major adverse cardiac events, defined as the composite of cardiac death, non‐fatal myocardial infarction, and rehospitalization for unstable angina, was assessed at follow‐up. We also assessed angina status using Seattle Angina Questionnaires summary score. We enrolled 310 patients (mean age, 60.6±11.9; 136 [43.9%] men; 169 [54.5%] stable NOCAD and 141 [45.5%] MINOCA). MB was found in 53 (17.1%) patients. MB and a positive acetylcholine test coexisted more frequently in patients with MINOCA versus stable NOCAD. MB was an independent predictor of positive acetylcholine test and MINOCA. At follow‐up (median, 22 months; interquartile range, 13–32), patients with MB had a higher rate of major adverse cardiac events, mainly driven by a higher rate of hospitalization attributable to angina, and a lower Seattle Angina Questionnaires summary score (all P<0.001) compared with patients without MB. In particular, the group of patients with MB and a positive acetylcholine test had the worst prognosis.ConclusionsAmong patients with NOCAD, coronary spasm associated with MB may predict a worse clinical presentation with MINOCA and a higher rate of hospitalization attributable to angina at long‐term follow‐up with a low rate of hard events.

The interplay between myocardial bridging and coronary spasm in patients with myocardial infarction and non-obstructive coronary arteries: pathogenic and prognostic implications

Abstract Funding Acknowledgements Type of funding sources: None. Background Myocardial bridging (MB) is associated with endothelial dysfunction and may represent a cause of angina in patients with non-obstructive coronary artery disease (NOCAD). Purpose Herein, we assessed the interplay between MB and coronary vasomotor disorders, evaluating also their prognostic relevance in patients with myocardial infarction and non-obstructive coronary arteries (MINOCA) or stable NOCAD. Methods We prospectively enrolled consecutive NOCAD patients undergoing intracoronary acetylcholine provocative test to assess the presence of epicardial or microvascular spasm in patients with suspected angina or MINOCA. Myocardial bridging was diagnosed by coronary angiography. The incidence of major adverse cardiac events (MACE), defined as the composite of cardiac death, non-fatal MI and rehospitalisation for unstable angina, was assessed at follow-up. We also assessed angina status using Seattle Angina Questionnaires (SAQ). Results We enrolled 310 patients (mean age 60.6 ± 11.9; 136 [43.9%] men; 169 [54.5%] stable NOCAD and 141 [45.5%] MINOCA). MB was found in 53 (17.1%) patients. MB was an independent predictor of spasm and MINOCA (p &amp;lt; 0.05). At follow-up (median 22 months, interquartile range [13-32]), patients with MB had a higher rate of MACE and a lower SAQ score (all p &amp;lt; 0.001) compared with patients without MB. The rate of MACE was considerably higher in patients with both spasm and MB than in the remaining patients (12/42 [28.6%] vs. 13/268 [4.8%], p &amp;lt; 0.001). Conclusion Among patients with NOCAD coronary spasm associated with MB predicts a worse clinical presentation with MINOCA and a worse clinical outcome at medium-long term follow-up, thus identifying a high-risk subset of patients with MB with relevant therapeutic implications. MB and clinical outcomesCharacteristicsOverall population(n= 310)Presence of Myocardial bridging(n= 53)Absence of Myocardial bridging(n = 257)p valueMACE [n, (%)]25 (8.1)12 (22.6)13 (5.1)&amp;lt;0.001CV Death [n, (%)]1 (0.3)0 (0.0)1 (0.4)0.649MI occurrence [n, (%)]6 (1.9)2 (3.8)4 (1.6)0.286Hospitalization for unstable angina [n, (%)]18 (5.8)10 (18.9)8 (3.1)&amp;lt; 0.001Recurrent angina [n, (%)]70 (22.6)20 (37.7)50 (19.4)0.004SAQ [median (IQR)]82 [78; 88]78 [68; 84]84 [78; 88]&amp;lt; 0.001Follow-up time [months, median (IQR)]22 [15;32]20 [15; 28]23 [15; 34]0.10CV Cardiovascular; MI: Myocardial Infarction; IQR: InterQuartile Range; MACE: Major Adverse Cardiovascular Event; SAQ: Seattle Angina Questionnaire.Abstract Figure Outcomes

A case report of coronary artery spasm and takotsubo syndrome: exploring the hidden side of the moon.

Background Takotsubo syndrome (TTS) is a disease characterized by an acute and reversible myocardial injury typically precipitated by stressful and/or emotional triggers. Despite extensive research, its pathogenesis remains incompletely understood. Spasm of epicardial coronary arteries has been proposed as a potential pathogenic factor in TTS.Case summary Herein, we report the case of a 68-year-old female admitted to the emergency department after developing chest pain in concomitance with an intense emotional stress. A diagnosis of non-ST-segment elevation myocardial infarction (NSTEMI) was made. Coronary angiography disclosed normal coronary arteries, and left ventriculography showed an inferior focal akinesia with basal and apical hyperkinesis, so that a diagnosis of ‘focal TTS’ was made. Two months later, the patient was re-admitted with NSTEMI, and repeat coronary angiography showed an irregular subocclusive stenosis of a well-developed first obtuse marginal branch. After intracoronary nitroglycerine infusion, a complete recover of the vessel patency was noted, and a diagnosis of epicardial spasm was made. Intracoronary optical coherence tomography was performed to assess a residual ‘hazy’ region, which confirmed a normal vessel morphology and a residual focal area of spasm without signs of instability.Discussion Whether TTS and coronary artery spasm are two expressions of the same disease, or rather two separate entities with overlapping mechanisms remains unknown, and further research is warranted to solve this issue. Meanwhile, the opportunity of performing provocative tests for coronary spasm in patients with suspected TTS might be considered to gain more insights into this hypothesis.

Effect of sarpogrelate and high-dose statin on the reduction of coronary spasm in vasospastic angina: A two by two factorial, pilot randomized study.

BackgroundVasospastic angina (VSA) is characterized by coronary spasm, which can be aggravated by vasoactive substances such as serotonin. Hypothesis Sarpogrelate, a selective serotonin receptor antagonist, and high‐dose statin have some effects on the reduction of coronary spasm in patients with VSA.MethodsWe recruited 100 patients with angiographically confirmed VSA, and randomly assigned them into four groups: sarpogrelate with high‐dose statin (Group A, n = 25), sarpogrelate with low‐dose or no statin (Group B, n = 25), placebo with high‐dose statin (Group C, n = 25), and placebo with low‐dose or no statin (Group D, n = 25). The primary endpoint was the remission of coronary spasm on 1‐year follow‐up provocation test.ResultsThe most common site of coronary spasm was left anterior descending artery (42%). Most patients (96%) took calcium channel blockers, and 46% were treated with vasodilators. Overall, 40% of patients reported no chest pain at 1 year, and 23% showed complete remission of coronary spasm on 1‐year follow‐up provocation test. No difference was observed in symptomatic and angiographically complete remission rate between the sarpogrelate and the placebo group. Although the apolipoprotein B level at the 1‐year follow‐up was significantly lower in the high‐dose statin group, symptomatic and angiographic outcomes were not different according to statin intensity. Distal thrombolysis in myocardial infarction (TIMI) flow on initial provocation test was independently associated with angiographically complete remission.ConclusionsSarpogrelate or high‐dose statin did not significantly improve the angiographic remission rate in patients with VSA. Distal TIMI flow on initial provocation test could predict the complete remission of coronary spasm at follow‐up.

Coronary artery spasm and dobutamine stress echocardiography in patients without known coronary disease: prevalence, predictors and outcomes

Background and objective Given its high diagnostic and prognostic value and good safety profile, dobutamine stress echocardiography (DSE) is widely used in patients with known or suspected coronary artery disease (CAD); it may however, occasionally induce coronary vasospasm. In this study, we aimed to evaluate the prevalence of dobutamine-related coronary spasm in patients without known CAD, to determine the potential predictors of spasm amongst those with positive DSE and to assess mid-term clinical outcomes.Methods 3,952 patients referred to our echocardiography laboratory for DSE between January 2010 and May 2012 were prospectively investigated. Those with positive DSE underwent coronary angiograms with systematic methylergometrine intracoronary injection in case of absence of significant coronary stenosis or spontaneous occlusive coronary spasm. Patients with spontaneous occlusive coronary spasm or a positive methylergometrine test but no significant stenoses were enrolled and compared with those with positive DSE and significant coronary lesions at angiograms but no history of CAD.Results Twenty-nine patients with DSE-related vasospasm (19.4% of positive DSE without known CAD) were compared with 64 patients with significant coronary lesions. They were significantly younger (56 vs 67.7 years; P < 0.001), had less frequently hypertension (27.6% vs 64.1%; P = 0.01) and diabetes mellitus (31% vs 68.8%; P = 0.01); conversely they had more frequently dyslipidaemia (79.3% vs 53.1%; P = 0.021); they also had a lower ischaemic area at peak DSE (< 4 involved segments) at 79.3% vs 48.4% (P = 0.006). On multivariate analysis, dyslipidaemia (HR = 21.3; 95% CI = [3.45-131.7]; P = 0.001), and less than 4 ischaemic segments at peak DSE (HR = 4.3; 95% CI = [1.14-16.23]; P = 0.034) were found to be independent predictors of coronary spasm rather than significant coronary lesions. Conversely, hypertension, DM and age > 60 were predictors of significant coronary lesions rather than spasm. Long-term actuarial survival free from adverse events was significantly higher in the group of patients with coronary spasm at 93% versus 70% (log rank P = 0.037) in patients with significant coronary disease.Conclusion DSE-induced coronary spasm is an important condition associated with a good mid-term prognosis; dyslipidaemia and lower ischaemic area at peak DSE predicted spasm rather than significant stenoses in patients with positive DSE and no history of CAD.

A report of two cases complicated with coronary spasm in patients with acute aortic dissection

A report of two cases complicated with coronary spasm in patients with acute aortic dissection

Le spasme coronaire lié à la dobutamine chez les patients avec des échocardiographies de stress faussement positives : prévalence et facteurs prédictifs

Background and objectiveDobutamine stress echocardiography (DSE) is being consistently used as an exercise-independent stress modality aimed at the detection of coronary artery disease (CAD) and the evaluation of myocardial ischemia. It may though occasionally induce coronary vasospasm. In this study, we aimed to evaluate the prevalence and predictors of dobutamine-related coronary spasm in patients without known CAD and false positive DSE (positive DSE but no significant coronary lesions on angiogram). MethodsThree thousand nine hundred and fifty-two patients referred to our echocardiography laboratory for DSE between January 2010 and May 2012 were prospectively investigated. Those with positive DSE underwent coronary angiograms with systematic methylergometrine intracoronary injection in case of absence of significant coronary stenosis or spontaneous occlusive coronary spasm. Patients with spontaneous occlusive coronary spasm or positive methylergometrine test but no significant stenoses were enrolled and compared with those with positive DSE but no coronary lesions nor spontaneous or induced spasm (“true” false positive DSE). ResultsTwenty-nine patients with DSE-related vasospasm (19.4% of positive DES without known CAD) were compared with 56 patients with no lesions and no spasm (“true” false positive DSE). They were more frequently smokers (72.4% vs 37.5%; P=0.003); they had more frequently dyslipidemia (79.3% vs 43%; P=0.001); they also had a larger ischemic area at peak DSE (3.4 segments vs 2.7 segments; P=0.05). On multivariate analysis, dyslipidemia (HR=10.7; 95% CI=[2.7–42.1]; P=0.001) and active smoking (HR=6.1; 95% CI=[1.7–21.1]; P=0.004) were found to be independent predictors of spasm-related DSE rather than “true” false positive DSE. ConclusionDSE-related coronary spasm is present in a significant proportion of patients with erroneously labelled “false” positive DSE and should systematically be ruled out. Dyslipidemia and active smoking were independent predictors of spasm rather than “true” false positive DSE.

0027: Dobutamine-related coronary spasm among patients with false positive dobutamine stress echocardiography: prevalence and predictors

Dobutamine stress echocardiography (DSE) is being consistently used as an exercise-independent stress modality aimed at the detection of coronary artery disease (CAD) and the evaluation of myocardial ischemia. It may though occasionally induce coronary vasospasm. In this study, we aimed to evaluate the prevalence and predictors of dobuta-mine-related coronary spasm in patients without known CAD and false positive DSE (positive DSE but no significant coronary lesions on angio-gram) 3952 patients referred to our echocardiography laboratory for DSE between January 2010 and May 2012 were prospectively investigated. Those with positive DSE underwent coronary angiograms with systematic methylergometrine intracoronary injection in case of absence of significant coronary stenosis or spontaneous occlusive coronary spasm. Patients with spontaneous occlusive coronary spasm or positive methylergometrine test but no significant stenoses were enrolled and compared with those with positive DSE but no coronary lesions nor spontaneous or induced spasm (« true » false positive DSE) 29 patients with DSE-related vasospasm (19.4% of positive DSE without known CAD) were compared with 56 patients with no lesions and no spam (« true » false positive DSE). They were more frequently smokers (72.4% vs 37.5%; p=0.003); they had more frequently dyslipidemia (79.3% vs 43%;p=0.001); they also had a larger ischemic area at peak DSE (3.4 vs 2.7 segments; p=0.05). On multivariate analysis, dyslipidemia (HR=10.7; 95% CI= [2.7-42.1]; p=0.001) and active smoking (HR=6.1; 95% CI= [1.7-21.1]; p=0.004) were found to be independant predictors of spam-related DSE rather than « true » false positive DSE. DSE- related coronary spasm is present in a significant proportion of patients with erroneously labelled « false » positive DSE and should systematically be ruled out. Dyslipidemia and active smoking were independant predictors of spasm rather than « true » false positive DSE

Abstract 14849: Gender Differences in Impact of CYP2C19 Polymorphism and Low Grade Inflammation on Coronary Spasm in Patients with Vasospastic Angina (VSA)

Background: Several cytochrome P450 (CYP) enzyme families have been identified in extra hepatic tissues such as heart, vasculature, kidney, and lung. CYP2C19 localized in vascular smooth muscle and endothelium contributes to the regulation of vascular tone and homeostasis. However, it is unknown whether CYP2C19 genotype is associated with the vascular tonus in patients with VSA. The aim of this study was to examine the impact of CYP2C19 genotype on coronary artery spasm in patients with VSA. Methods: We examined the distribution of CYP2C19 genotype in patients with VSA (n=129) who were diagnosed by intra-coronary acetylcholine infusion test and healthy subjects (n=455) as control group. CYP2C19 genotypes were divided into 3 groups; (1) CYP2C19*1/*1: EM, (2) one loss-of-function allele (*1/*2, *1/*3: IM), and (3) two loss-of-function alleles (*2/*2, *2/*3, *3/*3: PM). Moreover, we measured the level of high-sensitive CRP (hs-CRP) as a degree of low glade inflammation in each group. Results: The ratios of CYP2C19 genotype (EM, IM, and PM) were 30, 42, and 28% in VSA group, and 32, 49, and 19% in control group. In short, PM frequency was significantly higher in VSA than in control (28% vs 19%, P=0.026). In VSA group, the ratios of CYP2C19 genotype were 36, 44, and 20% in male, and 20, 39, and 41% in female, respectively. Briefly, the PM frequency was significantly higher in female than in male (41% vs 20%, P&lt;0.001). Moreover, the level of hs-CRP was significantly higher in VSA group than in control group (0.17±0.367 vs 0.10.±0.240, P=0.02). When patients were stratified by gender, the level of hs-CRP was significantly higher in VSA group in female (0.11±0.198 vs 0.06±0.105, P=0.031) and male (0.20±0.438 vs 0.12±0.277, P=0.044). Multivariate analysis for coronary spasm indicated high age, hypertension, and high level of hs-CRP as predictive factors among all subjects. PM is a predictive factor for coronary spasm in female group only (OR3.1, 95%RI 1.525-6.317, P=0.002), but not in male (OR0.829, 95%RI 0.453-1.518, P=0.543). Conclusion: The CYP2C19 two loss-of-function alleles (PM) and low grade inflammation may be associated with pathophysiology of coronary artery spasm and the regulation of coronary tonus, especially in female.

Coronary Artery Spasm in Multivessel ACS: What More Should We Know?

Coronary spasm may present as acute coronary syndrome (ACS), "which can be an ST segment elevation myocardial infarction (STEMI), non-STEMI, or unstable angina." However, the prevalence of coronary spasm in patients with ACS remains unknown due to scarcity of data. Concomitant coronary spasm may mask the true atherosclerosis burden in such cases, posing several management challenges. We illustrate the case of managing an ACS patient with concomitant spasm and atherosclerotic disease. We show that the routine use of vasodilator treatment in ACS cases may prevent inappropriate stenting by identifying concomitant coronary spasm, influencing the clinical outcomes associated with inappropriate stenting in the setting of coronary spasm.

High Prevalence of a Pathological Response to Acetylcholine Testing in Patients With Stable Angina Pectoris and Unobstructed Coronary Arteries: The ACOVA Study (Abnormal COronary VAsomotion in patients with stable angina and unobstructed coronary arteries)

This study aimed at determining the prevalence of epicardial and microvascular coronary spasm in patients with anginal symptoms, despite angiographically normal coronary arteries. Despite a typical clinical presentation with exercise-related anginal symptoms (chest pain or dyspnea) with or without occasional attacks of resting chest pain suggestive of coronary artery disease, 40% of patients undergoing diagnostic angiography have normal or "near" normal coronary arteriograms. Many of these patients are given a diagnosis of noncardiac chest pain, and some are considered to have microvascular angina. However, we speculate that abnormal coronary vasomotion (reduced vasodilatation with exercise = reduced coronary flow reserve and/or vasospasm at rest) might also represent a plausible explanation for the symptoms of the patient. This was a prospective study in 304 consecutive patients (50% men, mean age 66 ± 10 years) with exertional anginal symptoms undergoing diagnostic angiography. A total of 139 patients (46%) had ≥50% coronary artery disease in at least 1 coronary artery, 21 patients (7%) had luminal narrowings ranging from >20% to 49%, and 144 patients (47%) had normal coronary arteries or only minimal irregularities (<20% diameter reduction). One hundred twenty-four patients of the latter (86%) underwent intracoronary acetylcholine (ACH) testing, which elicited coronary spasm in 77 patients (62%), 35 patients (45%) with epicardial spasm (≥75% diameter reduction with reproduction of the symptoms of the patient) and 42 patients (55%) with microvascular spasm (reproduction of symptoms, ischemic electrocardiographic changes, and no epicardial spasm). Nearly 50% of patients undergoing diagnostic angiography for assessment of stable angina had angiographically normal or near normal coronary arteriograms. The ACH test triggered epicardial or microvascular coronary spasm in nearly two-thirds of these patients. Our results suggest that abnormal coronary vasomotion plays a pathogenic role in this setting and that the ACH test might be useful to identify patients with cardiac symptoms, despite normal coronaries. (Abnormal Coronary Vasomotion in Patients With Suspected CAD But Normal Coronary Arteries; NCT00921856).

Prevalence of the type 1 Brugada electrocardiogram in Caucasian patients with suspected coronary spasm

Sporadic cases have reported the coexistence of coronary spasm and Brugada syndrome. However, the prevalence of the Brugada phenotype in coronary spasm is unknown, particularly in non-Japanese populations. In this study, we sought to examine the prevalence of the type 1 Brugada electrocardiogram (ECG) in a large European patient population undergoing intracoronary provocation testing for suspected coronary spasm. We retrospectively evaluated ECG data for the presence of type 1, 2, and 3 Brugada ECGs from 955 consecutive German patients without obstructive coronary artery disease undergoing intracoronary acetylcholine (ACH) provocation (ACH-test). Eight hundred and twenty-seven patients (age 63 ± 12 years; 42% male) with complete ECG data were eligible for further analysis. The ACH-test revealed coronary spasm in 325 patients (39.3%). A Brugada ECG of any type was found in six patients (0.7%) at baseline and eight patients (0.9%) at any time. There was no difference in the prevalence of coronary spasm in patients with (37.5%) and without (39.3%) Brugada-type ECGs. The type 1 Brugada ECG was not seen at baseline, but two type 1 Brugada ECGs were observed during ACH-administration into the right coronary artery (RCA; 0.2%), one with simultaneous RCA spasm and one without. Ajmaline provocation testing reproduced the type-1 Brugada ECG in the patient without coronary spasm but she had no other features of the Brugada syndrome. This study reports a low prevalence of the type 1 Brugada ECG in the largest known European collection of intracoronary ACH provocation. In these patients, we found no evidence for the coexistence of Brugada syndrome and coronary spasm. This is in contrast to available Japanese data.

Spasm provocative test in troponin-positive patients with acute chest pain and no significant coronary artery disease: reply

We would like to thank Martinez-Selles et al. for their interest in our study1 and also to congratulate these authors on their VIRIATO registry which focuses on the incidence of coronary spasm in patients with chest pain but no significant coronary artery disease (CAD).2 We absolutely agree with the remark of these authors suggesting that (i) coronary spasm needs to be considered as a potential cause for troponin elevation in patients with acute chest pain but no significant CAD and (ii) provocative testing (e.g. using intravenous …

129 Dobutamine stress echocardiography and coronary artery spasm: a missed link

To assess whether abnormal dobutamine stress echocardiography (DSE) can be a consequence of dobutamine-induced coronary spasm in patients with angiographically documented vasospastic coronary arteries. Between January 2004 and April 2008, we prospectively evaluated all patients with known or suspected coronary artery disease (CAD) referred to the echocardiography laboratory for dobutamine stress tests (6061 examinations). Those with abnormal DSE underwent coronary angiogram with a systematic methylergometrine intracoronary injection in the case of absence of significant coronary stenosis or spontaneous occlusive coronary spasm. Patients who had spontaneous occlusive coronary spasm or positive methylergometrine test, but no significant stenoses, were ultimately included in this study. About 581 patients had abnormal DSE, among them only 20 (3.4%) fulfilled the inclusion criteria. There were 15 males and 5 females, and mean age was 64.35 years (range 52-85); 8 patients had a known history of CAD and all of them had at least two established cardiovascular risk factors. The culprit vessel was the left anterior descending artery in 10 cases (50%), right coronary artery in 8 cases (40%), and left circumflex in 2 cases (10%). There was a systematic correspondence between the culprit arteries and dobutamine-induced wall motion abnormality territories. No complications occurred during examination or during the provocation test. All the patients were discharged with a calcium channel blocker and were doing well after 13 months of mean follow-up. Coronary artery spasm can be induced at DSE, but is a rare finding; it could, though, be clinically relevant as it may partly explain some erroneously labelled ‘false-positive’ examinations. Methylergometrine provocation test is a safe and advisable approach in such situations.

Coronary artery spasm and dobutamine stress echocardiography

The aim of this article was to assess whether abnormal dobutamine stress echocardiography (DSE) can be due to a dobutamine-induced coronary spasm in patients with angiographically documented vasospastic coronary arteries. Between January 2004 and April 2008, we prospectively evaluated all patients with known or suspected coronary artery disease (CAD) referred to the echocardiography laboratory for dobutamine stress tests (6061 examinations). Those with abnormal DSE underwent coronary angiogram with a systematic methylergometrine intracoronary injection in the case of absence of significant coronary stenosis or spontaneous occlusive coronary spasm. Patients who had spontaneous occlusive coronary spasm or positive methylergometrine test, but no significant stenoses, were ultimately included in this study. About 581 patients had abnormal DSE, among them only 20 (3.4%) fulfilled the inclusion criteria. There were 15 males and 5 females, and mean age was 64.35 years (range 52-85); 8 patients had a known history of CAD and all of them had at least two established cardiovascular risk factors. The culprit vessel was the left anterior descending artery in 10 cases (50%), right coronary artery in 8 cases (40%), and left circumflex in 2 cases (10%). There was a systematic correspondence between the culprit arteries and dobutamine-induced wall motion abnormality territories. No complications occurred during examination or during the provocation test. All the patients were discharged with a calcium channel blocker and were doing well after 13 months of mean follow-up. Coronary artery spasm can be induced at DSE, but is a rare finding; it could, though, be clinically relevant as it may partly explain some erroneously labelled 'false-positive' examinations. Methylergometrine provocation test is a safe and advisable approach in such situations.

Predictors of coronary spasm in patients with chest pain and no significant coronary stenosis

We studied 346 patients with normal or near-normal coronary arteries using the ergonovine provocative test (EPT). EPT produced spasm in 69 patients (20%). Baseline ECG and ECG changes during chest pain had no relation with the presence of spasm. Vasospasm during follow-up (mean 39 ± 24 months) was more frequent in patients with a positive EPT (28 vs. 2%, P < .001).

Administration of the Rho-kinase inhibitor, fasudil, following nitroglycerin additionally dilates the site of coronary spasm in patients with vasospastic angina

The Rho/Rho-kinase signaling pathway is known to be involved in the pathogenesis of coronary artery spasm. Previous studies reported the efficacy of the Rho-kinase inhibitor, fasudil, in the prevention and relief of coronary spasm. The usefulness of fasudil in combination with conventional vasodilating agents, however, has not been fully examined in patients with vasospastic angina. A total of 26 patients (mean age, 61+/-11 years) with documented vasospasm in the left anterior descending coronary artery were examined by the acetylcholine stress test. Coronary diameter at the spasm site was measured at baseline and after the administration of vasodilator agents in the following order: intracoronary nitroglycerin (NTG) (300 microg), intravenous fasudil (30 mg, n=15, fasudil group) or saline (n=11, saline group), and again NTG during coronary angiography. The increase in diameter observed following the first NTG administration was found to be similar in the fasudil and saline groups (38.3+/-23.5% and 42.3+/-17.1%, respectively). The additional change in diameter on fasudil treatment (16.9+/-11.2% increase over the diameter after the first NTG administration) was significantly larger than that with saline (-2.8+/-7.6%, P<0.001). The second administration of NTG did not affect the diameter of the spasm site in either group. Fasudil further dilated the site of coronary spasm, which had already been treated with NTG in patients with vasospastic angina. These findings support and extend the previous results that showed the feasibility of employing fasudil as a novel therapeutic approach for coronary spasm.