A change in the pattern of vasospasm after stenting in a patient with vasospastic angina

We report an unusual case of a male patient with vasospastic angina in whom the pattern of coronary artery spasm changed after coronary stenting. The patient was admitted to our hospital with an acute coronary syndrome. Coronary angiography revealed an intermediate grade stenosis in the right coronary artery, and focal coronary spasm was provoked by intracoronary acetylcholine. A diagnosis of vasospastic angina was made, and the patient was followed medically. He subsequently was readmitted with refractory vasospastic angina and underwent coronary stenting. He was pain-free after stent implantation. Repeat angiography 6 months later showed no restenosis in the stented segment; however, coronary spasm was provoked in all areas except the stented segment by intracoronary acetylcholine injection.     

Prinzmetal's angina during cyclophosphamide therapy

The first case of cyclophosphamide-induced myocardial ischaemiawith electrocardiographically documented ST-segment elevation,T-wave inversion, arrhythmias, angina pectoris and cardiac decompensationis reported. The data suggest that cyclophosphamides inducesmyocardial ischaemia by eliciting coronary artery spasm.     

Sudden cardiac death from coronary artery spasm in a healthy subject

The true incidence of sudden cardiac death (SCD) from coronary artery spasm is unknown. The following case involves SCD in a previously asymptomatic young man with reasonable evidence to implicate coronary artery spasm as a potential cause for his clinical event. Ergonovine provocation may be warranted in patients who present with SCD and no discernable cause. © 1994 Wiley-Liss,Inc..     

Coronary vasospasm: A narrative review

Coronary artery vasospasm (CAVS) plays an important role in acute chest pain syndrome caused by transient and partial or complete occlusion of the coronary arteries. Pathophysiology of the disease remains incompletely understood, with autonomic and endothelial dysfunction thought to play an important role. Due to the dynamic nature of the disease, its exact prevalence is not entirely clear but is found to be more prevalent in East Asian and female population. Cigarette smoking remains a prominent risk factor, although CAVS does not follow traditional coronary artery disease risk factors. Many triggers continue to be identified, with recent findings identifying chemotherapeutics, allergens, and inflammatory mediators as playing some role in the exacerbation of CAVS. Provocative testing with direct visualization is currently the gold-standard for diagnosis, but non-invasive tests, including the use of biomarkers, are being increasingly studied to aid in the diagnosis. Treatment of the CAVS is an area of active research. Apart from risk factor modification, calcium channel blockers are currently the first line treatment, with nitrates playing an important adjunct role. High-risk patients with life-threatening complications should be considered for implantable cardioverter defibrillator (ICD), although timing criteria for escalated therapy require further investigation. The role of pharmaceuticals targeting oxidative stress remains incompletely understood.     

Recurrence of prinzmetal angina seven years following aortocoronary bypass surgery: A clinical and angiographic follow-up

A patient with Prinzmetal angina and ST segment elevation in the anterior ECG leads became asymptomatic after a 50% left anterior descending coronary artery stenosis was bypassed. However, seven years later Prinzmetal angina recurred but with ST segment elevation in the inferior ECG leads. Although the coronary bypass graft had remained patent, the proximal and distal left anterior descending coronary artery was occluded. No significant stenosis was present in the right coronary artery. Perhexiline maleate controlled his symptoms but when the drug was stopped because of side effects an acute inferior myocardial infarction occurred.     

Angiographic documented coronary arterial spasm in absence of critical coronary artery stenoses in a patient with variant angina episodes during exercise and dobutamine stress echocardiography

Dobutamine stress echocardiography is widely performed as a useful diagnostic tool in patients with known or suspected coronary artery disease. Dobutamine induced myocardial ischaemia is frequently associated with ST segment depression. ST segment elevation is uncommon and is almost always associated with prior myocardial infarction or transient total coronary occlusion. Dobutamine induced ST segment elevation in absence of significant coronary artery disease is a rare condition and is supposed to be a consequence of severe coronary artery spasm. The case of a 58 year old man with variant angina episodes at rest, during exercise test, and dobutamine stress echocardiography is reported, in whom coronary spasm without significant coronary artery stenoses was documented angiographically.


Keywords: coronary spasm; variant angina; Prinzmetal angina; dobutamine stress echocardiography; exercise test     

Coronary stent for variant angina: Atypical presentation

Pharmacological therapy remains the treatment of choice for Prinzmetal angina. We report an unconventional approach of coronary artery stenting to treat coronary artery spasm in variant angina refractory to triple drug therapy. Favorable clinical and angiographic results and a negative Ergonovine test, under less aggressive medical therapy, are valuable arguments for stenting. Four-month angiographic follow-up showed absence of intrastent restenosis with a negative Ergonovine test. However, long-term follow-up is necessary before advocating this as a systematic approach. Cathet. Cardiovasc. Diagn. 45:439–441, 1998. © 1998 Wiley-Liss, Inc.     

Vasospastic Angina with J‐Wave Pattern and Polymorphic Ventricular Tachycardia Effectively Treated with Quinidine

Background: Myocardial ischemia during coronary spasm may generate malignant ventricular arrhythmias. The J‐wave pattern was suggested to be a marker of a disorder associated with life‐threatening arrhythmias. Results: We report the case of a patient with vasospastic angina and J‐wave pattern in inferior and lateral leads associated with polymorphic ventricular tachycardia which was effectively treated only with quinidine—vasodilating drugs were not able to prevent the arrhythmia although they were effective in preventing ischemic events. Conclusion: The J‐wave pattern in inferolateral leads may be a sign of electrical vulnerability to lethal ventricular arrhythmia in patients suffering from vasospastic angina—quinidine can effectively prevent such arrhythmias in these patients.     

Multiple episodes of ventricular tachycardia induced by silent coronary vasospasm

We present a 46-year-old patient who suffered from cardiac arrest and subsequently underwent placement of an implantable cardioverter defibrillator (ICD). The patient underwent a cardiac catheterization which revealed no significant coronary artery disease. About 1 year later he experienced appropriated and frequent ICD discharges due to monomorphic ventricular tachycardia (VT) with left bundle branch block morphology. His prodromal symptoms were mild dizziness and lightheadedness with no chest pain. Amiodarone, mexiletine, sotalol and dofetilide as well as ablation of two inducible ventricular tachycardias in the electrophysiology studies were unsuccessful in controlling the arrhythmias and ICD discharges. During the last episode, he experienced a mild burning sensation in his chest and was given nitroglycerin 0.4 mg sublingually, which relived his symptoms and aborted the VT. This led to a second cardiac catheterization to investigate whether the VT was being induced by myocardial ischemia. This second coronary angiogram spontaneously revealed significant coronary vasospasm and simultaneously, the patient’s cardiac rhythm showed short runs of VT with left bundle branch block morphology. Intracoronary nitroglycerine relieved the coronary vasospasm and terminated the arrhythmia. The patient was treated with isosorbide mononitrate and diltiazem. He remained symptom free with no ICD discharges and no VT in ICD interrogations for more than 2 years. Coronary vasospasm may be silent and with no chest pain which creates a difficult clinical situation particularly if it is associated with ventricular tachycardia and sudden cardiac death. The mechanisms of VT in the setting of coronary vasospasm are not known and increased automaticity, focal discharges, functional unidirectional block with reentry, or a combination of these mechanisms may contribute to inducing the VT during the transient ischemia or rarely in the reperfusion phase. It is important to perform provocative tests to diagnose silent coronary vasospasm in unexplained sudden cardiac arrests.     

K(ATP) channels "vingt ans après": ATG to PDB to Mechanism

A multidisciplinary effort over twenty years has provided deep insight into the nature of K(ATP) channels. First discovered in cardiomyocytes and pancreatic beta-cells, as ubiquitous sensors of the ADP/ATP ratio they are implicated in multiple disorders characterized by the uncoupling of excitation from metabolism. Composed of two disparate subunits these large octameric channels present a formidable challenge to scientists interested in understanding mechanism in physical, chemical, and structural terms. Post-cloning studies have defined the domains and interactions, within and between the nucleotide-inhibited K(IR) pore and nucleotide-stimulated, drug-binding core of the ATP-Binding Cassette (ABC) regulatory subunits, that control channel assembly and gating. Determination of the three-dimensional structures of the bacterial prototypes of the channel subunits allowed homology modeling and has provided increasingly detailed mechanistic understanding. Here I review the early electrophysiology and molecular biology of K(ATP) channels, cover biophysical principles governing their single channel kinetics, integrate this with current efforts to understand ligand-recognition and gating within the pore and SUR core, and propose a mechanism of coupling based on recent identification of a SUR gatekeeper module and first composite models of (SUR/K(IR) 6.0)(4) complexes. This mechanism, based on interactions between inter-K(IR) subunit ATP-binding pockets and a unique bi-directional regulatory apparatus comprised of elements from the gatekeeper and K(IR) amino terminus, provides a molecular perspective for understanding the biophysical basis underlying the polar effects of pathogenic mutations in K(ATP) channel subunits.     

Giant R wave, convex ST-segment elevation, and negative T wave during exercise treadmill test

The giant R wave syndrome is characterized by giant R wave accompanied by widening of the QRS complex, marked ST segment elevation, QRS axis deviation, and the formation of monophasic QRS-ST complex with obliteration of S wave in leads facing the ischemic zone. This report describes a 65-year-old-man with variant angina who had a transient giant R wave syndrome during an exercise treadmill test. Initially, at peak exercise, there was a convex ST segment elevation ending in a negative T wave in the same (inferior) leads which showed giant R waves. Later, in the recovery period and coinciding with an amelioration of myocardial ischemia, there was a less marked increase of R wave amplitude associated with concave ST segment elevation and positive T wave in the inferolateral leads. Subsequently, a ST segment depression in the inferolateral leads preceded the ECG normalization. The patient had also a concave ST segment elevation and positive T wave in inferolateral leads during a spontaneous episode of variant angina at rest. An emergency coronary arteriography showed a dominant right coronary artery with an 80% and a 75% diameter stenosis of the middle and distal segment, respectively; the other arteries and left ventriculogram were normal. The underlying mechanisms of the different shapes of ST segment elevation and T waveform in the setting of acute transmural myocardial ischemia are discussed.     

Angor spastique réfractaire au traitement médical traité par angioplastie avec mise en place d’un stent. À propos d’un cas et revue de la littérature

Medical treatment of coronary spastic angina is based classically on the association of calcium channel blockers with nitrate derivatives. Some clinical forms of spastic angina remain refractory to these medications and can thus lead to serious complications (sudden cardiac death secondary to ventricular rhythm disturbance, myocardial infarction…). When the coronary spasm is focal, percutaneous coronary angioplasty with deployment of a stent can offer an interesting therapeutic alternative. We report in this article the case of a patient who had a focal spasm of the right coronary artery, which became refractory to optimal medical treatment. This patient was well improved by percutaneous angioplasty with deployment of a stent in the spastic segment of the right coronary artery. We propose also a review of the literature of the treatment of this pathology, which still remains not well codified.     

Does symptomatic stable coronary artery disease still exist in France?

In spite of the continuous growth of myocardial revascularisation techniques, stable angina remains an important clinical burden. In France, and based upon estimates from the European Society of Cardiology and from diverse epidemiological sources, 2 million people are likely to have stable angina. Though primary and secondary prevention are improving, this figure is likely to increase further, in particular because of the constant aging of the population (20% of patients more than 80 years of age have angina), but also because of the epidemics proportions that diabetes mellitus and obesity take.     

Angioplastie coronaire : indications, limites et résultats en dehors des syndromes coronaires aigus en 2009

Most of percutaneous coronary interventions are performed on stabilized patients. Although these procedures have recently been challenged for this type of patient following the publication of the recent Courage study in 2007 (which in fact has only confirmed previous studies), their efficacy is now well established for lowering the frequency of episodes of angina and increasing the performance under load in stabilized high risk patients. In practice, the evaluation of patients (case by case) is essential to establish their risk (low, intermediate or high) in order to offer the most suitable treatment. The aim of this paper is to overview the indications, limitations and results of coronary angioplasties performed in stabilized patients in France in 2009.     

Un cas une revue : syndromes coronariens aigus avec sus-décalage du segment ST à coronaire « coupable » angiographiquement saine

Acute coronary syndrome results in most cases of atherosclerotic plaque rupture. In a few cases, the physiopathological mechanism is different. This does not necessarily change the initial strategy but the subsequent treatments. We report three cases of clinical presentations of acute coronary syndrome whose pathophysiological mechanism is not or not mainly due to atherosclerotic lesions. Based on these cases and a review of the literature, two topics will be tackled: the diagnostic and therapeutic strategy in the management of Tako-tsubo cardiomyopathies and also acute coronary syndromes due to vasospastic angina.     

Premedication by thienopyridine before percutaneous coronary interventions in unstable angina

Ticlopidine or clopidogrel combined with aspirin decrease major cardiac events (Mace) after PTCA with stent implantation. It has not be proven yet that pretreatment by T or C was superior to conventional post-treatment, especially in unstable patients. The aim of the present study was to determine the influence of thienopyridine pretreatment on the risk of Mace (death, Q wave myocardial infarction, need for repeat PTCA or surgery, angina recurrence, stent thrombosis) during the hospitalization period in a population prospectively included in 2 multicentre registries of patients undergoing placement of a S670 or S7 stent (Medtronic) implanted in native coronary arteries (> or = 3.0 mm). Among the 2929 patients included into the registries, 1205 had unstable angina (41%). 50.2% of the patients were pretreated by T or C (T = 15.7%, C = 34.5%); 85.5% received aspirin before the procedure; definition of pretreatment was the administration of drug at least 6 hours before stent implantation. GPIIb-IIIa antagonists were administered in only 13.9% of patients. Mace were observed in 2% of the patients. Factors correlated with Mace by univariate and multivariate analyses were: age > 73 years (RR: 2.37; 95% CI: 1.05-5.36, P < 0.037), previous myocardial infarction (RR: 2.56; 95% CI: 1.08-6.11, P < 0.034), pretreatment by T or C (RR: 0.389; 95% CI: 0.16-0.95, P < 0.038). In patients who did not receive GPIIb-IIIa antagonists, age > 73, and pretreatment by T or C were the only independent predictors of Mace.     

Elevated plasma levels of interleukin-2 and soluble IL-2 receptor in ischemic heart disease

BACKGROUND: T-lymphocytes are present in significant numbers in the atherosclerotic plaque, but their role in the progression and pathogenesis of coronary syndromes remains poorly understood. HYPOTHESIS: We sought to determine the relationship between T-lymphocyte activation and ischemic heart disease by measuring plasma levels of cytokines related to T-lymphocyte function in patients with stable and unstable angina. METHODS: Plasma levels of interleukin-2 (IL-2) and soluble IL-2 receptor (sIL-2R) were measured in 105 patients: 66 with stable angina, 24 with unstable angina, and 15 healthy controls. Patients who presented to the cardiac catheterization laboratory with unstable or stable anginal syndromes for coronary angiography or percutaneous coronary intervention enrolled in the study. RESULTS: Mean levels of IL-2 were significantly higher in patients with stable angina than in those with unstable angina. The differences between stable angina and control groups, or between unstable angina and control groups, were not statistically significant. Mean levels of slL-2R were significantly higher in patients with stable angina than in either patients with unstable angina or control patients. CONCLUSIONS: Levels of IL-2 and sIL-2 receptor are significantly elevated in patients with stable angina, but not in patients with unstable angina. The contribution of T-lymphocytes to the development of both stable and unstable angina requires further investigation.     

Circulating Levels of IL-1β, a Prothrombotic Cytokine,are Elevated in Unstable Angina Versus Stable Angina

Background: Multiple studies support a role for inflammation in the pathogenesis of coronary atherosclerosis and unstable cardiac syndromes. However, of the known proinflammatory cytokines, only elevated plasma levels of interleukin-6 have been linked to unstable angina. We sought to examine the plasma levels of other major proinflammatory cytokines in similar clinical settings and to determine the extent of the relationship between inflammation and unstable coronary syndromes by measuring the levels of various proinflammatory cytokines in patients with stable and unstable angina.Methods: We measured plasma levels of interleukin-1 beta (IL-1), tumor necrosis factor alpha (TNF-), and interleukin 6 (IL-6) in 97 patients: 67 with stable angina, 24 with unstable angina, and 15 healthy controls.Results: Mean levels of IL-1 were significantly higher in patients with unstable angina as compared to patients with stable angina (p = .009). Levels of IL-6 were significantly higher than control patients for both stable angina and unstable angina patients (p = .031 and .006, respectively). No significant differences were found in the levels of TNF-.Conclusions: Our results suggest that both IL-1 and IL-6 contribute to the pathogenesis of unstable angina, and that the profile of circulating plasma levels of proinflammatory cytokines differs in unstable angina from that in stable angina.Abbreviated Abstract. Multiple studies support a role for inflammation in the pathogenesis of coronary atherosclerosis and unstable cardiac syndromes. We measured plasma levels of interleukin-1 beta (IL-1), tumor necrosis factor alpha (TNF-), and interleukin 6 (IL-6) in patients with stable and unstable coronary syndromes. Levels of IL-1 and IL-6 were found to be elevated in patients with unstable coronary syndromes. No significant differences were found in the levels of TNF-. Our results suggest that both IL-1 and IL-6 contribute to the pathogenesis of unstable angina.