Usefulness of implantable cardioverter-defibrillators in refractory variant angina pectoris complicated by ventricular fibrillation in patients with angiographically normal coronary arteries

Coronary artery epicardial spasm is involved in the pathogenesis of many cardiac disorders. Vasoreactivity testing, such as intracoronary injection of acetylcholine (ACH) or ergonovine (ER), is the gold standard method for the diagnosis of vasospastic angina. Provoked epicardial spasm phenotypes are classified as focal spasm and diffuse spasm. Multiple factors, including sex, ethnicity, and use of coronary vasoactive stimulators, are related to the provoked phenotypes of epicardial spasm. Diffuse-provoked spasm is often observed in females, where focal-provoked spasm is markedly more common in males. ACH provokes more diffuse and distal spasms, whereas ER induces more focal and proximal spasms. Yellow plaque and coronary thrombi are often observed in lesions with focal spasms, and intimal thickness with a sonolucent zone is significantly more common in lesions with focal spasm. Furthermore, clinical outcomes in patients with focal spasm are unsatisfactory compared with those in patients with diffuse spasm. However, the reproducibility and eternality of provoked spasm phenotypes by vasoreactivity testing is uncertain. Coronary atherosclerosis or endothelial damage may affect coronary vasomotor tone. Although coronary artery spasm may persist in the same coronary artery, provoked coronary spasm phenotypes may exhibit a momentary coronary reaction by intracoronary ACH or ER testing.

Sudden cardiac arrest survivors with a reversible cause are not eligible for implantable cardioverter defibrillator (ICD) implantation. This study aims to evaluate the risk of recurrent ventricular arrhythmia in sudden cardiac arrest survivors with a reversible cause and evaluate if ICD implantation increases survival.

We conducted a systematic review to identify studies evaluating ICD implantation in sudden cardiac arrest survivors with a reversible cause. Outcomes were mortality and appropriate device therapy. Sudden cardiac arrest patients were divided into 4 subgroups: due to acute myocardial infarction; due to coronary artery spasm; due to takotsubo cardiomyopathy; and studies with various reversible causes of cardiac arrest.

27 studies were included, evaluating 11,402 patients. A total of 2570 patients received an ICD. Studies evaluating coronary artery spasm and with various reversible causes showed a relatively high rate of appropriate device therapy (17% and 20%) and described an increased survival in ICD patients. Takotsubo cardiomyopathy was associated with a low mortality and none of the ICD patients received appropriate device therapy. Studies evaluating acute myocardial infarction survivors reported inconsistent results, with high numbers of appropriate device therapy (12–66%), but the mortality-rate of patients with and without an ICD varied.

This study shows that the recurrence risk of ventricular arrhythmia varies between different reversible causes of sudden cardiac arrest and should not be evaluated as one entity. Cardiac arrest survivors with a reversible cause can be at risk of recurrent ventricular arrhythmia and selected patients may benefit from ICD implantation.

A 52-year-old man was transferred to our hospital for ventricular fibrillation. He had no chest symptoms until then. After his full recovery, the administration of acetylcholine 20 μg showed the multiple spasm (left main trunk/left anterior descending artery/right coronary artery) without any chest symptoms or ischemic electrocardiographic changes. Subcutaneous implantable cardioverter-defibrillator (S-ICD) was implanted because of no chest symptoms during his-daily-life. We performed the pharmacological spasm provocation tests under the abundant medications. Sequential spasm provocation test provoked just focal spasm at mid left anterior descending artery. We convinced that medications and S-ICD suppress the next fatal event.

<Learning objective: LMT spasm may cause aborted SCD. Aggressive spasm provocation tests under the abundant medical therapy provoked spasm just at mid LAD artery focally in patient with VF survivor due to multiple spasm including LMT, while these medications blocked the LMT and RCA spasm. S-ICD implantation may be one of the selections in aborted SCD patients with silent LMT spasm under the abundant vasodilators in the future.>

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.

L’angor vasospastique (AVS) est une variante de l’angine de poitrine où l’angine se produit au repos, avec des modifications transitoires de l’électrocardiogramme et une capacité d’exercice préservée. Il peut être impliqué dans de nombreux scénarios cliniques, tels que l’angor stable, la mort subite, les syndromes coronaires aigus, les arythmies ou la syncope. Le vasospasme coronaire est un phénomène hétérogène qui peut survenir chez les patients avec ou sans athérosclérose coronaire, pouvant être focale ou diffuse, et pouvant affecter les artères coronaires épicardiques ou la microcirculation. Cette pathologie reste sous-diagnostiquée et les tests de provocation rarement pratiqués. Son diagnostic implique trois considérations: les manifestations cliniques classiques de l’AVS; la documentation de l’ischémie myocardique au cours des épisodes spontanés; et la démonstration du spasme de l’artère coronaire. L’approche diagnostique de référence utilise la coronarographie pour visualiser de manière directe le spasme coronaire en utilisant acétylcholine, ergonovine ou méthylergonovine comme stimulus provocateur. La modification du mode de vie, l’arrêt d’éventuels agents vasospastiques et la pharmacothérapie, tels que les inhibiteurs calciques, les dérivés nitrés, les statines, l’aspirine, les antagonistes des récepteurs alpha1-adrénergiques, les inhibiteurs de rho-kinase ou le nicorandil, pourraient être proposés aux patients atteints d’AVS. Cette revue traite de la physiopathologie, des aspects cliniques et de la prise en charge de l’AVS pour les cliniciens, ainsi que critères diagnostics et des tests de provocation disponibles pouvant être utilisés par les cardiologues interventionnels.

The long-term prognosis of vasospastic angina (VSA) patients presenting with aborted sudden cardiac death (ASCD) is still unknown. We sought to compare the long-term clinical outcomes between VSA patients presenting with and without ASCD by retrospective analysis of a nationwide population-based database.

A total of 6972 patients in the Health Insurance Review and Assessment database who were hospitalized in the intensive care unit with VSA between July 1, 2007 and May 31, 2015 were enrolled. Primary outcome was the composite of cardiac arrest and acute myocardial infarction after discharge.

Five hundred ninety-eight (8.6%) VSA patients presented with ASCD. On inverse probability of treatment weighting, ASCD patients had a significantly increased risk of the composite of cardiac arrest and acute myocardial infarction (adjusted hazard ratio, 2.52; 95% confidence interval, 1.72–3.67; p < 0.001) during the median follow-up duration of 4 years. The association of ASCD presentation with a worse outcome in terms of primary outcome was consistent across various subgroups, including comorbidity type and use of vasodilators (all p-values for interaction: non-significant). ASCD patients treated with an implantable cardioverter defibrillator (ICD) had a lower incidence of the composite of cardiac arrest and acute myocardial infarction during follow-up than those without an ICD (p = 0.009).

VSA patients that present with ASCD are at increased risk of cardiac arrest or myocardial infarction during long-term follow-up despite adequate vasodilator therapy. An ICD is a potential therapeutic option for secondary prevention.