Central Anticholinergic Syndrome Following Dobutamine–Atropine Stress Echocardiography

Wilson, Michael E.; Lee, Glenn K.; Chandra, Ankur; Kane, Garvan C.

doi:10.1111/j.1540-8175.2011.01509.x

Cited by 9 publications

(4 citation statements)

References 8 publications

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“…While vagolytic therapy would be difficult to carry out in CPVT patients because of systemic side effects, 41 overdrive atrial pacing could be performed in patients with dual chamber pacemakers or ICDs. In support of this concept is a recent clinical case report of the temporary overdrive suppression of bidirectional VT by a rapid atrial tachycardia in a young CPVT patient.…”

Section: Discussionmentioning

confidence: 99%

Accelerated Sinus Rhythm Prevents Catecholaminergic Polymorphic Ventricular Tachycardia in Mice and in Patients

Faggioni

Hwang

Werf

et al. 2013

Circulation Research

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Rationale Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT) is caused by mutations in cardiac ryanodine receptor (RyR2) or calsequestrin (Casq2) genes. Sinoatrial node dysfunction associated with CPVT may increase the risk for ventricular arrhythmia. Objective To test the hypothesis that CPVT is suppressed by supraventricular overdrive stimulation. Methods and Results Using CPVT mouse models (Casq2−/− and RyR2R4496C+/− mice), the effect of increasing sinus heart rate was tested by pretreatment with atropine and by atrial overdrive pacing. Increasing intrinsic sinus rate with atropine before catecholamine challenge suppressed ventricular tachycardia (VT) in 86% of Casq2−/− mice (6/7) and significantly reduced the ventricular arrhythmia (VA) score (atropine: 0.6±0.2 vs. vehicle: 1.7±0.3, p<0.05). Atrial overdrive pacing completely prevented VA in 16/19 (84%) Casq2−/− and in 7/8 (88%) RyR2R4496C+/− mice and significantly reduced ventricular premature beats in both CPVT models (p<0.05). Rapid pacing also prevented spontaneous calcium waves and triggered beats in isolated CPVT myocytes. In humans, heart-rate dependence of CPVT was evaluated by screening a CPVT patient registry for antiarrhythmic drug-naïve individuals that reached >85% of their maximum predicted heart rate during exercise testing. All 18 CPVT patients who fulfilled the inclusion criteria exhibited VA before reaching 87% of maximum heart rate. In six CPVT patients (33%), VA were paradoxically suppressed as sinus heart rates increased further with continued exercise. Conclusions Accelerated supraventricular rates suppress VAs in two CPVT mouse models and in a subset of CPVT patients. Hypothetically, atrial overdrive pacing may be a therapy for preventing exercise-induced VT in treatment-refractory CPVT patients.

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Section: Discussionmentioning

confidence: 99%

Accelerated Sinus Rhythm Prevents Catecholaminergic Polymorphic Ventricular Tachycardia in Mice and in Patients

Faggioni

Hwang

Werf

et al. 2013

Circulation Research

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“…8 The incidence of CAS in adults is reported to range from 0.03% to 7.1% and the following factors are associated with its development: atropine dose ≥1 mg, prior neuropsychiatric disorder, positive delirium observation screening, and body mass index <24 kg/m 2 . 9 Although CAS sometimes presents non-typical symptoms, atropine was used at a normal dose in each of the present patients and the present symptoms were different to those of typical CAS. Thus, we speculate that the cause of the transient worsening of OMS symptoms in these patients was not typical CAS.…”

Section: Discussionmentioning

confidence: 53%

“…Psychological symptoms are sometimes associated with its use, such as excitement, sedation, disorientation, and delirium, which are caused by central nerve toxicity, and are termed central anticholinergic syndrome (CAS) . The incidence of CAS in adults is reported to range from 0.03% to 7.1% and the following factors are associated with its development: atropine dose ≥1 mg, prior neuropsychiatric disorder, positive delirium observation screening, and body mass index <24 kg/m 2 . Although CAS sometimes presents non‐typical symptoms, atropine was used at a normal dose in each of the present patients and the present symptoms were different to those of typical CAS.…”

Section: Discussionmentioning

confidence: 99%

Transient symptomatic worsening by atropine in opsoclonus–myoclonus syndrome

Miyoshi

Nakamura

Yamaga

et al. 2017

Pediatrics International

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Opsoclonus-myoclonus syndrome (OMS) is characterized by abnormal eye and systemic involuntary movements, as well as cerebellar ataxia. Some sedatives and anesthetics worsen movements associated with OMS, while there is no known report of a negative effect of atropine. We report on sedation in two patients with OMS. Involuntary movements were transiently worsened after using atropine with midazolam or thiamylal in both, but were not seen when atropine was not used. We speculated that atropine has the potential to exacerbate involuntary movements in OMS due to vulnerability to this agent via unknown mechanisms.

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“…Although the importance of atropine in the treatment of organophosphate poisoning is generally recognized, numerous side effects of atropine have been reported, suggesting potential toxicity (7). Atropine used in dobutamine stress echocardiograms has been reported to cause morbidity (8). Atropine has been shown to be cytotoxic to human corneal epithelial cells via the induction of cell cycle arrest and death receptor-mediated mitochondrion-dependent apoptosis (9).…”

Section: Introductionmentioning

confidence: 99%

Alterations in ACE and ABCG2 expression levels in the testes of rats subjected to atropine-induced toxicity

Huang

Yang

et al. 2016

Molecular Medicine Reports

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Atropine-induced damage is associated with enzyme and protein alterations. The aim of the present study was to investigate atropine‑induced alterations in testicular expression levels of angiotensin‑converting enzyme (ACE) and adenosine 5'-triphosphate binding cassette sub‑family G member 2 (ABCG2) following atropine treatment. Male Wistar rats received 15 mg/kg/day atropine for 7 days; control rats received an identical volume of saline, Following treatment, the testes were harvested for immunohistochemistry and in situ hybridization to examine the protein and gene expression levels of ACE and ABCG2 by digital image analysis. ACE gene and protein expression levels were significantly reduced in the testes of atropine‑treated rats, compared with control rats (P=0.0001 and P<0.001, respectively). In addition, ABCG2 gene and protein expression levels were significantly increased in the testes of atropine‑treated rats, compared with control rats (P=0.0017 and P<0.001, respectively). Thus, the results of the present study demonstrate that testicular protein and gene expression levels of ACE and ABCG2 were altered as a result of atropine‑induced toxicity in the rats. These alterations may result in abnormal testicular function, and the proteins and genes identified in the present study may be useful to elucidate the mechanisms underlying atropine‑induced toxicity and provide a direction for further studies.

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Central Anticholinergic Syndrome Following Dobutamine–Atropine Stress Echocardiography

Cited by 9 publications

References 8 publications

Accelerated Sinus Rhythm Prevents Catecholaminergic Polymorphic Ventricular Tachycardia in Mice and in Patients

Accelerated Sinus Rhythm Prevents Catecholaminergic Polymorphic Ventricular Tachycardia in Mice and in Patients

Transient symptomatic worsening by atropine in opsoclonus–myoclonus syndrome

Alterations in ACE and ABCG2 expression levels in the testes of rats subjected to atropine-induced toxicity

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