Efficacy of Atropine as a Chronotropic Agent in Heart Transplant Patients Undergoing Dobutamine Stress Echocardiography

Kociolek, Larry K.; Bierig, S. Michelle; Herrmann, Steven C.; Labovitz, Arthur J.

doi:10.1111/j.1540-8175.2006.00223.x

Cited by 8 publications

(11 citation statements)

References 24 publications

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“…Furthermore, we observed substantial effects even with a very low dose of atropine (0.2 mg/kg twice daily for 7 days; Fig. 1 C-F), which was the same or less than the doses used in most studies of muscarinic signaling (Molinengo et al, 1989; Kociolek et al, 2006). Lastly, when we applied atropine at the lowest dose (0.2mg/kg once-daily for only 5 days; n=6 mice), we found milder defects that were confined to the synaptic area, and both preterminal axons and myelinating Schwann cells appeared completely normal (Supplemental Fig.…”

Section: Resultsmentioning

confidence: 70%

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Distinct Muscarinic Acetylcholine Receptor Subtypes Contribute to Stability and Growth, But Not Compensatory Plasticity, of Neuromuscular Synapses

Wright¹,

Potluri²,

Wang³

et al. 2009

J. Neurosci.

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Muscarinic acetylcholine receptors (mAChRs) modulate synaptic function, but whether they influence synaptic structure remains unknown. At neuromuscular junctions (NMJs), mAChRs have been implicated in compensatory sprouting of axon terminals in paralyzed or denervated muscles. Here we used pharmacological and genetic inhibition and localization studies of mAChR subtypes at mouse NMJs to demonstrate their roles in synaptic stability and growth but not in compensatory sprouting. M 2 mAChRs were present solely in motor neurons, whereas M 1 , M 3 , and M 5 mAChRs were associated with Schwann cells and/or muscle fibers. Blockade of all five mAChR subtypes with atropine evoked pronounced effects, including terminal sprouting, terminal withdrawal, and muscle fiber atrophy. In contrast, methoctramine, an M 2/4 -preferring antagonist, induced terminal sprouting and terminal withdrawal, but no muscle fiber atrophy. Consistent with this observation, M 2Ϫ/Ϫ but no other mAChR mutant mice exhibited spontaneous sprouting accompanied by extensive loss of parental terminal arbors. Terminal sprouting, however, seemed not to be the causative defect because partial loss of terminal branches was common even in the M 2 Ϫ/Ϫ NMJs without sprouting. Moreover, compensatory sprouting after paralysis or partial denervation was normal in mice deficient in M 2 or other mAChR subtypes. We also found that many NMJs of M 5 Ϫ/Ϫ mice were exceptionally small and reduced in proportion to the size of parental muscle fibers. These findings show that axon terminals are unstable without M 2 and that muscle fiber growth is defective without M 5 . Subtype-specific muscarinic signaling provides a novel means for coordinating activity-dependent development and maintenance of the tripartite synapse.

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Section: Resultsmentioning

confidence: 70%

“…These dramatic effects were unexpected because atropine is commonly used in the clinic (Das, 1989; Kociolek et al, 2006). The effects are unlikely to be indirect or due to overdosage.…”

Section: Discussionmentioning

confidence: 99%

Distinct Muscarinic Acetylcholine Receptor Subtypes Contribute to Stability and Growth, But Not Compensatory Plasticity, of Neuromuscular Synapses

Wright¹,

Potluri²,

Wang³

et al. 2009

J. Neurosci.

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“…4) We used the functional consequences of reinnervation (HR response to exercise) to infer reinnervation. This technique assesses sympathetic reinnervation only, and autonomic regulation involving parasympathetic and sympathetic innervation may be more accurately inferred from dobutamine stress testing with atropine (26). Additionally, there is direct evidence that reinnervation of the heart occurs after transplantation in animals (34), and there is growing evidence from clinical (40), physiological (3,8), and biochemical (2,24) studies in humans that partial reinnervation may occur at least 1 yr after transplantation.…”

Section: Ventricular-vascular Coupling and V O 2 In Htrmentioning

confidence: 99%

Cardiovascular responses to incremental and sustained submaximal exercise in heart transplant recipients

Scott¹,

Esch²,

Haykowsky³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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The cardiovascular response to exercise in heart transplant recipients (HTR) has been compared with that of healthy individuals matched to the recipient age (RM controls). However, no study has compared HTR with donor age-matched (DM) controls. Moreover, the cardiovascular response to sustained submaximal exercise in HTR requires further evaluation. We therefore examined cardiovascular responses during incremental exercise and sustained (1 h) submaximal aerobic exercise in 9 clinically stable HTR [63 +/- 10 yr of age, 24.2 +/- 10.9 ml x kg(-1) x min(-1) peak O(2) uptake (Vo(2peak))] and 11 healthy age-matched controls (60 +/- 11 yr of age and 36.3 +/- 10.7 ml.kg(-1) x min(-1) Vo(2peak) for 6 RM controls and 35 +/- 8 yr of age and 51.1 +/- 10.4 ml x kg(-1) x min(-1) Vo(2peak) for 5 DM controls). Heart rate (HR) and left ventricular systolic and diastolic volumes (2-dimensional echocardiography) indexed to body surface area [end-systolic and end-diastolic volume indexes (EDVI and ESVI)], cardiac output (CI), ejection fraction (EF), systemic vascular resistance (SVRI), end-systolic elastance index, and arterial elastance index were determined. Although systolic function was maintained during incremental exercise, peak CI was significantly reduced (6.7 +/- 2.4 vs. 11.6 +/- 1.4 l x min(-1) x m(-2)), secondary to blunted HR, EDVI, and increased peak SVRI, in HTR compared with DM controls. The lower peak CI in HTR than in RM controls was due to blunted peak EDVI (54.1 +/- 13.2 vs. 68.6 +/- 5.7 ml/m(2)). During sustained submaximal exercise, HTR exhausted their preload reserve, a response for which changes in ESVI, HR, or EF did not fully compensate. Thus it appears that HTR are limited by impaired preload reserve, HR reserve, and vascular reserve during exercise conditions.

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“…5,11,14–17 A retrospective study by Kociolek et al included 21 transplant patients who received atropine during DSE, and a similar study by Flox et al included 14 transplant patients who also received both agents. 11,16 The patient populations in those studies were similar to ours, though the study by Flox et al did not include patients using beta-blockers. Although there were slight protocol differences, such as higher doses of atropine and dobutamine in the study by Kociolek et al, no adverse events were reported in either study.…”

Section: Discussionmentioning

confidence: 59%

“…11,16 This difference could be due in part to protocol differences such as the maximum doses of dobutamine and atropine that were given. Doses of dobutamine and atropine for each patient in our study were determined by the supervising physician.…”

Section: Discussionmentioning

confidence: 99%

The Risk of Adverse Events Associated With Atropine Administration During Dobutamine Stress Echocardiography in Cardiac Transplant Patients: A 28-Year Single-Center Experience

Haythe

et al. 2013

Journal of Cardiac Failure

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Background Although dobutamine stress echocardiography (DSE) is performed in heart transplant patients, the safety profile of atropine administration in DSE in this setting is unclear. Methods and Results We identified heart transplant patients who received atropine during DSE from January 1984 to August 2011 at our institution and compared them with a propensity-scored matched control group of heart transplant patients who underwent DSE without atropine. Adverse events were defined as significant arrhythmias (sinus arrest, Mobitz type II heart block, complete heart block, ventricular tachycardia, or ventricular fibrillation), hypotension requiring hospitalization, syncope or presyncope, myocardial infarction, and death. Forty-five heart transplant patients (median age 62 years, 82% male) received 0.2–1 mg atropine during DSE. Of these, 1 patient (2.2%) developed temporary complete heart block. No adverse events were identified in the control group of 154 patients who received dobutamine without atropine. Conclusions Our findings suggest that complete heart block can occur infrequently with the administration of atropine in heart transplant patients undergoing DSE. Therefore, patients should be appropriately monitored for these adverse events during and after DSE.

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Efficacy of Atropine as a Chronotropic Agent in Heart Transplant Patients Undergoing Dobutamine Stress Echocardiography

Abstract: The adjunctive use of atropine in HTX patients during DSE aids in reaching 85% of maximum predicted HR in some patients. Furthermore, resting HR may predict the additional need of atropine during DSE.

Cited by 8 publications

References 24 publications

Distinct Muscarinic Acetylcholine Receptor Subtypes Contribute to Stability and Growth, But Not Compensatory Plasticity, of Neuromuscular Synapses

Distinct Muscarinic Acetylcholine Receptor Subtypes Contribute to Stability and Growth, But Not Compensatory Plasticity, of Neuromuscular Synapses

Cardiovascular responses to incremental and sustained submaximal exercise in heart transplant recipients

The Risk of Adverse Events Associated With Atropine Administration During Dobutamine Stress Echocardiography in Cardiac Transplant Patients: A 28-Year Single-Center Experience

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