Heart rate reserve during dipyridamole stress test applied to potential heart donors in brain death.


Journal

Minerva cardioangiologica
ISSN: 1827-1618
Titre abrégé: Minerva Cardioangiol
Pays: Italy
ID NLM: 0400725

Informations de publication

Date de publication:
Jun 2020
Historique:
pubmed: 27 2 2020
medline: 29 4 2021
entrez: 27 2 2020
Statut: ppublish

Résumé

A blunted heart rate reserve (HRR) during dipyridamole stress echocardiography (DSE) is a prognostically unfavorable sign of cardiac autonomic dysfunction. Short-term adjustments of heart rate (HR) are thought to rise from changes in neural input to the heart. DSE is applied in potential heart donors to rule out underlying coronary artery disease and left ventricular dysfunction. The aim of this study is to assess HRR during DSE in brain death. We enrolled two groups: group 1 (N.=49, 22 men, 54.6±8.8 years) with patients in brain death enrolled in the nationwide marginal donor heart recruiting program; group 2 (N.=49, 18 men, 66.4±12.0 years) referred to DSE for suspected or known coronary artery disease. All underwent DSE (0.84 mg/kg in 6') by quality-controlled readers certified via web-based training (1487/CE Lazio-1). We assessed left ventricular contractile reserve (LVCR) as stress/rest ratio of force (systolic blood pressure/end-systolic volume). HRR was calculated as the peak/rest HR ratio from 12-lead EKG. The two study groups were similar for prevalence of inducible ischemia (4/49 vs. 9/49, P=NS). Group 1 showed higher resting HR (group 1: 88.1±15.5 bpm vs. group 2: 66.5±11.5 bpm, P<0.01) and similar peak HR (group 1: 94.7±15.3 bpm vs. group 2: 89.5±19.3 bpm, P=0.144), with blunted HRR (group 1: 1.08±0.10 bpm vs. group 2: 1.36±0.31 bpm, P<0.01). HRR was unrelated to LVCR. HRR is almost abolished and unrelated to LVCR in brain-dead patients during DSE. The modulation of neural input to the heart is essential to determine HRR, and plays no significant role in determining the inotropic response during DSE.

Sections du résumé

BACKGROUND BACKGROUND
A blunted heart rate reserve (HRR) during dipyridamole stress echocardiography (DSE) is a prognostically unfavorable sign of cardiac autonomic dysfunction. Short-term adjustments of heart rate (HR) are thought to rise from changes in neural input to the heart. DSE is applied in potential heart donors to rule out underlying coronary artery disease and left ventricular dysfunction. The aim of this study is to assess HRR during DSE in brain death.
METHODS METHODS
We enrolled two groups: group 1 (N.=49, 22 men, 54.6±8.8 years) with patients in brain death enrolled in the nationwide marginal donor heart recruiting program; group 2 (N.=49, 18 men, 66.4±12.0 years) referred to DSE for suspected or known coronary artery disease. All underwent DSE (0.84 mg/kg in 6') by quality-controlled readers certified via web-based training (1487/CE Lazio-1). We assessed left ventricular contractile reserve (LVCR) as stress/rest ratio of force (systolic blood pressure/end-systolic volume). HRR was calculated as the peak/rest HR ratio from 12-lead EKG.
RESULTS RESULTS
The two study groups were similar for prevalence of inducible ischemia (4/49 vs. 9/49, P=NS). Group 1 showed higher resting HR (group 1: 88.1±15.5 bpm vs. group 2: 66.5±11.5 bpm, P<0.01) and similar peak HR (group 1: 94.7±15.3 bpm vs. group 2: 89.5±19.3 bpm, P=0.144), with blunted HRR (group 1: 1.08±0.10 bpm vs. group 2: 1.36±0.31 bpm, P<0.01). HRR was unrelated to LVCR.
CONCLUSIONS CONCLUSIONS
HRR is almost abolished and unrelated to LVCR in brain-dead patients during DSE. The modulation of neural input to the heart is essential to determine HRR, and plays no significant role in determining the inotropic response during DSE.

Identifiants

pubmed: 32100982
pii: S0026-4725.20.05093-8
doi: 10.23736/S0026-4725.20.05093-8
doi:

Substances chimiques

Vasodilator Agents 0
Dipyridamole 64ALC7F90C

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

249-257

Commentaires et corrections

Type : CommentIn

Auteurs

Tonino Bombardini (T)

Clinical Center of the Republic of Srpska, Faculty of Medicine, University of Banja-Luka, Banja-Luka, Bosnia and Herzegovina - tbombardini@yahoo.it.

Davide Pacini (D)

Department of Cardiac, Thoracic, and Vascular Surgery, S. Orsola-Malpighi Polyclinic Hospital, Bologna University, Bologna, Italy.

Luciano Potena (L)

Department of Cardiac, Thoracic, and Vascular Surgery, S. Orsola-Malpighi Polyclinic Hospital, Bologna University, Bologna, Italy.

Massimo Maccherini (M)

Heart Transplant Surgery Unit, Senese Academic Hospital, Siena, Italy.

Tamara Kovacevic-Preradovic (T)

Clinical Center of the Republic of Srpska, Faculty of Medicine, University of Banja-Luka, Banja-Luka, Bosnia and Herzegovina.

Eugenio Picano (E)

Department of Biomedicine, Institute of Clinical Physiology, National Research Council, Pisa, Italy.

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